NAVIGATING DIFFERENT DIETS IN CHILDREN WITH AUTISMBariah Dardari, M.D, FAAPAmerican Hospital Dubai

What the diet have to do with it??? Increased prevalence in

Autism>>environmental factors>>Diet Parents survey on ARI list diet as the most

successful intervention Global displacement of traditional foods

accompanied by malnutrition and chronic disease

When traditional people adopt modern diets there are increased rates of CVD, diabetes, cancer, hyperlipidemia,hypertension, and obesity.

we face the Dilemma where traditional high-fat foods also contain high amounts of PCBs, mercury, pesticides, and other contaminants.

What the diet have to do with it??? Ketogenic diet and

seizures Feingold diet and

ADHD : Pesller et al. 2010 pilot study in Netherland

Celiac disease

What the diet have to do with it??? previous reports indicate that the prevalence of GI

symptoms ranges widely in individuals with ASD, from 9 to 91% in different study populations

Macroscopic and histological observations in ASD include findings of ileo-colonic lymphoid nodular hyperplasia, enterocolitis, gastritis, and esophagitis

Associated changes in intestinal inflammatory parameters include higher densities of lymphocyte populations, aberrant cytokine profiles, and deposition of immunoglobulin (IgG) and complement C1q on the basolateral enterocyte membrane

Reported functional disturbances include increased intestinal permeability, deficient enzymatic activity of disaccharidases, increased secretin-induced pancreatico-biliary secretion , and abnormal fecal Clostridia taxa

Some children placed on exclusion diets or treated with the antibiotic vancomycin are reported to improve in cognitive and social function. Furthermore, a recent study found a strong correlation between GI symptoms and autism severity

Recent Data about the role of Diet Impaired Carbohydrate Digestion and Transport and

Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances. PLoS ONE 2011

Major findings in this study that may shed light on GI morbidity in ASD include the observations that: (1) levels of transcripts for disaccharidases and hexose transporters are reduced in AUT-GI children;

(2) AUT-GI children have microbial dysbiosis in the mucoepithelium;

(3) dysbiosis is associated with deficiencies in host disacharidase and hexose transporter mRNA expression.

propose a model whereby deficiencies in disaccharidases and hexose transporters alter the milieu of carbohydrates in the distal small intestine (ileum) and proximal large intestine (cecum), resulting in the supply of additional growth substrates for bacteria. These changes manifest in significant and specific compositional changes in the microbiota of AUT-GI children .

Nutritional Genomics

The human genome today is virtually unchanged from what it was 50,000 years ago. Yet today’s food supply bears little resemblance to that on which our ancestors evolved.

expectations for this field is to match foods to the individual’s genetically determined ability to digest, absorb, and use the nutrients within. Avoiding foods that are not an appropriate match and focusing on those with a positive impact on health

Nutritional Genomics

ex: MTHFR gene encodes enzyme 5,10-methylenetetrahydrofolate reductase that activates folate, which in turn serves as a critical methyl donor as well as being essential to maintaining desirable levels of homocysteine.

Individuals with the 677C>T variation in the MTHFR gene are at risk for impaired MTHFR

enzymatic activity when folate intake is low.

The Role of Nutritional Genomics in Developing an Optimal Diet for Humans Ruth DeBusk, PhD, Nutrition in Clinical Practice December 2010

The Gut Brain connection

The Gut Brain connection

The Gut Brain connection

The CF/GF Diet

The CF/GF Diet

Freidman 1999 certain ASD subjects deficent in enzyme Dipeptidyl peptidase DPP-IV responsible for breakdown of peptides

The specific Carbohydrate Diet The purpose is to deprive the microbial worlds of the intestine of

the food it needs to overpopulate, the sugars from the carbohydrates.

contains predominantly "predigested" carbohydrates allows maximal nourishement without overstimulation of the intestinal microbial population.

As the microbial population decreases due to lack of food (while being balanced by lactobacilli), its harmful by-products also decrease, freeing the intestinal surface of injurious substances. No longer needing protection, the mucus producing cells stop producing excessive mucus, and carbohydrate digestion improved.

many people with IBS and IBD are unable to split disaccharide sugars (lactose, sucrose, maltose, and isomaltose) into single molecule sugars.

The Specific Carbohydrate Diet also eliminates grains, which generally cause inflammation of the intestines in people with IBD. Leo Galland, MD, has found that the Specific Carbohydrate Diet works well for people with IBD."

The specific Carbohydrate Diet many research articles to show that the toxins

found in microorganisms play an important role in the suspected causes of ASD, in particular, lipopolysaccharide ( LPS) the bacterial toxins from gram negative bacteria that inhabit the guts of autistic children.

LPS toxicity works synergistically with mercury and other heavy metal poisonings to expand damage. These heavy metals increase harm from LPS.[1] In addition, LPS decreases glutathione levels making it even more difficult for the body to detoxify heavy metals.

