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Subscribe to RSSThe results of a new autism study published in the American Journal of Psychiatry offer hope for an early diagnosis. NBC's Chris Jansing reports.
By Karen Rowan
MyHealthNewsDaily
The early signs of autism are visible in the brains of 6-month-old infants, a new study finds, suggesting that future treatments could be given at this time, to lessen the impact of the disorder on children.
Researchers looked at how the brain develops in early life, and found that tracts of white matter that connect different regions of the brain didn't form as quickly in children who later developed autism, compared with kids who didn't develop the disorder.
"The way the wiring was changing was dampened" in the children with autism, said study researcher Jason Wolff, who studies developmental disabilities at the University of North Carolina, Chapel Hill. "It was a more blunted change over time, in how the brain was being wired."
In contrast, in the brains of infants who did not later develop autism, white matter tracts were swiftly forming, Wolff said. "Their brains were organizing themselves in a pretty rapid fashion."
The findings suggest that during a child's first year, "there is a potential to intervene, to disrupt autism before it becomes entrenched," Wolff said. "There are a lot of possibilities to improve outcomes for these children."
The study was published Friday in the American Journal of Psychiatry.
The first year of life is an important time in brain development, and is also when the first symptoms of autism start to appear, Wolff said.
In the study, the researchers looked at the brains of 92 infants, when they were 6 months, 1 year and 2 years old. All of the children had a sibling with autism ; research shows such children have a higher risk of developing the disorder themselves.
The researchers used a brain scan called diffusion tensor imaging, a type of MRI scan which allowed them to see changes in the brain's organization over time.
When the kids were 2 years old, 28 had developed autism, while 64 had not. The researchers looked back at the early brain scans, to see if there were differences between the groups.
"We looked at pathways that connect brain regions to each other, and 12 out of 15 were different in kids with autism," Wolff said.
Previous studies had found differences in brain volume in infants of this age, and other researchers had looked at white matter tracts in older children with autism, and adults, but the structures had not been examined before in infants so young, Wolff said.
The fact that so many of the tracts were affected shows that autism is a "whole-brain phenomenon," Wolff said. "There are widespread differences" in the brains of people with the disorder, he said.
Twins with autism: Parents wonder, did it have to happen?
As to what might be causing these brain differences, it's too early to say, Wolff said. But the findings are consistent with what researchers suspect about what triggers autism's development, he said, "there's a complex interaction between genes, and a child's experiences with the world."
And while the brain scans of the two groups of children certainly revealed their differences, those scans are not at the point where they could be used to diagnose the disorder in a 6-month-old, Wolff emphasized.
But the findings help researchers better understand how the disorder develops.
"It was really important to see that this was an evolving process," Wolff said. Kids don't just suddenly become autistic, "getting there is a journey," he said.
The researchers will continue to follow some of the children in the study until they are 3 years old, and will continue to enroll more children in the study, Wolff said.
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So...brain scans for every child now?
Autism is a spectrum. It does not describe every single case.
Regressive autism follows vaccination.
As a scientist I would want a lot more information.
Why do they not record the times in the kid's life when the multiple vaccinations are given and what they were for; And what about making scans of the brains of a large number of kids who have NOT received early vaccinations - What about records of which babies were nursed by their mothers and which were formula-fed and other questions - Without this information I think the research is very defective.
@Robert:
Total rubbish. Study after study has shown vaccination neither causes nor contributes toward any of the disorders in the autism spectrum.
That being said, vaccines pose a very low risk but the risk is substantially lower than that faced by being unvaccinated (especially if liing in a population of unvaccinated peers).
@Cecil: I have a thing for my children called a "shot record." It records the dates of vaccines, and what they are for. Imagine that. I wonder if these will catch on...
How does an epidemiological study on one vaccine determine if an individual child is harmed by ANY vaccine. You can "rubbish" all you want. You can't answer that question in a scientific manner. You can only speculate and give your opinionated answers. No study has ever been done that compares the health of the vaccinated vs. the unvaccinated
See above. I don't care about risk. What is the evidence. What is the result of the gold standard of science, the RCT research, that compares the health of the unvaccinated vs. the overall health of the vaccinated that shows the vaccinated are SOOOO much healthier and better off.
Good luck in your google search because such scientific evidence doesn't exist.
So do the parent's of children with vaccine induced regressive autism.
Robert, it is becoming clearer and clearer that autism is somehow mainly developed in the womb. A Recent study has shown that autistic children share certain distinct facial features. Yes, vaccines, in VERY RARE cases, can cause damage, but that is not the explanation for the current rise in autism. Personally, I don't think autism rates have risen. I think the medical profession has gotten better at diagnosing autism disorders. They aren't just labeled "retarded" or "mentally impaired" anymore.
Robert-1126350 your misinformed rhetoric on vaccines is dangerous because it is completely baseless. You either are too young to have grown up during a time when devastating childhood diseases were rampant (e.g. polio) and/or you have no understanding of science (specifically as it relates to pathogens). The original research linking autism and vaccines was retracted due to unsubstantiated findings and unethical practices by the researchers. The unvaccinated children are likely to encounter the dangerous pathogens (e.g. measles) at some point in their life and the sequelae can be devastating (e.g. neurological damage). Furthermore, unvaccinated children can spread the pathogen to children that are too young to be vaccinated, the immunocompromised and to those whose immunity has waned. Vaccines are the reason why we do not have serious childhood illnesses and debilitating complications in adulthood. Please refer to the 2010 Business Week article "Measles Outbreak Triggered by Unvaccinated Children" as a foundation for having a real discourse. I also recommend you watch the documentary on smallpox eradication and look up Edward Jenner.
So, Robert, where is your evidence that vaccines cause autism? Where is the study that shows vaccines increase the risk of autism? Not that ingredients in vaccines at high enough levels are neurotoxic. Not that some vaccines cause seizures or brain damage. A study that definitively shows that children who get vaccinated have an increased risk of developing autism.
Please provide that study. And if you can't then why should we listen to you or others like you who want to spread your opinion? If we have to have evidence, then where is yours?
UGH sorry for the double post.
Trip toe fan, you are asking for studies that will never be conducted. When vaccination injury results in neurological damage that manifests as symptoms of autism, this outcome will be labeled as something other than autism. This works well for the vaccination agenda. Not so well for the individuals whom have suffered from such harm. A study that examines these individuals would confirm that 100% of those vaccination injured were indeed vaccinated. Therefore, one could speculate that without receiving vaccinations, these individuals would not have been neurologically injured.
I would like to see such a study. We had the opportunity to examine Hannah Poling's vaccination injury. Of course her injury is not labeled as autism despite the fact that she displays enough autistic-like symptoms to be diagnosed as autistic. We also had the opportunity to examine the biomedical issues, but now those extensive tests results are locked away.
See how it works? When autistic -like symptoms result from vaccination injury, it is not autism. When extensive biomedical testing is conducted to provide answers towards understanding how this vaccination injury had resulted in neurological injury that manifests as autistic-like symptoms, we lock it away.
So show me the studies that include biomedical testing conducted on vaccination injured children that has resulted in autistic-like symptoms. Show me why this injury is not what is diagnosed as autism. I mean really, if autism is diagnosed based on autistic-like symptoms, then why don't these same symptoms that result from vaccination injury apply to this diagnosis?
Simply because we choose not to examine these issues does not mean that they do not apply.
Sorry Biff I don't completely follow your reasoning there.
Robert said that regressive autism follows vaccination. Now if that were true you could look at populations of vaccinated and non-vaccinated people and compare autism rates. If Robert is correct, then there should be a statistically significant difference in the two population's autism rates. Now Robert is correct that no study has done a comparison of totally non-vaccinated vs vaccinated groups. Instead, they've looked at a single vaccine, like MMR, or relative to an ingredient, like thimerosal. Those studies show MMR and thimerosal aren't linked to autism--i.e. the autism rates don't vary based on how much thimerosal a child receives or whether or not they had an MMR shot. So for Robert to be correct, I'd want to see a study that compared children who receive some subset of vaccinations to those who receive no vaccinations. If the no vaccination children have a lower autism rate, then I'd say there could be an autism-vaccine connection.
Sorry that statement is tautological and I don't get what you mean.
I guess my point is that there is no published scientific data to link vaccines to autism. So if Robert and others want to make statements, such as "Regressive autism follows vaccination," I'd like to see some published data to support their position. I have yet to see any. Instead I see several studies showing no link to specific vaccines or vaccine ingredients.
My whole point to Robert, who I've discussed this issue with many times, is that he demands the pro-vaccine side to pony up data all the time. But her has made a statement that needs data to support it and I'd like him to pony up the evidence this time.
"Robert said that regressive autism follows vaccination. Now if that were true you could look at populations of vaccinated and non-vaccinated people and compare autism rates."
It is true. Regressive autism has been reported to follow vaccination injury. You could look at these specific cases and determine the hows and whys. That's the point, we don't. We just claim that it does not occur.
"If Robert is correct, then there should be a statistically significant difference in the two population's autism rates."
In cases where vaccination injury had resulted in symptoms of autism and neurological damage, the injury resulted from vaccinations. To compare individuals whom do not experience this sort of injury because they were not vaccinated, and try to discredit the mechanism by which it happens simply because it doesn't apply to all cases of autism, is absurd.
"Now Robert is correct that no study has done a comparison of totally non-vaccinated vs vaccinated groups."
Or how autism from vaccination induced injury differs from other cases of causation. And why is that? It's because autism can not be linked to vaccination injury. It's an unacceptable risk that many would not take. It threatens the greater good. Some must be injured for the majority to be kept safe. Risk/benefit.
"So for Robert to be correct, I'd want to see a study that compared children who receive some subset of vaccinations to those who receive no vaccinations."
No, you should want to see studies based upon why some individuals were caused neurological damage and vaccination induced symptoms of autism. But you can't. They are not available. Like the Hannah Poling biomedical data, it gets hidden.
"I guess my point is that there is no published scientific data to link vaccines to autism. So if Robert and others want to make statements, such as "Regressive autism follows vaccination," I'd like to see some published data to support their position. I have yet to see any. Instead I see several studies showing no link to specific vaccines or vaccine ingredients."
I would like to see this as well. Why haven't we seen such studies? Are we to believe that no child has ever been vaccination injured and had acquired symptoms of autism as a result? None of these children, whom did not display these symptoms prior to injury, were later diagnosed as autistic? Is this what I am to believe? Sorry, I can't do that.
"My whole point to Robert, who I've discussed this issue with many times, is that he demands the pro-vaccine side to pony up data all the time. But her has made a statement that needs data to support it and I'd like him to pony up the evidence this time."
How do we show evidence when it is locked away? When specific studies are not done? When we label vaccination injury that manifests as autism as something else?
Again, no offense, but that is a meaningless tautological statement. It's like saying exercise-induced asthma attacks result from exercise. It doesn't prove anything. It just restates your position.
I'm sorry but comparing people who haven't been vaccinated to those who have is how you would do that study. I don't know if you have any science training, but when you want to know if variable X causes some condition you compare groups based on that variable: In this case, you'd compare vaccinated vs non-vaccinated.
No offense, but it sounds like you are assuming vaccines cause autism and then working backwards to show it does. Sorry, that's not how science works. Instead you start with a question: Do vaccines cause autism? And then you work forward trying to see if the evidence supports a connection.
So far there is no evidence supporting a connection. Some rare cases of vaccine injury have lead to brain damage that resembles autism, but that doesn't mean vaccines cause autism. Again to show that you would need to show that vaccinated kids have a higher risk of autism than do non-vaccinated kids.
I know this is a passionate issue, but science must be dispassionate. And the only way to prove an autism-vaccine connection is through scientific studies that compare vaccinated and non-vaccinated kids. Until then, you can not say vaccines cause autism. That's not how science works.
In cases where vaccination injury had resulted in symptoms of autism and neurological damage, the injury resulted from vaccinations.
"Again, no offense, but that is a meaningless tautological statement. It's like saying exercise-induced asthma attacks result from exercise. It doesn't prove anything. It just restates your position."
It proves that autistic-like symptoms can result from vaccination injury. How in the world is that meaningless? Autism is diagnosed from these symptoms. Children whom acquire them as a result of vaccination injury are diagnosed as autistic. Meaningless???
"No offense, but it sounds like you are assuming vaccines cause autism and then working backwards to show it does. Sorry, that's not how science works."
I'm not assuming anything. Some children, whom did not have neurological damage prior to vaccinations, experienced injury that was caused by their vaccinations. Soon after their injury they displayed symptoms of autism. Soon after that they were diagnosed as autistic. So one could make a strong argument that vaccination injury resulted in an autism diagnosis.
I guess you would have to work backwards. If an infant was brought to an ER would a physician ask for a population study to determine why the the infant was not breathing? No the physician would ask for details leading up to this problem. Back track and resolve what may have caused this condition.
Riddle me this-
IF VACCINATION INJURY DOES NOT RESULT IN AUTISM, ONLY AUTISTIC-LIKE SYMPTOMS, THE NUMBER OF CHILDREN WITH AUTISM FROM VACCINATION INJURY WOULD BE ZERO. SO HOW WOULD A STUDY EXAMINING THESE ENDPOINTS DETERMINE ANYTHING OTHER THAN VACCINATIONS DO NOT CAUSE AUTISM? ARE THESE THE STUDIES THAT YOU SPEAK OF? THE ONES THAT DO NOT INCLUDE CHILDREN WITH BRAIN DAMAGE AND AUTISTIC-LIKE SYMPTOMS.
I see how science works now. No child has ever become autistic after vaccination injury. Therefore when we compare those vaccinated with those whom are not, there is no difference in the rate of autism among the groups. I wonder what we would find if those whom acquired autistic-like symptoms after vaccination injury were compared to those whom did not get vaccinated and injured. You know the children who are now diagnosed with autistic-like symptoms that are not really autistic. I would also like clarification on what the actual difference between symptoms of autism and actual autism.
"And the only way to prove an autism-vaccine connection is through scientific studies that compare vaccinated and non-vaccinated kids. Until then, you can not say vaccines cause autism. That's not how science works."
I guess we'll never see those studies produce anything other than vaccinations don't cause autism. They can't. The number of children whom became autistic due to vaccinations is zero. The number of children with autistic-like symptoms is substantially higher. But they do not count.
Again, no offense, but that's not how science works. Also the statement you made was essentially this: Vaccines causes symptoms of X, therefore X is the result of vaccines. Both parts of that statement say the same thing and neither part proves vaccines caused X, they're just statements of your opinion. I don't want this to devolve into an argument over semantics, that is just a tautological statement and not proving anything. I suggest we move on, because there isn't much more to discuss.
Just because two events are related in time, doesn't mean the former caused the latter. That's a simple truth of reality. You have to develop evidence to show that causal link. When a physician asks about the events leading up to a child's illness, she does so because years of medical science have led to evidence and data showing how certain illnesses develop and are caused. So if a child is having trouble breathing and the parent says she was just eating a peanut butter sandwhich before she got ill, the doctor can start to think about a peanut allergy--just a simple example here.
Unfortunately, in the cause of autism, medical science doesn't have any good data on how the disease is caused. So doctors and researchers are now at the stage of making those causal links.
Yes there are children who suffer neurological damage from vaccines. That certainly happens every year. But those cases are extremely rare. Also symptoms that resemble autism don't always mean the child has autism. When you talk about spectrum developmental disorders, you're talking about a wide diagnosis net. In fact many doctors believe the spike in autism rates in the last couple decades has been due to the fact that psychiatrists widened the autism net. (Interestingly, the new DSM-V may shrink that diagnosis net and split conditions currently under autism into new categories.)
But even if you granted that those cases were vaccine-caused autism, you'd be left with an issue: The rate of severe neurological side effects of vaccines is far more rare than the rate of autism in society. The disparity is so large, that you'd have to accept that vaccines are not the main driving force for the disease.
Also if vaccines were a major driving force, you could easily prove it by comparing vaccinated vs non-vaccinated populations.
So what are we left with? We're back where we started: People claim vaccines cause autism but have no scientific evidence for it. They have anecdote, but not scientific data.
I am not debating that vaccines don't ever cause neurological damage. I can't. The data are clear, they do. But the data also show that these cases are rare.
What I'm saying is that if you want to link vaccines to autism, there is a very simple way to do it: Compare autism rates in vaccinated (to any degree) groups to non-vaccinated groups. A subset of studies like that have been performed and their data showed no connection.
Look, I have no horse in this race. If vaccines cause autism, then that's something we have to deal with. If a series of studies come out showing the link I'm talking about here, then I'll be on board with rethinking vaccination policy. But I see no evidence out there to support the link.
I never said that vaccination injury is a major driving force in autism causation. I am merely suggesting that some children may in fact succumb to autistic-like symptoms after vaccination injury. Later, a number of these children will display enough symptoms to be diagnosed as autistic. That being said, I also realize how little we understand about the development of the immune system and brain. Wherein exposure to the multitude of vaccinations children now receive may cause serious adverse reactions to occur during these critical stages of development.
Biff Loder what exactly are you arguing, that all children should not be vaccinated? You need to read more peer-reviewed journal articles (and I do not mean the ones that your anti-vaccine buddies write on their blogs) because you would see that scientists are trying to figure why a minor portion of children have sequelae from vaccines. However, the sequelae from not-vaccinating would be more devastating and widespread. Furthermore, not all sequelae are neurological in nature. No one is denying that there are potential and real consequences of any medical intervention, but the benefits far outweigh the risks in the case of vaccines. You can see from my previous post that autism is proving to be a multifactorial disease process. To help you better understand what I mean by that, take for example Celiac Disease (CD). CD is an autoimmune condition that has a genetic component but it requires an environmental trigger (e.g. gastrointestinal infection) to become active. Thus, autism might have a genetic component with the trigger being the environment (e.g. testosterone levels, infections). It does not mean that everyone predisposed to a condition will get it, they just have an increased risk. Science/medicine realize that fact and is moving toward a more personalized health care approach. Now that we have the tools to understand disease process from the micro/macro approach we can begin to individualize treatment options. This is how we treat certain cancers, by first identifying certain genetic makers and then picking the drug that is most effective. This is also true for HIV treatment.
Your rhetoric is based only on your emotions and not in actual fact. Some of the diseases that we are vaccinated from prevent us from developing serious neurological problems in the future (more devastating than autism). Polio and measles are 2 viruses that can present with minor symptoms initially but they either lay dormant for years or cause a slow disease process over years. After the disease process has taken over there is nothing you can do to stop it.
In the end you really have no argument seeing as the healthcare field is moving towards providing individualized care. This article was an example of that concept (intercept the disease process in those who are predisposed before it becomes permanent).
Great. So you agree that blaming vaccines for the spike in autism cases is unfounded? And that citing autism as a reason for parents to avoid vaccination for their children is unfounded?
"Biff Loder what exactly are you arguing, that all children should not be vaccinated? You need to read more peer-reviewed journal articles (and I do not mean the ones that your anti-vaccine buddies write on their blogs"
Excuse me. I have read thousands of peer reviewed publications. Where do you get off telling me that I am anti-vaccine or only read certain publications from "anti-vaccine buddies"? You have no idea of my understanding of neurodegeneration or neurobiology? So check your pompous comments at the door. At least trip toe fan is professional enough to not insult. I can respect his point of view and actually agree to some degree.
"Your rhetoric is based only on your emotions and not in actual fact."
Really? So you fully understand how the human body's neurological and immune system develops? You know that vaccinations will not interfere with this developmental process and result in adverse health issues? Spoken like a doctor whom specializes in arrogance. I can say this because some individuals are seriously harmed by vaccinations for many reasons. If we had all the answers, this harm would be eliminated. But we don't now do we?
"Thus, autism might have a genetic component with the trigger being the environment (e.g. testosterone levels, infections)."
Yeah. since we are comprised of DNA I would suspect a genetic component as well. Or wait... it could be something that adversely affects the protein expression post translationally that triggers dysregulation of protein signaling at the synapse. Really Doc? I mean really, if synaptic vessicle turnover is essential for proper neurotransmitter release and neuronal plasticity, couldn't adducts formed post translationally on lysine residues of these proteins inhibit degradation, extent the half life of its expression and deplete available.... awe forget it. You probably know all of this already.
But there it is. A doctor with all the answers except the ones needed to define what may contribute to autism. Arrogant and dismissive. It is something that so many parents have been exposed to when searching for answers. But take it for what is worth coming from a guy whom gets all his info from anti-vaccine buddies. That and thousands of hours studying neurobiology.
"Great. So you agree that blaming vaccines for the spike in autism cases is unfounded? And that citing autism as a reason for parents to avoid vaccination for their children is unfounded?"
What spike? I thought it was just better diagnosis these days? Did I suggest avoiding vaccinations? I said that some individuals are vaccination injured. These injuries have been shown to manifest as autistic-like symptoms. These symptoms are later diagnosed as autism. Stay with me here trip toe fan. Can I call you tryptophan for short?
2014md, I guess that you are not a doctor just yet based on your screen name. I guess the world can wait another 2 years for your arrogance. Tip of advice though....Don't think that you already know everything. You'll never be a good doctor with that attitude.
From what I've read, there is some serious doubt there is a spike. I was just making sure you weren't one of the people who blames the increase in autism diagnoses on increased vaccinations. It appears you aren't.
Also no serious person would debate you on the position: some people get injured by vaccines. As with all medical treatments, there are side effects, sometimes serious ones.
Do some rare set of kids develop neurological damage that leads to autism-like symptoms? I'm not a medical doctor, but that wouldn't surprise me. Does that mean vaccines cause autism? No. It means they can in rare cases lead to severe brain damage. Given how rare those side effects are I see no problem recommending all parents vaccinate their kids. Do you agree or disagree?
No offense, again, but I don't think you're fully understanding the systems you're talking about. For one thing, what do you mean by protein signalling at the synapse? G-protein signals? Neuropeptides? That's a broad term, you'll need to be more specific.
Also synaptic transmission and plasticity are really complex processes, so what specifically are you talking about?
And as I said on another thread, any thing that could from adducts on lysines that would block protein degredation pathways would have to be at extremely high concentrations in cells.
I guess my point is, that paragraph was more of a regurgitation of text book terms than a scientific hypothesis. I'd love to discuss it more, but you'll need to better explain what you mean.
"No offense, again, but I don't think you're fully understanding the systems you're talking about. For one thing, what do you mean by protein signalling at the synapse? G-protein signals? Neuropeptides? That's a broad term, you'll need to be more specific."
None taken. For openers I was looking at GAD60 and GAD65. I have to go to work, but look forward to a discussion.
OK. So how are you connecting vaccines to an enzyme in nerve cells?
I'm not connecting vaccines. I am connecting dysregulation of lipid metabolism and accumulation of hydroperoxides. I am looking at how excessive oxidation affects protein signaling post translationally. Looking at how glutathione synthesis may become impaired. Stuff like that.
OK I'm confused then. I was discussing vaccines with Robert and then you jumped in, but you don't want to discuss the connection between vaccines and autism?
Also, don't take this the wrong way, but I don't think you have a full grasp on some of these concepts. Just your use of the words suggests you're not completely understanding things.
For example, you don't call them hydroperoxides, just peroxides. Also you talk about how oxidation could affect protein signalling post translation. But all protein signalling occurs post translation, because translation is the process that produces proteins. I think you mean that oxidation could affect signalling through post translational modifications to proteins.
If so, then I guess I'd like to hear what your hypothesis.
"For example, you don't call them hydroperoxides, just peroxides."
Free radical-catalyzed peroxidation of docosahexaenoic acid (DHA, C22:6/ω-3) generates various lipid peroxidation products that covalently modify biomolecules such as proteins. Under a free radical-generating system, DHA significantly modified lysine residues in bovine serum albumin. Upon incubation of oxidized DHA with an amino-compound pyridoxamine or a lysine-containing peptide, N-propanoyl and N-succinyl adducts were determined to be the major modification products. The hydroperoxide levels in the oxidized DHA closely reflected the formation of the Nϵ-(succinyl)lysine (SUL) upon reaction with the peptide, indicating that the hydroperoxides of DHA represent a potential pathway for the formation of SUL. To detect the DHA-derived protein modification in vivo, we developed a monoclonal antibody (mAb2B12) specific to SUL and found that the antibody specifically reacts with the SUL moiety. The formation of SUL was then immunochemically demonstrated in the liver of mice fed with DHA followed by intraperitoneal injection of carbon tetrachloride (CCl4), a hepatic lipid peroxidation model. Immunoreactive materials with mAb2B12 were observed in the DHA + CCl4 group, but were not significant in the control, DHA-alone, and CCl4-alone groups. These data suggest that the formation of DHA-derived adducts such as SUL may be implicated in the oxidative damage observed in DHA-enriched tissues.
During the lipid peroxidation reaction, lipid hydroperoxides are formed as primary products. Several lines of evidence suggest that lipid hydroperoxides can trigger cell death in many cell types, including neurons. In a screening of lipid hydroperoxides which can induce toxicity in neuronal cells, we found docosahexaenoic acid hydroperoxides (DHA-OOH) induced much severe levels of reactive oxygen species generation and cell death in human neuroblastoma SH-SY5Y cells compared to the hydroperoxides of linoleic acid and arachidonic acid. Therefore, we focused on DHA-OOH, and demonstrated that DHA-OOH apparently induced an apoptosis in the neuronal cells through several apoptotic hallmarks including nuclei condensation, DNA fragmentation, poly (ADP-ribose) polymerase cleavage and increased activity of caspase-3. We also found the signaling changes in mitochondria-mediated apoptosis, such as cytochrome c release and increased expression of Bcl-2, as well as a dose-dependent attenuation of mitochondrial membrane potential in the DHA-OOH treated cells. These data indicated DHA hydroperoxide as a potential inducer of apoptosis in human neuroblastoma SH-SY5Y cells, which may be mediated by mitochondria dysfunction pathway.
