In the last post I wrote about how beneficial bacteria shapes our immunity. Today I want to review some studies in children examining the association between gut dysbiosis and allergic diseases.
As I’ve mentioned, commensal gut flora not only maintain the integrity of the gut wall preventing endotoxins and other antigens from entering systemic circulation, they are essential in maturing the immune system and shaping its responses.
Studying how beneficial bacteria, or its absence, affects rodents is a great place to begin generating hypotheses. However, we need to know whether this holds true for humans.
Allergies and Dysbiosis in Children
In a 1999 cross-sectional study of sixty-two 2-year old children in Sweden and Estonia, those suffering from allergies were found to have fewer lactobacillus, bifidobacteria and Bacteroides species than healthy controls. They also had higher counts of pathogenic gram negative bacteria and Staphylococcus aureus. And since they had higher levels of gut pathogens, I can assure you they had increased intestinal permeability or “leaky gut”.
In another Swedish cross-sectional study published in 2000, twenty-five allergic 13-month old infants were compared to forty-seven nonallergic babies to assess differences in fatty acid profiles. Because fatty acids are produced as a byproduct of fermentation by colonic bacteria, determining what fatty acids were present gave the researchers some idea of the types of bacterial populations resident in the guts of these children. Allergic babies were found to have more Clostridium difficile than non-allergic children. C. difficile is commonly acquired in hospital environments and is prevalent in those born through Caesarean section or exposed to early antibiotic treatment.
A 2001 longitudinal Finnish study of seventy-six infants also examined fatty acid composition. It too found that allergic infants at twelve months of age had increased counts of the Clostridium difficile pathogen.
A 2007 longitudinal study in the Netherlands of nine hundred fifty-seven children examined bacteria in feces. The presence of Escherichia coli (E. coli) was associated with increased risk of eczema. Clostridium difficile was also associated with an increased risk of eczema as well as dermatitis, asthma and allergic reactions at two years of age.
A case-controlled UK study examined thirty-seven matched pairs of children with or without allergies with a mean age of 4.4 years. No difference in Lactobacillus or Bifidobacterium was found. However, the presence of Clostridium difficile was associated with an elevated risk of eczema and allergies at two years of age.
In a 2008 longitudinal Belgium study that looked at one hundred fifty-four children, increased levels of harmful anaerobic bacteria was associated with increased odds of wheezing. Paradoxically, increased levels of Clostridium difficile were found to be protective against wheezing in the first year of life.
In a 2008 case-controlled study conducted in the United States, twenty-one pairs of infants with and without eczema were examined. Stool samples were analyzed at one and four months. The higher the diversity of gut flora, the lower the incidence of eczema.
Finally, a Finnish longitudinal study examined the microbial culture of amniotic fluid in four hundred sixty children delivered by C-section. Intrauterine growth of anaerobic bacteria and Streptococcus was highly associated with an higher risk of asthma.
All of these studies have their limitations. Some of the associations border on non-statistically significant. Stool samples are notoriously unreliable as many types of bacteria may exist in the gastrointestinal tract but may not appear in feces because they are attached to the gut wall. And a good number of bacteria cannot be cultured in a lab.
Other studies failed to control for diet of either the mother or the child. Nor did many examine the bacterial composition of the mother’s gut and vaginal flora, control for mode of delivery or determine whether the child was breast-fed or for how long. Nevertheless, in all these studies some form of gut dysbiosis was evident.
As we know, dysbiosis will tip the immune system to an allergic or Th2 response. Increased intestinal permeability brought about by an overgrowth of gut pathogens is no doubt a factor. In the future I would like to see studies that measured the level of lipopolysaccharides in the blood of those afflicted with allergies.
Speaking from personal experience, a number of life-long allergies to dust mites, cat dander, smoke, recurring sinus infections and rosacea disappeared after I resolved my gut dysbiosis.
Is there a role for probiotics in the treatment of these disorders?
In a study that treated one hundred thirty-two infants with a genetic predisposition to allergies and asthma, supplementation with Lactobacillus rhamnosus GG given to pregnant mothers and their newborns halved the risk of eczema, but not allergies before the age of two. These results were pretty much constant at four and seven years of follow-up. Surprisingly, at age seven, the incidence of allergic nasal symptoms and asthma was more common in the L. rhamnosus group than the placebo group. I suspect this was due to unresolved yeast overgrowth.
In another study of infants, supplementation with the same probiotic increased the production of non-inflammatory treg cells and reduced the severity of dermatitis.
