Antigluten therapy is the elimination of gluten from the body by dieting and/or supplemental enzymes. This entry will examine enzyme supplements that break down gluten. (For elimination diets, see “Gluten-Free Diet.”)
In 1979, Jaak Panksepp hypothesized that the symptoms of autism may be caused by an opiate excess, although he was unsure how such an excess might come about. Starting in the 1980s, some investigators reported abnormal peptide concentrations in the urine of children with autism and proposed that enzyme deficiencies caused this abnormality (Trygstad et al. 1980; Reichelt et al. 1981, 1990). Additionally, these investigators speculated that the abnormal peptide concentrations reflected abnormal levels of opioid peptides in the brain (Trygstad et al. 1980; Reichelt et al. 1981). More recently, Andrew Wakefield (Wakefield et al. 1998) described intestinal abnormalities in several children with autism and hypothesized that this abnormality could provide another explanation for the opiate-excess theory. More specifically, he hypothesized that children with autism have a leaky gut that results in the release of opioids that enter blood vessels and circulate into the brain. However, Wakefield’s study has since been retracted by The Lancet and is considered to be unreliable.
Rationale or Underlying Theory
Antigluten therapy is based on the opioid-excess, enzyme deficiency, and leaky gut theories. According to the opioid-excess theory, the core symptoms of autism may be explained by disrupted opiate activity in the brain (Panksepp 1979). One proposed explanation for this theory is that children with autism have deficient peptidase enzymes (Trygstad et al. 1980; Reichelt et al. 1981). However, Hunter et al. (2003) did not find dipeptidyl peptidase IV to be defective in children with autism. A “leaky gut” or increased intestinal permeability has also been theorized to cause an opioid excess and to be associated with autism. The theory suggests that undigested proteins and peptides leak into the bloodstream through the intestines, eventually causing damage and/or disrupted opioid receptor activity in the brain. However, this theory lacks empirical support as it is based on a discredited study (Wakefield et al. 1998) that found intestinal abnormalities in several children with autism and that has not been replicated by other investigators (Buie et al. 2010; Fernell et al. 2007; Sandhu et al. 2009).
Another uncorroborated theory that has been adduced to support antigluten therapy is that children with autism have a wheat allergy and other symptoms similar to celiac disease (Lucarelli et al. 1995). However, there is no evidence for increased co-occurrence of wheat allergies or celiac disease and autism spectrum disorders (Fitzgerald et al. 1999; McCarthy and Coleman 1979).
Goals and Objectives
The goals of antigluten therapy include administering digestive enzymes to assist in the breakdown of gluten and preventing undigested gluten and gluten derivatives from affecting the body.
For information on the efficacy of gluten-free diets, see “Gluten-Free Diet.”
To date, there are only two empirical studies examining the efficacy of enzyme supplements to break down gluten for individuals with autism. Brudnack et al. (2002) placed 46 patients on a combination of several enzymes for 12 weeks. Several behavioral parameters were measured every 2 weeks for the entire 12 weeks. The authors report improvement on every measure including core symptoms. However, there was no control group, the baseline measures were assumed to be zero rather than measured directly, and behavioral evaluators were aware that the children had received a supplement. Additionally, behavioral measurements were collected from an “SOS” form (not shown or explained in the manuscript) in addition to scoring by an observer, and it is not clear whether the observer was distinct from a teacher, parent, or guardian who completed the SOS form. No standardized instruments (i.e., ADOS, Vineland, Mullen, etc.) were used. Despite the reported improvements, the numerous methodological weaknesses in the study make the results unreliable.
Munasinghe et al. (2010) conducted a more scientifically rigorous study that incorporated a randomized, double-blind, crossover design. Only food selection improved significantly at the month 2 measurements. Improvements were not sustained at 3 months. Thus, the two available studies provide insufficient information to recommend antigluten therapy in the form of enzymatic supplements at this time.
Antigluten treatment is intended to reduce autism symptoms and improve adaptive functioning. Therefore, if clinical trials of antigluten therapy are undertaken, outcome measures should include measures of autism symptoms such as the ADOS and measures of adaptive behavior such as the Vineland. Also, because digestive enzymes are administered, measures of nutrition and vital signs should be included.
Qualifications of Treatment Providers
Caregivers should consult a board-certified physician before beginning antigluten therapy. Additionally, the use of enzyme supplements should be supervised by a physician.
References and Readings
- Reichelt, K. L., Ekrem, J., & Scott, H. (1990). Gluten, milk proteins and autism: Dietary intervention effects on behaviour and peptide secretion. Journal of Applied Nutrition, 42, 1–11.Google Scholar