"I think you mean that oxidation could affect signalling through post translational modifications to proteins."
Yes, that is what I mean. Why do I suggest this as implicated in autism?
Home » Publications » Science and Technology journals » Biology journals » American Journal of Biochemistry and Biotechnology »
The autistic phenotype exhibits a remarkably localized modification of brain protein by products of free radical-induced lipid oxidation.(Clinical report)
American Journal of Biochemistry and Biotechnology
March 22, 2008 | Evans, Teresa A.; Siedlak, Sandra L.; Lu, Liang; Fu, Xiaoming; Wang, Zeneng; McGinnis, Woody R.; Fakhoury, Evelyn; Castellani, Rudy J.; Hazen, Stanley L.; Walsh, William J.; Lewis, Allen T.; Salomon, Robert G.; Smith, Mark A.; Perry, George; Zhu, Xiongwei | Copyright
Abstract: Oxidative d
In this study, to substantiate the role of oxidative
stress in autism brain, we used antibodies against two
distinct lipid-derived oxidative protein modifications.
One of these, carboxyethyl pyrrole (CEP) is derived
exclusively from free radical-induced oxidative
cleavage of docosahexaenoates, e.g., the docohexaenoic
acid (DHA) ester of 2-lysophosphatidylcholine (PC)
DHA-PC, to afford HOHA-PC that then reacts with
protein to generate CEP modifications of the e-amino
groups of lysyl residues
And why may GAD65 and GAD 67 be of importance?
"Children with autism often present with abnormal
immune and digestive systems, such as inflammation of
the bowel, and changes in digestive enzymes, and often
suffer from bowel problems and constipation, and
occasionally liver problems[7]."
Glutamate is the major excitatory neurotransmitter in the
mammalian central nervous system (CNS). Packaging and
storage of glutamate into glutamatergic neuronal vesicles
require ATP-dependent vesicular glutamate uptake
systems, which utilize the electrochemical proton gradient
as a driving force. Three vesicular glutamate transporters
(VGLUT1-3) have been recently identified from neuronal
tissue where they play a key role to maintain the vesicular
glutamate level. Recently, it has been demonstrated that
glutamate signaling is also functional in peripheral
neuronal and non-neuronal tissues, and occurs in sites of
pituitary, adrenal, pineal glands, bone, GI tract, pancreas,
skin, and testis. The glutamate receptors and VGLUTs in
digestive system have been found in both neuronal and
endocrinal cells. The glutamate signaling in the digestive
system may have significant relevance to diabetes and GI
tract motility disorders. This review will focus on the most
recent update of molecular physiology of digestive VGLUTs.
Wow. Cut and paste overload! (Just a pet peeve of mine, but you should really cite the source of text you paste into your posts--I'm referring to the text on hydroperoxides. I'm a crazy academic so unattributed text makes me go cross-eyed.)
OK peroxides versus hydroperoxides. A peroxide is any chemical with a oxygen-oxygen bond, like RO-OR, where R can be anything from a hydrogen to some organic molecule. It is a general term that encompasses many types of molecules based on those R groups. When you use hydroperoxide in a chemical name, you're saying that one of those R groups is a hydrogen. You wouldn't say hydroperoxides are accumulating in a cell, because the term hydroperoxide is incomplete. You'd say lipid hydroperoxides or tert-butyl hydroperoxides were accumulating. Basically you need to explain what the other R is in the peroxide. If you meant the other R was also a hydrogen then you'd say hydrogen peroxide is accumulating. I don't make the rules, long dead chemists do.
As for the paper, I don't know if it's all that interesting to find oxidative damage in the brain cells of autistic patients. Obviously, something has gone wrong in the brains of autistic people--their brains don't work like "normal" people. But if you looked at other patients with brain damage, I'd wager that you'd also find oxidative damage, because oxidative damage is a very common cause when things go awry in a cell. Basically all of our cells oxidize things to create energy--a cell can't live unless its mitochondria or oxidizing organic molecules. But having a lot of oxidants around isn't safe for the other organic molecules floating around in the cell. Our cells set up several systems to control and monitor these oxidizing agents. Basically, our cells live next to a creaky levy with a torrent of oxidizing chemicals on the other side. So when you look at dead or dying cells, you'll find that that levy has broken, leading to oxidative damage.
Now some of their controls had brain damage or diseases that involve brain damage, but not all. I think the better study would have been to compare autistic patients to a cohort of parkinson's/alzheimer's patients. That way you could see if the oxidative damage was unique to the damage leading to autism opposed to general brain diseases. Also I'd control what part of the brain I looked at too. In this study, it looks like they took samples from mainly the hippocampus but also other brain parts. I would have done a more systematic sampling and compared like parts to like parts. Obviously, the relevant damage in a parkinson's brain is going to be different from the damage in an autistic brain.
So all of those issues lead me to be not so impressed with the paper's finding. And I'd guess that's why the paper appears in a pretty low tier journal. I don't think I've really ever read a paper from the American Journal of Biotechnology and Biochemistry until right now. It doesn't pop up in PubMed, so I don't know how many citations it has. But I doubt it's been a highly cited one, because, like I said, it's conclusions aren't earth-shattering.
First of all, GAD65 and GAD67 are different forms of the same enzyme. So for the level of this discussion, we can just say glutamate decarboxylase, or GAD, is important.
So you go on to say point out two facts: autistic children often have digestive issues and glutamate is involved in signalling in some parts of the digestive system. Now it is a giant--superhero-sized--leap to then say glutamate signalling is behind the problems in autism. Do you have any evidence to even begin to make that connection?
2. Novel plasma phospholipid biomarkers of autism: mitochondrial dysfunction as a putative causative mechanism
Pastural E, Ritchie S, Lu Y, Jin W, Kavianpour A, Khine Su-Myat K, Heath D, Wood PL, Fisk M, Goodenowe DB.
Prostaglandins Leukot Essent Fatty Acids. 2009 Oct;81(4):253-64.
Autism is a neurological disorder that manifests as noticeable behavioral and developmental abnormalities predominantly in males between the ages of 2 and 10. Although the genetics, biochemistry and neuropathology of this disease have been extensively studied, underlying causal factors to this disease have remained elusive. Using a longitudinal trial design in which three plasma samples were collected from 15 autistic and 12 non-autistic age-matched controls over the course of 1 year, universal and unambiguous alterations in lipid metabolism were observed. Biomarkers of fatty acid elongation and desaturation (poly-unsaturated long chain fatty acids (PUFA) and/or saturated very long chain fatty acids (VLCFA)-containing ethanolamine phospholipids) were statistically elevated in all autistic subjects. In all 8 of the affected/non-affected sibling pairs, the affected sibling had higher levels of these biomarkers than the unaffected sibling. Exposure of neurons, astrocytes and hepatocytes in vitro to elevated extracellular glutamate levels resulted in lipid biomarker changes indistinguishable from those observed in autistic subjects. Glutamate stress also resulted in in vitro decreased levels of reduced glutathione (GSH), methionine and cysteine, in a similar way to the decreases we observed in autism plasma. Impaired mitochondrial fatty acid oxidation, elevated plasma VLCFAs, and glutamate toxicity as putative causal factors in the biochemistry, neuropathology, and gender bias in autism are discussed.
Sorry to cut and paste. Many researchers have suggested glutamate toxicity may play a role in autism. It appears to play a role in symptoms that develop after traumatic brain injury. Just showing where aberrant glutamate signaling may play a role in digestive disorders as well. I'm no superhero, but I often wear tights and a cape.
Well the problem is that you're just pasting whole abstracts. It's a flood of information and I have no idea what you want me to take from it. A better way would be to make your point and then point to an article that supports that point. Or select an informative quote from the paper.
Also, you're all over the place. What is your point? You said you don't want to connect vaccines to autism. Then you post papers about lipid metabolism, oxidative stress, and glutamate signalling? What is your point? I can't make heads or tails of what you're trying to tell me.
I have no problem discussing things with you, but you need to sit down and write a post that explains what you're trying to get at. Because, right now, I'm just scratching my head.
Now to the paper you just cited. First off, any study like this has a chicken-egg problem, and the authors would likely tell you that. Is the difference in lipid composition the cause of the damage that leads to autism? Or is it just a symptom of the real cause of autism? We can't know from this paper. We just have an observation: Some autistic children have differences in lipid composition.
Next, they looked at 20 something subjects. Nowhere sufficient to make any definitive conclusion. The best it could do is suggest more study.
Also did you purchase the article and read all of it? I don't plan to, but I'm curious what test they ran that led them to say: "Exposure of neurons, astrocytes and hepatocytes in vitro to elevated extracellular glutamate levels resulted in lipid biomarker changes indistinguishable from those observed in autistic subjects." Do you know what test they ran there?
"Then you post papers about lipid metabolism, oxidative stress, and glutamate signalling? What is your point? I can't make heads or tails of what you're trying to tell me."
My point would be that dysregulation of lipid metabolism could initiate oxidative stress and this could result in aberrant glutamate signaling during stages of neurodevelopment.
I didn't read all of the publication. I just assumed that you hadn't come across glutamate toxicity as implicated in traumatic brain injury or autism. Just quickly posted that publication.
OK, fine. But what is your point in bringing that up? You don't want to blame vaccines for autism. Then you present a bunch of papers that you think suggest a linkage between lipid metabolism, oxidative stress, glutamate signalling, and neurodevelopment.
Remember this whole discuss started after you were talking to 2014MD:
I think you were trying to say that something in environment could be at play in autism. Is that correct? Nothing you've presented me so far supports that hypothesis, though. All you've really shown me is that autistics have higher levels of oxidative damage and possibly different lipid compositions in some cells.
So again, I'll ask: What is your point? Can you summarize what you're getting at in a simple paragraph. When I apply for grants I need to do just that to explain the project I want funding for. Pretend I'm the NIH and explain what you're thinking about.
Sure. I would like to investigate DHA supplementation of infant formulas. Being that the triacylgycerol structures used are much different from naturally synthesized sources. The structural differences adversely affect the oxidative stability. This becomes problematic when incorporated in to a developing brain. DHA is found esterified in all three positions among the glycerol backbone of these novel infant formula supplements. Free DHA will be available towards oxidation after digestive hydrolysis of the SN-1 and SN-3 positions. So I would start by examining how exogenous altered DHA triacyclyglycerols may affect antioxidant defense. Perhaps the NRF2/ARE pathway, or glutathione synthesis,etc.
Interesting when we discuss DHA, a few names are intimately associated. I'll list two and see if you can make the connection.
Jon Poling
Norman Salem Jr.
How are these two individuals associated with DHA?
Oh yeah, keep in mind that Hannah Poling was vaccination injured. Her injury resulted in autistic-like symptoms due to an underlying mitochondrial dysfunction. A condition that predisposed her towards encephalopathy after vaccinations. And by the way, Norman Salem worked at the NIH before he left to work for........
And what does infant formula have to do with this discussion? Sorry still grasping at your point.
How do the structures of the fatty acids differ and why does that make them more susceptible to oxidation?
I thought I just explained that. The positioning among the glycerol backbone will either allow rapid absorption in the SN-2 position or cleavage as free fatty acids. Free DHA fatty acids are vulnerable towards oxidation. So more DHA positioned in the SN-1 and SN-3 positions will result in more free DHA available towards oxidation after digestive hydrolysis.
Better yet, novel diacylglycerols will be formed with unknown triggering effects on cellular pathways. You know, alterations in lipid metabolism.
Hey, that's what the Institute of Medicine had warned about.
I thought you would be interested in the whole Jon, Norman DHA thing.
You started talking about a fatty acid in infant formulas and TAG positions. But why? Are you saying you think fatty acids in infant formula cause autism? If that's what you mean, then just spell it out. Talking in mysteries doesn't really make for a good discussion.
"How do the structures of the fatty acids differ and why does that make them more susceptible to oxidation?"
I have to explain this to you? How does the structure of fatty acid triacylglycerols differ and how does this compromise oxidative stability? Look it up. I was unaware that I was talking in mysteries. Sorry, I won't waste anymore of your time.
Look, at no point have you said what all the papers, talk of DHA, and oxidative stress all have to do with what we were talking about: autism.
I would discuss things with you but I started to lose the point of our discussion. I didn't mean to offend you.
Now as for the fatty acid discussion, I'm trying to understand what you're talking about. All fatty acids get oxidized in some way at some point. I'm trying to figure out what you mean that DHA is more susceptible to oxidation.
If you want to discuss more, I'll listen.
No, I mean DHASCO is more vulnerable towards oxidation. Synthetic DHA triacylglycerols, not DHA from elongation and desaturation of ALA and EPA.
OK but why are the synthetic ones more vulnerable than natural ones?
And what does that difference have to do with autism?
"OK but why are the synthetic ones more vulnerable than natural ones?"
The DHA molecules occupy different positions. Many of theses TAGs have DHA occupy 2 or all three positions. Since bio-similar is not bio-identical, these fats will not be digested, absorbed or oxidized in the same fashion. I suggest reading up on palm olein. Where fatty acid position is revealed to cause adverse effects on digestion and absorption. It is now known that DHA is more stable towards oxidation when esterified in the SN-2 position.
"And what does that difference have to do with autism?"
If oxidative stress and altered levels of LCPUFAs play a role as suggested by many researchers, increasing cellular levels via supplementation may be problematic. Natural synthesis is tightly regulated. It's not a more is better type of situation.
Since the TAG structure is different, different diacyglycerols and monacyglycerols will be formed. In theory, these unique DAGs could exert different cellular effects. Which had been warned by the Institute of Medicine. Since DHA exerts numerous diverse cellular effects via oxidation, we could predict alterations in these signaling cascades.
Create yourself a punchlist of what has been found as a co-morbid condition of autism. Mitochondrial abnormalities, dyregulation of immune response, neuroinflammation, digestive disorders, food intolerances, cholesterol depletion,glutathione deficiency..etc.
Could excessive accumulation of DHA initiate oxidative stress and cause any of the above mentioned?
Well the only responsible scientific answer is "I don't know." You've obviously read a lot about this subject, but at the moment you have what my PhD adviser would have called a table full of vaguely compatible puzzle pieces. If you just starred at them all, you could imagine how they all fit together. But until you start to move them around and try to connect them, you don't really know if they all fit into the same puzzle.
Of course, the chicken-egg issue pops again all over the place here. We have no idea if the oxidative stress, inflammation, etc are causes of the damage that leads to autism or just symptoms of the real cause. But that is an issue that haunts any work on this subject.
But I guess I have some questions about the fatty acids part of your post:
Do we know for sure synthetic DHA doesn't get metabolized in the same way? What does the literature say about how these molecules get metabolized? Also, forgive my ignorance, how is synthetic DHA different from the natural fatty acid? Is it a case of stereochemistry differences?
OK so say for sure synthetic DHA is more prone to oxidation. You still need an oxidizer present to do the oxidizing. And if you're conjecture is that increasing levels of synthetic DHA leads to oxidative stress, I guess my question becomes: Where do the excess oxidizing agents come from?
"I guess my question becomes: Where do the excess oxidizing agents come from?"
Perhaps from the ferrous sulfate added as a source of iron at very high levels. How about exposure to heat, air and light once the formula is prepared? I have read reports from parents whom have described the smell of diesel fuel after opening a can. So I would imagine extended shelf life may also affect this process.
From the IOM's report in 2004-Evaluating the safety of new ingredients
Another example is the long-chain polyunsaturated fatty acids (LC-PUFAs) that have been determined as GRAS for addition to infant formulas. These LC-PUFAs are derived from genetically selected algae that produce triglycerides with a high content of either arachidonic acid or docosahexaenoic acid onto two or three of the fatty acid chains of the triacylglycerol molecule. This contrasts to the triacylglycerol makeup of human milk, where LC-PUFAs rarely form two-thirds of the fatty acids of a single triacylglycerol molecule. In this case, diglycerides resulting from hydrolysis of the algae triglycerides in infant formula would be different than those produced from human milk and different biological effects could occur (e.g., specific diglycerides have very different effects in cell signaling pathways and could have different “triggering” effects on certain cellular pathways).
But that's not what the manufacturer described in 2002 when applying for a GRAS status from the FDA-
"Martek describes published information about the digestion of triglycerides by infants. Martek describes published information relevant to the biodisposition of ARASCO and DHASCO, focusing on a comparison of the biodisposition of ARASCO and DHASCO to that of ARA- and DHA-containing triglycerides in human milk. Martek concludes that the digestion and absorption of DHA from DHASCO, and ARA from ARASCO, would be the same as that of DHA and ARA from triglycerides present in human milk."
I had a few discussions with the individuals involved with writing this report at the IOM. They have stated that it was not their position to evaluate the safety of DHASCO as an infant formula ingredient. Not only had they used Martek's information that was applied to their GRAS application, but they corrected their misinformation that explains the digestion and absorption of DHASCO.
So which cell signaling pathways were the IOM referring to? I would guess those involved with brain development since DHASCO supplementation was aimed at improving this developmental process. What do they mean by triggering effects? Since DHA oxidizes to exert triggering effects, are they suggesting that the differences in the DHASCO TAGs may create unique diglycerides after hydrolysis that will oxidize differently?
Does this seem appropriate safety for infant formula ingredients? Ingredients that are highly vulnerable to oxidation and are incorporated in to a developing brain. Ingredients that may exert unknown triggering effects on cell signaling pathways.
You are an intelligent person with a solid understanding of biochemistry. In your opinion, what should have been done after the IOM corrected the flawed safety description given in regards to the digestion and absorption of DHASCO? Is that what has become of the standard of safety applied towards infant formula ingredients? We aren't quite sure what effects this ingredient may exert on signaling pathways, but we'll just have to wait and see.
I love the IOM's response. We were not asked to evaluate the safety of new infant formula ingredients in our report entitled Evaluating the safety of new ingredients. It actually reminds me of a discussion I had with an individual at the FDA. Where he had stated that palm olein can and does cause constipation and malabsorption due to the fatty acid positioning differences. But positioning differences of DHASCO will not exert adverse effects.
Remember when I asked you if you knew how Norman, Jon and DHA were all associated? It's really interesting. Norman worked at the NIH for@30 years. Jon's passion for neurology was sparked from his interest in fatty acid metabolism, specifically DHA. Norman and Jon had written publications together on DHA and potassium channels. Jon goes on to become a neurologist. Norman leaves the NIH to become the chief scientific officer at Martek Biosciences. Martek manufactures > 90% of all DHA (DHASCO) used in infant formulas world wide. Jon becomes the first to be awarded compensation for vaccination injury that resulted in autistic-like symptoms. Then the biomedical information that confirmed what had happened get sealed away. Martek sells it's DHASCO manufacturing platform overseas. True story. What are the odds?
Now if I were a conspiracy theorist, which I am not, I could interpret the facts above differently. I could suggest that at the time, pre-DHA supplementation of infant formula, Jon and Norman knew of the purported benefits of DHA supplementation towards improvements in brain development.More is better right? Who wouldn't want their infant to benefit from such improvements? Problem being, if your infant had an underlying mitochondrial dysfunction, and one decided to supplement with DHA, could exogenous supply of DHA worsen this pre-existing condition? I can not say that this is what had transpired. I don't know anything about the biomedical data that was collected or whether or not DHA supplements were used. I guess we will never know what really happened. This information is unavailable.
OK now I see what you're talking about. But I have to say I don't see any there there.
Sorry, but ferrous sulfate, Fe(II) sulfate, is a reducing agent. Iron (II) gives up an electron to become Fe(III). So there is no way DHA is being reduced by ferrous sulfate.
Also even if there were an oxidizer in the formula can, the result wouldn't be children digesting DHA hydroperoxides. Peroxides are unstable molecules just sitting around. If you put a bunch of alkane peroxides, which DHA peroxides would be, in a vessel and let them sit around, the long chain would break down leading to aldehydes. By the time you'd open the can, you'd no longer have DHA.
So if you're going say oxidized fatty acids are the cause, they have to be oxidized in the body, not the can. Where in the body are those oxidizing agents coming from?
Now to the IOM document:
So from that sentence it sounds like they're acknowledging DHASCO/ARASCO digestion could be different, because of the fatty acid positions--make sense since enzymes usually care about things like that. But they don't say the digestion will be different. That tells me there is no literature data on the subject. Have you seen any studies looking into that issue?
Until there is data, you can't say one way or the other whether DHASCO/ARASCO gets digested differently than those TAGs in human milk. Hence their use of the word "could be."
I also highly doubt that if they do differ in how they're metabolized that the synthetic TAGs would lead to more oxidized products, such as lipid peroxides. It seems more likely that the difference would be in rate of digestion: either the enzymes involved are less likely to digest them or are more likely, not that they produce different products. I say that because any digestion of a TAG is going to start by cleaving the fatty acids from the glycerol backbone. So with different fatty acids present, the cleaving enzyme may either be more prone to cleave or less prone, depending on their active site. But the result of that cleavage is the same: free DHA or ARA. Sorry I don't see how the synthetic TAGs would lead to more oxidized DHA/ARA. Do you have a paper that suggest otherwise?
Honestly, I don't think the different fatty acid composition of the TAGs matters all that much. Yeah you could see some people have trouble digesting them, because of what I just said above. But I don't see the composition differences leading to any toxic consequences.
But as a scientist, I'd of course want to run the experiment and see how the metabolism differs. Feed it to some rats, see what happens. So probably the best thing would have been to do the test. But as I say above, I doubt anything super serious would happen.
You suggest constipation and malabsorption as possible consequences. Like I said, possibly. But that's a far cry from oxidative damage leading to autism. Of course, we have no way of knowing until some does the experiments. So we're both just shooting in the dark.
Oops just realized I had a typo:
I mean there is no way DHA is being oxidized by ferrous sulfate.
Also now that I think about it, it is highly unlikely that the fatty acids would get oxidized with, what you call, very high levels of a reducing agent present. So again I think it is not possible to find oxidized DHA in formula, given what you've told me.
"So again I think it is not possible to find oxidized DHA in formula, given what you've told me."
Yeah, the DHA won't oxidize in the formula. That's why they add tocopherols to limit oxidation and increase shelf life. Doesn't DHA auto-oxidize?
"EPA and DHA are highly polyunsaturated and easily undergo auto-oxidation.5,6 In fact, it is very difficult to avoid the oxidation of these very labile fatty acids. More importantly, in vivo, a large increase in tissue and plasma accumulation of both omega-3 fatty acids and fatty acid oxidation products is noted in subjects consuming fish oil, even after addition of antioxidant supplements to the diet."
What are you talking about? Are you suggesting that the DHA in formulas will not oxidize? Why does quality control monitor for deterioration? Sensory evaluation?
"So again I think it is not possible to find oxidized DHA in formula, given what you've told me"
Of course this is present. They go to great lengths to minimize oxidative deterioration. They measure TBAR levels. What are you talking about?
Look, Biff, you said ferrous sulfate would oxidize DHA in formula. It is a fact ferrous sulfate won't reduce DHA, ARA, or anything in forumla or anywhere else. Ferrous sulfate is a reducing agent! You seem to have avoided me pointing out that simple fact in your last post. Why is that?
Also many preservatives act as agents to control oxidization. Go look at the ingredients list of many products that sit on pantry shelves and you'll see the compound BHA. It is an antioxidant that is in there to prevent oxidation. So yes formula manufacturers add compounds into their products to prevent oxidation, but so do cookie manufacturers, pancake mix manufacturers, etc.
OK if you look at the paper that quote comes from, you'll see that they're talking about in vivo--aka in the body--effects. Not in the bottle. Look at this quote from the disucssion section:
But I think pointing out that paper doesn't help your argument. The whole point of that paper is to find the antiinflammatory mechanism for DHA. And they find that the oxidized fatty acids inhibit an inflammation pathway. In a previous post, you cited neuroinflammation as a component of the link between these formula additives and autism. But this paper would suggest that the oxidized DHA would protect against that inflammation. According to this paper, having more oxidized DHA is a good thing with respect to inflammation.
No. I made two points in my previous post: 1) Ferrous sulfate will not oxidize DHA in formulas and 2) If DHA does get oxidized it will break down into aldehydes.
My second point is that when you oxidize double bonds, especially with peroxides, you get aldehydes. Ask any synthetic chemist. So if rampant oxidation were a problem in infant formula, you wouldn't see lipid peroxides floating around, you'd see aldehydes and other break down products of the lipids. Do you have any data that shows infant formula contains high levels of lipid peroxides? I mean a study that analyzed the contents of random formula bottles and found the peroxides?
Now Biff, why didn't you respond to my ferrous sulfate critique? You specifically pointed to ferrous sulfate as the culprit behind DHA oxidation. I told you a simple chemical fact: ferrous sulfate doesn't oxidize anything, it's a reducing agent. What's your response to that?
Now Biff, let's look at what your last few posts have contained.
You said ferrous sulfate would oxidize DHA in formula. And your hypothesis is that these oxidized fatty acids lead to oxidative stress and other conditions that eventually lead to autism.
1) Ferrous sulfate doesn't oxidize anything. Simple chemical fact. Iron does most of its chemistry moving between Fe(ii) and Fe (iii). Fe(ii) -> Fe(iii) is when it reduces things. Fe(iii) -> Fe(ii) is when it oxidizes things. Ferrous sulfate is Fe(ii), thus it reduces things.
2) You have yet to present any data that shows infant formula has high levels of oxidized DHA.
