NEW HARVARD/COLUMBIA U. STUDY SIGNALS NEED FOR ENZYMES FOR COMPREHENSIVE CARBOHYDRATE BREAKDOWN

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  • 8/3/2019 NEW HARVARD/COLUMBIA U. STUDY SIGNALS NEED FOR ENZYMES FOR COMPREHENSIVE CARBOHYDRATE BREAKD

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    NEW HARVARD/COLUMBIA U. STUDY SIGNALS NEED FOR ENZYMES FOR

    COMPREHENSIVE CARBOHYDRATE BREAKDOWN

    I am going to tell you about an important new study and what it means to me as a parent. But first I am

    going to tell you about an "oldie-but-goodie" study.

    The 2005 study "Gastrointestinal symptoms and intestinal disaccharidase activities in children withautism," which was by Drs. Tim Buie, Rafail Kushak, and colleagues, was published in the Journal of

    Pediatric Gastroenterology and Nutrition. Having previously reported preliminary findings at a biomedical

    conference in New Orleans in 2004 ("Disaccharidase deficiencies in patients with autistic spectrum

    disorders"), Drs. Buie and Kushak now provided this landmark study indicating legitimate underlying

    physiological reasons for gastrointestinal symptoms and food sensitivities in children diagnosed with

    autism. But it also, quite importantly, gave us insight into what we could do about it. A helpful avenue

    that became apparent concerned the use of supplemental digestive enzymes.

    In the 2005 paper, researchers measured the activity of disaccharidases, which are enzymes that break

    down carbohydrates in the intestine, in tissues obtained from duodenal biopsies from 308 individuals with

    autism. Now, I pretty closely report what the study says sans all of the abbreviations: Autistic individuals

    with diarrhea [206 individuals] demonstrated significantly lower maltase activity than nonautistic

    individuals with diarrhea. Frequency of lactase deficiency in autistic individuals with failure to thrive [5

    individuals] was significantly higher (80% vs. 25%) than in non-autistic individuals with failure to thrive,

    and frequency of palatinase deficiency in autistic individuals with diarrhea was significantly higher than in

    nonautistic individuals with the same gastrointestinal problem. Autistic and nonautistic individuals with

    other gastrointestinal problems exhibited similar frequencies of disaccharidase deficiencies.

    This study supports an autism/GI link, and the paper's results are consistent with clinical evidence of

    many children with autism improving both physically and behaviorally when they are placed on a

    gluten/casein-free (gf/cf) diet along with supplemental disaccharidase digestive enzymes.

    And now, we have a new study, which was just published in September 2011 in PLoS One titled

    "Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with

    Autism and Gastrointestinal Disturbances." The eminent Dr. Tim Buie is again among the study authors,

    who hail from Columbia University and Harvard.

    Hearkening to previous reports of deficiencies in disaccharidase enzymatic activity and of beneficial

    responses to probiotic and dietary therapies, the authors now investigated "expression of human genes

    involved in carbohydrate digestion and transport along with bacterial community composition in intestinal

    biopsies from children with autistic disorder and GI [AUT-GI] disease ... compared to children with GI

    disease alone...." In addition to deficient disaccharidase enzymatic activity, other reports had included

    abnormal fecal Clostridia taxa (that is, abnormal bugs in the stool). When the bugs were addressed and

    when the diet was altered, improvement was seen in cognitive and social function. To me, this looks like

    when you address the enzymatic activity, you'll address digestion, and when you address digestion, you'll

    address the bugs. And when you do THAT, you'll help cognition and behavior.

    What the authors did find was that children with autism and GI problems had abnormalities in levels of

    genes for enzymes that break down sugars and for molecules that take them from the lumen of the

    intestine into the blood. Furthermore, the composition of the bacteria in the gut of these children was also

    out of balance for good and bad bacteria .

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    These conditions can lead to maldigestion, malabsorption, and dysbiosis. And, in fact, in the "Discussion"

    section of the paper, the authors do describe a chain of events where there are reduced enzymes and a

    vicious cycle of maldigestion and dysbiosis. The authors state: ". . . we 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."

    We know that abnormal gut flora can affect the rest of the body by affecting the immune and central

    nervous systems, such as brain development and behavior; therefore, addressing this situation in an

    affected child is a matter of great urgency.

    This study reinforces what I, as a parent, can do. I can feed my child a healthful, special diet that

    excludes items that my child cannot process well, while consulting with a nutritionist to make sure that all

    nutrients are supplied from the diet or supplements, and I can use digestive enzymes to mitigate my

    child's lack of enzymes. By using the enzymes, I will reduce the amount of undigested food that festers

    and feeds additional bad bacteria, thereby halting additional damage to the gut in that manner and

    mitigating undigested substances from entering the blood stream, and I will increase digestion of good

    nutrients from food that my child does need to fuel the brain and body. Of particular note in my mind, the

    study reported that "[The study authors] examined transcript levels for three primary brush border

    disaccharidases (sucrase isomaltase [SI], maltase glucoamylase [MGAM], and lactase [LCT]) in ileal

    biopsies of AUT-GI and Control-GI children by real-time PCR. Levels of mRNA for all three enzymes were

    significantly decreased in AUT-GI children." This means that, optimally, I would want to use a

    supplemental digestive enzyme that had isomaltase activity. Kirkman exclusively provides that enzyme,

    which is offered under the trade name of Isogest. Isogest has the ability to split isomaltose into two

    molecules of glucose (and also to split palatinose into one molecule of glucose and one molecule of

    fructose). The result of this is better, more complete carbohydrate digestion (and fewer bad bugs!).

    Here's my summary of the article:

    IFenzymes down

    THEN

    digestion down

    bad bugs up

    symptoms up

    (cognition down , behavior "down" )

    GI pathology up

    behavior "down"

    And the take-home message is, in my opinion, that since objective scientific evidence has revealed aproblem, we can take positive measures to fix it that will improve health, happiness, and behavior for

    affected children and, by extension, their families.