Why Does Gluten-free Improve Autism?

[veggienft]

I just visited Doug Kaufmann's Friday video:

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At about 9 minutes Kaufmann interviews nurse Linda May (sp?). Nurse May cites some research implicating "teratogens" as a possible cause of autism.

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"TERATOGEN?!!!!" ........I said. What the heck is "teratogen".

So I did a little research. Teratogen seems to describe the process by which an environmental stimulus (teratogen) affects a mother, and that effects the future health of her child. The teratogen can be anything, an infection, a chemical...... And the process can take any of many routes. DNA changes, blood flow.....

The theory of teratogens causing autism flies in the face of the predominant theories which blame direct environmental effects ........an infant ingests something, or gets an inoculation, and becomes autistic.

There have been several small scale studies recently attempting to identify teratogenic processes which could cause autism. One teratogenic hypothesis is passing experimental challenges. It blames autism on a deformation of the GSTP1 mitochondrial DNA marker.

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I have no idea what the GSTP1 mitochondrial DNA marker does. I'll be researching it. However, a gluten-free diet improving autism fits the teratogenic mitochondrial deformation hypothesis. And that has pretty amazing implications.

Human mitochondrial DNA is not the DNA which replicates in the nuclei of our cells, and forms new cells. Mitochondrial DNA is DNA which we inherit from our mothers. It gets passed on to us in the fluid contained in the egg which she contributes. We have our mothers' mitochondrial DNA in most of the fluids of our bodies, and as far as I know, in every cell of our bodies.

Epigenetics describes the proteins on the surface of our DNA. Epigenitic proteins mostly (if not totally) come from the mitochondrial DNA of our mothers. In the 20th century, mapping the human genome was touted as the holy grail of identity. Cracking each person's DNA code would supposedly tell everything about a person's makeup. Now we know that epigenetic proteins add volumes to our makeup.

Epigenetic proteins turn genes on and off .......tell our cells which genetic traits to express, and which ones not to express. We inherit this capacity directly from our mothers. And that's key to the teratogenic effect. Our mothers inherit mitochondrial DNA at birth, and place it in their eggs early in life. It's easy to see how an environmental stimulus applied to a girl could change the mitochondrial DNA she passes to her eggs, and to her children. And that change affects the operation of her child's epigenetic proteins.

Humans have only consumed agrarian grains in the last 10,000 years of our evolution. Survival of the fittest dictates that major evolutionary changes can only occur when environmental hardships reduce a species down to a breeding pair. A genetic mutation allows that pair to propagate the species with changed attributes. Agrarian grains expand human populations, meaning that humans have no ability to genetically adapt to agrarian grains.

We have developed epigenitic abilities to adapt. But epigenetic adaptations are fleeting. We are predators with only temporary ability to survive on grains.

So humans inherit an epigenetic method of digesting grain proteins and starches. Celiac disease and autoimmune disease occur when those substances, in combination with environmental stimuli defeat our inherited epigenetic method of digesting agrarian grains.

Gluten is a harmful opioid which mimics human endorphin. It can plug into the endorphin receptors of our central nervous system. Some immune systems recognize gluten as an invading antigen. Those immune systems attack gluten and attack all the human tissue it may have come in contact with. Where the tissue is nerve tissue, the attacks can change mood, cause emotional instability, and degrade socialization in children.......

......autism.

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It is imperative that humans digest gluten before it goes into the bloodstream. People who fail to digest gluten include people with celiac disease, people with other autoimmune diseases, and people with......

.......autism.

Autism shows itself in subjects upon initial attempts at socialization, between one and two years old. Many studies have found that a gluten-free diet remarkably improves the symptoms of people with autism.

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Autism's link to maternally inherited mitochondrial DNA, combined with its link to failure to digest gluten, tends to confirm that autism represents a breakdown in the epigenetic codes which allow us to digest glutenous grain.

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[veggienft]

Okay, I'm not the best closer. Here are the last two paragraphs in English:

Celiac disease and autoimmune disease result when gluten, in combination with environmental stimuli defeat our inherited epigenetic method of digesting gluten. Autism seems, via teratogenic mitochondrial DNA deformation, to represent the total absence of the epigenetic-ly inherited means of digesting gluten.

Autism's link to maternally inherited mitochondrial DNA, combined with its link to failure to digest gluten, tends to confirm that autism represents a breakdown in the epigenetic codes which allow us to digest glutenous grain.

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[veggienft]

Revision #2:

Sorry. Apparently I crossed the genes and causes in two experiments.