3) In your last post, you quote a paper that shows that oxidized DHA is actually protective against inflammation, one of the conditions you claim leads to the damage that causes autism.
From these three points, it's pretty clear that your hypothesis is on very shaky ground. Not only do you have no proof that children would be consuming oxidized DHA in their formula, you just provided a paper saying that those oxidized fatty acids are how they protect against inflammation.
What is becoming abundantly clear is that you have a tenuous grasp on these scientific concepts. I mean the simple fact that you'd point to ferrous sulfate as the oxidizing culprit, suggests to me that you don't really understand basic chemistry. Also you cut and paste quotes from papers and obviously don't read the full paper to understand the quotes' context. I mean why else would you pull a quote from a paper that goes against your argument to argue for your position?
A quick glance at your posts made me think you knew what you're talking about: You talk about well-known pathways. But on closer inspection, it's clear you know the words to the song, but not the tune.
I guess that's why you've been kicked out of court twice, huh, Mike?
Oh, Biff, before you start denying you're Mike Pescatore, do me a favor and do a google search on "dha ferrous sulfate autism." You'll find a bunch of links to blog posts by Mr. Pescatore and no other links where people talk about ferrous sulfate oxidizing DHA. So save me the denials.
Of course, the reason no one else talks about ferrous sulfate oxidizing DHA is because ferrous sulfate isn't an oxidizer--a point you appear to not understand.
"In your last post, you quote a paper that shows that oxidized DHA is actually protective against inflammation, one of the conditions you claim leads to the damage that causes autism."
Oxidized DHA is protective as well as essential for numerous cellular processes. That's how it exerts its anti-inflammatory effects. Protectins/resolvins etc. Controlled and tightly regulated. But I'm talking about excessive and uncontrolled oxidation. You know the bad stuff that becomes neurotoxic when antioxidant defense is overwhelmed. You know.. when it forms secondary products of lipid peroxidation.
Let me get this straight. Oxidation of DHA is benefical towards inflammation at any level? It won't cause inflammation and damage to DNA, proteins etc.? Really? This oxidation and products formed haven't been implicated in neurodegeneration other serious health conditions? Really? So oxidative stress is a theory that has yet to be proven?
Docosahexaenoic acid (C22.6 ω-3, DHA) is a fatty acid that is highly enriched in brain, particularly in gray matter, where it comprises ∼25-35% of the total fatty acids in aminophospholipids, such as phosphatidylserine (8-10). Oxidation of DHA in the central nervous system has been implicated in various neurodegenerative disorders, including, importantly, Alzheimer disease. DHA is highly susceptible to autoxidation because it has six double bonds. We have previously shown that analogous to arachidonic acid, IsoP-like compounds can be generated from the free radical-catalyzed peroxidation of DHA both in vitro and in vivo. These compounds are termed neuroprostanes (NPs) (11-14). The first class of NPs discovered contained F-type IsoP rings and four double bonds and are designated F4-NPs. We have found that that F4-NPs are markedly increased in the brain tissue of humans with Alzheimer disease supporting the contention that oxidation of DHA is increased in this disorder.
"I guess that's why you've been kicked out of court twice, huh, Mike?"
Now my name is Mike? I've been kicked out of what court twice? Are you alright?
"Oh, Biff, before you start denying you're Mike Pescatore, do me a favor and do a google search on "dha ferrous sulfate autism." You'll find a bunch of links to blog posts by Mr. Pescatore and no other links where people talk about ferrous sulfate oxidizing DHA. So save me the denials."
Did it ever occur to you that I may be related to Mike? You know, like a brother or cousin, but not actually Mike. I'm sure that thought never crossed your mind. Mike actually deleted his NV account. I didn't. He actually knows far more than I do on the topics we discuss. So spare me from your nonsense.
Oh, Biff, I see you still haven't responded to my questions about ferrous sulfate. Do you still stand by your assertion that DHA is oxidized by ferrous sulfate? Yes or no? Still waiting for that answer.
Excellent point. Uncontrolled oxidation would be bad. But I have yet to see any evidence from you that the synthetic DHA/ARA will lead to excessive oxidation. Got any of that data?
Oxidative stress as a cause of autism is definitely a hypothesis people have. But it hasn't been proven to cause the disease. And again, you have shown me no evidence that synthetic DHA will lead to such oxidative stress.
Again quoting papers without citing them. Nice work. But let's look at the last bit of that paragraph:
OK so increased oxidation of DHA may be associated with Alzheimer's. Let's quickly go over what that quote doesn't mean to a scientist: 1) All patients with Alzheimer's will have increased levels of oxidized DHA. It just says it supports the idea that may be true. 2) Oxidized DHA leads to Alzheimer's disease. Again chicken-egg issue. We don't know what causes what here.
Also if increased oxidation of DHA is a problem, and that problem can lead to autism, where are the excess of oxidating agents in the formula? Again don't say ferrous sulfate, because that's not an oxidizer!
As for the Mike Pescatore connection, you're right I have no proof you're Mike. Sorry. You could be a relative. But it's kind of odd you'd make the same chemistry mistake as he has made all over the internet (namely, the ferrous sulfate one).
And if he knows more about this than you and still thinks ferrous sulfate is an oxidizer, that doesn't bode well for either of you.
Seriously, respond to my ferrous sulfate critique. I'd like to hear how you wiggle out of that one.
"Seriously, respond to my ferrous sulfate critique. I'd like to hear how you wiggle out of that one"
I thought I said "perhaps" as in maybe. Since we are talking about ferrous sulfate now, wouldn't that react with vitamin C? I ask because I don't have all the answers. I don't understand why you are getting rude all of a sudden.
Also if increased oxidation of DHA is a problem, and that problem can lead to autism, where are the excess of oxidating agents in the formula? Again don't say ferrous sulfate, because that's not an oxidizer!"
Who said it had to happen in the can. Auto-oxidation can occur. Also, there are several other infant formula ingredients that could react. Don't transition metals react with DHA? I Believe they do because they remove them during the manufacturing process.
So auto-oxidation won't occur? That not what I have read. Moving on... So DHA oxidation will be controlled in every infant that consumes dietary supplementation of DHA regardless of their redox status.
I guess you're right. Exogenous altered sources of DHA TAGs that are vulnerable towards oxidation are not problematic. Every infant is completely capable of dealing with bypassing homeostatic synthesis of DHA and controlling excessive oxidation. This includes those with mitochondrial abnormalities and other issues that affect cellular redox. What was I thinking? I mean when has fatty acid structure ever cause adverse health conditions?
Have we ever increased the DHA levels in infant directly via supplementation? No we haven't until formula supplementation.
Is homeostatic synthesis tightly regulated? Why yes it is.
So dietary supplementation by passes this tight regulation? Yes it does.
I guess insulin is important. Should we alter its levels? Supplement with synthetic versions? No, that could be dangerous. Not DHA though.
At least you're not calling me Mike again.
Co-supplementation of ferrous salts with vitamin C exacerbates oxidative stress in the gastrointestinal tract leading to ulceration in healthy individuals, exacerbation of chronic gastrointestinal inflammatory diseases and can lead to cancer. Reactive oxygen and nitrogen species (RONS) have been ascribed an important role in oxidative stress. Redox-active metal ions such as Fe(II) and Cu(I) further activate RONS and thus perpetuate their damaging effects. Ascorbic acid can exert a pro-oxidant effect by its interaction with metal ions via a number of established RONS generating systems which are reviewed here. Further studies are required to examine the detrimental effects of nutraceuticals especially in chronic inflammatory conditions which co-present with anaemia.
I guess ferrous salts will react with vitamin C and exacerbate oxidative stress. Is vitamin C and ferrous sulfate in formula?
I thought DHA hydroperoxides didn't exist. Isn't that what you said? They would be called something else. I guess you were wrong there as well. Know it all.
No I said using the term hydroperoxides the way you were was incorrect. I never said DHA hydroperoxides don't exist. They of course exist.
Now in your post you again quoted a paper, without citing it. You do that often. I don't know why. But it is a bad habit.
But that paper doesn't say ferrous sulfate oxidizes anything. Actually that paper isn't a scientific study, it's a perspective citing other literature. If you actually read the paper, you'll see them discuss the Fenton reaction, in which Fe(ii) interacts with hydrogen peroxide. In that reaction hydrogen peroxide oxidizes Fe(ii) to Fe(iii) to form a hydroxyl radical. Again ferrous sulfate (aka Fe(ii)) isn't oxidizing anything there. The hydrogen peroxide is. And the oxidative stress comes from the resulting hydroxyl radical.
So let's summarize that paper for a second: 1) not a scientific study, a literature review of sorts. So it doesn't show that Fe and Vitamin C leads to oxidative stress, it just suggests it could, 2) it never mentions ferrous sulfate as an oxidizing agent, 3) it has only been cited 4 times, so not a very important paper at all.
Now you call me a "know it all." What is the point of that? Look, Biff, it's clear you're over your head in this situation. You clearly don't have a solid grasp on this subject. Your knowledge solely comes from using google or using Pubmed to find terms and concepts that you think are connected. Then you find their connection in the paper and cut and paste them without looking at the entire context of the paper. That's why you previously posted a paper that showed oxidized DHA protected against inflammation to prove the opposite point. That's why you pointed to ferrous sulfate as an oxidizer, when any chemist will tell you it is used a reducing agent.
I started this conversation cordial, because I thought you knew what you were talking about and just needed some help to get things straight. But now you're calling me names for pointing out that you have made blatant missteps in scientific reasoning. Why can't you just admit you made a mistake in calling ferrous sulfate an oxidizing agent?
Seriously, I have no problem talking with you about this subject and helping you understand this stuff. Who knows what causes autism. If you have a good idea and need some help understanding the biochemistry better, I'm willing to help. That's why I went into science: To think about big problems. But don't call me names. And just admit you don't understand some of these things.
Biff, if you think excess oxidized DHA is a problem, where is the oxidation occurring? what is doing the oxidizing? and where is the proof that it is happening/could be happening?
Simple questions that any scientist looking at your hypothesis would ask. If you'd like to discuss this further, let's start with those three questions. And I won't call you Mike anymore.
People who take insulin take insulin made by microbes. They splice in human genes and the bacteria ferment and synthesize the human insulin. That's exactly what people do with DHA and algae!
So in fact the process you're complaining about is being used to make human insulin all the time. Also some of those insulins are slightly modified human insulins. Meanwhile, the DHA made by algea is the same, it's just that the TAG structure is different.
"People who take insulin take insulin made by microbes. They splice in human genes and the bacteria ferment and synthesize the human insulin. That's exactly what people do with DHA and algae!"
People whom take insulin do so to regulate/normalize their levels. Healthy individuals don't just take insulin as supplements. Again, that would be dangerous.
They splice human genes and bacteria to ferment algae in DHA production? Could you show me that literature?
"Meanwhile, the DHA made by algea is the same, it's just that the TAG structure is different."
Yeah and TAG structure isn't important?
You brought up insulin and asked should we use synthetic versions of it. We do.
Also DHA is normally in human breast milk.
Do you have any evidence that the TAG structure in DHASCO or ARASCO has any deleterious effects?
"Also DHA is normally in human breast milk."
So is palmitic acid. But the source of palmitic acid used in formulas is as palm olein. The structural changes made to palm olein cause constipation and absorption issues. These issues arise because the palmitic acid in the SN-1,SN-3 positions react with cations of calcium and magnesium. So would DHA found in these positions react with calcium and magnesium?
Also, there is evidence that when oleic acid is esterified with DHA, the oxidative stabilty of the TAG is decreased. It's difficult to find info on DHASCO. I would guess that is because they claim it is the same as natural DHA. I showed where the info by the manufacurer was in contrast to that of the IOM.
So I ask you if cations of calcium and magnesium may react with DHA.
Do you have a link to a paper that says that? Do you know if DHASCO has TAGs with DHA and oleic acid?
Also if TAG structural changes lead to things like malabsorption, you are a long way from oxidative stress and neurodevelopmental damage. I mean if a TAG is poorly absorbed, the result is fatty feces. Do you have any evidence that poor absorption of DHA-containing TAGs leads to oxidative stress?
I can't think of a chemical reaction between Ca2+ or Mg2+ and unsaturated fatty acids. I'd imagine for any redox chemistry to occur you'd need a strong oxidator present.
"Also if TAG structural changes lead to things like malabsorption, you are a long way from oxidative stress and neurodevelopmental damage. I mean if a TAG is poorly absorbed, the result is fatty feces. Do you have any evidence that poor absorption of DHA-containing TAGs leads to oxidative stress?"
So the poorly digested DHA will only result in fatty feces? This DHA will not oxidize before being excreted in stools? I guess infant nutrition isn't all that important in regards to neurodevelopment. I mean fatty acids that are poorly absorbed and prone towards oxidation are not problematic. They are simply removed in feces. But wait....What if the poorly digested palmitic acid TAGs cause constipation? What happens to the excess DHA in these stools?
Biff, you raise interesting questions. I don't know what happens to the undigested TAGs. But neither do you.
You also don't know that the DHASCO/ARASCO TAGs are undigested in infant stomachs, or at least you haven't show me any definitive evidence to support that idea.
And my question still stands: Do you have any evidence that poor absorption of DHA-containing TAGs leads to oxidative stress?
Raising questions are great. But the existence of questions doesn't mean anything until you start to get answers.
As I've said before, I haven't seen anything in your posts that suggests to me that there's a link between DHASCO/ARASCO in infant formula and any neurodevelopmental damage.
I don't know exactly what you want from this conversation. If you were an actual scientific researcher, I'd love to help you hone your questions so you could write a good grant proposal. But from your posts, I doubt you have much actual scientific training. Instead you seem to be a well-read, intelligent guy who can google or PubMed pretty well, but who lacks the background to fully understand all the concepts he throws around. So what do you want from me?
Biff, if you're interested in research on the causes of autism, I'd suggest this article that I just saw today: http://cen.acs.org/articles/90/i10/Inner-Workings-Autism.html
They discuss some of the cutting edge research on mutations in proteins that are involved in brain cell signaling. Enjoy.
To the authors' knowledge, this is the first time that TAG regio-isomerism has been shown to be a factor influencing lipid oxidation in emulsions. This effect has previously been demonstrated for bulk oil oxidation, where PUFA was observed to oxidize more slowly when attached to the sn-2 position compared with the sn-1(3) position in TAG (Wada and Koizumi 1983; Endo et al. 1997; Wijesundera 2008; Wijesundera et al. 2008). The present study has shown that this regio-isomeric influence on oxidative stability extends to oil-in-water emulsions stabilized with Tween 40. Further studies are required to determine whether the same regio-isomeric effect occurs with other emulsifiers used by the food industry. Furthermore, the present study was conducted with model TAG in which DHA occurred in combination with two saturated fatty acids. In natural fats and oils, PUFA occur in combination with monounsaturated fatty acids as well as saturated fatty acids. Natural oils also contain TAG molecular species, which are entirely made up of PUFA. For bulk oils, it has been shown that the superior oxidative stability of sn-2-bound PUFA also applies for TAG in which PUFA occurs in combination with two monounsaturated acids (Hoffmann et al. 1973; Wijesundera et al. 2008). Further studies are needed to determine regio-isomeric effects on the oxidative stability of oil-in-water emulsions of other TAG species abundant in natural oils.
Although experimental evidence has clearly shown that TAG regio-isomerism influences lipid oxidation in both oil-in-water emulsion and bulk oil, the reason for this effect is not known. The reaction mechanism and factors influencing lipid oxidation are substantially different between emulsified and bulk lipids (McClements and Decker 2000), and the mechanisms by which regio-specificity influences oxidation in the two systems need not be the same. In oil-in-water emulsions, lipid oxidation occurs at the interface, and it is possible that sn-2-bound DHA are able to orient a greater portion of its unsaturated groups inside the interior of the oil droplets rather than at the interface compared with sn-1(3)-bound DHA, thus making them less available for the oxidation reaction. However, there is no direct experimental evidence to support such a hypothesis.
Biff, two things to start: 1) Why can't you provide citations when you cut and paste quotes from papers? Doing so gives credit to the people behind those ideas and allows a reader to look at the context of the quotes. It's an annoying habit of yours. Please start providing links to the paper when you cut and paste parts of it.
Also posts that are completely other people's words are truly useless. It shows you haven't put any thought into the argument you're trying to make. A more effective strategy would be to grab key quotes and use them as examples of the points you make in your own words.
2) You didn't answer my more important question: What do you want from this discussion? Do you just want to keep cutting and pasting things from papers you google, and then have me point out that you're not fully understanding the context of the quote or that you need to consider some other factors? I can do that, no problem. But I don't know what we get out of it. Can you please answer that question before proceeding to address any of my other points?
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OK now to the cut and paste quote.
So I'll say this first: You're right. This paper--and a couple others I quickly searched for--show that FA position in a TAG have different levels of stability toward oxidation. From this paper, it's pretty clear that DHA at position 3 is less stable than at position 2.
But the next question is how much of DHASCO has DHA in position 3? Well the editor-in-chief of the journal that this paper comes from, Journal of Food Lipids, wrote a book about specialty lipids, like DHA: http://www.amazon.com/Nutraceutical-Specialty-Co-Products-Science-Technology/dp/1574444999
In the section on DHASCO, he has answer to that very question: About 45% of DHASCO TAGs have DHA at the 2 position, while in human milk the fatty acid is in that position 50 to 60% of the time. He concludes that makes DHASCO's TAG structure "nearly identical to that of human milk." And he goes on to say that digestion and absorption of DHA in algal oil should be the same as in human milk.
Earlier in the DHASCO section, the editor also remarks that a study in rats showed that feeding large amounts of DHASCO didn't lead to any adverse effects on animal growth or lipid metabolism. He adds that DHASCO has "remarkable oxidative stability," and that it is stable for months.
Want to check for yourself? Here is that page (269) in his book: http://books.google.com/books?id=-DasysmU7V0C&pg=PA269&lpg=PA269&dq=tag+structure+DHASCO&source=bl&ots=fN6PSJVPdh&sig=ldaQbGYqSg_Bu0rOfJMLiWN5TJ4&hl=en&sa=X&ei=R71XT8P5AuqniQKUh-SHCw&ved=0CCEQ6AEwAA#v=onepage&q=tag%20structure%20DHASCO&f=false
So an expert on lipids--and editor-in-chief of the journal you just cited--concludes that the TAG structure of DHASCO is essentially the same as that of those in human milk, that DHASCO is remarkably stable to oxidation, and, in animal tests, shows no differences in lipid metabolism.
No offense, Biff, but that single book page is basically the kill shot on your hypothesis. We have spent days talking about synthetic DHA leading to oxidative stress being a possible environmental cause of autism. Yes TAG structure does influence oxidative stability, but it appears that the TAG structure of DHASCO is so similar to that of human milk TAGs, that its stability isn't all that different. Also an actual study of the effect of an organism digesting the oil shows none of the effects you predicted: namely adverse lipid metabolism.
Before you go and google something and cut and paste here, think for a second. Think about all the things I have shown you. I think it's time to admit that you need to scrap your hypothesis.
"In the section on DHASCO, he has answer to that very question: About 45% of DHASCO TAGs have DHA at the 2 position, while in human milk the fatty acid is in that position 50 to 60% of the time. He concludes that makes DHASCO's TAG structure "nearly identical to that of human milk." And he goes on to say that digestion and absorption of DHA in algal oil should be the same as in human milk."
Nearly identical and should be are guesses. Nowhere in human milk is DHA found to be esterified in all three positions as in the case of DHASCO. Show me where DHA found esterified in all three positions "is in fact" digested and absorbed identically as TAGs found in human milk. Should be doesn't cut it.
As for posting links to publications-I can't because Newsvine won't allow me to.
"Before you go and google something and cut and paste here, think for a second. Think about all the things I have shown you. I think it's time to admit that you need to scrap your hypothesis."
I guess you knew that the DHA used in formulas was different than natural sources. You already knew that this unique structure wasn't problematic. I have thought for a long time and done extensive reading on the subject. I'm sorry that I google these topics. I have to find this info somewhere.
There is nothing conclusive with statements such as "nearly identical" and "should be". So in no way should I scrap anything. I believe such phrases were used when the manufacturer described the digestion and absorption of DHASCO to the FDA. Then these statements were corrected by the IOM. You have already admitted to not knowing what becomes of the unabsorbed DHA after digestion. It could become available for oxidation. So before I scrap my whole theory, understand that there is much more to understand.
Sorry about the link issue. I think you said that before and I forgot. My bad.
Biff, I didn't say those things, an expert on lipids said those things. You and I are both not lipid experts. He said that the two are nearly identical. He said that their digestion are suspected to be similar. He is the one that described DHASCO as remarkably stable to oxidation. He is the one that pointed out that tests in rats showed no adverse lipid metabolism.
Look, you showed me a quote from a paper that said TAGs are more stable to oxidation when DHA is at the 2nd position compared to the 3rd position. Then I showed you evidence that the amount of DHA in the more stable position in DHASCO is roughly equal to that of human milk. You do this all the time, instead of taking in new evidence and learning from it, you refuse to accept it or ignore the facts someone presents to you.
And you still haven't explained what you want from this conversation. It is pretty darn clear you're not in this to learn anything. When presented with evidence that is counter to your hypothesis, you become inflexible and opposed to considering it. So why keep chatting with me? What is your goal?
I realize you have. And I don't want to belittle that work. But I think what you need to start to acknowledge is that you don't fully understand all of the topics you've read about. The fact that within 5 minutes I found that book chapter on DHASCO that contradicts the foundation of your hypothesis suggests your reading has been selective or not thorough enough. The fact that when asked for an agent responsible for oxidizing DHA, you pointed to ferrous sulfate, a reducing agent, suggests your background in chemistry is lacking.
I imagine this is a very personal issue for you. But if you think persisting on this formula issue is getting anywhere, I'm here to tell you it isn't. I have worked in biochemistry for my entire career. Nothing you have presented me or anything I've looked up in the course of our conversations suggests that synthetic lipids are a concern in the context of autism.
Biff, a quick search of "infant formula autism" leads you to this study: http://www.internationalbreastfeedingjournal.com/content/1/1/16
Now the study is based on a web-based survey, so it has problems with confirming autism diagnoses and you have the self-reporting biases to consider. But what they found in a survey of 900 people or so is this:
Like I said, I wouldn't say this study means DHASCO/ARASCO protects children from autism or even that breast-feeding does. This study is far from perfect. But a study like this is what you need to start to connect synthetic lipids to autism. If you could point to a study like this one--albeit with a better experimental design--that showed kids who took formula w/ DHASCO/ARASCO were more likely to be autistic than kids that did, then you'd be on your way to proving your point.
But you haven't presented such a study. And the one that I found suggests the exact opposite of your hypothesis.
I have read that study several times in the past. Web based self reporting? Imagine if you had such a study with vaccinations/non vaccinations and autism? But then again it would be just as worthless. Correlation doesn't equal causation right?
Funny though, if DHA/ARA supplementation were to protect from autism, you would think that the manufacturers would conduct such studies. Really, imagine how this information would propel sales. Why bother breast feeding and risk autism. A mother could have low DHA levels.
"But you haven't presented such a study. And the one that I found suggests the exact opposite of your hypothesis."
Let's take a look at what DHA/ARA supplementation provides towards benefits in brain development-
Reviewers' conclusions
The results of most of the well conducted RCTS have not shown beneficial effects of LCPUFA supplementation of formula milk on the physical, visual and neurodevelopmental outcomes of infants born at term. Only one group of researchers have shown some beneficial effects on VEP acuity. Two groups of researchers have shown some beneficial effect on mental development. Routine supplementation of milk formula with LCPUFA to improve the physical, neurodevelopmental or visual outcomes of infants born at term can not be recommended based on the current evidence. Further research is needed to see if the beneficial effects demonstrated by Dallas 2005 trial of Birch et al can be replicated in different settings.
That's odd. This study was published the same year that non supplemented formulas were removed from the market. Birch et al in Dallas 2005? She was paid well for her results by Mead Johnson. So have they replicated the beneficial effects? No.
"Previous in vitro and in vivo studies suggest DHA/AA ratios in commercially prepared infant formulas are potentially toxic for normal brain development. At ratios of .56 or less, negative effects on health were detected in vivo, with critical levels for safety at a ratio of 1.8 in vitro. Abbott, the makers of Similac, as well as Mead Johnson, the makers of Enfamil, offer commercially prepared infant formula with DHA to AA since 2002 with ratios of approximately .37 and .50 respectively. Abbott representatives state Similac established DHA to AA ratio to replicate American women’s breast milk, a DHA/AA ratio .74 lower than the top 10 countries for concentration of DHA/AA in breast milk worldwide. Abbott’s PediaSure and Mead Johnson’s Enfagrow Premium (vanilla and chocolate) contain DHA without AA. Excess DHA, without adequate antioxidant such as vitamin E, induces apoptosis through a translocation of phosphatidylserine (PS), heightened bax and capase-3 activity subsequent to disruption of mitochondrial transmembrane potential, and activation of peroxisome proliferator-activated receptors (PPARs) via the p38 signalling pathway. Chronic neuroinflammation may lead to non-enzymatic oxidation of DHA which produces highly reactive neuroketals and results in generation of further toxic metabolites. Pseudogenes, competitive endogenous RNA, and microRNA represent genomic and transcription level sources of dysfunction not examined in existing literature. Abnormal cytochrome P450 genes contribute to neuroinflammatory damage leading to behaviors of the autism spectrum. Postnatal gonadotropin and sex steroids surge by 3 months of age resulting in hormonal expression above pubertal levels. In males, the hypothalamic-pituitary-testicular axis generates high serum androgens, though testosterone is a neurotoxin within the developing CNS. This author suggests P450arom on chromosome 15q21.2 represents a biomarker for autism as its enzyme converts testosterone to estradiol through mechanisms similar to the conversion of excess DHA and AA by cytochromeP450 enzymes into feed-forward neurotoxic inflammatory metabolites. Estradiol is a powerful neuroprotective agent, a modulator of oxytocin receptors known deficient in classical autism, and regulates conversion of precursors into neuroprotective DHA. Males do not produce DHA above dietary background. A recent study indicates high-dose DHA (1% total fatty acids) administered to pre-term infants improves Bayley Mental Development (MDI) scores at 18 months corrected age in female infants only. Therefore, converging evidence indicates a system linking environment, gender, and both translation and transcription level genetics. Serious disturbances within this system are capable of inducing autism, yet autistogenesis paradoxically grants selectively advantage in an inhospitable environment, as playing well with others is undesirable in a high stakes environment. Infant physiology provides adaptive processes targeted to sexually dimorphic males. Environmental stressors cannot induce gene-based adaptation in the same generation. Therefore, this systems theory explains the ontogeny and phylogeny of classical autism."
