Archive for the ‘GFCF Diet’ Category

So many diets to choose from… What does it all mean?

Friday, August 19th, 2011

[The following comment is to help you understand the complexities of choosing one diet over another, combining them, or interpreting lab results correctly.  Because of the complexity of the problem, the comment is given for educational purposes.  However, you will need to discuss the specific application(s) with your clinician.]

Frequently Dr. Neubrander is asked what diet is the best or in what order the diets should be added. Please note that diets are an individualized thing and there is no simple answer. A few general rules that will apply to most patients the majority of the time (with major exceptions, of course!) are as follows: Begin with the GFCF diet first and observe for clinical benefits. The next diet is usually the SCD followed by the diets that eliminate special foods (elimination and rotation), food chemicals, e.g. phenolics, salicylates, glutamates, excitotoxins, etc. This can be followed by a “limited” low oxalate diet (not yet strict), the Body Ecology diet or the GAPS diet (Gut and Psychology Syndrome diet). The last diet many parents move to is a very “strict” low oxalate diet. NOTE THAT THERE IS NO ‘PERFECT ORDER’ AND DIFFERENT CHILDREN WOULD DO BETTER TO SWITCH THE ORDER.  This is something that parents and their clinician could do together, though more often than not parents experiment on their own as they watch what works and what does not work for their child.

As stated, there are reasons that a child may need to skip over “the next usual diet to be added” to go farther down the list. These “skips” or “exceptions” are usually based on a child’s symptoms, a discussion too big and too specific to be covered in this comment. Trial and error is the tried and true method. Lab tests are very often misleading and confusing. In addition, lab tests are not always available for many of the different “mechanisms of action” that may be operative. Even if a lab test was possible to do, because there are so many different lab tests to look at all the different mechanisms — IgE “true” food allergy, IgG non-allergic “delayed” hypersensitivity, difficulty breaking down peptides, gastrointestinal enzymatic deficiencies, cytotoxicity, direct chemical reactions, toxic or intolerance reactions to food components or contaminants, etc — it is financially impossible and impractical to do them all. Therefore, the CLINICAL TRIAL IS THE BODY’S BEST LAB TEST, but only if done in a systematic and progressive manner.

In general the casein-free, gluten-free diet helps over 60% of children on the autism spectrum according to ARI data.  Though such a diet has been historically mocked by our detractors as unproven, unhealthy, and ineffective, as time marches on more and more peer reviewed articles are appearing in respectable journals documenting this diet works for a significant subset of the children on the spectrum.  The reasons discussed in the published papers why this diet works has a spectrum of its own ranging all the way from “unknown but definite” to “gastrointestinal” all the way to “immunological” reasons.  One recently described but definite reason that milk may be playing a negative role in children on the spectrum is because of a cerebral folate deficiency.  In the “absolute” deficiency syndrome there is an autoimmune reaction whereby the body produces antibodies against the folate receptors found at the choroid plexus, thus blocking the body’s ability to get reduced folic acid molecules across the blood brain barrier into the cerebral spinal fluid and ultimately into the neurons.  It is becoming apparent that every child does not need to meet the criteria to be diagnosed with an “absolute” cerebral folate deficiency to be suffering similar negative neurological symptoms due to a “partial or incomplete” blockade of the same biochemical pathway.  Cerebral folate deficiency studies show that when milk is present, the blocking antibodies rise, that when milk is taken out of a child’s diet the blocking antibodies fall substantially, and that when milk is reintroduced, the blocking antibodies once again rise very quickly!  Research also shows that the longer one is exposed to milk, the higher the antibody levels become.  Of special interest at the time of this post (August 2011) is that out of the 120 children we have tested so far in our clinic for folate receptor autoantibodies, 2/3 of them (65.8%) have been positive to either the blocking and/or binding folate receptor autoantibodies.  Of even greater interest is that we can often do something to treat the problem effectively, occasionally even to the ‘Wow-degree’!