The GSTP1 marker I listed above goes with the corresponding link and experiment. However, GSTP1 is a human gene, and not a mitochondrial marker. It is theorized that the presence of an acid at birth, contributed by the mother, causes a mutation of the gene in the offspring. How can that happen? I don't know.

Here is the link:

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......to the nih experiment which associates the mitochondrial marker with autism. The mitochondrial marker is SLC25A12.

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[ChemistMama]

veggienft-

Two errors: your tetratogen and opioid definitions aren't quite correct.

A tetratogen is a compound which interferes with the way the fetus develops, but doesn't necessarily affect the mother. The best known tetratogen is thalidomide, the morning sickness drug which helped the moms but then caused the fetuses to develop abnormally.

Also, gluten and casein are not opioids, see here:

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"Individuals who have a gluten or casein allergy are not able to fully metabolise food containing gluten or casein proteins and so small units called peptides remain undigested. ... The undigested harmful peptides are said to leak into the bloodstream and are able to cross the blood brain barrier which protects the nervous system. The consequences can be quite hazardous as some of these peptides are casomorphine and gliadinomorphine peptides (they contain high levels of opioids, a drug like heroin and morphine); which are believed to mimic neurotransmitters and therefore can cause chaos in the sensory system. "

The issue here is that in some individuals, the gluten and casein are not properly broken down by the intestines, and the pieces of the gluten and casein proteins are the opioids.

glutathione S-transferase P1 (GSTP1)? I have a PhD in chemistry, and I still couldn't find a clear nontechnical definition of what that it does. The wikipedia entry is sufficiently vague. The few searches I've done show that it's being studied to look for cures for asthma, cancers, and a few other illnesses.

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There is always a problem with looking at the literature online; usually they don't post the full text of the medical journals and when it comes to genetics, it's especially difficult to comprehend what's going on. I wish you the best of luck. If you live near a University and are really interested in learning about these things, I would suggest talking to a biochemistry or genetics professor so he/she can explain some of the details to you. Good luck!

[veggienft]

veggienft-

Two errors: your tetratogen and opioid definitions aren't quite correct.....

Thanks for your reply, especially your explanation of a teratogen. I was kinda hoping my posts would die a quiet death, because via further research, I found they contain yet another error.

Your clarification of gliadorphin and casomorphin as opioids are valuable. I did not include them because my post was already excessively long.

The other error in my above posts concerns the nature of mitochondrial DNA, and its relationship to epigenetic proteins. To repeat, mitochondrial DNA is not base human DNA. It comes in our mother's egg.

The correction:

I claimed that epigenetic proteins are mitochondrial DNA. Wrong.

Epigenetic proteins surround base human DNA within the cell nucleus. Mitochondrial DNA lies in sort of additional small nuclei in the cytoplasm outside the cell nucleus. The relationship between mitochondrial DNA and epigenetic protein is not well understood, but is the subject of much research. The research I was able to find points to strong chemical communication bonds between mitochondria and epigenetic proteins. Some of the studies I read even point to mitochondria as the engines which maintain the structure of epigenetic proteins.

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.......In which case, my point still stands. Our ability to form body chemistry in a way which digests foods like gluten comes from our mothers, and was formed in them when their eggs were formed.

What I've read says you are correct, that the teratogens I'm referring to, which affect the formation of the mother's egg mitochondria, do not necessarily affect the mother.

It's interesting reading that scientists decades ago formed the theory of "mitochondrial disease". If you read through the elusive symptoms, many are the exact same symptoms now associated on these pages with celiac disease .....heart arrhythmia, thyroid disease, diabetic ketosis, renal failure, recurring mucosal infection, digestive dysfunction and pain.......

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In my opinion celiac disease and mitochondrial disease are the same disease. The question is, how do they fit together?

But mitochondria also perform other vital functions. Right now I would like information on the rolls and relationships of SOD protein formed by the mitochondria and the SOD1 aggregate protein whose mis-folded mutation is implicated in pituitary dysfunction, ALS (Lou Gehrig's disease), and macular degeneration. The casein and gluten opioids you mentioned have also been implicated in these diseases.