So increasing levels of DHA and sidestepping natural synthesis isn't problematic? Let's look at research that reveals how DHA may be implicated with disease-
Background
The transmissible spongiform encephalopathies, otherwise known as prion diseases, occur following the conversion of the cellular prion protein (PrPC) to an alternatively folded, disease-associated isoform (PrPSc). Recent studies suggest that this conversion occurs via a cholesterol-sensitive process, as cholesterol synthesis inhibitors reduced the formation of PrPSc and delayed the clinical phase of scrapie infection. Since polyunsaturated fatty acids also reduced cellular cholesterol levels we tested their effects on PrPSc formation in three prion-infected neuronal cell lines (ScGT1, ScN2a and SMB cells).
Results
We report that treatment with docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) or the cholesterol synthesis inhibitor simvastatin reduced the amounts of free cholesterol in membrane extracts from prion-infected neuronal cells. Simvastatin reduced cholesterol production while DHA and EPA promoted the conversion of free cholesterol to cholesterol esters. Crucially, while simvastatin reduced PrPSc formation, both DHA and EPA significantly increased the amounts of PrPSc in these cells. Unlike simvastatin, the effects of DHA and EPA on PrPSc content were not reversed by stimulation of cholesterol synthesis with mevalonate. Treatment of ScGT1 cells with DHA and EPA also increased activation of cytoplasmic phospholipase A2 and prostaglandin E2 production. Finally, treatment of neuronal cells with DHA and EPA increased the amounts of PrPC expressed at the cell surface and significantly increased the half-life of biotinylated PrPC.
Conclusion
We report that although treatment with DHA or EPA significantly reduced the free cholesterol content of prion-infected cells they significantly increased PrPSc formation in three neuronal cell lines. DHA or EPA treatment of infected cells increased activation of phospholipase A2, a key enzyme in PrPSc formation, and altered the trafficking of PrPC. PrPC expression at the cell surface, a putative site for the PrPSc formation, was significantly increased, and the rate at which PrPC was degraded was reduced. Cholesterol depletion is seen as a potential therapeutic strategy for prion diseases. However, these results indicate that a greater understanding of the precise relationship between membrane cholesterol distribution, PrPC trafficking, cell activation and PrPSc formation is required before cholesterol manipulation can be considered as a prion therapeutic.
And how about this-
Chronic ingestion of diets enriched in SFA commonly causes vascular dysfunction, including in capillary vessels of the brain. The effects of SFA could be described as a response-to-injury phenomenon induced by exaggerated exposure to plasma triglyceride, cholesterol, NEFA, or harmful inflammatory products of lipid metabolism, such as lipid peroxides. Many studies support a role of n3 and n6 fatty acids in the prevention of vascular, based disorders primarily via suppression of inflammatory cascades. Less clear however are the benefits of polyunsaturated oils in the presence of profound inflammation, because of the propensity to generate lipid peroxidation products. In an established model of cerebrovascular dysfunction induced by chronic ingestion of an SFA-enriched diet, provision of DHA amplified the harmful effects. Probable mechanisms include hypercholesterolemia and perhaps fatty acid-induced cytotoxicity. The data suggests that introduction of n3/n6 fatty acids in metabolic conditions that are characterized by heightened systemic inflammation needs to be carefully considered in the context of paradoxical detrimental effects that could occur.
Oxidative stress appears to be directly involved in the pathogenesis of the neurodegeneration of dopaminergic systems in Parkinson disease. In this study, we formed four dopamine modification adducts derived from docosahexaenoic acid (C22:6/ω-3) and arachidonic acid (C18:4/ω-6), which are known as the major polyunsaturated fatty acids in the brain. Upon incubation of dopamine with fatty acid hydroperoxides and an in vivo experiment using rat brain tissue, all four dopamine adducts were detected. Furthermore, hexanoyl dopamine (HED), an arachidonic acid-derived adduct, caused severe cytotoxicity in human dopaminergic neuroblastoma SH-SY5Y cells, whereas the other adducts were only slightly affected. The HED-induced cell death was found to include apoptosis, which also seems to be mediated by reactive oxygen species generation and mitochondrial abnormality. Additionally, the experiments using monoamine transporter inhibitor and mouse embryonic fibroblast NIH-3T3 cells that lack the monoamine transporter indicate that the HED-induced cytotoxicity might specially occur in the neuronal cells. These data suggest that the formation of the docosahexaenoic acid- and arachidonic acid-derived dopamine adducts in vitro and in vivo, and HED, the arachidonic acid-derived dopamine modification adduct, which caused selective cytotoxicity of neuronal cells, may indicate a novel mechanism responsible for the pathogenesis in Parkinson disease.
Oh yes, and autism?
Abstract: Oxidative damage has been documented in the peripheral tissues of autism patients. In this
study, we sought evidence of oxidative injury in autistic brain. Carboxyethyl pyrrole (CEP) and
iso[4]levuglandin (iso[4]LG)E2-protein adducts, that are uniquely generated through peroxidation of
docosahexaenoate and arachidonate-containing lipids respectively, and heme oxygenase-1 were
detected immunocytochemically in cortical brain tissues and by ELISA in blood plasma. Significant
immunoreactivity toward all three of these markers of oxidative damage in the white matter and often
extending well into the grey matter of axons was found in every case of autism examined. This striking
threadlike pattern appears to be a hallmark of the autistic brain as it was not seen in any control brain,
young or aged, used as controls for the oxidative assays. Western blot and immunoprecipitation
analysis confirmed neurofilament heavy chain to be a major target of CEP-modification. In contrast, in
plasma from 27 autism spectrum disorder patients and 11 age-matched healthy controls we found
similar levels of plasma CEP (124.5 ± 57.9 versus 110.4 ± 30.3 pmol/mL), iso[4]LGE2 protein adducts
(16.7 ± 5.8 versus 13.4 ± 3.4 nmol/mL), anti-CEP (1.2 ± 0.7 versus 1.2 ± 0.3) and anti-iso[4]LGE2
autoantibody titre (1.3 ± 1.6 versus 1.0 ± 0.9), and no differences between the ratio of NO2Tyr/Tyr
(7.81 E-06 ± 3.29 E-06 versus 7.87 E-06 ± 1.62 E-06). These findings provide the first direct evidence
of increased oxidative stress in the autistic brain. It seems likely that oxidative injury of proteins in the
brain would be associated with neurological abnormalities and provide a cellular basis at the root of
autism spectrum disorders.
Of course, I raised the same objection in my post. Not disagreeing that this study has serious problems. Just showing you want type of study, in general, you should be looking for to start to verify the DHASCO-autism connection.
Also, a study that compared vaccinated and non-vaccinated kids is exactly that type of study you need to show a connection between autism and vaccines. And that isn't a correlation. A correlation says the amount of variation in one variable depends on variation in another variable. That's not what this study is looking at. So the correlation-not-causation criticism doesn't apply here.
As I said in my previous post, I don't think that study really makes a strong argument that DHA/ARA protects against autism.
Yes let's look at what you just quoted. It's this: http://asa.confex.com/asa/2011/webprogram/Paper1750.html
That's not a study or a paper, it's the summary of a presentation at a conference. Also from that summary, you'll see that the author didn't actually run any experiments, he just reviewed the literature. So what you presented to me isn't a study at all. It's a review of the literature, followed by someone's hypothesis. Not what I was asking for. You need to have data collected and presented in a paper before any one will take your hypothesis seriously. Just connecting the dots through a literature review isn't going to cut it for real scientists.
Also let's look at the author: A doctoral candidate at Walden University, which is an online degree university. So not really the kind of "expert" you want to be quoting.
--
OK Biff, you haven't said what you want to get out of this conversation--despite me repeatedly asking you the question. So I now assume you don't hope to get anything out of this from me. You just want to tout your infant formula hypothesis.
But as I have shown repeatedly, that hypothesis is dead on arrival. Let's look at it and what we've discussed for weeks now:
You think that additives to infant formula are an environmental cause in some autism cases. You think that synthetic DHA and ARA (DHASCO/ARASCO), when ingested by infants, lead to oxidative stress, inflammation, and other conditions, that then cause neurodevelopmental deficits, leading to autism.
Now the second part of that hypothesis (oxidative stress and inflammation connected to autism) has some support. Of course, you didn't come up that. Some autism researchers have pointed to those two factors before.
But the main problem with your hypothesis is connecting the synthetic TAGs to oxidative stress and inflammation.
You say that DHASCO/ARASCO are more prone to oxidation than DHA/ARA TAGs in human milk. When asked for the source of this oxidation, you told me ferrous sulfate. But as I've pointed out, that compound is a reducing agent. You also have said that the DHASCO/ARASCO TAG structure is less stable to autoxidation compared to the TAGs in human milk. You supported that with a paper that showed DHA position in a TAG changes its oxidation stability. But I showed you a book chapter written by a lipids expert that says 1) DHASCO TAG structure is nearly identical to that of TAGs found in human milk (45% in position 2 compared to 50-60%) and 2) DHASCO is remarkably stable to oxidation, lasting for months in storage.
So you have shown me no scientific that DHASCO/ARASCO has a significant oxidation problem. In fact, from what I've read, they don't seem to be any different than natural TAGs in that regard.
Of course, a point I haven't raised enough is that if we're talking about DHASCO/ARASCO oxidizing in the formula can, we're not talking about children ingesting the kinds of compounds that lead to oxidative stress. When biochemists talk about oxidative stress, they talk about reactive oxygen species, such as peroxides or oxygen radicals. If DHASCO/ARASCO were oxidation instable, the result wouldn't be compounds that lead to reactive oxygen species. The result would be a break down of the fatty acid carbon chains. The carbon-carbon double bonds in the fatty acids would oxidize, eventually break, and form smaller molecules. When people talk about fats going rancid, that's what they're talking about: oxidative breakdown of the fatty acid chains. So if oxidation was a problem, the result would be infants ingesting smaller carbon chains, not compounds that lead to reactive oxygen species.
Biff, it's abundantly clear now that you really don't have a tight grasp on what you're talking about and you have no desire to actually understand the biochemistry you talk about. You seem to be interested only in shoving your hypothesis down other people's throats.
But that won't work with me or anyone else who actually understands biochemistry. Sorry, but if you've spent years looking into this topic, the only thing you have to show for it is a series of links to papers you googled.
You obviously don't fully understand the science going on here. And you have made it clear you don't care. When presented with evidence that contradicts your hypothesis, you either ignore it or try to explain it away with quotes lifted out of context from other papers.
At the start of this thread you were talking to 2014MD and said this:
You used a sarcastic tone to imply that 2014MD didn't understand the science you did. Actually, I've seen you do this before--and your relative Mike Pescatore did it too. You try to bully people by tossing around big scientific terms and insinuating that they are clueless to the scientific insights you've made.
Well, Biff, I have spent my career studying biochemistry and from our weeks of conversation, it's clear you don't really understand much about biochemistry. And you have no grand insights into the cause of autism. You have a poorly thrown together series of ideas lifted out of context from papers you've skimmed.
I don't know what else there is to say on this topic. I tried to be patient with you and explain where you were wrong, but I see you don't really care. So I'll leave you with this suggestion: Don't quit your day job.
So now you present me with three papers trying to link DHA to oxidative stress. But we're not talking about DHA, we're talking about DHASCO. If DHA were the problem, then human milk would be a problem.
Now if you're saying that excess DHA via supplementation is the problem, that is different. Of course, that would be yet another explanation you've thrown out--first it was metals and DHASCO in formula leads to oxidation, then it was DHASCO's TAG structure leads to more oxidation. Basically you just keep moving the goal posts when I critique one of your arguments. It shows you only care about connecting infant formula to autism, not that you want to know the truth. Of course, no good scientist thinks that way.
Also I can do a quick Google Scholar search of "Docosahexaenoic acid oxidative stress brain" and find many papers that talk about how DHA protects against oxidative stress. So feel free to keep finding papers that agree with you. I can find ones that don't.
Again, if you wanted to know the truth, you wouldn't keep looking for papers that supported your position and ignored those that don't. You'd look at the entire literature and assess the validity of your hypothesis. Of course, you don't do that, because you're not actually a scientist and you're not really interested in the truth.
"So now you present me with three papers trying to link DHA to oxidative stress. But we're not talking about DHA, we're talking about DHASCO. If DHA were the problem, then human milk would be a problem."
Human milk is far more complex than formula. The levels of DHA vary in human milk during lactation and are dynamically regulated. So don't go down that road. DHA and ARA are derivatives of essential LCPUFAs. There is a reason that the human body regulates elongation and desaturation of precursors fatty acids. As an example, formulas were supplemented with ALA in an attempt to increase levels of DHA. They found that increasing ALA only resulted in minor increases in DHA. This was quickly labeled as inefficient synthesis rather than tightly controlled synthesis. So they then attempted DHA supplementation without ARA. They quickly realized that too much DHA had undesirable consequences. They found that balanced levels of n-3 and n-6 fatty acids were required. So it becomes clear that supplementation of DHA and ARA is not a static, one size fits all answer.
"Again, if you wanted to know the truth, you wouldn't keep looking for papers that supported your position and ignored those that don't. You'd look at the entire literature and assess the validity of your hypothesis. Of course, you don't do that, because you're not actually a scientist and you're not really interested in the truth."
What papers am I ignoring? I understand that DHA and ARA oxidation is essential for numerous cellular processes. I understand how synthesis is dynamically regulated. I suggest that deviating from natural synthesis by supplementation may lead to increased levels beyond what can be afforded protection from excessive oxidation. How is that not being interested in the truth? Are you suggesting that every infant is capable of dealing with increased levels of DHA and ARA?
I don't recall implying infant formula was exactly the same as human milk. So don't get your issue here. I'm just pointing out that you moved from discussing the TAG structure of DHASCO to pointing to papers that suggest DHA supplementation is the problem.
Basically, my whole point in my last post is that you constantly move the goal post in this discussion. First it's metals in the formula that oxidize DHASCO. Then it's the TAG structure. Not it's simply that formula may provide too much DHA. When I point out problems with one form of your hypothesis you retreat to another. That's what a person does when their sole goal is proving the connection between a variable and a condition and not understanding what causes the condition. You are focused on connecting formula additives to autism, you don't care what that connection is.
So this is your new hypothesis. Do you have any evidence that the levels of DHA an infant receives from formula supplementation would lead to such a situation? Is there any evidence out there that the levels of DHA in formula are harmful?
"So this is your new hypothesis. Do you have any evidence that the levels of DHA an infant receives from formula supplementation would lead to such a situation? Is there any evidence out there that the levels of DHA in formula are harmful?"
My new hypothesis? I have been saying all along that bypassing natural synthesis,a tightly controlled process, results in increased levels. Since we have only been doing this since 2002, and neurological issues such as autism are increasing, rather than decreasing, we should probably investigate. We have evidence that structural alterations in palmitic acid TAGS result in adverse effects on digestion and absorption. We have evidence that reveals DHA is more prone to oxidation when esterified in the SN1, SN3 positions of TAGs, as found in DHASCO. Since oxidative stress has been implicated in several neurological diseases as well as autism, it is important to understand how supplementation may affect infants. There are infants that may be harmed from increased levels of LCPUFAs. Believe it or not, some children may have underlying medical conditions such as a mitochondrial abnormality that could result in deleterious effects from increased levels of LCPUFAs.
"Basically, my whole point in my last post is that you constantly move the goal post in this discussion. First it's metals in the formula that oxidize DHASCO. Then it's the TAG structure. Not it's simply that formula may provide too much DHA."
I suggested ferrous sulphate. I was wrong. So does that mean that other metals found in the human body will not react with DHA and initiate oxidation? If this was to occur, are you suggesting that all infants are capable of controlling this oxidation? Does excessive oxidation cause neurological damage? Has excessive DHA oxidation been implicated at all?
So let me get this straight, because I don't understand what I am talking about. DHA synthesis isn't all that important. The balance between N-3 and N-6 fatty acids isn't important. Altering the TAG structures of DHA and ARA will not affect digestion and absorption. Any undigested or unabsorbed DHA and ARA will not be available to react with metals and oxidation will not initiate. The excess will be simply removed and result in fatty feces. All infants are capable of increasing LCPUFA levels and providing adequate antioxidant protection.
You're right. There aren't any issues with supplementing bio-similar TAGs of LCPUFAs that are highly susceptible towards oxidation. They will be metabolized the same as natural sources, and if not, they will simply be excreted in feces.
In prefacing their study the researchers noted, “Neuropathological studies in autism have shown increased microglial activation, decreased cerebellar Purkinje cell density and abnormal brain swelling, particularly in white matter. Biochemical studies have shown increased oxidative stress, abnormal glutathione metabolism, decreased melatonin, and increased docosahexaeonic acid (DHA) in autistic subjects. Although there is debate as to whether autism has a pre- or post-natal origin, it is generally accepted that the symptoms and pathology persist through the life of the subject. These studies suggest that there is an underlying and ongoing biochemical abnormality in autism, regardless of its origin.”
The study conducted by the researchers was designed to find evidence of metabolic dysregulation and toxicity, regardless of the initial cause. Their plan was to collect three plasma samples over the course of a year from 15 autistic and 12 non-autistic age-matched controls. 8 out of the 12 controls were siblings of autistic children, some of whom had impairments in social relations not rising to the level of autism.
The researchers found “consistent alterations in the levels of very long chain fatty acid (VLCFA)-containing phosphatidylethanolamines (PtdEtns) and in DHA-containing ethnalomine plasmalogens (PlsEtns). . . These findings are reported herein and suggest a possible disruption of fatty acid metabolism due to compromised mitochondrial function. Mitochondrial stress was assessed through measurements of reduced glutathione (GSH) and related metabolites. In addition, we investigated and compared the in vitro effects of glutamate toxicity on neuronal, astrocyte and hepatocyte cell cultures to biomarker changes observed in the autistic subjects. Impaired mitochondrial fatty acid oxidation as the underlying cause of elevated plasma levels of VLCFA-containing PtdEtn is hypothesized.”
In plain English, what does this mean? First, the researchers found abnormal levels of very long chain fatty acids in children with autism. Second, it may be due to the mitochondria not working as well as it should (I'd also suggest involvement of the peroxisome). Last, the glutamate derangement which would result from this situation would have different effects on different parts of the brain.
So again, could DHA supplementation be problematic for certain infants? I ask because I simply don't understand what I am talking about and choose to ignore everything else.
Well it seems we've spent most of our time talking about the fatty acids oxidizing in the can. So if you brought that up earlier, I apologize.
The number of cell towers in cities and towns have increased since 2002 too. Should we investigate if that is leading to more autism cases too? Here is the correlation-causation fallacy.
But I showed you evidence from a lipids expert that in rats DHASCO has similar metabolism to natural TAGs with DHA.
True but that same lipids expert pointed to the fact that amount of position 2 DHA in DHASCO isn't all that dissimilar from human milk. And, on top of that, described DHASCO as remarkably stable toward oxidation. So I think focusing on the TAG structure of DHASCO is a no go, if you want to connect it to oxidative stress.
1) Thank you for finally admitting you were wrong about that.
2) There are possibly other metals that could oxidize it. But metals don't just float around in cells so they could bump into DHA molecules. They often form complexes with organic molecules or proteins. But in those complexes, they're regulated as part of the redox processes of the cell. What I'm trying to say is that, for a cell to experience run away oxidation of DHA you would need the cell to have a surplus of oxidants. What about excess DHA is causing that surplus of oxidants?
Never said. I just said that you don't know much about biochemistry.
Again rat studies showed DHASCO didn't change lipid metabolism.
Again DHASCO is not that different from human milk TAGs, is remarkable stable to oxidation, and doesn't lead to differences in lipid metabolism in rats. So again if you are attacking this problem from the TAG structure alone, you have nothing to stand on.
Fine. But how does DHASCO supplementation have anything to do with this? Are you saying that the levels of DHA in infant formula are higher than those in human milk and that leads to these lipid metabolism issues?
If so, then what is the range of DHA concentrations in human milk and what is the range in infant formula. Are we talking a std deviation greater? Half a std dev? How much more DHA is an infant getting when they eat formula compared to human milk?
That is the question you need to focus on here. If DHA concentrations are not that abnormal in formula, your hypothesis is a no go. If they are quite high relative to human milk, then you need to find out if excess fatty acids disrupt lipid metabolism in cells with mitochondrial deficits.
"Fine. But how does DHASCO supplementation have anything to do with this? Are you saying that the levels of DHA in infant formula are higher than those in human milk and that leads to these lipid metabolism issues?"
You are still thinking that DHA levels are the same in every individual. Yes, DHA levels are higher in formulas than some mother's breast milk. These levels vary from mother to mother, infant to infant. It's not some fixed level, it's dynamically regulated. I'm surprised that you don't understand this.
"If so, then what is the range of DHA concentrations in human milk and what is the range in infant formula. Are we talking a std deviation greater? Half a std dev? How much more DHA is an infant getting when they eat formula compared to human milk?"
I guess that would depend on the mother's levels during lactation as well as the infant's levels before receiving dietary DHA. The level used in formulas is calculated from an average of levels found world wide. But DHA levels are dynamically regulated, not just some average number. Again, not quite getting the whole bypassing of natural synthesis thing.
"That is the question you need to focus on here. If DHA concentrations are not that abnormal in formula, your hypothesis is a no go. If they are quite high relative to human milk, then you need to find out if excess fatty acids disrupt lipid metabolism in cells with mitochondrial deficits."
See what I mean? Explain DHA concentrations that are not that abnormal. What is the optimum level of DHA? Does it vary from different cell types? Is it incorporated at different rates in different cell types? Which human milk are we examining? Mothers from Japan or from the U.S.? I see, take an average of all these values and use that as a safe level. Change its esterification positions and claim it will be metabolized in an identical fashion of natural sources.
I thought you understood what has been revealed in regards to DHA and mitochondrial membrane potential. I thought excessive DHA incorporated into cells could disrupt protein palmitoylation and displace signaling proteins in lipid rafts.
Tell me what the optimal level of DHA should be when used as a dietary supplement. I am curious as to how one would calculate such a figure when such endogenous levels are dynamically regulated. When you explain how much is just right for every infant, I'll admit my argument is moot.
I never said they were the same for every one. I would never say such a thing. What I was asking is what is the range of DHA concentrations in breast milk versus the range found in formulas. That would tell us how much different the two are.
If you're correct that the DHA levels in formulas are in the range of those found in breast milk worldwide, then sorry your hypothesis is dead. If the DHA concentrations in infant formula are within the range of physiological concentrations, then you're not talking about abnormal levels of the lipid.
If you have the data, I'd love to see the range of DHA concentrations in human milk vs those in formula.
It's like worrying about the salt concentrations of contact lens saline solution and then saying the manufacturers use a concentration based on worldwide concentrations in human tears. Sure the exact salt concentration may be higher than your own tears, but they are within the normal physiological range.
Sorry you're talking nonsense now.
You know what accounts for variation in DHA levels in human milk? Diet. Does that mean we should expect children of women who eat a lot of fish and seafood to have higher rates of autism? That would be in keeping with your hypothesis.
I love when you do things like this, Biff. I never once said anything like that. But you like to drop those things in to insinuate you have made an insight I've missed. Sorry, I never said that.
Are you seriously saying that you think that by basing the levels of DHA in infant formula on levels found in human milk worldwide, that manufacturers are causing autims in some children? Is that your hypothesis? That since they don't know how much to match your mother's milk, they are causing harm? Seriously?
Sorry but this is your most absurd hypothesis yet. You are really grasping at straws here. Time to admit you're out of your element.
Really? I thought the difference between benefit and harm were calculated from dosage. So here we don't understand the proper dosage of DHA as a supplement and you have determined that there will not be any toxicity. Genius. I guess supplement dosage levels can't cause toxicity in this case. Make sure you notify all your colleagues. You have determined that LCPUFA supplementation is safe at any level.
"You know what accounts for variation in DHA levels in human milk? Diet. Does that mean we should expect children of women who eat a lot of fish and seafood to have higher rates of autism? That would be in keeping with your hypothesis."
Oh so fish oil DHA is the same as DHASCO? I thought excessive DHA would only be excreted? You seem to understand the differences between TAG DHA, Phospholipid DHA and esters of DHA. I guess DHA is DHA. Tell me more.
But you just said that the levels of DHA in the formula are similar to ones found in breast milk worldwide. So you receive roughly the same dose of DHA, whether you breast feed or eat formula. So are you saying that DHA levels in breast milk can cause problems? If so, then formula isn't the problem, DHA is.