The GAPS Diet

An altered Abnormal intestinal permeability in children with autism P D'Eufemia JAN 2008 Acta Paediatrica

intestinal permeability was found 43%) autistic patients, but in none of the 40 controls. We speculate that an altered intestinal permeability could represent a possible mechanism for the increased passage through the gut mucosa of peptides derived from foods with subsequent behavioural abnormalities.

Elimination Diet

Low Oxalate Diet

Low phenol Diet

Effects of Phenol-Depleted and Phenol-Rich Diets on Blood Markers of Oxidative Stress Hwa-Young Kim, MSc J AM college of nutrition June 2003

Evidence of difference in phenol metabolism in patients with ASD>>causing oxidative stress in CNS ( Evans 2008, Waring 2000)

Some individuals show reaction to phenol containing foods( spinach, berries, soya, cocoa…) and Salycalate due to Phenolsulfotransferse enzyme which seems to function abnormally in some ASD patients.Waring 1993 UK

Low Glutamate/ Aspartame diet Glutamic acid excitatory

Neurotransmitter in Brain Glutamine is found in the following foods: Beans,

brewer's yeast, brown rice bran, caseinate, dairy products, eggs, fish, lactalbumin, legumes, meat, nuts, seafood, seeds, soy, whey, whole grains. Hydrolysis of gluten, beet root or other proteins

In 2005 Tebartz et al of Germany reported "increased prefrontal and hippocampal glutamate concentration in schizophrenia".

Reynolds (1991) In 1991 Reynolds of the UK reported glutamate concentrations to be high

Serotonin Diet

Dietary increase in Serotonin ( e. g Banana, avocados, pineapple, papaya, walnuts) decreased self injury behavior in Developmentally delayed and Down’s patients

Gedye, A. Biological Psychiatry. 1991: Placebo controlled study: Buspirone was more effective in reducing aggressive/ self injury behavior when combined with serotonin diet.

The Body Ecology Diet

Started by Donna Gates 2006. no published data about its efficacy

Draws on different dietary approaches ( Macrobiotic diet, D’Adamos Eat for your blood type diet, the Raw food diet..)

Low carbohydrate, low sugar, low dairy, emphasis on raw/ minimally processed foods, fermented foods

Provide high probiotic support, may be beneficial for patients with Dysbiosis.

Supplemental Diet

Low urine Calcium level in autistic patients with eye poking behavioral

Clinical pilots Studies showed that ASD and related neurological disorders in adults stems from lack of circulating nutritional neural lipids.

Lipidomics: the function of Vital lipids in embryogenesis preventing ASD. T.Tallberg, J Lipids: 2011

Recommendation of high vital lipids diet for pre and post pregnancy and during BF to secure normal development and enhance IQ in offspring.

Supplemental Diet

MIND institute A proteomic study of serum from children with autism showing differential expression of apolipoproteins and complement proteins

Children with autism 4–6 years of age (n = 69) were compared to typically developing children A total of 6348 peptide components were

quantified. Of these, five peptide components corresponding to four known proteins had an effect size > 0.99 with a P < 0.05 and a Mascot identification score of 30 or greater for autism

compared to controls. The four proteins were: Apolipoprotein (apo) B-100, Complement Factor H Related Protein (FHR1), Complement C1q and Fibronectin 1 (FN1). In addition, apo B-100 and apo A-IV were higher in children with high compared to low functioning autism.

Apos are involved in the transport of lipids, cholesterol and vitamin E. The complement system is involved in the lysis and removal of infectious organisms in blood, and may be involved in cellular apoptosis in brain.

How do I know if my child will benefit? Hyperactivity, sleep problems Bloating, constipation, diarrhea Recurrent OM, Eczema, shiner, AR Craving food, Pica, Fatigue, excessive sweating Family history of Allergies, Celiac Dx, GI

diseases.

Laboratory Assessment

Casomorphine, Gliadomorphine Food RAST ( IGG, IGE) Iron, Ca, Vit D, Oxalate, Zinc, Mg. Lipid profile Comprehensive Stool analysis OAT, AA profile Celiac disease panel

How to assess results

Do it with guidance of physician/dietitian Do it right But be flexible Assess every 3 month Not every diet work for every patient Keep a food dietary Remember that it’s only part of the

biomedical/ behavioral therapy

Avoid pitfalls

CF/GF diet: osteoporosis, lethargy, retinal degeneration, kidney stones.

Low phenol diet: low cholesterol, low antioxidant

Low phenylalanine diet: low Omega 3-6-9

SCD: : osteoporosis, lethargy, retinal degeneration, kidney stones, high copper

Books to read

Dietary interventions in ASD. By Kenneth Aitken

Food and the Gut Reaction by Elaine Gottschall, B.A., M.Sc.