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[dally099]

hi, as a mom with 2 autistic kids i have had this proposed to me numerous times. i refuse to put my kids on a gluten-free diet, being on it myself i know how restrictive and difficult it can be, i figure my kids have a hard enough time in the world as it is. as well there is not one study, (not one trust me ive looked) that shows any deffinitave positive results for gluten-free diets in autistic kids. a lot of the time when there is improvement after the diet is introduced there is also the additon of speech and OT therapies in the childs life as well. and something that i notice it is very wealthy and famous people who push this a lot and these are the people who can truly afford some amazing services for there kids so you know there is going to be drastic changes within those children.

this is only my thoughts all parents of autism have there own thoughts on this, but my son and daughter eat very picky as it is and i cant imagine further restriciting them, as well there docs and dieticians do not reccomend it for them.

hope this helps

nadine

[Rachel--24]

and something that i notice it is very wealthy and famous people who push this a lot and these are the people who can truly afford some amazing services for there kids so you know there is going to be drastic changes within those children.

this is only my thoughts all parents of autism have there own thoughts on this, but my son and daughter eat very picky as it is and i cant imagine further restriciting them, as well there docs and dieticians do not reccomend it for them.

hope this helps

nadine

Just wanted to say that although I dont have any children...the doctors that I see for my own condition are primarily treating autistic children. They do put these kids on the gluten-free/cf diet and it does help them....somtimes very dramatically.

These arent children of wealthy famous people.....just regular folks who keep their kids on the diet because they've had positive results.

I realize that many parents choose not to try the diet....and that it can be difficult since most of these kids are picky eaters and crave the gluten/casein foods. Another option is enzymes such as Peptizyde and Zyme Prime. Alot of parents who dont want to do the diet have reported improvement with the use of these enzymes.

All of the Dr.'s I've ever spoken to would strongly recommend the diet for ASD kids....as well as for adults like myself who have similar problems.

[veggienft]

My point above is that maternally inherited mitochondrial DNA can dictate the mental development of children by impeding their response to carbohydrates and glycoproteins like gluten. You would have to start your children on a selected elimination diet before or as they start mental development to get a full benefit.

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Autism. The etiology of autism is uncertain and might vary among individuals (e.g., Gilberg, Trygstad, & Foss, 1982; Trottier, Srivastava, & Walker, 1999). Hypotheses regarding etiology include genetics, environmental toxins, infectious agents, enzymatic problems, and dietary factors. In this section we discuss some evidence related to the hypothesis that digestive and dietary factors may be involved. Particular interest has been directed to the relation between childhood autism, as well as schizophrenia, to problems with the proteins that occur in dairy and grain products (Dohan, 1983; Horvath, et al., 1999). Such problems involve immune responses as well as gastrointestinal symptoms. For example, researchers at the University of Minnesota have found T-cell reactivity to the dietary proteins in soy, milk, and wheat in 75 to 80% of a group of 83 children with autism (Reuters Medical News, 2001b). Others have related problems with dietary proteins to the gastrointestinal symptoms frequently found among these populations (e.g., Goodwin, Cowen, & Goodwin, 1971; Hovrath, et al., 1999; Wakefield, et. al., 1998; Quigley & Hurley, 2000).

One explanation for the relation between gut and brain problems is intestinal permeability. Intestinal permeability can allow passage of the opioid peptides from food proteins such as glutens and caseins to pass into the blood stream and enter the brain. Some hypothesize that the behaviors seen in autism and schizophrenia could be the result of exogenous peptides affecting neurotransmission and the neuro-regulatory role normally performed by the endogenous opioid peptides such as enkephalins and endorphins (e.g., Dohan, 1988; Singh & Kay, 1976; D'Eufemia, et al., 1996; Mehl-Madrona, 2000; Shattock & Savery, 1996). An argument in support of this hypothesis, often referred to as the opioid excess hypothesis, is that some symptoms of autism (e.g., diminished sensitivity to pain, limited clinging behavior, unpredictable response to stimuli, reduced socialization, repetitive stereotyped behavior) can be simulated in animals by administering opiates during infancy (Panksepp, 1979, as cited by Deutsch, 1986; Sher, 1997). Moreover, when gluten exorphin, a fragment from wheat gluten, was injected into mice it suppressed pain-inhibition and influenced emotionality and memory processes affecting both peripheral and central nervous system (Takahashi, et al., 2000). These are all, of course, symptoms found in autism. Moreover, unique urinary peptide patterns have been found among autistic children as compared with those of normally developing peers and children who have mental retardation without psychoses (Gilberg, et al., 1982; Reichelt, Hole, Hamberger, et al., 1981). Some suggest that many of the peptides found in the urine are derived from the incomplete breakdown of food and that they may well result in enhanced opioid activity (Shattock & Savery, 1996).