First of all, I didn't say that DHA would be safe at any level. Again you put words in my mouth. But I also love your attempt at being flippant. Big words for the man who doesn't know the difference between a reducing agent and an oxidizing agent. I love the chutzpah.
The DHA molecule found in fish oils is the same DHA molecule found in DHASCO. DHA is DHA. It's a fatty acid that is the same no matter where it comes from. The difference in DHASCO is in the TAG structure, which DHA is a part of. Also TAGs with DHA and phospholipids with DHA are all esters of DHA. Ester just means the fatty acid is attached to a organic compound, which in both cases is glycerol. Again it appears you're struggling with simple chemical nomenclature.
Also you didn't answer the question: Will women who eat more fish be more likely to have autistic children, since their breast milk will have higher DHA levels?
"The DHA molecule found in fish oils is the same DHA molecule found in DHASCO. DHA is DHA. It's a fatty acid that is the same no matter where it comes from. The difference in DHASCO is in the TAG structure, which DHA is a part of. Also TAGs with DHA and phospholipids with DHA are all esters of DHA. Ester just means the fatty acid is attached to a organic compound, which in both cases is glycerol. Again it appears you're struggling with simple chemical nomenclature."
I understand that DHA is DHA. I was referring to how it may be incorporated differently. As in the case of TAG v egg phospholipid or human milk phospholipids.Does the head group of phospholipids play a role?
On a per-weight basis, the brain is the organ richest in lipids, including a remarkable proportion of polyunsaturated fatty acids (PUFAs) of the omega 3 series, namely eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. The cerebral effects of exogenous DHA likely depend on its degree of incorporation into neuronal phospholipids and on its distribution among the various brain structures, after intake. Hence, because PUFAs are not evenly distributed among the brain phospholipid classes and because the existence of class-specific phospholipases that regulate their turnover, we sought to investigate the incorporation of omega 3 PUFAs in selected brain areas regions and specific phospholipid classes. Rats (n=7) were administered, by oral gavage, 100mg/kg/d of a commercially available fish oil (containing ∼84% of long-chain omega 3 fatty acids, of which ∼38% of DHA and ∼46% of EPA). Control rats (n=7) received liquid paraffin. This treatment was continued for 30 days. Thereafter, we dissected three areas, namely the hippocampus, the striatum, and the cortex. Quantization of individual phospholipid classes and their molecular species was performed by ESI-MS/MS. Principal component analysis was used to examine the variation of the molecular lipid profiles (as percentage) induced by omega 3 supplementation. Our results show that provision of omega 3 fatty acids to rats results in their incorporation into brain phospholipids, the extent of which is lower in the striatum as compared with cortex and hippocampus. These data might in part explain the mixed therapeutic results obtained in neurological disorders, many of which are likely region-specific.
Dietary n-3 fatty acid supplements including DHA, α-linolenic acid and eicosapentaenoic acid are widely recommended for various populations, especially the infants, elderly, and patients with neurological and mental disorders [8–10]. The amount of DHA that is actually taken up by brain after ingesting various types of supplements, however, is not clearly established. Unlike other tissues, the brain uptake needs to overcome the blood-brain barrier (BBB), and the transport mechanisms involved for DHA uptake through this barrier are poorly understood.
Studies with whole animals as well as with in vitro systems showed that DHA and other long chain polyunsaturated fatty acids (PUFA) are transported across the BBB more efficiently when they are esterified to lysophosphatidylcholine (lysoPC), compared to free PUFA [11–13]. Interestingly, this was specific for the PUFA, because the saturated fatty acids were transported to the same extent whether they were in the free form or esterified to lysoPC [14]. However, the pathways by which the DHA-lysoPC is formed in plasma compartment are not fully understood. The long chain PUFA are exclusively in the sn-2 position of plasma phospholipids, and therefore the action of phospholipases A2 (PLA2) would not generate DHA-lysophospholipids. We have previously shown that plasma lecithin-cholesterol acyltransferase (LCAT), which is quantitatively the most important enzyme in the hydrolysis of plasma PC, alters its positional specificity in the presence of sn-2 DHA-PC species, resulting in the formation of the sn-2 DHA-lysoPC [15,16]. In addition, Brossard et al. [17], and Lemaitre-Delaunay et al. [18] reported that DHA ingested as triglycerides and phospholipids appear as lysoPC in plasma at higher specific activities than PC, suggesting the presence of pathways that secrete DHA-lysoPC from liver or other tissues. Direct hepatic secretion of unsaturated lysoPC has also been reported in rats [19].
An additional source of sn-2 DHA-lysoPC may be through the action of endothelial lipase (EL), which is expressed in several tissues, and is anchored at the endothelial surface. Recent investigations show that it has more phospholipase activity than lipase activity, but unlike the phospholipases, it specifically hydrolyzes the sn-1 acyl groups from diacyl phosphoglycerides [20]. Thus the PUFA, which are mostly present in the sn-2 position of phospholipids, end up in lysophospholipids rather than in free fatty acids. This enzyme therefore could provide an alternate mechanism by which the sn-2 DHA-lysoPC can be generated in plasma. Furthermore, EL has been shown to be expressed and secreted by brain endothelial cells [21] and astrocytes, the major components of the BBB, and therefore could be involved in the generation of DHA-containing lysophospholipids at the BBB.
Although EL has been shown to be relatively more specific for phospholipids than triglycerides, studies on its phospholipid specificity are limited. Duong et al. [22], employing reconstituted HDL composed of single species of PC, reported the preferential hydrolysis of PC containing DHA. Gauster et al. [20] reported that in addition to exhibiting PLA1 activity, EL hydrolyzed some 2-acyl lysoPC generated during the reaction, thus releasing both saturated and unsaturated fatty acids. They also showed that the enzyme did not hydrolyze fatty acids from sn-1 ether PC, confirming the positional specificity of the enzyme for sn-1 acyl ester. However, the specificity of the enzyme for the polar head group of phospholipids was not analyzed. Furthermore, there is no information on the relative specificity of the enzyme in the natural mixtures of PC species. In this study we first analyzed the head group specificity of the enzyme using deuterated phospholipids of identical fatty acid composition. In addition, we studied the fatty acid specificity of the enzyme using phospholipids from a natural source that is rich in DHA-lipids, namely the shark liver lipids. The results presented here show that EL preferentially hydrolyzes PE compared to other phospholipids, and it preferentially releases DHA-containing lysophospholipids from the natural mixture of phospholipid molecular species.
Biff, there were 1002 words in your last post. 87 of those words were mine that your quoted. 37 of those words were yours. And 878 words were from papers. So you contributed about 4% to that last post. The other 96% came from other people.
How is anyone supposed to take your ideas seriously when most of what you write in a post is other people's words? What anyone would take from your last post is that your are a person who doesn't actually understand the science being discussed. From that post, it looks like you can't take the ideas you get from papers, digest them, and then summarize them in your own words. Seriously, if you ever want to be taken seriously by a real scientist you need to start using your own words to explain your points.
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OK, but the DHA in infant formula is from DHASCO, a TAG. In fact, the second paper you cite is focused on understanding how much of the supplement DHA, like DHASCO, makes it into phospholipids in the brain:
They're concerned with how effectively the DHA supplement you digest becomes DHA in your brain cell membranes. From that paper, the problem doesn't appear to be that too much of that DHA goes to your brain, it's that the DHA must overcomes some significant hurdles to do so. You're worried about the DHA supplement leading to too much DHA, but this paper seems to suggest only a fraction of it does. Again, reading the entire paper, not just hunting for quotes will let you understand the full context of the study.
So, let's see you said formula with DHASCO may present infants with more DHA than they can handle. But then you point out that the DHA levels in formula are no different than DHA levels found in mother's milk worldwide. Then you show me a paper that talks about the barriers DHA in the diet must overcome to make it to the brain. So if DHA in DHASCO were incompatible with the enzymes that help get DHA into the brain, the resulting problem wouldn't be an excess of DHA in brain cells--as your hypothesis suggests--but a problem of too little DHA getting there.
Again nothing you have shown me suggests DHASCO is going to lead to an excess of DHA in infant brains. I know you want so badly to finger infant formula as the culprit behind autism. But you haven't made a convincing argument, and we've spent weeks discussing this. All I'm convinced of is that you have no idea what you're talking about.
I await your next post filled with text from papers you googled.
"Again nothing you have shown me suggests DHASCO is going to lead to an excess of DHA in infant brains."
I thought I was concerned with excessive accumulation and oxidation. Therefore, if DHASCO is not efficiently transported across the BBB and incorporated in to the brain, what happens to it? That's right, you said it would simply be excreted in feces. So the dietary TAGs of DHASCO that are not efficiently transported across the BBB and incorporated in to the brain will not oxidize in the digestive tract. If they were to oxidize, the breakdown components would not be able to cross the BBB as well. So I guess that oxidative stress could not begin in the digestive system. So I can rule DHASCO supplementation out in the cases of serious digestive issues reported to the FDA. Wherein, stools were reported to be extremely foul smelling and oily in appearance. Digestive issues that were reported to stop immediately after the infant was switched to a non supplemented formula.
I'm sure that this more than likely represents the natural digestion of DHA. Afterall, DHA is DHA. Just because there is evidence that supports that esterification position affects how it will cross the BBB and be incorporated in to the brain and how it may be more prone to oxidation, there is no reason for concern. I'm sure that there is nothing in the digestive tract that may initiate oxidation, and if there is, this oxidation would be controlled. So DHA hydroperoxides will not form in the digestive tract and cross the BBB.
"So if DHA in DHASCO were incompatible with the enzymes that help get DHA into the brain, the resulting problem wouldn't be an excess of DHA in brain cells--as your hypothesis suggests--but a problem of too little DHA getting there."
Ok, so what happens to the DHA that doesn't make it to the brain? Oh yeah, its pooped out.
Did you know that exogenous supply of DHA inhibits natural synthesis?
Relevant animal studies use a variety of study designs. The results show the need to consider ω-3/ω-6 ratios, species differences, and maturational development in interpreting the available data. The majority of studies show a negative effect on neurodevelopment and visual acuity with either supplementation of DHA and ARA or with DHA and ARA deficiency. Most studies (animal, human) have not evaluated long-term effects of supplementation. In long-term deficient monkeys (36 weeks) adverse effects seen with short-term deficiency are neutral with respect to long-term outcome. This suggests a lack of benefit and possible harm of excess supplementation.
Lifetime studies with excess supplementation in rats revealed long-term sensory–neural adverse effects (acceleration of age related hearing loss) as well as a 30% reduction in lifespan. Infant monkeys given excess supplementation had a neutral effect on visual acuity long term, whereas supplementation at repletion levels to correct an earlier deficiency state had a negative effect on visual acuity after short-term treatment (<4 weeks). None of the animal studies in this review regardless of DHA/ARA levels administered demonstrated a positive effect on neurologic or visual endpoints assessed. The animal studies reviewed were negative or neutral with regard to neurodevelopment and visual acuity outcomes across species (Table 2). This is despite studies demonstrating that tissue accrual of DHA/ARA in the brain and retina was increased by dietary supplementation. The ratio, timing, duration, and concentration of DHA given in conjunction with ARA are thought to influence functional outcome because it affects tissue specific membrane incorporation of these fatty acids. There are few studies that directly measure functional outcome relative to changes in physiologic pools of DHA/ARA after supplementation. Clinical studies that have shown benefits were more likely to measure electrophysiological outcomes, or use specific rather than global measures to assess cognitive development (Carlson, 2009a).
There are few studies that directly measure functional outcome relative to changes in physiologic pools of DHA/ARA after supplementation. Clinical studies that have shown benefits were more likely to measure electrophysiological outcomes, or use specific rather than global measures to assess cognitive development (Carlson, 2009a).
I would think that these studies would have been conducted since we have decided to increase levels via supplementation. Not only conducted, but revealing a positive effect. But as I have said before, sidestepping natural synthesis has serious safety concerns. But then again, I simply don't understand what I read.
Oh, Biff, sarcasm isn't going to make you more correct or insightful about biochemistry. It just makes you seem petty and mad. Not attractive.
OK maybe DHASCO leads to digestive problems. You'd have to show me more than anecdotal evidence to prove it, but it's possible. But we're not talking about digestive problems, are we? We're talking about autism. And if we're talking about autism, we need to link DHASCO to problems in the brain, not the digestive track. "But some autistic kids also have digestive problems," you say. True. But just because they have digestive problems doesn't mean the digestive problems caused the autism. It could be the cause of autism also caused the digestive problems.
Well you have shown me no evidence that DHASCO in fact leads to less DHA crossing the blood brain barrier. But even if it did, we already now the DHASCO's oxidative stability isn't different from milk TAGs--remember our lipids expert saying that? Even if it did lead to oxidized DHA, what evidence do you have that DHA-hydroperoxides can cross the blood-brain barrier. If DHA needs to be in a specific form to facilitate facile BBB crossing, then it seems unlikely that an oxidized molecule is just going to slip through without a struggle.
Now you're next to posts talk about a review, not an actual study again. Let's see what those authors conclude:
So I see a lot of no effect/we don't know in that conclusion. What I don't see is infants get too much DHA from formula and that leads to oxidative stress. Also there is a lot of talk in the review about excess DHA. But you told me that infant formula has DHA concentrations equal to those in breast milk worldwide. So they're not getting excess DHA with formula.
Look, Biff, why do you keep posting? It's obvious you're wrong and it's obvious you're miffed that I keep pointing out flaws in your arguments. This has gone past the comical stage and is now becoming sad. You're clearly obsessed about this topic--maybe your relative Mike Pescatore has convinced you that formula caused his son's autism. But, as a person who knows much more about biochemistry than you, may I suggest finding a more healthy past-time. You;re on the wrong track here.
Docosahexanoic acid (DHA) and arachidonic acid (ARA) are long chain essential fatty acids used as supplements in commercial infant formula. DHA/ARA deficient states are associated with adverse neurological outcomes in animals and humans. Preterm infants are at risk for DHA/ARA deficiency. A few clinical reports on the effects of fatty acid supplementation have shown benefit in preterm, low birth weight, and normal infants in the first year of life, whereas others did not. Studies in animals have reported shortened gestation, fetal growth retardation, reduced infant body mass, and increased fetal mortality with consumption of fatty acids during pregnancy. To understand the data that support fatty acid supplementation in infant formula, a review of the animal model literature was undertaken, to examine the effects of DHA/ARA on neurodevelopment, including the effects on visual acuity. Several points emerged from this review. (1) Animal studies indicate that requirements for DHA/ARA vary depending on developmental age. Alterations of the ratio of DHA/ARA can impact developmental outcome. (2) The available studies suggest that while supplementation of DHA/ARA in an appropriate ratio can increase tissue levels of these fatty acids in the brain and retina, tissues sensitive to depletion of fatty acids, the benefit of routine supplementation remains unclear. Few studies measure functional outcome relative to changes in physiologic pools of DHA/ARA after supplementation. (3) Animal literature does not support a clear long-term benefit of replenishing DHA/ARA tissue levels and administration of these fatty acids at concentrations above those in human milk suggests adverse effects on growth, survival, and neurodevelopment. Birth Defects Res (Part B) 92:240–250, 2011. © 2011 Wiley-Liss, Inc.
So in the the U.S what is the average DHA level found in human milk? What level is found in formulas?
"Also there is a lot of talk in the review about excess DHA. But you told me that infant formula has DHA concentrations equal to those in breast milk worldwide. So they're not getting excess DHA with formula."
So levels found in Asian women are not higher than found in American women? I see. I thought Asian women had substantially higher levels and women from the U.S. had among the lowest. So if we take an average of these levels, those on the lower end would by default would receive a larger increase in DHA after supplementation. Just common sense. Just not getting the whole average dosage v. natural synthesis thing are you?
I have already asked you what the optimal level of DHA should be for an infant. You couldn't answer because it hasn't been established. That's because it is different for every infant and natural synthesis is dynamically regulated. So where is your evidence that some infants will not receive excessive DHA after supplementation? We see evidence where this excess is excreted in feces. That would suggest the body is eliminating what it does not need, wouldn't it?
"Look, Biff, why do you keep posting? It's obvious you're wrong and it's obvious you're miffed that I keep pointing out flaws in your arguments. This has gone past the comical stage and is now becoming sad."
I have no issue with someone pointing out flaws. I don't think altering DHA levels in infants without understanding the potential danger is comical at all. But it is indeed sad.
"Look, Biff, why do you keep posting? It's obvious you're wrong and it's obvious you're miffed that I keep pointing out flaws in your arguments. This has gone past the comical stage and is now becoming sad."
Ok, show me where they have examined DHA hydroperoxides and determined that they can not cross the blood brain barrier if formed in the gut, as well as how they could not be transported to the brain. Then I'll say I'm wrong. Until then, who knows what's right or wrong.
You keep saying it's dynamically regulated. What does that mean to you? Don't cite a paper, pleas use your own words.
Sorry in science the onus is on you to show it does happen, not on me to show it doesn't. You think DHA-hydroperoxides make it to the brain and lead to damage. Then you need to show they can cross the blood-brain barrier. You again show you know nothing about science.
It's funny, if I invited you to my institution to give a symposium about your hypothesis, you would be laughed out of the lecture hall. People would tell you what I'm telling you: You don't know what you're talking about.
So keep your day job and leave the science to real scientists, Biff.
"You keep saying it's dynamically regulated. What does that mean to you? Don't cite a paper, pleas use your own words.'
The natural synthesis of DHA and ARA from elongation and desaturation of essential precursor fatty acids is well established. If you don't understand this, then perhaps you should google it. But since we are supplementing infant formulas with preformed DHA and ARA in an effort to normalize/increase levels, please explain what this desired target level should be.See, this is right up your alley. The difference between benefit and harm of any supplement is dosage.So what is the level that may result in toxicity?
"Sorry in science the onus is on you to show it does happen, not on me to show it doesn't. You think DHA-hydroperoxides make it to the brain and lead to damage. Then you need to show they can cross the blood-brain barrier. You again show you know nothing about science."
I know nothing about science because I haven't proved that excess DHA from dietary TAGs may oxidize in the digestive tract and form DHA hydroperoxides? I know even less about science because if this were to happen, I don't know whether or not these DHA hydroperoxides could cross the BBB and be incorporated in to a developing brain. This area of science is very complex. But since I don't understand everything like you do, I know nothing about what I am talking about.
"It's funny, if I invited you to my institution to give a symposium about your hypothesis, you would be laughed out of the lecture hall. People would tell you what I'm telling you: You don't know what you're talking about.
So keep your day job and leave the science to real scientists, Biff."
Oh, you own an institution? Would those same people laughing be able to describe what would happen to excess DHA found in an infant's digestive system? I suppose they would reach the same conclusion as you- It would be excreted in feces.
I'll be waiting for your answer regarding the levels of DHA that provide benefit/toxicity based on dosage. Maybe you can ask all the people in your institution.
I don't know what a beneficial level and a toxic level would be. But I'm not the one claiming that DHASCO in infant formula is causing neuorological damage leading to autism. You are, so you're the one who needs to have those data.
What I do know is that you told me that the DHA levels in infant formula match those found in human milk worldwide. If you're correct, then I would expect the formula levels to not be toxic, because they are levels found in normal people's milk. If you told me that infant formula had DHA levels 10x the worldwide average, then I'd be less sure they weren't toxic.
From a quick search of Mead Johnson formulas, it looks like their DHA concentrations are all right around 0.32% of total fats. The worldwide average for DHA concentrations in human milk is 0.32%: http://www.ajcn.org/content/85/6/1457.full.pdf. So are you telling me that the fact some women's breast milk is 0.17% DHA and they give their baby 0.32% in formula, they're putting the baby at risk? Do you have any evidence that such a small change has a large effect on neurological development? We're talking about a few mg of DHA here. Do you have any evidence that such small amounts can cause harm or disrupt redox controls in the body?
Also how does a mother's body know what the right amount of DHA is for her baby? What if she just changed her diet to one with lots of fish? Is there a way for a woman's milk glands to know what the beneficial and toxic levels are for her baby?
I didn't ask what it meant, as in I don't know what that means, can you explain it to me? I asked what it meant to you. Basically I wanted you to explain it to me in your own words. Why? Because I've noticed you make two kinds of posts. One type, like your last post, is mainly in your own words. You ask sarcastic questions using scientific terms in a way that implies you know something the other person doesn't. In the other type of post, you respond to my questions by posting paragraphs cut and pasted from scientific papers. So the only time you really explain any science is through other people's words. I'd like to see you do it without cutting and pasting others words. See I don't think you can do it, because I don't think you actually understand most of the science you talk about. That's why I asked you what the concept of dynamic regulation of DHA levels in human milk meant to you--to see if you could answer in your own words.
But you have refused, so I guess I was right: You don't really know what you're talking about. You just parrot what you read in scientific papers. That's OK. I started to assume you weren't very knowledgeable about these topics the minute you offered ferrous sulfate as an oxidant.
Did I say I owned one? No. I referred to my institution, as in my university or my company--the one I work at. You love to put words in other people's mouths, Biff. I guess it's only fair, since most of the words in your posts are other people's written words.
"I don't know what a beneficial level and a toxic level would be. But I'm not the one claiming that DHASCO in infant formula is causing neuorological damage leading to autism. You are, so you're the one who needs to have those data."
I know you don't. I am the one claiming that not understanding the difference between benefit/toxicity in regards to levels of supplementation may cause numerous health issues.
"What I do know is that you told me that the DHA levels in infant formula match those found in human milk worldwide. If you're correct, then I would expect the formula levels to not be toxic, because they are levels found in normal people's milk. If you told me that infant formula had DHA levels 10x the worldwide average, then I'd be less sure they weren't toxic."
Levels in formula? There is a specific level used in each formula. How can one specific level match all levels found worldwide? They can't match. Levels of DHA vary significantly among women worldwide. These levels change during periods of lactation, tapering off towards the end. Vary from feeding to feeding. So right away, the levels supplemented are almost 2x higher in U.S. formulas if we use the average of .32% vs. .17%. Of course some mothers may have higher levels, and some may be lower. So if a mother had a level of .10% and her infant was given .32% as a supplement, that infant would receive @ 3X the level that would be found in mother's milk. If mother's DHA levels naturally tapered off substantially over the lactation period, supplementation at .32% could be many times higher than what would be naturally transferred from milk. So it isn't quite as simple as you suggest. Therefore the importance of understanding benefit/toxicity in regards to dosage. You would also have to account for the gender difference in natural synthesis, where females are known to have a higher efficiency to convert ALA to EPA to DHA.
"Also how does a mother's body know what the right amount of DHA is for her baby? What if she just changed her diet to one with lots of fish? Is there a way for a woman's milk glands to know what the beneficial and toxic levels are for her baby?"
I don't know how mother's milk would adjust to such a dietary change. I would expect DHA levels to increase dramatically. I would also expect increased levels of EPA. I wouldn't advise such a dietary change. There is also mercury in fish. I thought that a pregnant mother should limit servings of fish due to mercury, but I could be wrong.
"You ask sarcastic questions using scientific terms in a way that implies you know something the other person doesn't."
I asked how structural changes to TAGs of DHA may compromise its oxidative stability, be digested and absorbed differently and may dysregulate natural synthesis. Nothing sarcastic about that. Since excessive oxidation of DHA has been shown to be implicated in numerous health issues, as well as neurological disease, I feel the dietary sources of supplementation should heed some caution. I try to support the safety issues that I raise by posting peer-reviewed publications relevant to what I suggest. This bothers you, so in return you say I don't know anything about what I am talking about. At least I got you to admit that you can't determine what level of DHA supplementation will provide benefit or harm.
I wonder what would happen if we supplemented insulin in formulas based on an average level found worldwide. Supplemented without understanding which infant would benefit and which would be harmed. Disregarded natural insulin regulation and used a one size fits all dosage.
Well, of course you don't either. And that's my point. Look, there is a difference between pointing out people don't have a good grasp on what DHA levels are beneficial and which are harmful, and saying the levels in formula now cause harm. I readily admit that I have no idea what level of DHA consumption could lead to harm--I'm not a lipids expert.
But I find it highly unlikely that the harmful level for a child would lie within the range of normal DHA levels found in breast milk worldwide. That would mean that either 1) some mothers' bodies will unintentionally feed their babies harmful levels of the nutrient or 2) the range of safe DHA levels for each child is quite narrow and somehow mothers' bodies can titrate DHA levels in their milk accordingly.
Option #1 seems highly unlikely for evolutionary reasons. If high levels of DHA can cause neurodevelopmental problems, as you say, then there would be intense selective pressure to regulate how much DHA gets into mothers' milk. So you'd expect the ranges of DHA found in mothers' milk worldwide would be within the reasonable range for normal development, and thus the high end of DHA levels in mother's milk worldwide wouldn't be harmful to developing brains.
Option #2 also seems quite implausible, especially given that we know that diet has such a significant influence on DHA levels. If the window for every child was unique and narrow, then why would the milk production system evolve to allow diet to have such a sway on DHA levels? Wouldn't it make sense that if the range of acceptable DHA levels was small and small variations outside that range could lead to significant neurological harm, that the milk gland cells would tightly regulate how fats from the diet got into the milk?
So for those reasons, I find it extremely unlikely that the range of DHA levels found in breast milk worldwide would be harmful to infants. I can't say for sure that is universally true, but you have shown me no evidence to make me think that it isn't true in the vast majority of cases.
You only have to worry about some fish RE mercury levels. Also do pregnant women breast feed their fetuses?
