What are the implications for selective/restrictive diets (ie: great white diet) for children with autism? Consider physiological (such as impact of protein imbalance or limited ingestion of lysine, etc) and activity restrictions.
Many articles have researched the food selectivity/restriction via questionnaires to the caregivers. It has been determined that the fewer food items the family eats, the fewer food items the child will eat. Studies conflict as to whether sensory affects the selectivity. (Shreck and Williams2006)
Food preferences of children with autism are usually related to high sugar content like cake, cookies, white bread, grapes, pizza, ice cream. Most of these foods are on the high glycemic index, which measures how quickly digestion of carbohydrates triggers a peak in blood sugars. Further research to explore how food consumption, change in blood sugar results in immediate behavioral changes was recommended. (Shreck and Williams2006)
Another theory is the sensitivity could be related to physiological component that the composition of the tongue may be extremely sensitive to bitter taste which may result in an aversion and food selectivity. (Shreck and Williams2006)
A research article had 31 children go on a gluten free diet with urinalysis prior and after removal and then the return of gluten. 22 children were successful in completing the diet. Behavior rating was done prior to the diet and then five months of being gluten-free. Behaviors may worsen up to 21 days after starting a GF diet like anxiety, clinginess, crying, flu-like symptoms, and increased urination. Behaviors that showed the most significant differences after the five months was the increased desire to interact, increased curiosity/interest and increased number of “good days”, increased smiling, eye contact and play behavior, increased attempts to communicate and an increased number of initiations of interactions, decrease in self-injurious behaviors. Behaviors worsened upon re-introduction of gluten. The urinalysis showed an overall reduction in the urinary IAG excretion and creatinine levels except in one case. There is no correlation between the reduction in IAG and improvements in behaviors. (Whiteley 1999) Another study looked at levels of IAG in children with ASD to TD children and found no difference in the amount that is secreted showing that IAG levels are not correlated with autism. (Wright 2005) Research is questioning the relationship of opioid-SIB relationship through a possible reorganization of abnormal functioning of pain receptors, governed by the presence of elevated levels of opioid peptides. (Whiteley 1999) A more recent case study believes that gluten and casein are triggers for neurodevelopmental dysfunction. Further theories are exploring the pathophysiologic mechanisms that may provoke the central nervous system. The leaky gut is one theory; another is that casein and gluten trigger inflammation in the gut leading to autoimmune illness or cross reactivity with other potential CNS antigens. Another theory is the gut inflammation in celiac patients can precipitate underlying malabsorption of nutrients required for the CNS functions. Certain essential nutrients can result in brain malfunction, potentially manifesting as a developmental disorder. This study recommends testing for celiac disease in children diagnosed with autism even if there are no symptoms which conflicts with earlier reports.
A study that looked at the amino acid profile of TD children, children with autism-no diet restrictions, children with autism on a gluten free casein fee diet. Both autistic groups had frequent essential amino acid deficiency suggesting of poor protein intake. Children with autism on unrestricted diets compared to control group had deficiencies in valine, isoleucine, leucine, phenylalanine, and lysine. Lysine and Leucine were significant difference. Children with autism on restricted diet in addition had defiency in tryptophan than children with autism on unrestricted diet. These restrictive diets can put the developing brain under increased risk secondary to protein malnutrition. There may also be a link between decreased tryptophan (amino acid) which would decrease serotonin (neuro transmitter) levels. Many of the amino acids are preceptors to the neurotransmitter of serotonin.
Many Asperger Syndrome will complain of being confused or having difficulty concentrating when drinking milk. Other will “hate milk” or say it is “slimy”. Some people don’t have the enzyme to complement or metabolic processing ability (sunderlandprotocol). A child that reacts to milk may vomit, eczema (especially behind the knees or in the crook of the elbow), early ear infections, constipation, diarrhea and respiratory problems resembling asthma are all side effects.
If a diet is restricted (gfcf) and the child doesn’t expand their diet, it may mean that the offending food is still part of the diet. Without appropriate levels of essential nutrient elements the normal metabolic process of digestion and absorption will be severely impaired in any case.
Zinc helps to decrease aluminum and also is desirable for normal metabolic reactions.
