The implications on function with these GI issues can vary greatly. It has been shown to impact behavior, feeding, and overall participation in daily activities. When thinking about how we feel when our GI system is “acting up”, it is clear that chronic GI problems can lead to impacts on daily life. Children with autism have been shown repeatedly to have communication disorders or are non-verbal; 50% of children with autism will remain functionally mute in adulthood (Tincani 2004). This also impacts their own ability to identify what is wrong, or that they are having difficulties.
In reviewing the literature there are really mixed results. Many of the studies have very small numbers (participants), the trials are uncontrolled have been unable to show a true relationship to GI issues and autism (Erikson, et al., 2005). Therefore, it is up to the practioner to discern theory from firm evidence, and pay attention to uncontrolled observations from rigorously tested treatments.
Shearer et al., (1982) evaluated nutrient and mineral intake of autistic children by looking at hair samples. The minerals that were examined in this study included calcium, zinc, magnesium, copper, lead, and cadmium from 12 children with autism and 12 controls. They also evaluated a 3-day food diary. There was only one statistically significant mineral difference between the groups, which was lower cadmium level in the children with autism (Cadmium is a mineral and does the same job as zinc). The clinical significance of this result is unclear. When looking at their 3-day food diaries, the children with autism had a lower intake of calcium and riboflavin than the control group. However, they were noted to still have equal or greater than their recommended daily requirements of all nutrients (including calcium and riboflavin).
A critical review by Erikson, et al. (2005) showed that much of the research on the GI tract physiology of autistic children yielded information in three categories: gross pathology (such as reflux esophagitis), histopathology, and microbial abnormalities. Torrente et al. (2002) looked at frozen tissue samples from duodenum from 25 children with autism. These children were selected due to previous issues with diarrhea, constipation, and/or pain, all associated with sever fecal retention with acquired megarectum. The samples from the children with autism were compared with 11 children with celiac disease, as well as other children with cerebral palsy (5) and typical controls (19). Overall, there were no abnormalities in the histopathology (routine) analysis of the children with autism. However, as noted in a previous study (Horvath et al. 1999), the children in this study also had increased Paneth cells (these cells excist within the intestinal epithelial lining and contain granules which exert bacteriocidal effects when released). The children with autism (92%) had a deposition of IgG at the basolateral enterocyte surface, which differed from those children with celiac disease. The further staining agree again with the Horvalth et al. (1999) study in finding duodenitis, again suggesting the possibility of an autoimmune process. One must remember though, that this study was subject to selection bias as all of the children were suffering from sever GI complaints, and it is not a good generalized sample of the autistic population.
Further research has been completed looking at the intestinal permeability. Multiple studies have utilized lactulose and mannitol recovery rates, looking at alpha-1-antitrypsin levels, and then providing information about increased intestinal wall permeability. Horvath et al. (1999) found that there was evidence of increased protein loss from the gut of autistic children, and the Alpha-1antitrypsin is used for the marker for increased gut permeability to protein and subsequent protein loss in the stool. However, none of the autistic children (15) in this study had any evidence of celiac disease.
Horvath et al. (1999) also looked at malabsorption concerning intestinal carbohydrate digestive enzyme levels in children with autism. In a study of 36 children with autism (all whom had sever GI complaints), they also evaluated the child’s disaccharides levels with an upper endoscopy. The results were that 21 (58%) of the children had the activity of one or more disaccharidases noted to be more than one standard deviation below normal values, with lactase being the most frequent. The results of this study are difficult to interpret due to the fact that the children with enzymatic deficits were also those with chronic diarrhea.
Medical and therapy interventions are many. When looking at it through the thought of disrupted GI flora, there was a study where oral vancomycin was given in an attempt to reduce gut flora (Sanders et al., 2000). There were communication and behavior gains noted by trained psychologists in 8 of 10 children during the trial. However, after the drug was discontinued, these gains did not persist, therefore, not making a broad recommendation of this treatment protocol. There was also the use of secretin for treatment of GI issues with children with autism. Secretin is a peptide secreted by S cells, of the duodenum, in response to falling pH within the duodenal lumen as the stomach contents enter the small intestine. It then stimulates the secretion of water and bicarbonate from the pancreas and it supports the activity of cholecytokinin, further activating pancreatic secretion. This was a very popular treatment in the late 1990’s as case reports indicated significant behavior (decreased self stim) and language improvement (increased social interaction and communication) after administering secretin. However, when further studies were done (more controlled) there were not “major” differences on testing scores in the areas of language and behavior, when compared to placebo groups.
Shearer et al., (1982) evaluated nutrient and mineral intake of autistic children by looking at hair samples. The minerals that were examined in this study included calcium, zinc, magnesium, copper, lead, and cadmium from 12 children with autism and 12 controls. They also evaluated a 3-day food diary. There was only one statistically significant mineral difference between the groups, which was lower cadmium level in the children with autism (Cadmium is a mineral and does the same job as zinc). The clinical significance of this result is unclear. When looking at their 3-day food diaries, the children with autism had a lower intake of calcium and riboflavin than the control group. However, they were noted to still have equal or greater than their recommended daily requirements of all nutrients (including calcium and riboflavin).