You did earlier, yes. And I showed you evidence from a lipids expert that 1) DHASCO is remarkably stable to oxidation and 2) is metabolized like "natural" DHA TAGs in rat studies.
You know very well that you employ heavy doses of sarcasm in your posts--I do too sometimes.
No what I am criticizing is that you just dump paragraphs of text from other papers without explaining how it pertains to your argument or which particular facts argue in your favor. Basically, you just regurgitate text without processing it in any way that indicates you understand the text you pasted.
I say you don't know what you're talking about for many reasons: you don't the difference between a reducing agent and an oxidation agent, you only explain the science behind your argument using cut and paste paragraphs from papers, when asked to explain a scientific concept in your own words, you refuse. It is quite clear you are just a parrot who reads papers online and then spits out that text without really understanding it. If you truly understand what you're talking about, why can't you explain, in your own words, what you mean by dynamic regulation of DHA levels in mother's milk?
When I teach undergrads, I don't let them just cut and paste text from papers or their text book on exams. They have to use their own words to show they understand the material. It seems you don't and you won't indulge me to prove otherwise. So I'll continue to assume you're just a scientific parrot.
No one would advocate putting insulin in formulas for many reasons, one of which is that digesting insulin won't get it into your blood stream. Also insulin isn't a nutrient, like DHA, it's a regulatory protein, so it makes no sense to supplement a regulatory protein unless someone has a pathological deficit of it--such as in diabetes.
The very fact that you have brought up insulin multiple times to make your DHA argument again shows a true lack of understanding of biochemistry. You're just embarrassing yourself in this argument. (BTW I'm forwarding our posts to some colleagues and they're getting a big kick out of it. Thanks for the entertainment.)
"No one would advocate putting insulin in formulas for many reasons, one of which is that digesting insulin won't get it into your blood stream. Also insulin isn't a nutrient, like DHA, it's a regulatory protein, so it makes no sense to supplement a regulatory protein unless someone has a pathological deficit of it--such as in diabetes."
I was making an analogy towards how insulin levels also vary among individuals and there isn't an average measurement that could be used to determine how much was safe for every person whom was diabetic. I guess that's why they constantly measure their blood/sugar levels. BTW, DHA formula has been shown to adversely affect insulin sensitivity in female children. Is that funny as well?
". (BTW I'm forwarding our posts to some colleagues and they're getting a big kick out of it. Thanks for the entertainment.)"
I'm glad you find this amusing. Wouldn't it be hysterical if science reveals that excessive DHA TAGs that were not digested and absorbed did in fact oxidize in the digestive system and caused inflammation and tissue destruction. What if these DHA hydroperoxides were able to cross the BBB and be incorporated in to a developing brain? Would that be funny as well? Really?
You understand more than I do about biochemistry. If the above situations could happen, and at this point you don't know for sure, how is that funny? Now you're just being arrogant.
Diabetics don't test their blood sugar because everyone has naturally different insulin levels. They test so they can see how what they ate, what meds they took, etc affect their blood sugar levels. The point being that they want to avoid too high/too low blood sugar levels. Their bodies can't properly regulate their levels, so they test their blood sugar to see how the things they do change those levels. Basically, they're acting as their own blood sugar regulation system, since their biological one is out of whack.
So your insulin analogy makes no sense in this case. You're trying to compare levels of a regulatory protein in people with a disease to levels of nutrient in the average person. Apples and oranges. Again showing a true lack of understanding in some fundamental concepts here.
I guess I am being a little arrogant. But you have to understand that you are amusing from my perspective. You keep posting, trying to wiggle away from the onslaught of clear evidence that your hypothesis has no real basis to stand on.
A normal person would listen to someone with more experience and knowledge and realize that they're hypothesis needs a serious overhaul, if not scrapped all together. But you seem unphased, as if you didn't care what the reality of the situation was and that you only cared about showing the world DHA in infant formula is harmful.
Now yes I don't know for sure that DHASCO isn't causing neurological harm in infants. But just because I don't know something for sure, doesn't mean the alternative is plausible. Go look through the annals of science and medicine and you'll find thousands of hypotheses that posited X caused Y, but the linkage was never proven or some other variable was found to cause Y. Those X->Y hypothesis makers could have easily said what you said: "You don't know for sure that X doesn't cause Y." But it turned out they were wrong.
That's why in science, before anyone takes you and your hypothesis seriously, you need to pony up some evidence. You clearly haven't done that. So I wouldn't hold your breathe for scientists to take you seriously.
Finally, I guess I'm being arrogant because I see you and your "relative" Mike Pescatore do it on here time and time again. You even did it earlier in this thread to 2014MD. You did your word salad of scientific terms and used a flippant tone to imply he didn't get the deep insight you'd made about the topic. That made me want to find out how much you really knew. I've found out you don't know much at all, so I guess I'm being a bit arrogant to give you a little taste of your medicine back.
Not fun, huh? So maybe you should treat people with respect, especially when you really don't have a clue of what you're talking about.
Relevant animal studies use a variety of study designs. The results show the need to consider ω-3/ω-6 ratios, species differences, and maturational development in interpreting the available data. The majority of studies show a negative effect on neurodevelopment and visual acuity with either supplementation of DHA and ARA or with DHA and ARA deficiency. Most studies (animal, human) have not evaluated long-term effects of supplementation. In long-term deficient monkeys (36 weeks) adverse effects seen with short-term deficiency are neutral with respect to long-term outcome. This suggests a lack of benefit and possible harm of excess supplementation.
Lifetime studies with excess supplementation in rats revealed long-term sensory–neural adverse effects (acceleration of age related hearing loss) as well as a 30% reduction in lifespan. Infant monkeys given excess supplementation had a neutral effect on visual acuity long term, whereas supplementation at repletion levels to correct an earlier deficiency state had a negative effect on visual acuity after short-term treatment (<4 weeks). None of the animal studies in this review regardless of DHA/ARA levels administered demonstrated a positive effect on neurologic or visual endpoints assessed. The animal studies reviewed were negative or neutral with regard to neurodevelopment and visual acuity outcomes across species (Table 2). This is despite studies demonstrating that tissue accrual of DHA/ARA in the brain and retina was increased by dietary supplementation. The ratio, timing, duration, and concentration of DHA given in conjunction with ARA are thought to influence functional outcome because it affects tissue specific membrane incorporation of these fatty acids. There are few studies that directly measure functional outcome relative to changes in physiologic pools of DHA/ARA after supplementation. Clinical studies that have shown benefits were more likely to measure electrophysiological outcomes, or use specific rather than global measures to assess cognitive development (Carlson, 2009a).
I'm sure you have all the missing information as to how DHA and ARA supplementation will affect infant development. As you can see, there is an absence of available studies measuring long term effects. Tens years of formula supplementation, and an absence of studies examining long term effects. These supplements were added to correct/normalize deficient levels and improve brain and eye development. It appears that long term effects do not result from supplementation...well at least beneficial effects can not be substantiated. It also appears that adverse effects have been reported.
You're right, this is funny. It is a joke. There is nothing more entertaining than altering an infant's levels of LCPUFAs without understanding long term effects. Hillarious.
We're not talking about excess supplementation. We already discussed that. We're talking about DHA levels found in normal levels of mother's milk. Here is what that paper says about that:
OK back to my main point: Just because you have questions, doesn't mean something bad is actually happening. All it means is that people need to study the issue more.
The absence of data doesn't mean DHA in infant formula is bad.
And what is funny about this isn't the science, it's you. You don't stop even though it's clear you have no idea what you're talking about. You keep cutting and pasting the same text from the same papers and have yet to make a single argument in your own words. You need to start to show me that you actually understand this material and can form your own arguments. Until then, I find this whole continuing discussion to be comical. I don't see what's in it for you. You keep pushing the door marked pull.
"We're not talking about excess supplementation. We already discussed that. We're talking about DHA levels found in normal levels of mother's milk."
Define normal levels of mother's milk. I thought these levels varied during the course of lactation. I thought these levels varied from one mother to another. So from what you are saying, it doesn't matter when these levels were measured, or what the change over the course of lactation represents as a natural way of regulating these levels.
So if we found higher levels during the first month of lactation, and we established an average level among women worldwide, that would be the ideal level of supplementation. If we continued to supplement at this desired level through periods when this level would naturally decline ( later months of lactation), this increase in DHA levels (levels above what would normally be supplied from human milk) would not result in excessive levels?
Let me put it another way, because I don't think you are really understanding what "normal" levels represent. If a mother naturally had low levels of DHA (low in comparison to the ideal supplemented levels established by taking an average of women worldwide and not accounting for variation during lactation), her infant would receive DHA levels above what would be naturally supplied from her milk. This important because human milk from this mother is a biological match for her infant. As this is true, the infant is then unnaturally receiving more DHA from formula supplementation. You could argue that is safe if you could determine the difference between benefit/harm of increased levels. So far, there has been little or no benefit established for supplementation.
As a scientist, you should understand the danger of supplementation in regards to dosage. Are you seriously suggesting that DHA supplementation does not apply in this case? What I think you are saying is that supplying a fixed dosage that is based on an average level ( a level that naturally changes during the optimal source of nutrition) will not have adverse effects on some infants. The infants whom may receive DHA levels above what would be naturally supplied in milk would only be ensured that a deficiency would not result. If the body was supplied with higher amounts that were not needed, this DHA would not oxidize before being excreted in feces.
I know this is comical to you. I don't think supplementation of DHA has proven to be beneficial towards infant development. If anything, we are experiencing an increase in children with neurological issues. We understand a great deal more about the cellular effects of DHA. Substantially more than we did before we decided to increase levels via formula supplementation. But we are far from understanding everything about these effects. To me, this should suggest that caution should be taken when we decide to increase DHA levels during critical stages of development. To you, this is amusing and a joke.
You should find some humility and lose some of your arrogance. There may come a day when science reveals that increased levels of DHA via supplementation are problematic for some infants. There may come a day when we reveal that excessive DHA oxidation results in digestive inflammation and creates neurotoxic by products that may cross the BBB and create neurological issues. So I guess until that day comes I'll continue to push the door marked pull and be mocked by real scientists that find unknown effects of infant formula supplements comical.
"Chronic ingestion of diets enriched in SFA commonly causes vascular dysfunction, including in capillary vessels of the brain. The effects of SFA could be described as a response-to-injury phenomenon induced by exaggerated exposure to plasma triglyceride, cholesterol, NEFA, or harmful inflammatory products of lipid metabolism, such as lipid peroxides. Many studies support a role of n3 and n6 fatty acids in the prevention of vascular, based disorders primarily via suppression of inflammatory cascades. Less clear however are the benefits of polyunsaturated oils in the presence of profound inflammation, because of the propensity to generate lipid peroxidation products. In an established model of cerebrovascular dysfunction induced by chronic ingestion of an SFA-enriched diet, provision of DHA amplified the harmful effects. Probable mechanisms include hypercholesterolemia and perhaps fatty acid-induced cytotoxicity. The data suggests that introduction of n3/n6 fatty acids in metabolic conditions that are characterized by heightened systemic inflammation needs to be carefully considered in the context of paradoxical detrimental effects that could occur."
Is there anything in infant formulas that could cause intestinal inflammation? Carrageenan perhaps? Let's see-
"Multiple studies in animal models have shown that the commonly used food additive carrageenan (CGN) induces inflammation and intestinal neoplasia. We performed the first studies to determine the effects of CGN exposure on human intestinal epithelial cells (IEC) in tissue culture and tested the effect of very low concentrations (1–10 mg/L) of undegraded, high-molecular weight CGN. These concentrations of CGN are less than the anticipated exposure of the human colon to CGN from the average Western diet. In the human colonic epithelial cell line NCM460 and in primary human colonic epithelial cells that were exposed to CGN for 1–8 d, we found increased cell death, reduced cell proliferation, and cell cycle arrest compared with unexposed control cells. After 6–8 d of CGN exposure, the percentage of cells reentering G0-G1 significantly decreased and the percentages of cells in S and G2-M phases significantly increased. Increases in activated p53, p21, and p15 followed CGN exposure, consistent with CGN-induced cell cycle arrest. Additional data, including DNA ladder, poly ADP ribose polymerase Western blot, nuclear DNA staining, and activities of caspases 3 and 7, indicated no evidence of increased apoptosis following CGN exposure and were consistent with CGN-induced necrotic cell death. These data document for the first time, to our knowledge, marked adverse effects of low concentrations of CGN on survival of normal human IEC and suggest that CGN exposure may have a role in development of human intestinal pathology."
So if carrageenan were to cause intestinal inflammation, would DHA supplementation amplify this inflammation?
I know how much you enjoy cutting and pasting. I also know how little I actually understand. So tell me if carrageenan and DHA will cause increased intestinal inflammation in infants as a result of formula feeding.I asked you before if any other formula ingredients could react with DHA and cause adverse effects. You didn't know, so I'll ask again. Is it possible for some infants to experience carrageenan induced intestinal inflammation that is amplified by DHA supplementation?
Is that comical question? Wouldn't it be hysterical if an infant were to die from NEC because of these two infant formula ingredients? Time for a condescending and arrogant response on your behalf. Share this joke with your colleagues, maybe they'll find it entertaining as well.
Oh yeah, there are hundreds of reports of infants whom have suffered from serious digestive issues when fed DHA/ARA supplemented formulas. Digestive issues that were miraculously resolved when weaned to a non supplemented formula. By non supplemented, I mean the same formula brand without the DHA/ARA. Isn't that funny? How funny would it be if you had a child that had experienced this? You're right, not understanding how formula ingredients may react and cause serious harm or death is funny.
Do you have any scientific evidence that the level of DHA in a mother's milk is matched to her infant's needs/metabolism?
I do not deny that when formula makers produce formula with 0.32% DHA to match the worldwide average, that some babies are getting more DHA than their mother's milk would give them. Won't get any debate from me on that point. In fact, a quick scan of U.S. averages (http://www.ajcn.org/content/85/6/1457.full.pdf) shows that mothers in the U.S. have about 0.2% DHA in their milk, below the worldwide average.
But my point is and has always been that I seriously doubt that getting 0.32% DHA when your mother would give you 0.2% DHA leads to any harm. Why? Because it doesn't make any evolutionary sense.
You are proposing that DHA levels in mother's milk are controlled to match her infant--so there is a tight window of DHA levels before you start hitting concentrations that do harm.
I think that is a ridiculous idea, solely based on the fact that we know diet is a huge contributor to DHA levels in mother's milk. (It's the whole reason why Japanese mother's milk has DHA levels around 1% and U.S. mothers have it around 0.2%. U.S. moms eat way less fish than Japanese moms.) Why would the milk production system evolve to allow diet to have such a sway on DHA levels, when the window for safe DHA levels is so small?
Imagine for a second a distant past and there are two groups of women: those whose bodies tightly regulate the amount of DHA that goes into their milk and those whose bodies are more laissez-faire. The first group of women pump out milk with a small, consistent range of DHA levels. The DHA levels in the other group's milk can fluctuate, particularly when their diet changes. A string of fish dinners leads to higher levels of DHA.
Now if you're correct that DHA levels must be matched for every baby and that small increases can lead to significant neurological damage, then what happens to the fitness of those two group's offspring? Obviously the first group's offspring will be significantly more fit than those of the second group. So over time, you should see the genes that lead to tight regulation of DHA levels predominate in the population. But today, we don't see that. We see DHA levels strongly dependent on diet. Therefore, I think your hypothesis that slightly higher DHA levels than usual leads to significant harm doesn't seem to fit what we see around us.
Does that make sense to you? Do you understand what I am saying? Yes or no. Please respond directly to this argument.
But you have zero evidence linking childhood neurological issues to infant formula DHA levels. So to suggest to others there is a link is not scientific, it's fear-mongering.
Once again, I did not say the science or this issue is a joke. I said that I find your persistent disregard for basic facts and simple logic are comical. You consistently try to put words in my mouth. That is an annoying rhetorical tick on your part.
As for finding humility and dropping the arrogance, I believe you may want to take some of your own advice. You are clearly not a trained scientist. And you clearly do not understand most of the scientific concepts you write about. But when you encounter people who do have such training and do understand those concepts, you ignore them or treat them with flippant dismissal. You seem to think you have made some grand insight into this topic and that people who are experts are blind to your insights. That sounds pretty arrogant, if not a tad delusional.
Totally possible. But nothing you have said to me in the past few weeks suggests that will happen. So I'm not worried about DHA levels in infant formula. And it is fear-mongering on your part to tell parents to worry about it.
I thought I would add that carrageenan has a Citizen's Petition filed at the FDA due to causation of intestinal cell damage. This petition remains unresolved since it was filed in 2008. It appears that carrageenan safety concerns have alluded scientists such as yourself and are deemed acceptable as formula ingredients. In fact, there is a label for this level of safety. It's called Generally Regarded As Safe. I know two other formula ingredients that share this level of safety-DHASCO and ARASCO. I wonder if a petition were filed again them, how long it would remain unresolved.
So there we have it. A non scientist such as myself can show genuine safety concerns based on available information found on the internet. How does it feel to realize that a non scientist can ask you a specific question that you can not answer? I'll ask again-
Can carrageenan ingestion and digestion cause inflammation in an infant's digestive system? Could this inflammation be amplified be dietary supplementation of LCPUFAs? Could this result in formation of neurotoxins that could cross the BBB and result in neurological injury?
There are two possible responses from you.
1. Based upon the information available, yes it is possible and we don't know yet.
2. It is not possible because neither carrageenan can cause intestinal inflammation, nor could DHA amplify this condition.
Which one is it professor, and why? You're right. This is becoming comical.
Where to start, Biff? Where to start?
Let's start with your latest post.
1) There are many questions I can't answer. Possibly more than I can answer. That doesn't bother me. The unknown doesn't bother me. I want to know those answers, but I also realize that questions don't always get answered.
2) Also who cares if you can ask a question I can't answer? Unless you have the answer--which in this case, you obviously don't--why do I care? Why should anyone care? I can raise questions without answers too. But people only care when the questions have a basis in reality. From what you've shared with me, your questions don't.
Here's an example of a good question without an answer: Do nanoparticles in consumer products cause any long-term health issues? No one knows the answer to that one yet. But it's a good question because we know these particles have unique chemical properties that could cause trouble in living systems. They could be completely safe, in the end. But it's worth asking that question, because of what we know about nanoparticles.
Your questions aren't that valuable, because based on what you have shown me, there is no smoking gun that says "hey something about this DHASCO and its concentrations could cause trouble."
OK now carrageenan.
You cut and pasted from two papers: one that showed diets with high levels of DHA could exacerbate BRAIN inflammation; and the other connected carrageenan may promote inflammation in the INTESTINES.
Well first off, I've set up my first point: We're talking about two different systems of cells. Look, I don't doubt carrageenan could cause intestinal inflammation in some infants--it's a complex polysaccharide and those molecules can wreak havoc on intestinal cells, especially in people with pre-existing sensitivities. But to then say that inflammation in the intestines will lead to inflammation in the brain is a stretch, or to then say that the same mechanism in which DHA exacerbates brain inflammation will happen in the intestines is a stretch. To make that leap, you will need to show some actual scientific evidence. Until, then I see no reason to think either happens.
Also look at the DHA paper. Look at the amount of DHA in the mice's diet. The fat composition of the DHA-enriched diet was 8.22% DHA. And they were comparing those mice to animals that had no DHA in their diet. What you're talking about in terms of humans and milk formula is DHA at 0.32% of total milk fat. So we're talking about diets uber-enriched with DHA. Not really an apples and orange comparison, now is that?
So to summarize: Yes carrageenan could cause intestinal inflammation in children. But the papers you showed me do not lead me to conclude that DHA in infant formula would exacerbate that, because 1) you showed me no evidence of DHA and intestinal cells and 2) the levels of DHA in the study you showed me were incredibly high, greater than what we're talking about in formula.
Also to take it a step further, to then say that DHA-exacerbated inflammation in the intestines would then lead to inflammation and the oxidative stress in the brain is another giant leap. You still haven't shown me one piece of evidence that these inflammed intestines would excrete lipid hydroperoxides or that those lipid hydroperoxides could then cross the blood-brain barrier and start inflammation int he brain.
So once again, I must conclude that your hypothesis is on seriously shaky ground. Only one piece of it--that carrageenan causes intenstinal inflammation--seems legit to me.
Finally, once again, I'm not calling the science or infants with intestinal inflammation funny. I'm saying you and your quixotic postings are comical.
"1) There are many questions I can't answer. Possibly more than I can answer. That doesn't bother me. The unknown doesn't bother me. I want to know those answers, but I also realize that questions don't always get answered."
It really bothers me that these answers are not known. That's because if the answers prove to show serious harm, think of how many infants were put at risk.
"2) Also who cares if you can ask a question I can't answer? Unless you have the answer--which in this case, you obviously don't--why do I care? Why should anyone care? I can raise questions without answers too. But people only care when the questions have a basis in reality. From what you've shared with me, your questions don't."
So carrageenan induced intestinal inflammation doesn't have a basis in reality towards the safety of infants? I'm not sure that I agree with you on that statement.
And how this inflammation may be amplified due to DHA supplementation is also irrelevant towards the safety of infants? You're kidding right?
So before I brought this info to your attention, you never questioned the safety of infant formula ingredients, right? So I show that formulas contain an ingredient known to cause inflammation. I take it a step further to show how this inflammation may be amplified by DHA. I suggest that this may create neurotoxic by products capable of crossing the BBB and you basically say-"you don't know that, and you can't prove it.
I heard of this brain/gut theory in regards to autism. Maybe this falls in line with that nonsense. I mean really, when did diet ever adversely impact health?
True if the answers are as bad as you think they are, then that's terrible. But, again, and I can't stress this point enough: Nothing you have shown me in weeks--actually a full month--suggests the answers is that bad. I go back to the nanoparticles question. There are plenty of preliminary studies on nanoparticles to make me think there could be something toxic we should be worried about with them. But that isn't the case here. You haven't convinced me in anyway that something similar is happening with DHA in infant formula. Do you get that distinction? You keep pointing to unanswered questions and expect us to be horrified. Nothing you have told me suggests I should be horrified.
Woah, woah, Biff. Again you have put words in my mouth. Please stop doing that. It makes you look like a rhetorical weasel. When I said your questions don't have basis in reality, I was referring to the ones about DHA levels--the topic we'd been discussing for weeks until you suddenly jerked the steering wheel and started bring up carrageenan. In my last post, I admitted, not begrudgingly either, that carrageenan may cause intenstinal inflammation issues. My problem was you connecting it to DHA and then brain damage. I think those connections are baseless and unsupported by any science you've shown me.
I addressed the DHA-carrageenan connection in my last post. You have chosen not to respond to my arguments--as you usually do. Let me summarize my points again, and maybe this time you'll be able to muster some sort of retort:
Actually you almost never address my points head on: In the last couple days, I've made several arguments refuting your position that DHA levels would be too high for infants, that DHA exacerbates carrageenan inflammation and in turn causes brain damage, and in none of those cases you chose to pick apart my argument. Why not? In a normal debate, someone would find a hole in my argument. Instead you just keep asking your sarcastic questions or you bring up another topic. It seems to me that you're incapable of refuting my arguments and so you ignore them. That is what makes you so comical. It's almost as if convincing me I'm wrong isn't your goal. It's more that you just like to hear yourself squack.
If you want to continue this discussion with me, explain to me how my counterargument above (my respose to your claim that DHA could exacerbate carrageenan inflammation in the intestines leading to brain damage) is flawed. If you don't, then I'll assume you don't actually want to debate and just want to hear yourself talk and I'll end this discussion.
To be clear, that's not what I said. I said that you couldn't say DHA would amplify carrageenan-induced inflammation in the intestines by pointing to a paper looking at the brain. And I said that the levels of DHA that that paper looked at were significantly higher than those you get in infant formula--or breast milk for that matter!
I then pointed out that even if you could point to a paper that said infant formula levels of DHA could amplify carrageenan inflammation, you still can't connect it to the brain. You have no evidence that lipid hydroperoxides or other inflammatory molecules would build up and then travel to the brain, where they would cause neurological damage.
That is what I said. Once again you have put words in my mouth after I have completely destroyed your argument. You are starting to get on my nerves with your childish debating tactics.
Now either respond to my actual argument in your next post or I'm finished with you.
"Actually you almost never address my points head on: In the last couple days, I've made several arguments refuting your position that DHA levels would be too high for infants"
We went over this many times. I did address this. I asked you what the optimal level of DHA would provide benefit and not result in harm. You didn't know.I asked if DHA could react with other ingredients in formula. You didn't know. I asked if DHA did oxidize in the digestive system and create by products such as DHA hydroperoxides, could they cross the BBB and cause neurological damage. You didn't know.
"You have no evidence that lipid hydroperoxides or other inflammatory molecules would build up and then travel to the brain, where they would cause neurological damage."
That's right, lipid hydroperoxides can cause neurological damage. DHA is very vulnerable towards formation of lipid hydroperoxides, isn't it? I know it's a stupid question, but I'll ask again. Can DHA oxidize in the digestive system and form DHA hydroperoxides? Can these DHA hydroperoxides cross the BBB and cause neurological damage?
I showed you were it has been suggested that if ongoing inflammation was occuring, DHA has been shown to amplify it. Then I suggest that if carrageenan were to promote inflammation in the digestive system, DHA supplementation may amplify it.
"I then pointed out that even if you could point to a paper that said infant formula levels of DHA could amplify carrageenan inflammation, you still can't connect it to the brain."
What level of DHA is required to oxidize? Are you suggesting that the levels in formulas will not oxidize? Are you suggesting that all infants have the same levels of antioxidant protection. You seem to be an expert on the proper DHA levels that will provide benefit and not result in excessive oxidation in the digestive system. What is that level? That's right, you don't know.