The use of sulphate in the system affects the immune system, the effectiveness of hormones and maintaining integrity of the intestinal function, kidney function and detox of systems. Sulphation in chemical bodies of glycosaminoglycans have implications on brain development. Inflammation would deplete the sulphar. Sulphar is better absorped through the skin (Epsom salt water baths) sunderlandprotocol
Lysine is an essential amino acid. That means that we can’t synthesize it, we need to get it from our dietary intake. It is a building block for all protein in the body. It helps with calcium absorption, hormones, enzymes and antibodies. It also serves to decrease serotonin receptors in the intestinal tract. This will help to decrease anxiety and anxiety induced diarrhea. Lycsine defiency also leads to an increase of serotonin in the amygdala which affects emotional regulation.
Coeliac disease is an autoimmune disorder of the small intestine. Symptoms include chronic diarrhea, failure to thrive, fatigue. Changes in the bowel may make it harder for the body to absorb nutrients and minerals and fat soluble vitamins (A,D, E,K). Untreated can have symptoms like cerebellar ataxia, peripheral neuropathy, schizophrenia, and autistic like features.
Iron deficiency or anemia may cause malabsorbtion of folic acid and vitamin B12. Iron deficiency may have symptoms that include constipation, sleepiness, depression, twitching muscles, poor appetite, and restless leg syndrome. During infant development, Iron deficiency would affect neurological development by decreasing learning ability, altering motor function and reducing the number of dopamine receptors and serotonin levels. It can also lead to reduced myelination of the spinal cord and affect the growth hormone.
Emerging evidence confirms that deficiency of assorted nutrients such as folate, vitamin D, or essential fatty acids41 may impair various biological processes required for normal metabolic and neurological functioning.
If a child has GI issues, this may affect all levels of functioning. They will be irritable, tired, have decreased concentration, decreased retention of information. Malabsorbtion can lead to nutrional defiency and the body will start to break down due to malnourishment. Many behavioral signs may be worsened. Since diet affects all levels of functioning in the body, looking into the nutrient involvement of the child is important. Studies are conflicting as to the lack of nutritional input the child with ASD receives. But a minor change in the essential amino acids or vitamins could have symptoms that mirror ASD. Many caregivers do a “shot gun” approach to treatment (different diets, vitamins, supplements) rather than a biochemical approach. This is not optimal as they don’t identify the nutritional status of the individual and may not target specific biochemical deficiencies that may be causing abnormalities responsible for the central nervous system dysfunction.
Genuis and Bouchard have 3 recommendations based on the emerging information that micronutrient deficiency may be a determinant of central nervous system dysfunction:
1. All children with developmental, behavioral, and inexplicable central nervous system disorders should be routinely screened for celiac disease.
2. Considering the escalating public health problem with pervasive developmental disorders, further study into the correlation between micronutrient deficiency and neuropsychiatric problems is in the public interest and should be undertaken.
3. Recognizing that neuropsychiatric dysfunction exacts an enormous cost both financially and personally, micronutrient screening is recommended for all children with significant central nervous system dysfunction. Such screening should include plasma amino acid status, serum screen for coenzyme Q10 and fat-soluble vitamins, red blood cell mineral status, serum folate, plasma fatty acid profile, and urine organic acids to assess functionality of nutrient physiology.
Arnold, G., Hyman, S., Mooney, R. Kirby, R., (2003) Plasma Amino Acids Profiles in Children with Potential Risk of Nutritional Deficiencies. Journal of Autism and Developmental Disorders 33:4 449-454
Genuis, S., Bouchard, T. (2010) Celiac Disease Presenting as Autism. Journal of Child Neurology 25:1 114-119
Schreck, K.A., Williams, K. (2006) Food preferences and factors influencing food selectivity afor children with autism spectrum disorders. Research in Developmental Disabilities 27: 4: 353-363
The Sunderland Protocol: A logical sequencing of biomedical interventions for the treatment of autism and related disorders. (2000) Autism Research Unit
Whiteley, P., Rodgers, J., Savery, D., Shattock, P.(1999) A gluten-free diet as an intervention for autism and associated spectrum disorders: preliminary findings. Autism 3:1 45-65.
Wright, B., Brzozowski, A.M., Calvert, E., Farnworh, H., Holbrrok, I. Imrie, G. etal. (2005) Is the presence of urinary indolyl-3-acryloylglycine associated with autism spectrum disorder? Developmental Medicine and Child Neurology 47: 190-192