What is not well understood is that there are many different “mechanisms” as to why a certain food may cause problems in different subsets of individuals that look alike and have the same types of symptoms.  Let’s use casein as one good example.  Some patients cannot tolerate casein well because of the “OPIOID” MECHANISM which causes a drug-like reaction.  This opioid-like phenomenon is due to the inability of “specific” enzymes that break down key bonds that occur between the molecules holding together certain parts of a casein molecule [also certain parts of a gluten molecule].  Therefore, “if” a patient lacks this specific enzyme, DPPIV ["DPP-four"], casein may not be broken down into its smallest common denominator (single amino acids named “peptides”) and thus remain as polypeptides or “dipeptides,” which are then absorbed and subsequently “misread” by the body’s opioid receptors with which they cross react as opioids [morphine-like drugs].  This “OPIOID REACTION” to casein/milk products is only “ONE SPECIFIC MECHANISM” to a host of mechanisms why dairy may not be good for a certain subset of children.  The “ADENOSINE CONNECTION” is “ANOTHER SPECIFIC MECHANISM” whereby dairy products from milk (not eggs), acting through the DPPIV pathway, blocks the effectiveness of methyl-B12.

“ANOTHER SPECIFIC MECHANISM” why some children will do better without dairy products is because the child may have “TRUE FOOD ALLERGIES”, e.g. the IgE antibody response [accepted by all conventionally trained physicians].  Still “ANOTHER SPECIFIC MECHANISM” why some children will do better without dairy products is because the child may have “FOOD SENSITIVITIES/INTOLERANCES” e.g. the IgG antibody response [accepted by most alternative medicine practitioners but only a small percentage of conventionally trained physicians].  “ANOTHER SPECIFIC MECHANISM” would include AN ABNORMAL CYTOTOXIC RESPONSE when the nuclei of cells are directly incubated with casein.   When this is done, the nuclei “get angry” by taking in a lot more blue dye and the nuclei look just like the sky before a thunderstorm instead of a pretty blue sky on a summer day.  Still “ANOTHER SPECIFIC MECHANISM” would include LACTOSE INTOLERANCE whereby “a different enzyme” than the one described above cannot break down milk sugar.  When this happens, the undigested milk sugar bypasses absorption in the small intestine and travels down to the large intestine where bacteria and yeast say, “Yippee, beer and pretzel time!” and have a party on the front lawn of the large intestine.  Unfortunately the byproducts of bacteria and yeast being “overfed” is the production of hydrogen and methane gases resulting in the child feeling bloated, having flatulence, and possibly abdominal pain.

Many similar mechanisms are happening with a child that may be better on a gluten-free diet, e.g. the DPPIV opiod-mechanism, the IgE and IgG mechanisms, and the cytotoxic mechanism.  An ADDITIONAL MECHANISM comes into play with gluten, that being the AUTOIMMUNE PHENOMENON known as CELIAC DISEASE.  In this disorder the body makes an antibody against its own intestinal mucosa.  The mucosal lining becomes damaged and therefore the absorptive surface becomes compromised which impairs the body’s ability to absorb.  This can be pictured by opening one’s hand to observe the fingers and knuckles which we will define as absorptive surfaces.  When antibodies destroy the surface lining, picture this by making a fist.  Now compare the two – the first one has a tremendous surface area while the second one has very little.  So it is with celiac disease.

A popular diet right now for children on the autistic spectrum is the Specific Carbohydrate Diet (SCD).  The “mechanism” at work in this diet is still another enzyme deficiency — a specific class of enzymes that are supposed to break down starches or “two-part, two-molecule sugars.”  The food classification known as “carbohydrate” is comprised of individual biochemical units known as sugars [these are "biochemical sugars" that are not the same as the lay term "sugar"].  These biochemical sugar molecules have common names, e.g. glucose, fructose, and galactose.  Biochemically these individual units of biochemical sugars are called mono ["one"] saccharides ["sugar molecule"].  When two of these individual sugar molecules are combined, they are now called dissacharides ["two" "sugar molecules"].  When a single “glucose” biochemical sugar molecule combines with a single “galactose” biochemical sugar molecule, the result is the disaccharide lactose, commonly known as “milk sugar.” When a single glucose biochemical sugar molecule combines with a single fructose biochemical sugar molecule, the result is the disaccharide commonly known as “fruit sugar.”  When a single glucose biochemical sugar molecule combines with another single glucose biochemical sugar molecule, the result is the disaccharide commonly known as a “starch.”  Clinically it seems that there is a subclassification of enzymes that is unable to break down the “starchy” disaccharides [names like isomaltase -- a disaccharidase; palitinase -- a dissacharidase, etc].  These types of disaccharidases are especially hard on the intestinal tract [remember "ase" added to the end of a word just means an enzyme that digests the similarly named substrate, e.g. lactase digests the substrate lactose, etc.].  By simply removing these “relatively hotter disaccharides” from a child’s diet, the child may improve significantly.