"And I said that the levels of DHA that that paper looked at were significantly higher than those you get in infant formula--or breast milk for that matter!"
True, the levels were higher. So what level of DHA will amplify inflammation, and what level will be anti-inflammatory. Again, are you suggesting that low levels of DHA will not oxidize? If they did, they would only result in anti-inflammatory effects?
While we are on the topic of proper DHA levels, you do understand that prenatal DHA supplements are widely used today, right? I wonder what impact they have on desired levels. Wouldn't an infant have higher levels if mom took these supplements prenatally? I'm just trying to get my head around the proper dosage that will provide benefit. What is that level?
Chronic ingestion of diets enriched in SFA commonly causes vascular dysfunction, including in capillary vessels of the brain. The effects of SFA could be described as a response-to-injury phenomenon induced by exaggerated exposure to plasma triglyceride, cholesterol, NEFA, or harmful inflammatory products of lipid metabolism, such as lipid peroxides. Many studies support a role of n3 and n6 fatty acids in the prevention of vascular, based disorders primarily via suppression of inflammatory cascades. Less clear however are the benefits of polyunsaturated oils in the presence of profound inflammation, because of the propensity to generate lipid peroxidation products.
In an established model of cerebrovascular dysfunction induced by chronic ingestion of an SFA-enriched diet, provision of DHA amplified the harmful effects. Probable mechanisms include hypercholesterolemia and perhaps fatty acid-induced cytotoxicity. The data suggests that introduction of n3/n6 fatty acids in metabolic conditions that are characterized by heightened systemic inflammation needs to be carefully considered in the context of paradoxical detrimental effects that could occur.
So if autism is in fact a condition resulting from neuroinflammation and digestive inflammation (brain gut theory), this publication suggests that DHA and ARA could paradoxically result in worsening this systemic inflammation.
What levels of DHA and ARA are safe if systemic inflammation was occurring in an infant? What level in the digestive system? What level incorporated in to the brain?
Let me guess, you don't know.
Biff, thanks for responding to my arguments directly. But, unfortunately, you continually miss my main point.
Yes I don't know what a toxic level of DHA would be. And I don't know if lipid hydroperoxides can cross the blood-brain barrier and accumulate in brain tissue.
But guess what? Neither do you. And that is my whole point. You seem to think that if you can come up with a question that others can't answer then you have supported your argument. That can't be further from the truth.
A question without an answer--or even a hint of answer--isn't support for your hypothesis. It just means we have a gap in our knowledge. And you don't get to fill in knowledge gaps with whatever you want. This is what creationists do:
Creationist: How did life start on Earth?
Scientist: I don't know for sure.
Creationist: Then God started it.
A question mark doesn't support one side or the other. So you have done nothing to further your cause by coming up with questions that have no answers. You can only support your hypothesis with answers. Currently, you have zero answers and so your hypothesis has zero support.
Do you understand that simple point? You have not provided any support for your DHA supplement hypothesis in these past weeks. All you have done is ask questions without answers. If you went to the NIH and asked for money to study your hypothesis, know what they'd say? "Come back to us when you start to answer some of your questions."
Now when confronted with questions that have no answers, scientists sometimes attack the situation by trying to rule out answers. You may not be able to find the exact answer, but you can start to figure out what isn't the answer.
I have done that with some of your questions, most notably the question of what is a harmful level of DHA in infant formula.
You ask: What is a harmful level of DHA? I think we can reasonable respond: I don't know for sure, but it is reasonable to assume it isn't 0.32% of total fat, the level found in most infant formulas.
Why can I reasonably exclude that level? I've made this argument twice already, but will make it again.
You have proposed that mothers tailor their DHA levels in their breast milk to match their infant. So if that means they would normally produce 0.17% DHA and the formula gives 0.32%, that could be too much and harmful. I think that doesn't make an ounce of sense.
We know diet is a huge contributor to DHA levels in mother's milk. (It's the main reason why Japanese mother's milk has DHA levels around 1% and U.S. mothers have it around 0.2%. U.S. moms eat way less fish than Japanese moms.) Why would the milk production system evolve to allow diet to have such a sway on DHA levels, when the window for safe DHA levels is so small?
Imagine for a second a distant past and there are two groups of women: those whose bodies tightly regulate the amount of DHA that goes into their milk and those whose bodies are more laissez-faire. The first group of women pump out milk with a small, consistent range of DHA levels. The DHA levels in the other group's milk can fluctuate, particularly when their diet changes. A string of fish dinners leads to higher levels of DHA.
Now if you're correct that DHA levels must be matched for every baby and that small increases can lead to significant neurological damage, then what happens to the fitness of those two group's offspring? Obviously the first group's offspring will be significantly more fit than those of the second group. So over time, you should see the genes that lead to tight regulation of DHA levels predominate in the population. But today, we don't see that. We see DHA levels strongly dependent on diet. Therefore, I think your hypothesis that slightly higher DHA levels than usual leads to significant harm doesn't seem to fit what we see around us.
Does that make any sense to you? How do you respond to that specific argument?
So you keep referring to this paper: http://www.hindawi.com/journals/ijvm/2012/647689/
The problem with using that paper to support your argument is many-fold.
1) We don't know for sure that inflammation is at the root of autism. Yes some autistic children have higher levels of inflammation, especially in their digestive systems. But that doesn't mean the inflammation causes the autism or if some other condition causes both.
2) Just because DHA can exacerbate inflammation in the brain, doesn't mean it can do it in the digestive system. If you want to make that claim, you need to show evidence of DHA doing it to intestinal cells. So you can't link DHA to amplifying inflammation in the intestines.
3) This paper is talking about a very specific type of inflammation brought on by high saturated fat diets. The inflammation pathways involved in that condition may be different from the inflammation pathways involved in autism--of course, if autism is caused by inflammation. So you would need to study DHA's role in amplifying inflammation with respect to that inflammation pathway, before you could begin to connect DHA to exacerbating autism-inducing inflammation.
4) You can't take this paper and say DHA levels in infant formula could be harmful. Why? Because the DHA levels used in this paper are 25 times greater than those found in formula. Yes I don't know what level of DHA could still cause this inflammation amplification, but you can't point to a paper using 25x DHA levels of infant formula and claim that formula levels are dangerous. That doesn't make a lick of sense.
How do you respond to my four simple points?
"1) We don't know for sure that inflammation is at the root of autism. Yes some autistic children have higher levels of inflammation, especially in their digestive systems. But that doesn't mean the inflammation causes the autism or if some other condition causes both."
Back to the chicken and the egg thing. We don't know if inflammation can cause autism or autism causes inflammation. We can measure this intestinal inflammation in autistic individuals, but we don't know whether it is just a co-morbid condition.
"2) Just because DHA can exacerbate inflammation in the brain, doesn't mean it can do it in the digestive system. If you want to make that claim, you need to show evidence of DHA doing it to intestinal cells. So you can't link DHA to amplifying inflammation in the intestines."
I see. So if oxidative stress were to initiate in the digestive system, it would not cause tissue destruction and inflammation. There is no evidence that supports this? Why do they recommend antioxidants with DHA supplementation? Why bother? Make some sense please. Next you will be debating whether or not DHA oxidizes at all.
"3) This paper is talking about a very specific type of inflammation brought on by high saturated fat diets. The inflammation pathways involved in that condition may be different from the inflammation pathways involved in autism--of course, if autism is caused by inflammation. So you would need to study DHA's role in amplifying inflammation with respect to that inflammation pathway, before you could begin to connect DHA to exacerbating autism-inducing inflammation."
I read the paper. It suggests that if ongoing system inflammation is occurring, caution is advised with n3/n6 supplementation. Hence my concern with this supplementation in formulas. If autism is caused by systemic inflammation, it could be worsened by supplementation. But since we don't know for sure, we should just dismiss this concern.
"4) You can't take this paper and say DHA levels in infant formula could be harmful. Why? Because the DHA levels used in this paper are 25 times greater than those found in formula. Yes I don't know what level of DHA could still cause this inflammation amplification, but you can't point to a paper using 25x DHA levels of infant formula and claim that formula levels are dangerous. That doesn't make a lick of sense."
I would think that increasing DHA and ARA via supplementation would result in higher levels in the digestive system. It is ingested. And if inflammation was ongoing, it may amplify this condition. But we don't know for sure so it doesn't heed caution right?
Very true. So before you can talk about DHA amplifying inflammation and that leading to higher risks of autism, you need to show that inflammation causes autism. And in particular, inflammation in the digestive track.
I didn't say that oxidative stress wouldn't lead to tissue damage or inflammation. I never said anything like that. Can you for once respond to my arguments without putting words in my mouth? Seriously, your reliance on that rhetorical technique suggests you have no actual intellectual ammo to respond to my arguments directly.
My specific point was that you showed me a paper about DHA exacerbating inflammation in the brain. I pointed out that you needed to show that it could do the same thing in the intestines. I didn't say inflammation couldn't happen in the intestines. I just said that the next step a scientists must take is show that what they found in the brain happens in the intestines with respect to DHA.
So again my point remains. Can you respond to it and not a straw man point you make up for me?
Obviously you didn't read the paper. Because that paper was talking about mice brains, not systemic inflammation. Here see for yourself:
I see words like cerebral, brain, cerebrovascular. Those are all talking about the brain! Not systemic conditions! So I must conclude you either didn't read this paper or you don't understand what terms like cerebral mean.
But you have provided no evidence to raise concern! That is my whole point. It has been for weeks now. You have presented no data that suggests people should be concerned with DHA levels in formula. Not a shred. Questions aren't data for concern. They're just questions.
OK now I'm getting frustrated. You appear incapable of understanding a very simple point. Yes the paper showed that a diet enriched in DHA can exacerbate brain inflammation. But that is a meaningless statement unless you consider what they meant by "enriched." In this case, it is a diet with a fat content that was 8.22% DHA. Now in infant formula, a baby receives fat content that is 0.32% DHA. Do you see any difference there? Any difference at all?
It's a 25-fold difference! Before you can start fingering infant formula DHA levels for exacerbating brain inflammation, you must show a study that is talking about DHA levels that approach formula levels. This isn't me being a pest. It's what any scientist would say.
Say you have a 10 kg infant. The LD50 for water is 90 g/ kg body weight. That means 900 g of water kills 50% of 10 kg infants. (900 g of water is 0.9 L.) So because a liter of water will kill an infant, should we assume that 3 tablespoons of water--less than a cup--is dangerous? Three tablespoons is about 40 mL, which is 1/25 of a liter--the same ratio of 0.32% DHA to 8.22% DHA.
Do you see how dosage matters here? Do you see how a conclusion about the toxicity of one dossage doesn't always hold for a lower one? Does that make any sense to you?
"OK now I'm getting frustrated. You appear incapable of understanding a very simple point. Yes the paper showed that a diet enriched in DHA can exacerbate brain inflammation. But that is a meaningless statement unless you consider what they meant by "enriched." In this case, it is a diet with a fat content that was 8.22% DHA. Now in infant formula, a baby receives fat content that is 0.32% DHA. Do you see any difference there? Any difference at all?"
I thought you said dietary DHA wouldn't do anything in respect to brain inflammation. So what does it matter? I guess I do have to understand what is meant by enriched.
"Now in infant formula, a baby receives fat content that is 0.32% DHA."
Yes, per feeding. On average @ 5x a day x several months. That's most likely enrichment being that before supplementation, an infant's DHA levels are not null.
"Do you see how dosage matters here? Do you see how a conclusion about the toxicity of one dossage doesn't always hold for a lower one? Does that make any sense to you?"
I understand how dosage matters. I keep harping on it. You don't know what represents a toxic or beneficial level, yet you can explain a absence of toxicity @ .32% per feeding. You have no idea what each infant has as a baseline level before supplementation and claim .32% will not result in levels that cause toxicity. That's not very scientific.
"Obviously you didn't read the paper. Because that paper was talking about mice brains, not systemic inflammation. Here see for yourself:"
Chronic ingestion of diets enriched in SFA commonly causes vascular dysfunction, including in capillary vessels of the brain. The effects of SFA could be described as a response-to-injury phenomenon induced by exaggerated exposure to plasma triglyceride, cholesterol, NEFA, or harmful inflammatory products of lipid metabolism, such as lipid peroxides. Many studies support a role of n3 and n6 fatty acids in the prevention of vascular, based disorders primarily via suppression of inflammatory cascades. Less clear however are the benefits of polyunsaturated oils in the presence of profound inflammation, because of the propensity to generate lipid peroxidation products.
In an established model of cerebrovascular dysfunction induced by chronic ingestion of an SFA-enriched diet, provision of DHA amplified the harmful effects. Probable mechanisms include hypercholesterolemia and perhaps fatty acid-induced cytotoxicity. The data suggests that introduction of n3/n6 fatty acids in metabolic conditions that are characterized by heightened systemic inflammation needs to be carefully considered in the context of paradoxical detrimental effects that could occur.
Maybe you should read it again. They are warning about supplementation of n3/n6 fatty acids in individuals with metabolic conditions characterized by heightened systemic inflammation.
Now you are just being silly. You can understand the author's conclusion, can't you. I'll explain in my own words. Be careful with supplementation of n3/n6 fatty acids if you are suffering from a health condition that is caused by high levels of inflammation. These supplements may further increase this ongoing inflammation.
You explain what the conclusion meant. Maybe I didn't understand it correctly. I'm not a real scientist such as yourself.
Biff, you don't get it.
OK say a baby eats formula that has a fat content that is 0.32% DHA. And that baby eats that formula 5x a day. What percentage of that baby's fat intake is DHA? Guess what it is? 0.32%!
It doesn't matter how many times that baby eats that formula in a day, the DHA % is still 0.32%.
And 0.32% is still 25 times smaller than 8.22%, what the rats got in your study.
I already explained the reason why I think 0.32% won't be toxic. You have never once responded to that argument. I won't repeat it again, because you obviously don't understand it.
Jesus Christ! The paper is talking about inflammation in the brain. You are just picking and choosing sentences out of context. Read the damn paper and you will see they are talking about inflammation in the brain. I have no desire to have a debate with you over something that is written in plain english.
Look, I'm tired of trying to explain simple reading comprehension, math, and biology to you. You're clearly willfully ignorant and only interested in pinning the blame for autism on infant formula supplements. Debating with you is futile. I'm reminded of the old saying: Don't wrestle with pigs--you only get dirty and the pig likes it.
So let's put our money where our mouths are. I propose a bet. You write up a summary of your research and hypothesis and submit it to a scientific conference. If it gets accepted, I'll pay your way to the conference. If it doesn't get accepted, I don't want your money. I just want you to post at the end of this thread the following message: "I, Biff Loder, and my relative Mike Pescatore are fools. We know very little about biochemistry, but like to pretend we do on the Vines. Our posts are full of conspiracy theories and unsubstantiated claims. I apologize for my ignorance in scientific matters and acknowledge I'm way over my head when it comes to issues like biochemistry and medicine."
We have to agree on the conference. No crazy psuedoscience conferences. I'm talking hardcore science conference.
Sound like a deal?
"It doesn't matter how many times that baby eats that formula in a day, the DHA % is still 0.32%."
If .32% of Dietary DHA gets incorporated in to the body, a percentage of that will get accreted in to the brain. That's the whole point of DHA supplementation. To increase levels. So you are saying that DHA supplementation will not result in higher brain levels? And it doesn't matter how many feedings of DHA supplementation an infant receives?
"Jesus Christ! The paper is talking about inflammation in the brain. You are just picking and choosing sentences out of context. Read the damn paper and you will see they are talking about inflammation in the brain. I have no desire to have a debate with you over something that is written in plain english."
Yes, and this inflammation is worsened by n3/n6 supplementation.
I got a better idea. I'll contact our friend whom is a pharmacology professor and tell him that I found someone willing to pay for the experimental study he has designed. His study will examine the effects of DHA supplementation on glutathione synthesis. Let me know.
Also, I can contact a few autism researchers that we have conversed with and explain the hypothesis in detail. But I'm sure you consider autism conferences as psuedoscience conferences.
So you want to put your money where my mouth is? That's a deal. Let me know. The study will cost @ 5-10k.
Once again you do not get it. What is going to increase DHA levels more: ingesting a diet in which 0.32% of the fats are DHA or eating a diet in which 8.22% of the fats are DHA? (Also I checked the percentage of calories from fats are about the same in the rats' diet, 40%, as in Mead Johnson formula, 48%.) It appears to be futile to get you to understand simple mathematics. So I will stop trying.
Holy jeez, you don't even understand my flippant bet for you. Why would I pay you money to test a hypothesis I think is baseless? The whole point of my bet was that I don't think any scientific conference would accept your hypothesis. So if a conference did accept it, then I would have been wrong and I would pay your way to the meeting. That's how a bet works: Someone takes a position and if that position is wrong, they pay. A bet doesn't just involve a person paying for something they don't agree with.
So I'm ignoring your offer because that isn't a bet and makes zero sense. If you'd like to prove me wrong and find a conference--it could be an autism conference, I have no problem with a legit autism conference, I am willing to pay your way if they accept your hypothesis. Basically, with my bet, you stand to lose almost nothing. If you don't get accepted by the conference, you just have to post on this thread, which no one will ever read. Basically, I'd be the only person who would see that post.
Are you willing to take that challenge?
Also the whole point of sending your hypothesis to a scientific conference is to get a neutral third party to assess it. Asking researchers you know or have talked to before isn't going to a neutral party, now is it?
Look, if you believe in your heart that this hypothesis is legit, what do you have to lose? Basically, nothing. And if you're right, then you get a free trip to a conference where you can talk to scientists about your hypothesis and get some good feedback.
What are you scared of, Biff?
Actually paying the five or 10 grand for the study would be what you would do to put your money where your mouth is, not me. You're the one who thinks the hypothesis is legit, so putting your money where you mouth is would involve you paying for the research, technically.
I can see it now... Hey trip toe fan, my hypothesis is going to be discussed at the upcoming DAN conference. Can I get those plane tickets? Hello? Hey where did he go?
I might as well make an online bet with the Easter bunny. No, but thanks for the fictitious offer.
I bet you can not tell me how every infant will be affected by DHA formula supplementation. How many will experience digestive issues? How many didn't need supplementation? How many had a metabolic condition that would be worsened by supplementation? Tell me what the ideal level of DHA should be in a developing infant. We are trying to establish this level through formula supplementation. What is it? This should be a simple question, yet you can not answer it. What level is ideal to ensure benefit and not result in toxicity? No more tap dancing around this question. DHA is a very powerful fatty acid. It is highly vulnerable towards oxidation. Its natural synthesis and oxidation must be tightly controlled for proper cellular processes. Surely there is a level that may be reached from supplementation that would require a heightened antioxidant response to control oxidation. What is that upper level that may overwhelm antioxidant responses and result in oxidative damage? Stop pretending that this is irrelevant. Answer the question. And don't say average levels found worldwide in breast milk.
I stand by my word. If you were accepted by a legit conference, I'd pay your way.
But I can understand your lack of trust. So how about this: Instead of paying, I have to post a message on this thread. Something like, "Biff and his relative, Mike Pescatore, have made an insight about the cause of autism that I could not have made. My arrogance blinded me to this insight and I apologize for belittling Biff on the Vines. Obviously, I don't know as much about this topic as I have claimed."
So if you get accepted, you just have to show me the acceptance email and I'll post that message on this thread. Then if you want to go to the conference, I'll still pay your way. Or you can turn down the invite. Your choice. But I'd promise to post that message on this thread, no matter what, as long as a legit conference accepted.
Seriously, you lose nothing by taking me up on this offer. Only someone who wasn't confident they'd get accepted would decline this bet. So, Biff, are you confident a real scientific conference would accept your hypothesis?
I don't think of this as a bet or a game. I really don't care what you will admit on Newsvine. You are not that important. There are legit safety issues that I have asked you. Answer the questions. No more sidestepping or tap dancing. At what levels of DHA incorporation in to a developing brain via supplementation will provide benefit or toxicity?
Oxidative damage in the brain is a legit concern. DHA readily oxidizes. So forcing more DHA in to the brain via supplementation will also require greater antioxidant protection. At what level of DHA incorporation will result in an overwhelmed antioxidant response and oxidative damage?
Additionally, if neuroinflammation was present, could increased levels of DHA amplify this inflammation?
You like to think that you can rule out the possibility of these events actually happening. But since you can't establish a DHA level that is neuroprotective v neurotoxic, you can not determine either way. I am suggesting that brain DHA levels may be increased high enough to overwhelm antioxidant protection via supplementation at .32%. Not in every infant, but some. It is very possible. Are you suggesting that an infant's redox staus is unimportant as well in regards to DHA supplementation? What would result in an infant had an underlying mitochondrial abnormality? Would supplemental DHA be problematic in this situation?
Fine. Then we have nothing more to talk about. You think your questions are legit. I think they're not.
Nothing you have shown me convinces me you're correct. You ignore my arguments.
That's an impasse if I've ever seen one.
Good luck and goodbye.
I ask a relevant question in regards to the level of DHA incorporated in to a developing brain via supplementation that will provide benefit or toxicity. You don't know. So I guess we don't have anything else to talk about.
All supplements have an effective dosage. It's the difference between benefit and harm. When a supplement is prone to oxidize, and excessive oxidation is detrimental, harm may result from such supplements. You don't understand what an effective dosage represents in this case, but are convinced the levels used will not cause harm. That's not very scientific. Good bye.
hahahahaha omg biff you really stuck it to that guy...another hater shut down!
when will people acknoledge theres questions that need answers...you and mike p have really shown the truth on here...people just hate the truth sometmes
ive been watchin you guys go at it off n on and you really nailed him...its cool to watch someone like you stand up against know-it-alls
later
Hey thanks mfoed. You know it's funny that the scientists have all the answers except the ones to easy questions. It was a simple question that haunted trip toe fan.
How much DHA would be too much as a supplement? A question that really should have been answered and understood before we started feeding it to infants. For the past 10 years we have been supplementing formulas in an effort to increase DHA levels and improve brain and eye development. Never did this before in the history of evolution. And what have we accomplished? Increased rates of children with neurological impairments. If anything, we should see somewhat of a decrease if DHA supplementation did what it was claimed to do. In this 10 years, we have discovered that DHA can create neurotoxic by products of peroxidation. Then we see evidence where these components of lipid peroxidation are implicated with neurodegenerative diseases as well as autism.
I asked trip toe fan if DHA was to oxidize in the digestive tract, and form such products of lipid peroxidation, would they be able to cross the blood brain barrier and be incorporated in to the brain. He didn't know that either. It's important because first you would see digestive issues as reported in autistic individuals. Then these neurotoxic components could cause extensive damage to the brain.
Hey, I'll keep asking the questions until the know it alls have the answers-later
well i wouldnt call him a knowitall...doesnt seem to know much at all to me...if he cant answer those questions then he should keep quiet...you have the questions he dont have the answers
so whats next? where do you see your reserch goin next?
Very funny, mfoed.
I wonder if Biff really stuck it to me, why couldn't he respond to my evolutionary arguments about why worldwide milk DHA levels should be acceptable for formula levels? Why couldn't he understand the simple issue that the DHA dossage in the rat study was not applicable to formula levels? Why did he finger a reducing agent, ferrous sulfate, as the chemical responsible for oxidizing DHA in formula cans?
Also don't forget the questions I couldn't answer, Biff couldn't answer either.
But you are like most Americans, happy to applaud the willfully ignorant for standing up against people who know more. Enjoy standing by the ignorant and the irrational.
wait wait mr know it all...biff is just raising the questions...you're dismissing them without knowing the answers...how does that work? what if people did that with cigarettes? people didnt know they were bad and what if people said stop asking questions?
im happy to stand with biff...he is standing up for truth...who are you standing by? big pharma?
Ugh. You and your friend, Biff, keep making the same mistake: You think simply coming up with a question means everyone should be worried about something.
That's absurd. Here's an example:
Does letting your child use an iPad or other tablet negatively affect their normal mental development? For centuries, children haven't had access to such content literally at their fingertips. Sure there's been TV for several decades, but nothing like an iPad. The way they can manipulate things on an iPad are alien to how things work in the real world. Does that harm their normal cognitive development?
See I came up with a question. Now are you going to yank iPads from your kids' hands? Petition Washington to ban children's use of iPads until researchers can answer my question? Or at least storm onto the Vines and shout at people about the dangers of the iPad in children's hands, like Biff and Mike Pescatore do about infant formula?
I hope not. That would be ridiculous. Why? Because we have no reason to think iPads harm children. There is no evidence to make us think that way.
Similarly, there is no evidence to make us think DHA in infant formula is a concern. Just because Biff has questions doesn't mean we sound the alarm. If he had questions and data to suggest there is a concern, then I'd say he has a point. But he doesn't have such evidence--or at least never showed it to me--and so his questions are as silly as my iPad one.
Does that make any sense?
As for cigarettes, people started to accumulate data on their harm during the period when people started raising their questions. So it was wise to listen to those questions because they had data to support their concerns, not just questions.
Mfoed, He'll argue black is white. At the end of the day he still doesn't know any more about what causes autism than anyone else. I could suggest that there may be life on other planets. He would argue that there is no study available to support my theory.
"As for cigarettes, people started to accumulate data on their harm during the period when people started raising their questions. So it was wise to listen to those questions because they had data to support their concerns, not just questions."
How exactly does one start to accumulate data without first asking questions? It starts with a concern. Questions are asked. Answers to the questions are revealed. These answers accumulate and determine the facts. If no questions were asked and answered, there would not be any data. You would have a bunch of unanswered questions.