A critical review by Erikson, et al. (2005) showed that much of the research on the GI tract physiology of autistic children yielded information in three categories: gross pathology (such as reflux esophagitis), histopathology, and microbial abnormalities. Torrente et al. (2002) looked at frozen tissue samples from duodenum from 25 children with autism. These children were selected due to previous issues with diarrhea, constipation, and/or pain, all associated with sever fecal retention with acquired megarectum. The samples from the children with autism were compared with 11 children with celiac disease, as well as other children with cerebral palsy (5) and typical controls (19). Overall, there were no abnormalities in the histopathology (routine) analysis of the children with autism. However, as noted in a previous study (Horvath et al. 1999), the children in this study also had increased Paneth cells (these cells excist within the intestinal epithelial lining and contain granules which exert bacteriocidal effects when released). The children with autism (92%) had a deposition of IgG at the basolateral enterocyte surface, which differed from those children with celiac disease. The further staining agree again with the Horvalth et al. (1999) study in finding duodenitis, again suggesting the possibility of an autoimmune process. One must remember though, that this study was subject to selection bias as all of the children were suffering from sever GI complaints, and it is not a good generalized sample of the autistic population.
Further research has been completed looking at the intestinal permeability. Multiple studies have utilized lactulose and mannitol recovery rates, looking at alpha-1-antitrypsin levels, and then providing information about increased intestinal wall permeability. Horvath et al. (1999) found that there was evidence of increased protein loss from the gut of autistic children, and the Alpha-1antitrypsin is used for the marker for increased gut permeability to protein and subsequent protein loss in the stool. However, none of the autistic children (15) in this study had any evidence of celiac disease.
Horvath et al. (1999) also looked at malabsorption concerning intestinal carbohydrate digestive enzyme levels in children with autism. In a study of 36 children with autism (all whom had sever GI complaints), they also evaluated the child’s disaccharides levels with an upper endoscopy. The results were that 21 (58%) of the children had the activity of one or more disaccharidases noted to be more than one standard deviation below normal values, with lactase being the most frequent. The results of this study are difficult to interpret due to the fact that the children with enzymatic deficits were also those with chronic diarrhea.
Medical and therapy interventions are many. When looking at it through the thought of disrupted GI flora, there was a study where oral vancomycin was given in an attempt to reduce gut flora (Sanders et al., 2000). There were communication and behavior gains noted by trained psychologists in 8 of 10 children during the trial. However, after the drug was discontinued, these gains did not persist, therefore, not making a broad recommendation of this treatment protocol. There was also the use of secretin for treatment of GI issues with children with autism. Secretin is a peptide secreted by S cells, of the duodenum, in response to falling pH within the duodenal lumen as the stomach contents enter the small intestine. It then stimulates the secretion of water and bicarbonate from the pancreas and it supports the activity of cholecytokinin, further activating pancreatic secretion. This was a very popular treatment in the late 1990’s as case reports indicated significant behavior (decreased self stim) and language improvement (increased social interaction and communication) after administering secretin. However, when further studies were done (more controlled) there were not “major” differences on testing scores in the areas of language and behavior, when compared to placebo groups.
duodenum, pancreas, and spleen
There are also dietary interventions and elimination diets, looking specifically at eliminating gluten and casein from the diets of children with autism. The gluten free diet is often utilized with children who have abnormal urinary protein patterns. It was hypothesized (Reichelt et al., 1990, 1991) that the patterns represented gluten or casein protein absorption abnormalities, which allowed more proteins to be absorbed and therefore excreted in the urine. Children have been reported to exhibit improved behavior and communication skills after 1 and 4 year periods. Urine peptide levels often normalized after one year of this type of diet. However, again, it is unclear, because of multiple interventions going on at the same time (other therapies, natural maturity) if the improvements in these areas (behavior & communication) are purely from the elimination diet. (www.autism.com)
Another dietary intervention includes the use of the ketogenic diet. The ketogenic diet “is a high fat, adequate protein, low carbohydrate diet, primarily used to treat difficult-to-control (refractory) epilepsy in children. The diet mimics aspects of starvation by forcing the body to burn fat rather than carbohydrate. Normally, the carbohydrates in food are converted into glucose, which is then transported around the body and is particularly important in fuelling the brain. However, if there is very little carbohydrate in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. When the body produces ketone bodies—a state known as ketosis—this has an anticonvulsant effect” (Wikipedia). A study by Evangeliu et al. (2003) found that 60% (of 30 children with autism) tolerated the diet and demonstrated improvement in the Childhood Autism Rating Scale.
Therapy interventions/implications for treatment for children with autism and feeding issues tend to revolve either in the sensory-based approach or the behavior-based approach. The literature supports a behavior-based approach, as the articles and outcomes are numerous. It is apparent that as therapists, we also need to balance behavioral issues around feeding with the child’s sensory system function/dysfunction, and continue to also address the intrinsic drive to participate in mealtimes and feeding/eating activities. It is of most importance to be aware of the variety in treatment approaches and respect the decision of the family on which approach they are choosing for their child. It is helpful to be versed in both aspects (sensory/behavior) as to then utilize clinical reasoning and experience to assist the family and child.