Other diets include elimination diets based on “true allergy tests — IgE tests,” on “intolerance/sensitivity allergy tests — IgG tests,” “cytotoxic sensitivity tests — lymphoblastic activation,” or “chemical reactions to food substances,” e.g. the Feingold diet and other similar diets, “metabolic disorders,” e.g. avoidance of foods containing items like phenols, sulfur pathway offenders, tyramines, nightshades, the oxalate diet, etc.  Each of these diets may work because of single mechanisms or alternatively because of combined synergistic mechanisms working together.

PLEASE NOTE THAT THE SINGLE MOST VALUABLE LABORATORY TEST is a child’s specific reaction to the introduction, restriction, and then reintroduction of a potentially offending substance.  Therefore, When In Doubt, Cut It Out of the child’s diet and observe clinically for results.  Understand that the removal of an item may not give clinical results that are easily observable.  However, with the reintroduction of the food, symptoms or decompensation may then occur.

The only real exception to the general principle stated above is to the “big baddies,” things that are known to be life-threatening, things like peanuts, shrimp, etc.  These are true IgE allergies and could have serious consequences if not respected.  To these substances one should not consider reintroducing them just to see if the child has improved or can tolerate the substance or not.  The problem is that if reintroduced, two things could happen.  With the first reintroduction after being off the food for a period of time, the body may not have an outward reaction, though internally the body will lose what was a “temporary amnesic response” because it had avoided the food for a long period of time while it sets itself up for a serious reaction should the food be ingested again within a relatively short period of time.  The second thing that could happen is that the child may react to the first reintroduction of the food and have a potentially life-threatening anaphylactic emergency.

Remember that each child is different and that each diet is different. The best way to determine when to start and when to stop a diet will be different, one child to the next.  Therefore I always recommend professional help in these matters.  As is standard for my practice, if I believe a result to starting a diet could be “very important,” or have significant benefits or side effects, I will recommend that the diet be started at a time when no other variables are being added or removed from the child’s program.  The same general principle applies to the discontinuation of a diet.

Diets are very frustrating, no doubt.  They are not “The American Way”!  The right diet is not easy to find.  And no diet is ever easy to do.  It takes commitment by the parents and alters the family’s lifestyle, one of the hardest things for all of us to do – change!  However, diets are worth investigating by every parent because when the correct diet is found, many of the troublesome symptoms associated with the autism spectrum will diminish or disappear completely~!  Good luck on your journey.  We are here to help you in any way we can along the way.


Parents are right again! Scientific proof at last showing the GFCF diet works!

Sunday, August 14th, 2011

Remember how all those studies came out a few years ago telling us that the diet did not help/cure autism. Parents were imagining this as the studies showed that diet had no effect.  The gut has nothing to do with the brain.  Studies on well children prescreened to make sure that they had no bowel issues were administered the diet and wonders of wonders the diet did nothing for autism in children with no bowel issues. Well lately things are looking up for parents.  So after years of being patronized by physicians and the scientific community, it is now being shown that the parents may not be crazy after all. Here are a few of the more recent articles to come out.

Nutr Neurosci. 2010 Apr;13(2):87-100.

The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disorders.

Whiteley PHaracopos DKnivsberg AMReichelt KLParlar SJacobsen JSeim APedersen LSchondel MShattock P.


Dept of Pharmacy, Health & Well-being, Faculty of Applied Sciences, University of Sunderland, UK.


There is increasing interest in the use of gluten- and casein-free diets for children with autism spectrum disorders (ASDs). We report results from a two-stage, 24-month, randomised, controlled trial incorporating an adaptive ‘catch-up’ design and interim analysis. Stage 1 of the trial saw 72 Danish children (aged 4 years to 10 years 11 months) assigned to diet (A) or non-diet (B) groups by stratified randomisation. Autism Diagnostic Observation Schedule (ADOS) and the Gilliam Autism Rating Scale (GARS) were used to assess core autism behaviours, Vineland Adaptive Behaviour Scales (VABS) to ascertain developmental level, and Attention-Deficit Hyperactivity Disorder – IV scale (ADHD-IV) to determine inattention and hyperactivity. Participants were tested at baseline, 8, and 12 months. Based on per protocol repeated measures analysis, data for 26 diet children and 29 controls were available at 12 months. At this point, there was a significant improvement to mean diet group scores (time*treatment interaction) on sub-domains of ADOS, GARS and ADHD-IV measures. Surpassing of predefined statistical thresholds as evidence of improvement in group A at 12 months sanctioned the re-assignment of group B participants to active dietary treatment. Stage 2 data for 18 group A and 17 group B participants were available at 24 months. Multiple scenario analysis based on inter- and intra-group comparisons showed some evidence of sustained clinical group improvements although possibly indicative of a plateau effect for intervention. Our results suggest that dietary intervention may positively affect developmental outcome for some children diagnosed with ASD. In the absence of a placebo condition to the current investigation, we are, however, unable to disqualify potential effects derived from intervention outside of dietary changes. Further studies are required to ascertain potential best- and non-responders to intervention. The study was registered with, number NCT00614198.

