A Look at 'Leaky Gut' Theories of Autism

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" Healing Autism: No Finer a Cause on the Planet "

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October 25, 2000

A Look at ‘Leaky Gut’ Theories of Autism

* The Concept of Increased Intestinal Permeability

* Gastrointestinal Abnormalities Among Children with Autism

* Binstock's Anterior Insular Cortex Hypothesis for Linkage

Between Gut and Brain

[These summaries of “Leaking Gut Theories” of autism are written and

maintained by Mehl-Madrona, M.D., Ph.D., Medical Director of The

Center for Complementary Medicine. Email coyotemd@... Other

theory of autism summaries are also available at the website below.

References have been deleted but are available at the website. This

material contains technical language.]

http://www.healing-arts.org/children/

The Concept of Increased Intestinal Permeability

The concept of increased intestinal permeability is key to many

theories of autism. Just how important is the integrity of the intestine's

mucosal lining to good health? In children in remote tropical regions

without access to adequate medical care, progressive damage to the gut's

barrier function can eventually lead to life-threatening conditions,

requiring them to be airlifted for emergency medical treatment.

Aboriginal children in Australia, for example, have high rates of

severe intestinal diseases, or enteropathies, that cause chronic diarrhea.

These conditions can lead to dehydration, acidosis, and hypokalaemia -

serious complications associated with central nervous system damage and even

death.

To shed more light on how these conditions develop, researchers from

Australia evaluated intestinal permeability (IP) in Aboriginal children,

measuring the rate that two nondigestible sugars are excreted in urine after

ingesting a challenge drink. This noninvasive test indicates the gut's

ability to absorb nutrients and to block toxins, bacteria, allergens, and

other potentially harmful molecules from penetrating into the systemic

circulation.

The IP ratio for Aboriginal children with diarrhea was, on average,

more than twice as high as that found in their healthy Aboriginal peers.

When compared with healthy non-Aboriginal children, these Aboriginal

children with diarrhea showed an IP ratio over three times higher than

normal. An elevated ratio of larger molecules such as lactuolose to smaller

sugar molecules such as mannitol or rhamnose, recovered in the urine sample,

indicates increased permeability and mucosal damage. This value is known as

the IP ratio.

Surprisingly, a higher IP ratio was found even in healthy Aboriginal

children without diarrhea. Researchers speculated that this increased

permeability - double that normally found in healthy non-Aboriginal

children - was " consistent with an underlying partial villous atrophy, " a

wearing down of the finger-like projections on the intestine's mucosal

layer, caused by environmental factors. For this reason, the Aboriginal

children were more susceptible to gastrointestinal diseases and their

complications.

How does this all happen? One possible mechanism involves the body's

digestion of milk products. Increased IP may reflect damage to the

microvilli, which can reduce levels of lactase, the enzyme needed to digest

milk sugar, eventually triggering osmotic diarrhea. Once this disease

process starts, small bowel mucosal damage, indicated by higher IP ratios,

remains " an important factor " associated with increased acidosis,

hypokalaemia, iron deficiency, dehydration, and parasitic infection.

Great Smokies Diagnostic Laboratory offers an Intestinal Permeability

Assessment. This test is a noninvasive and convenient way to evaluate gut

mucosal barrier function in patients with chronic gastrointestinal disorders

or in those individuals with a higher likelihood of developing such

problems, including patients with chronic inflammatory conditions,

especially those using NSAIDS. I use it with my autistic children and

monitor the effectivenes of my treatment to reduce intestinal permeability.

Two physicians have written articles that are posted on the Great

Smokies' web site: Inflammatory Conditions and the Gastrointestinal Tract,

by Myron Lezak. M.D., and Leaky Gut Syndrome: A Modern Epidemic, by Jake

Fratkin, O.M.D. Both discuss aspects of intestinal permeability and the

conditions related to impaired mucosal function.

I suspect intestinal permeability is very important for autistic

children, and that the assay should be routinely used as a means of

following the success of therapies for autism.

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Gastrointestinal Abnormalities Among Children with Autism

Horvath, et al. (1999)29 evaluated the structure and function of the

upper gastrointestinal tract in a group of patients with autism who had

gastrointestinal symptoms. Thirty-six children (age: 5.7 ± 2 years, mean ±

SD) with autistic disorder underwent upper gastrointestinal endoscopy with

biopsies, intestinal and pancreatic enzyme analyses, and bacterial and

fungal cultures.

The most frequent gastrointestinal complaints were chronic diarrhea,

gaseousness, and abdominal discomfort and distension. Histologic examination

in these 36 children revealed grade I or II reflux esophagitis in 25

(69.4%), chronic gastritis in 15, and chronic duodenitis in 24. The number

of Paneth's cells in the duodenal crypts was significantly elevated in

autistic children compared with non-autistic control subjects. Low

intestinal carbohydrate digestive enzyme activity was reported in 21

children (58.3%), although there was no abnormality found in pancreatic

function. Seventy-five percent of the autistic children (27/36) had an

increased pancreatico-biliary fluid output after intravenous secretin

administration. Nineteen of the 21 patients with diarrhea had significantly

higher fluid output than those without diarrhea.

The authors concluded that unrecognized gastrointestinal disorders,

especially reflux esophagitis and disaccharide malabsorption, may contribute

to the behavioral problems of non-verbal autistic patients. The observed

increase in pancreatico-biliary secretion after secretin infusion suggested

an upregulation of secretin receptors in the pancreas and liver.

* *

Binstock's Anterior Insular Cortex Hypothesis for Linkage Between Gut

and Brain.

Binstock (http://www.jorsm.com/~binstock/insular.htm) has developed a

hypothesis to explain the gut-brain relationships for autistic children.

The anterior insular cortex (aIC) links visceral sensation from the

gastrointestinal tract with the amygdala and the hypothalamus. The anterior

insular cortex also participates in oral phenomena, object recognition, and

naming along with " apraxia of speech " .

Twenty-five stroke patients with articulatory deficits all had a

lesion within " a discrete region of the left precentral gyrus of the

insula " , whereas this area was " completely spared " in 19 stroke patients

without these deficits.

Autism-spectrum children with atypical oral habits and/or disorders of

naming and of language also tend to have a typical gastrointestinal

symptoms. There is also a growing volume of anecdotal data that a small

subgroup of autism-spectrum children experiences improved sound production

and language use in response to treatments whose focus and effects are

gastrointestinal. These treatments include gluten-free and casein-free

diets, anti-Candida therapies, anti-viral therapies, and antibiotic

therapies suggesting that the underlying neuronal circuitry is intact.

Binstock suggests that the aIC and associated nuclei could become

disrupted by at least two mechanisms: (I) intraneuronal migration of a

neurotropic virus and/or (II) chronic hyperstimulation of the

gastrointestinal tract.

Gesser and colleagues have documented (I) the translocation of HSV

from the gastrointestinal tract into the mesenteric nervous system (rats and

humans), and (II) the migration of mesenteric HSV as far as theamygdaloid

nuclei in rats. In this theory, viruses could migrate from the

gastrointestinal tract through neural pathways into the central nervous

system.

Given a high rate of stimulation of neuron pathways reporting

gastrointestinalconditions to limbic regions and cortex, neurotransmitter or

intracellular-messenger use in excess of their production or recirculation

could occur, thereby inducing a change of function of neurons within the

aIC.

This hypothesis provides a basis for helping autistic children through

treating their gastrointestinal disturbances.

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