Trip toe fan believes my questions have no merit based solely on the fact that the questions haven't been asked. The answers haven't accumulated data. He needs to see a study that has determined autism can be caused DHA supplemented formulas. A study that may never be conducted until safety questions are asked and answered. Until then, he'll use the "you can't prove that" rebuttle.
Autism affects boys and men at over 10x the rate it affects women. Not a single word in this story is used to communicate that autism is primarily a male brain phenomenon.
It could have something to due with the fact the rate is actually 4.3 to 1 not 10 to 1.
http://idea.library.drexel.edu/bitstream/1860/2632/1/2006175339.pdf
Not a single word is said that ethyl methyl mercury found in toxic amounts in the 'required' shots your helpful robo-doc wants to inject in your 6 month old child is in there either. How long will this corporate farce be allowed to continue?? Read "Evidence of Harm" and see the truth the corporations who are avoiding the largest class action lawsuit EVER don't want you to see!
Research has found the neuron differences between the second and third trimester of pregnancy. The behavior symptoms show up later because that's when the brain is wiring up those neurons. No vaccinations necessary or fraud doctor's research necessary. California eliminated the vaccine preservatives 10 years ago - autism still went up not down.
JApan stopped the MMR vaccinations altoghther for a while as well... autism rates rose as well.
Let me guess, Allen, you conveniently misplaced all those peer-reviewed citations you were going to use to back up your statement...
It has nothing to do with vaccines. My son, several nephews and 1 grandson all have autism in varying degrees. They are all on my son's father's side of the family. I believe firmly that it is genetic, at least in the case of our family's children.
Yup Midway-same in my family-all cases of Aspergers...my father,quite possibly 1 or more of his brothers,at least 1 if not both my male cousins,my son,at least 1,possibly both, of my sisters sons....
I don't know if there is an actual increase in cases of autism,i know in my fathers case he did not receive a diagnosis until his grandson participated in a study..how many cases are now correctly diagnosed where in the past they would have been dismissed as the weird nerdy kid that could recite you all there ever was to know about airplanes(example only)but could not handle social interaction with his peers or the strange nonverbal kid with ticks or ocd like behaviour or the one that,when agitated,would only calm down if hugged tightly,and all the variations in between?
I'm not sure it's a men and boys thing...more likely it is just more difficult to diagnos in Women and girls because of the prevalent, and numerous psychoses
I firmly believe that the rise in autism is tied to the rise in the use of fertiity drugs.
based on what?
Do you not think researchers would have spotted something so simple? Do you think that only women who have used fertility drugs have autistic babies?
Links to supporting studies please...
And if there were true children of women who took the fertility drugs should have higher rates of autism...but they don't. Sorry. Nor would the mothers be daughters of mothers who took them in any rate to be significant. Sorry.
One more idiotic, false myth about autism to go along with the vaccine hoax. There are too many people out there who spread misinformation that need to be stopped, or at least held responsible for the consequences of their actions. I would love to see idiots like Jenny McCarthy made to take responsibility for every child that was harmed by a preventable disease because of her spreading lies about vaccines causing autism. Far more children have suffered permanent injury due to not being properly immunized because of this myth than have been harmed by vaccines.
My wife has never used fertility drugs and we have two autistic children. I look more at Monsato's GM food. It's banned in other countries around the world but we can't even get labeling here. Don't worry though, they have solved the epidemic but changing the Autism definition. I know that will help my son even though he can't speak and stims constantly. As soon as that goes into affect I expect him to instantly become not autistic. Thanks again Obama for putting the head of Monsato in charge of food safety, love that one. We subsidize our farmers crops now because the rest of the world won't buy the crops, they won't eat it...........because it's dangerous. They grow spermicide and plastics in corn now......really. Spermicide taco anyone? Nice. Even the Chinese won't eat it. wow
Also, Nano particles are in everything now. They have no regulations because they aren't drugs. They are 1000 times smaller than a human hair. They have no idea what this does to the human body but it's in toothpaste, makeup, lotion...hell even golf balls? My wife did work with Nano particles....so did some other girls at her plant. They all have Autistic children now. Studies? regulations? not in the good ol USA. That might put a crimp in the economy.
Oh wait then there's chem-trails. Those planes flying grids over your head leaving long "vapor" trails that spread out all day long. Yeah, whatever that is. Commercial jets don't fly grid patterns and crisscross in X patterns. Google that then start looking up. Nice.
Well at least we're not pumping millions of gallons of chemicals into the drinking water supply....oh wait...that would be fracking. I guess we're all fracked.
Oh yeah it's those damn fertility drugs right?
I think that if it had any correlation to fertility drugs, its not a direct causal relationship, but probably tied more closely to the fact that fertility drugs are often used in assisting older women in getting pregnant.
Anyway, as for the subject of the article, this is really cool if we are approaching the point where we can interfere with autism and maybe even reverse its course in early brain development!
As a clarification on your point and to elevate the discourse above unsubstantiated statements, autism does have link to maternal and paternal ages. Please follow the link for more information (). The age of the parents plays a role in a variety of developmental disorders; however, age is not the only factor in some disorder. Testosterone has been hypothesized to potentiate the development of autism (either through increased in utero exposure because of PCOS or other causes). If interested you can read more information about testosterone and autism in this article
It would not let me paste the links so here are the articles:
Sex hormones in autism: androgens and estrogens differentially and reciprocally regulate RORA, a novel candidate gene for autism. PLoS One, 2001 6(2): e17116. doi:10.1371/journal.pone.0017116
Maternal and Paternal Age and Risk of Autism Spectrum Disorders. Archives of Pediatric and Adolescent Medicine, 2007;161(4):334-340.
Sex hormones in autism: androgens and estrogens differentially and reciprocally regulate RORA, a novel candidate gene for autism. PLoS One, 2001 6(2): e17116. doi:10.1371/journal.pone.0017116
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0017116
Maternal and Paternal Age and Risk of Autism Spectrum Disorders. Archives of Pediatric and Adolescent Medicine, 2007;161(4):334-340.
http://archpedi.ama-assn.org/cgi/content/abstract/161/4/334
2014MD: I believe these are the articles you were trying to link to - please double check the links, if they aren't the right research articles, please let me know - and I'll try again. When you're relatively new to newsvine, it won't let you post links. Thanks for the information on the articles. I will have to read them later, as I need to get back to studying for my endocrine final. But, as a medical student and a mother of a child on the autism spectrum, I am always interested in reading journal articles from reputable, scientific journals.
Thank you Summer-1597193, those are the articles. Good luck with your endocrine final.
2014MD: No problem, and thanks :)
I totally disagree. I have a 13 year old son who is high-functioning autistic and I got pregnant with him naturally. 4 years later, I had twins (boy and girl) that I got pregnant with through fertility drugs and neither of them have ever shown any signs of autism at all.
kaykay969, you make a great case for shortening education to grade 6.
At the end of the day is always the same story: We do not really know what causes Autism, or are even close to really find out.
So, what else is new? All the money used for political trashing could go to help fund research, and find a cure for this and other diseases of the brain.
....Oh! how naive of me to think that!
We (the researchers) have not yet asked the right questions.
Not at all surprised or mad about that, since really we're just getting out of the dark ages when talking about autism.
Waaaaashuuuuuuu!
Don't believe.
It's ok, you don't need to believe, this is being tested, there's no faith-based "reasoning" here
Please continue your mission to preserve a fertile breeding ground for preventable childhood diseases
Nano particles? Jet contrails? Actually, much is probably faith-based as empirical evidence is lacking. Maybe it's the parents?
I agree to an extent. There could be something in the genes but environmental triggers could play a strong roll. Nano particles are heavy metals. Not really so far fetched.
I firmly believe the rise in autism is closely linked to the increase in the use of fertility treatments.
You said that already.
It isn't any truer this time than it was the first time you said it:)
You firmly believe that someone who took fertility treatments is causing autism in babies of mothers who didn't?
Haven't you heard? That sort of thing can be spread through casual contact. You only need to have spoken to someone who has taken a fertility pill to be at risk. I have a friend who knows a scientist and she confirmed it was true.
Autism used to be blamed on emotionless mothers, and that was back in the 1960's. Pre-fertility drugs, and a number were pre-vaccines, too.
They used to park a lot of the kids in institutions and forget them, including ones that had that awful illness called "illegitimacy." Some doctors got kick-backs.
ElkMeadow wrote "Autism used to be blamed on emotionless mothers, and that was back in the 1960's."
In the terms of today, genetic pre-disposition to extreme maleness is blamed on mothers with a female body and a male brain.
Fibromyalgia, ADHD, some depression---over-diagnosed, over-prescribed, over-studied money machines. I cite ALL the studies. The prevalence doesn't make sense. Surprised they don't include low self-esteem by MRI.
I have low-esteem because I haven't had an MRI; everyone else has had one.
I agree with melodic.
It's the food additives. And I believe the chemicals in the food we eat is responsible for the bizarre behavior that is on the rise in children and teens and young adults.... the breakdown of moral restraint that results in unbelievable cruelty and death, whether by suicide or murder.
well duh!
it's obviously the food additives that warp the moral compasses of children these days, not sucky parents!
From Bewilder53 - "It's about one thing;Money! Taxpayer Money! ADHD has fizzled out. Autism/Aspargers is a new way to get it"
I would pay any amount of money to see my kids not have this any amount of money. Every cent I have.This is the most ignorant post post I've ever read. Someday this will touch someone you know,someone you love. You'll sing a different tune then
Now please go back to listening to Rush Limbaugh and come back when you have an original thought.
Gee,how many kids do you have w/it? How much taxpayer money do you guys suck-up? Bet they're your meal-ticket!
I have two and work for a living. clearly your an old fool
Rest my case.
Goodnight, case...sleep well
Wake up people!!! Everything that has been manufactured in the past 100 plus years causes this and other problems in children and adults. Don't expect a change until everyone( in the world ) goes back to nature. We can't point the finger at any one source. Except mankind.
Life is fatal. Ban it.
It's probably all the plastic.
I agree with melodic
I do believe it is the food it's the gmo's of monsanto. They are going to kill the whole world off . This is because they are aloud to play God and no one says a word about it, but if you don't say something it will be to late. They also intimidate the small farmers, trying to make them buy ther poison round up and then they sell round up ready corn seeds because they are the only things that will grow after using round up. This is making it hard for those of us who want to have a backyard garden and it is also harming the organic farmer. We need to take a stand against these bad practices. Go to Care too and other web site to find out more information and to sign petitions to fight them. Also the latest thing is fracking the chemicals they put into the ground will distroy our water. Check it out people the water burns.
Thank you Mariann.
The terminator seed scares the hell out of me. Seeds that won't grow without an activation spray? Let that gene loose in nature.
There is zero evidence to backup any claims either of you make regarding GMO. You can have your opinions of course, and agree with each other, but the data shows otherwise.
The MOA you describe is simply impossible, end of story. A gene is nothing more than a long string of nucleotides, naturally occurring in nature, easily digested by our stomachs. These genes are typically only expressed in the root system and stalk of the crop, rarely (if ever) in the end food product. That means your body never ingests the gene product. I have never heard of any mechanism whereby a metabolite you never come in contact with is able to affect progeny.
Furthermore, Monstanto's first GM-trait crop was launched in the 1970's. If there was indeed a direct cause-effect relationship, we would have begun to seen evidence after the first generation, not some 40 years later.
People may not "like" GMO or even understand what is going on at a genetic/protein/metabolite level. People may hate Monsanto and its business/patent practices, and they/you have full right to do so. But that does not create a direct causal relationship between eating GM foods and increased risk of autism, and you should not present your opinion as fact.
Vaccines....Vaccines....vaccines....Stop taking the vaccines...
Maternal age and male children. Stop it !
Medical science is what matters. If you're not a medical scientist what you believe doesn't matter. Furthermore, it's people spouting their beliefs that hinder science.
Everyone's opinion matters. I'm not a physicist but I wish I had a vote when the brilliant scientists developed nuclear weapons.
I also would have voted against biological weapons and genetic engineering. Just because you're a medical scientist doesn't mean all your opinions or work benefit the rest of us.
Melodic
Sorry, but in medical matters you opinion is meaningless as to the cause. Now if you have an opinion on the uses of something that's different. But just because your 'opinion' is that something is a cause doesn't make it correct, Only the science matters.
It's about one thing;Money! Taxpayer Money! ADHD has fizzled out. Autism/Aspargers is a new way to get it.
bewildered53, obviously by your comment you dont have a child with autism. There is no money given to us for having a child with autism.
Now since you have demonstrated you KNOW NOTHING about autism STFU and sit down and let the grown ups talk.
Not yet maybe,bet your trying for one. Subject really pissed you off,a little sensitive about it;better get some anger-management!
I do wonder, if autism is such a burdensome disorder, then why are the parents (at least in this study) having additional children (siblings)?
I never considered having a second child until I finished the highly demanding toddler stage with the first. If you have a child that never gets past that highly demanding stage, then you're setting yourself up for a real challenge by having another at all!
JLM the average age that a child is officially diagnosed with autism is 4-5 yrs old. Well past when toddler stage is over. Nice to be so judgemental since you obviously also do not have a child with autism.
As to bewildered, he's off his meds and cant find his tinfoil hat. The men in the nice white coats are looking for you. maybe you should go with them.
Presumably the autistic child's behavior is a "handful" before they are officially diagnosed with autism. Having another child while your first one is still demanding - whether it's because they're toddlers, have autism, or are just spoiled - makes no sense. I didn't want a second child to care for until mine were PAST the gruesome toddler stage. I don't understand parents who complain about how difficult it is, but obviously felt they had room in their lives for additional children.
Again JLM that lack of ACTUAL experience raising a child with autism or being the parent of a child with autism is so VERY telling.
STFU douchebag
We all wish we had your experience, so we could be as bright and articulate as you are, with the ability to read and understand various viewpoints and provide insightful, research-based feedback in intelligent and respectful dialogue!
I am not going to claim to know which chemical, environmental poison, or even which genetic factor caused my child's autism. I will tell you as a mom that I knew there was something wrong with my baby before he ever left the hospital after his birth. You can't imagine what its like to have a baby who prefers to not be held, to not be fussed over, who screams when he sees regular baby toys (because the lights and sound scared him). To have a toddler who doesn't speak, and freaks out when he is around more than a few people at a time. To constantly be asked "what is wrong with your kid?" If I could have know at six months instead of three years I could have at least given an explanation, instead of saying I am sorry I don't know.
I know. I knew there were issues with my grandson from the time he was 6 months old. But his parents denied it until he was 4. I finally insisted they get him tested. It created some really hard feelings for a while. But now they realize I was right. I just wish they had listened for the three years prior. My grandson would be better off and their lives would have been a bit easier.
Thankfully he's 'high functioning' and things are beginning to go better. I have hope for his future.
Good luck with your struggles. It's hard. Too many people still think its 'bad parenting'.
And don't ever say 'I'm sorry'. You can't control stupid people. My daughter-in-law still struggles with it.
I sympathize with the parental heartache and abhor the disability suffered by autistic children. I do not doubt autism exists. When a brain altering disease becomes more common than green eyes, I question the frequency of diagnoses and question the implication of vaccines, jet contrails, genetically engineered foods, nano-particles, plastics etc.
There is no defining diagnostic lab test. The increase could be from shaping a clinician's opinion. If it is an environmental poison, then those never exposed should not get afflicted.
Mother nature, evolution, whatever, would not favor an unbeneficial trait to such a great extent. I support all studies and efforts to understand autism.
Not sure what you're getting at in your last paragraph by implying natural selection. What kind of selection pressure would reduce autism (even if it were entirely genetic) in our modern society? Traditional concepts of competing for food resources and surviving are almost entirely phased out. An autistic person, and certainly a family with an autistic member, has a pretty much equal chance of acquiring enough food to survive and eventually reproduce, with or without austim genes. It isn't the jungle any more.
If the autistic adult is socially affected, asocial or aberrant behavior would reduce mating behavior (even if it were only shyness). If an autistic adult has a desire not to risk having autistic children, that would reduces mating behavior. If a community observed certain individuals with autistic traits and found them negative, that community may inhibit mating opportunity.
It does seem to be a mostly male-dominated disorder. My daughter happens to be one of the few females who are affected with autism. Though, my daughter is on the spectrum as "functioning", I really have to disagree with the term. Yes, she can talk and do other things that some with full-blown autism can't do. However, her mind doesn't grasp things well, and we endure screaming fits on a daily basis. God forbid we have a change in routine, because that is a nightmare to deal with! Plus, we get to deal with her having OCD, ADHD, and oppositional defiant disorder. I think every doctor we've been to since she was 3 years old (she is now almost 11) has been baffled by how she can have so many disorders at one time. I'm baffled. It doesn't mean I love her any less, though.
As for bewildered53's comment: You obviously don't know anything about autism. Autism is NOTHING about money. I guess you have the idea that everyone who has a child with autism is going to be on SSI or something. Well, I know we don't get any type of government funds to help out. We pay monthly for insurance, we pay taxes just like every other US citizen should, and it's not like when I got pregnant with my daughter, I thought "Oh, I want to have an autistic child so we can get money." That is a completely idiotic statement that you made, bewildered53. I can't stand when people try to turn any and every story into something political. It isn't about politics, and it isn't like we as parents of autistic children are looking for welfare. In fact, maybe you should look up the name Temple Grandin sometime. You might be surprised at how intelligent those with autism are, and how there are many who want to help make a difference in the world.
1brightmommy: I know exactly how you feel. My daughter squirmed at feedings, would pull back a lot of times, even. She was late to start talking, and always wanted (and still wants) to pretty much play on her own. She has a hard time making friends at all, because no other kids understand her. We would get calls from every school we had her attend (we are military family), to let us know that she was just too much to handle. There have been so many times that we had to get her from school, because she would have fits and disrupt the class. She flat out punched a kid once because he pulled her hair. Thankfully, he wasn't hurt, but still. We tend to have either myself or my husband stay home with her when we need to get groceries, because every trip to the grocery store or anywhere turns into a scene. As anyone with an autistic child knows, they have a one-track mind. If they want something, they will do everything in their power to make sure they get it, or they will have a fit. My daughter is known for having a full-blown temper tantrum in the middle of Walmart, with everyone in the area looking at us like we are horrible parents, or like she is a rotten brat. They don't understand she has a disorder.
A sample size of 92 cannot possibly be statistically significant. Doesn't autism occur in about 1 in every 150 children? So the chances of getting even 1 autistic child in this study would be hit-or-miss, and you can't make conclusions based on 1 autistic child anyway.
It seems the researchers tried to improve their odds by selecting children with autistic siblings, though they didn't quantify how much this changes the probability of autism. Furthermore, by loading the study this way, they risk contaminating it with outside factors. If you want to be sure you are only looking at genetic predisposition, then you need a sample group that is representative of the population at large, not just children from autism-inclined families. A number of factors in these families could influence the children's brain development and risk of autism separately... such as environmental contaminants, parenting styles, even the amount of attention these children get simply because their parents are already occupied with the increased demands from the autistic sibling.
One should also consider that autism is frequently accompanied by heightened skills in other areas, and so treating it as a disorder is tricky. Are you forcing a child to be more verbal and less mathematical, for example? I know that autism itself can be so debilitating in some that it cancels out the odds of being successful in life with any such talents, but not always. I wonder how telling a 6-month-old's brain scan can really be in determining how severe or debilitating their autism will be, and whether it's worth trying to "treat" preemptively. Besides, studies have shown very mixed results on the effectiveness of early intervention for autism - from very effective to virtually worthless. (In California, these studies seem to mimic whatever is fiscally convenient!)
JLM, they picked those 92 children from families that already had a child dx with autism. The chances of having autism are MUCH greater than the normal odds when a sibling has it.
The recognized odds in the general population for autism is 1:110 , or 1:70 boys.
So you read my first paragraph.
and you're a douche.
As the mother of an 18 yo son with Aspergers, and a 3 yo granddaughter I have no doubt is on the spectrum, it constantly amazes me to see the comments some people make regarding the diagnosis of this disorder. Normally, they are the people who not only dont have a Spectrum child, they have no children at all.
I was an infertility patient for over 10 years. My 22 yo daughter is not on the spectrum, her daughter, concieved naturally is.
My son was 'normal' until he recieved his 18 month shot. Seven days later, he was walking on tippy-toes and spinning in circles. When I questioned his pediatrician, I was told I was paranoid. I watched as day by day, month by month, it became more and more obvious he was no longer 'normal'. Brilliant? absolutley. But certainly not normal.
I see so many similarities between he and my father. Whereas my da is able to function in society, my son cannot.
I believe that one has to be 'predisposed' to the spectrum, but that enviornmental and medical factors come into play. Of the ten children gestated within an eight house block in the last 23 years, nine are on the spectrum, so predisposition aside, there are outside factors at work.
That being said, does it matter who or what causes spectrum disorders? Not even remotely. Does finding a cure, method of assisting these children matter? Beyond a shadow of a doubt. Arguments, opinions and theories aside, all that matters is finding a way to help.
My family receives not a penny in Local or Federal financial aid. It would have been a Blessing more times than not. The physical ( I currently have a fractured tailbone due to an 'outburst') and emotional costs far outweigh the financial 'burden' of a Spectrum disorder.
All parents with a child in this condition want, need, are answers, and help and understanding. It is difficult to have a 'disabled' child, when there is nothing on the outside to show a 'disability'. People would not dream of slamming a parent of a child in wheelchair, or in leg braces. But we, the parents without an outward 'sign' are labeled, just as much as our children, and somehow, someway, it needs to change
This article does nothing but prove that they really don't know anything! But of course lets try to label these kids younger and younger...so the insurance companies can deny them coverage younger and younger.
"The findings suggest that during a child's first year, "there is a potential to intervene, to disrupt autism before it becomes entrenched"
Oh Jason...That sounds wonderful! Now explain to me how that would work exactly....uh huh...go ahead...um, didn't think so.
As father of an autistic child, these sort of stories piss me off.
"As to what might be causing these brain differences, it's too early to say, Wolff said."
"The findings suggest..."
Tell you what Mr. Wolff, get some solid findings first, then publish your papers and call reporters. And then someday, when you discover how to intervene and disrupt autism before it becomes entrenched, we'll all enjoy watching you receive the Nobel Prize.
I agree John. Just another piece of worthlessness.
I don't see any articles mentioning infant formula companies experimenting with brain development. You know, the synthetic DHA added to improve brain and eye development. The fatty acid that is forced to ferment and is extracted from algae with hexane. They actually manufactured a structurally different triacylglycerol containing DHA and added it to infant formulas before they understood how it exerts its biological effects. Think about it. They didn't fully understand how DHA affects cell signaling, changed this fatty acid's esterification position and added it to the sole source of nutrition during critical stages of development.
Come to find out that DHA will oxidize and form breakdown components of lipid peroxidation. These DHA hydroperoxides actually form adducts on protein residues. A recent publication reveals protein damage found exclusively among the autistic brain due to adducts formed by peroxidation of DHA.
But I'm sure that synthetic long chain polyunsaturated fatty acids are beneficial to brain and eye development. Just because the Institute of Medicine had warned of unknown biological triggering effects due to the structural differences of these novel triacylglycerols, doesn't mean that they will be problematic for neurodevelopment.
If new findings weren't published then research on all levels would just stop. If you expect applicable treatments fully developed to suddenly appear then you will be waiting forever.
Research builds on each other and that is just how it is. If you don't like "small" studies, ignore them but when one that you deem important comes out, it will be the small studies that will have allowed it to happen.
"there is a potential to intervene, to disrupt autism before it becomes entrenched"
As an independent, functional member of society with a professional diagnose of Aseperger's Syndrome, I find this to be highly offensive. Many who call themselves scientists and academics take a stance that Autism Spectrum Disorders are diseases to be cure. Not only is this condescending and misleading, it tends to cause improper treatment of people with ASDs. It is not a disease, nor is it something to be cured. Given some accommodation and support early in life, we can adapt and integrate in to society with ease. Even my closest friends did not know I was on the spectrum until I told them directly. In addition, I know several other people on the spectrum who have had just as much success as I have in becoming part of society. If you truly care about helping those with autism, do not allow the current attitude to continue.
Nsc109, what a Blessing for you, and those you know, who are able to function and suceed in society. I agree totally with you, ASD is NOT a disease. It is however a disorder. I believe that many use the word 'cure' (sometimes myself included) as a benign term for help, assistance, answers. Please remember though there are many who are not as Blessed as you. Try as they might some parents cannot seem to help thier children adjust and assimilate into our society without sever, often devastating, results.
I would give all I have, will ever have, to help my son. I have spent 15 of his 18 years fighting for the support and accommodations you speak of. Begged, pleaded and fought. Our family, like many, had not the funds to enlist assistance. Through the schools I have seen my son excluded, ridiculed, denied and abused. NONE of which falls under 'support' or accommodation'.
Sometimes the help parents of children on the spectrum get from the schools have devastating results. One call to Social Services can ruin not just the child, but the entire family structure.
Like you, many do not know my son is on the spectrum. But then, they see the bruises some of which cannot be hidden, and explanations have to be made.
You my friend, are one of the lucky ones. Most are not. please do not be offended, just understand the heartbreak, fear and desperation that drives the ones less fortunate.
Best wishes
Nsc109, agreed. Anyone with experience in technology R&D understands that those with the "male syndrome" are the only lot willing and able to invent in conditions of solitary confinement. A "cure" will only return us to plucking termites from the dirt mound for lunch.
The illness is being male, according to females.
Pass that bowl over here Vincent.