The opioid excess hypothesis has also been tested by examining the effect of various treatments on the behavior of children with autism including the use of opiate antagonists and the dietary exclusion of gluten and caseins. Level of beta-endorphin has been correlated with severity of stereotypic behavior in children with autism (Ernst, Devi, Silva et. al., 1993). Naltroxone is a specific opiate antagonist that blocks the action of endogenous opioids at opiate receptors and is an approved treatment for substance abuse such as heroin addition. It has been reported to have positive effects in schizophrenia and on impulse control in animals (Deutsch, 1986; Soderpalm & Svensson, 1999). A number of studies have examined its effect on children with autism. Some case studies and small clinical trials have reported that a some autistic children treated with naltroxone show significant reduction of symptoms including hyperactivity, self-injurious behavior, aggressiveness, poor attention, inappropriate social and play behavior with no improvement in learning skills (e.g., Bouvard, Leboyer, Launay, et al., 1995; Campbell, Anderson, Small, et al., 1993; Cazzullo, Musetti, Musetti, et al., 1999; Kolmen, Feldman, Handen & Janosky, 1997; Leboyer, Bouvard, Launay, et al., 1993; Scifo, Cioni, Nicolosi, et al., 1996; White & Schultz, 2000). In contrast to these findings, other studies report little effect of naltroxone on maladaptive and social behavior including communication skills (e.g., Feldman, Kolmen, & Gonzaga, 1999; Willemsen-Swinkels, Buitelaar, & van Engeland, 1996; Willemsen-Swinkels, et al., 1995; Zingarelli, Ellman, & Hom, 1992). These data could be interpreted as weak evidence in support of the opioid excess theory.

Studies on dietary intervention come mainly from Europe, primarily Norway and Great Britain. Some success with removal of gluten and casein from the diet has been reported for patients with schizophrenia (e.g., De Santis, Addolorato, Romito, et al., 1997; Singh, & Kay, 1976). In fact, Dohan and colleagues point out that schizophrenia is rare in cultures where grain is rare in the diet (Dohan, Harper, Clark et al., 1984). Dietary changes suggested for children with autism are most often reduction or removal of casein and/or gluten. Parents of children with autism have reported that such dietary intervention had a significant impact on their child's behavior (Shattock, 1995). In a summary of seven group studies, plus three case studies and two surveys on dietary intervention with autistic children, Knivsber, Reichelt and Nodland (2001) report positive changes in autistic behavior in all but one study, as well as a reduction in number of epileptic fits and changes in urinary peptide abnormalities in all studies that considered these latter two factors. For example, in a case study of an 8-year-old boy with autism, investigators found that certain foods (such as wheat, corn, sugar and dairy products) produced behavior disorders (O'Banion, Armstrong, Cummings, & Strange, 1978). One study found that autistic patients had higher levels of antibodies to casein than controls and that an 8-week period of a diet free of cow's milk yielded marked improvement in symptoms (Lucarelli, Frediani, Zingoni, et al., 1995). Some researchers report dietary intervention with autistic children brought about improvement in the urinary peptide pattern as well as in educational and developmental measures (Knivsberg, Reichelt, Hoien, & Nodland, 2002; Knivsberg, Wiig, Lind, et al., 1990). In contrast, others found no change in urinary profile, although they also reported improvement on a number of behavioral measures (Whiteley, Rodgers, Savery, & Shattock, 1999). At the 12th International Conference on Autism, Kniker reported that elimination of dairy, grains, food additives, and caffeine dramatically changed behavior of about one-third of the autistic children observed, however, half of these children improved whereas half deteriorated (Reuters Medical News, 2001b). Finally, one study reported no association between ingestion of gluten and symptoms of autism and concluded that gluten-free diet could be just another way to isolate the individuals in this group (Sponheim, 1991). Thus, results are mixed but some preliminary evidence supports Hypothesis D, that dietary intervention involving removal of casein and gluten may help a few children with autism. Unfortunately, many of the studies reporting on dietary intervention are difficult to obtain through the usual sources (e.g., PubMed) and many are not reported in peer-reviewed journals. Clearly more research is needed to clarify whether the opioid excess theory can be supported and if changes in diet are the most appropriate intervention.

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Without knowing the father's DNA DQ patterns, the list of gluten-disease genetics in your signature would potentially give each of your children a 50% chance of gluten disease genetics. If the father has gluten disease genetics, the chances rise upward from 50% that your children will have that potential. But roughly 1/3 of people of European ancestry have gluten genetics. What makes the difference in whether or not an offspring actually contracts celiac disease or a related autoimmune disease like autism? .......their maternally inherited mitochondrial DNA, and its relationship to their inherited base DNA.

You have celiac disease, which means there's a very good chance you passed on mitochondrial DNA capable of "activating" gluten-related disease in your children.

.......and two of your children are autistic.

.......food for thought.

The choices you face are difficult, and I can't make them for you. However, as the celiac son of a schizophrenic mother I have good reason to be biased. Try the diet on your children.

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