Knowing potential GI issues (symptoms) is key in assisting the families in appropriate referrals. With this knowledge, we as therapists can develop and utilize core/key questions that will then assist us with our own clinical reasoning to make those referrals. Often GI issues have not been at the “forefront” of the parents’ concerns, as their child has “always had diarrhea” and they don’t think twice about it. Or, they are more concerned with speech/communication and don’t mind making the same foods day in and day out for their child (again, not seeing it as a problem). It is our role, as therapists to assist the families with these issues, and addressing them, as it becomes a priority in their family. The bottom line is, educate yourself, so that you can better serve your families; get to know the specialists in your area or surrounding areas, so that you can make appropriate referrals.
Take home strategies for OT's/SLP's
Another dietary intervention includes the use of the ketogenic diet. The ketogenic diet “is a high fat, adequate protein, low carbohydrate diet, primarily used to treat difficult-to-control (refractory) epilepsy in children. The diet mimics aspects of starvation by forcing the body to burn fat rather than carbohydrate. Normally, the carbohydrates in food are converted into glucose, which is then transported around the body and is particularly important in fuelling the brain. However, if there is very little carbohydrate in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. When the body produces ketone bodies—a state known as ketosis—this has an anticonvulsant effect” (Wikipedia). A study by Evangeliu et al. (2003) found that 60% (of 30 children with autism) tolerated the diet and demonstrated improvement in the Childhood Autism Rating Scale.
Therapy interventions/implications for treatment for children with autism and feeding issues tend to revolve either in the sensory-based approach or the behavior-based approach. The literature supports a behavior-based approach, as the articles and outcomes are numerous. It is apparent that as therapists, we also need to balance behavioral issues around feeding with the child’s sensory system function/dysfunction, and continue to also address the intrinsic drive to participate in mealtimes and feeding/eating activities. It is of most importance to be aware of the variety in treatment approaches and respect the decision of the family on which approach they are choosing for their child. It is helpful to be versed in both aspects (sensory/behavior) as to then utilize clinical reasoning and experience to assist the family and child.
Knowing potential GI issues (symptoms) is key in assisting the families in appropriate referrals. With this knowledge, we as therapists can develop and utilize core/key questions that will then assist us with our own clinical reasoning to make those referrals. Often GI issues have not been at the “forefront” of the parents’ concerns, as their child has “always had diarrhea” and they don’t think twice about it. Or, they are more concerned with speech/communication and don’t mind making the same foods day in and day out for their child (again, not seeing it as a problem). It is our role, as therapists to assist the families with these issues, and addressing them, as it becomes a priority in their family. The bottom line is, educate yourself, so that you can better serve your families; get to know the specialists in your area or surrounding areas, so that you can make appropriate referrals.
Take home strategies for OT's/SLP's
Education/reading. This is of utmost importance. I chose this topic because though I address feeding as related to children with autism, it is out of our scope of practice (meaning we don’t get it in our OT/SLP curriculums) to be prepared with all of the medical/gi issues. In reading numerous journal articles, it is very apparent that many of the studies have limitations, but clearly, some of the treatments (e.g., elimination diets) have worked extremely well for some, but not all children with autism. Knowing what is available and who can provide it will allow families opportunities to make their own informed decision on a treatment approach.
Understanding “both worlds” – that being sensory and behavior. Clearly, as evidenced in the literature and multiple feeding centers in the US, a behavioral approach can increase feeding/eating for children with autism. Knowing that there are often underlying sensory issues, which then manifest into behavioral issues, you need to be able to address both. For some, it is an “either or”, personally, I find it best to try and balance both, and try to preserve that intrinsic motivation for wanting to eat, having a pleasant mealtime, while not completely melting down. Definitely the strategies that we discussed in earlier modules regarding behavior have been a benefit.
Listen to the family and ask key questions. After you have a broader understanding of potential GI problems (absorption, allergies, etc.) you will be better able to ask questions in your evaluation process and on-going assessment during your treatments. You can identify potential signs/symptoms of allergies, help the parent understand the nutritional needs, and/or that their child’s responses are not typical (e.g., chronic diarrhea, constipation). In the long run, you will have a much more well rounded approach to treatment.
When working with feeding, specifically and especially those kids who have major sensory-based issues, don’t forget to have fun! Make it enjoyable, comfortable, not threatening. This can be done through sensory-based play, with or without food. Helping the child engage, initiate, and participate in meal preparation, mealtimes, and social events in the big picture will contribute to improved self-esteem as well as overall happiness (and less stress) in the family.
Joan,
ReplyDeleteI appreciate the information provided. It is such a challenging area to approach when I feel there is not physician support. This provides information on questions to ask families during interview them and guide them as they express distress or interest in these issues. The take home strategies are beneficial and remind us to have fun. I try to keep in mind that a key concept is increasing flexibility in all areas of functioning, include oral intake. Thank you!
Kirsten