PMID: 20406576

Notice there is increasing interest. For years parents have said… but only now is there increasing interest.  Also the cover your butt conclusion “unable to disqualify potential effects”.  So are there any other studies out there? it appears so. More and more studies are coming out showing that the GFCF diet does have a scientific reason for the reduction in symptoms.

J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.

Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives.
de Magistris LFamiliari VPascotto ASapone AFrolli AIardino PCarteni MDe Rosa MFrancavilla RRiegler GMiliterni RBravaccio C.

Department Magrassi-Lanzara, Gastroenterology, Second University of Naples, Italy.


Intestinal permeability (IPT) was investigated in patients with autism as well as in their first-degree relatives to investigate leaky gut hypothesis. Faecal calprotectin (FC) was also measured in patients with autism, either with or without gastrointestinal symptoms, and in their first-degree relatives.

IPT results, assessed by means of the lactulose/mannitol test, were compared with adult and child controls and with FC values.

A high percentage of abnormal IPT values were found among patients with autism (36.7%) and their relatives (21.2%) compared with normal subjects (4.8%). Patients with autism on a reported gluten-casein-free diet had significantly lower IPT values compared with those who were on an unrestricted diet and controls. Gastrointestinal symptoms were present in 46.7% of children with autism: constipation (45.5%), diarrhoea (34.1%), and others (alternating diarrhoea/constipation, abdominal pain, etc: 15.9%). FC was elevated in 24.4% of patients with autism and in 11.6% of their relatives; it was not, however, correlated with abnormal IPT values.
The results obtained support the leaky gut hypothesis and indicate that measuring IPT could help to identify a subgroup of patients with autism who could benefit from a gluten-free diet. The IPT alterations found in first-degree relatives suggest the presence of an intestinal (tight-junction linked) hereditary factor in the families of subjects with autism.

PMID: 20683204

There are more but this one is one of my favorites.

Ann Clin Psychiatry. 2009 Oct-Dec;21(4):205-11.
The possibility and probability of a gut-to-brain connection in autism.
Reichelt KLKnivsberg AM.
Department of Pediatric Research, Rikshospitalet Medical Centre, University of Oslo, Oslo, Norway.
We have shown that urine peptide increase is found in autism, and that some of these peptides have a dietary origin. To be explanatory for the disease process, a dietary effect on the brain must be shown to be possible and probable.
Diagnosis was based on DSM-III and DSM-IV criteria. We ran first morning urine samples equivalent to 250 nm creatinine on high-performance liquid chromatography (HPLC) reversed phase C18 columns using trifluoroacetic acid acetonitrile gradients. The elution patterns were registered using 215 nm absorption for largely peptide bonds, 280 nm for aromatic groups, and 325 nm for indolyl components. We referred to a series of published ability tests, including Raven’s Progressive Matrices and the Illinois Test of Psycholinguistic Ability, which were administered before and after dietary intervention. The literature was also reviewed to find evidence of a gut-to-brain connection.
In autistic syndromes, we can show marked increases in UV 215-absorbing material eluting after hippuric acid that are mostly peptides. We also show highly significant decreases after introducing a gluten- and casein-free diet with a duration of more than 1 year. We refer to previously published studies showing improvement in children on this diet who were followed for 4 years and a pairwise matched, randomly assigned study with highly significant changes. The literature shows abundant data pointing to the importance of a gut-to-brain connection.
An effect of diet on excreted compounds and behavior has been found. A gut-to-brain axis is both possible and probable.

PMID: 19917211

The gut and diet CAN influence the brain!   Shocking I know. Such a recent discovery except for the part of disregarding parental testimonies for 15 years or so. Maybe in the future, science will pay attention to parents and try to design studies that look for the why parents are seeing something rather than looking for the why a treatment could  not  work.