Another small trial saw reduced dermatitis in infants aged six to eighteen months when given Lactobacillus fermentum.
In a recent study of 925 mother-infant pairs, prenatal probiotic supplementation containing four bacterial strains during the last month of pregnancy as well as postnatal supplementation of infants with both probiotics and prebiotics for six months, resulted in short-term changes in infant gut flora. Eczema was reduced in these children, but no effect on allergy occurrence was noted at two years of age.
In the same trial, 891 children who had a complete follow-up at five years of age showed that this six-month course of probiotics did not prevent eczema, allergic rhinitis or asthma. However, children born via Cesarean section who supplemented with probiotics had fewer allergic reactions.
The results of studies using probiotic supplementation are contradictory or disappointing. The problem is that science has yet to find how different species of beneficial bacteria affect our immune system. While there is no doubt that some probiotic strains tip the scale against allergies, others may offer no protection whatsoever.
A major issue I have with these trials is that am I not a fan of supplementing with just one or a few strains of bacteria as doing so may crowd out other good bacteria. A healthy gut flora is a complex ecosystem so a great diversity of commensal organisms should be the goal. While using one or a few strains may help researchers determine which strains are effective, it may not do the child suffering from allergies much good in curing their dysbiosis.
I’m a big believer in taking probiotics with many different strains. Nevertheless, the more strains contained in a probiotic, the fewer the colony forming units of each found in a capsule or tablet because of size limitations.
There is another major confounder with all the studies that showed either no improvement or a worsening of symptoms with probiotic supplementation and that’s food. No probiotic or prebiotic will totally compensate for a lousy diet and that is doubly true for children.
Those dietary factors I identified in my small intestinal bacterial overgrowth (SIBO) series that predispose to SIBO will also predispose to allergies. While these factors certainly can’t be blamed for the onset of symptoms in infants before the introduction of solid food, they play a big role in perpetuating or aggravating these diseases after weaning.
As anyone who has read this blog for any length of time knows, I’ve not been shy in expressing my concerns about wheat, the staple grain of the Western diet and along with refined sugar and vegetable oils, the mainstay of practically every processed food under the sun. Because of its negative effects on GI motility, intestinal permeability, promotion of gut-wall inflammation and gut-trashing lectin, it’s number one on my list of foods to avoid when trying to overcome allergies.
The introduction of genetically engineered wheat with higher protein content over the last half-century means more people are consuming higher amounts of gluten and its lectin than ever before. In the last post I highlighted the important role both vitamins A and D play in shaping the immune system. Eating lots of gluten grains is an efficient way to encourage small intestinal dysbiosis that will in turn prevent the proper absorption of these fat-soluble vitamins as well as other nutrients.
Another disastrous dietary trend over the past 50 years is the decrease in consumption of foods that are most abundant in these fat-soluble, immune-strengthening vitamins: cod-liver oil, full-fat milk, especially from pastured animals, liver, organ meats, eggs and shellfish. Unfortunately, many parents of allergic children are too afraid to feed these foods to their kids because of advice against consuming foods containing saturated fat and cholesterol.
However, few people know, and that includes the overwhelming majority of medical professionals, that all transporters of blood fat or lipoproteins—chylomicrons, VLDL, LDL and HDL—bind to and inactivate toxic lipopolysaccharides from gram negative bacteria preventing the very inflammatory responses responsible for metabolic endotoxemia and allergic reactions. Any increase in lipoproteins after a fatty meal is a protective mechanism we evolved to neutralize endotoxins that hitch a ride on the very transporters that supply us with these fat-soluble nutrients. I’ll have more to say on this when I blog on heart disease, endotoxemia and cholesterol.
While fermented probiotic-rich foods like yogurt and kefir are not likely to lead to a quick resolution of dysbiosis due to the low survival rate of viable organisms transiting the stomach, it’s still imperative that these foods be included in the diet when trying to resolve allergies.
No probiotic company will ever know better than mother nature when it comes to replenishing our gut flora with beneficial organisms. While I could not have overcome my dysbiosis without prebiotics and probiotics, yogurt and other fermented foods also played an important role.
Other foods that may need to be limited or eliminated include non-fermented dairy and nightshades. It may be possible to reintroduce these foods at a later date once the gut has sealed and healed. Because we’re also dealing with leaky gut, any food has the potential to act as an allergic trigger. While eliminating these foods will help in the short-term, one should concentrate on clearing the overgrowth of gut pathogens and yeast. Once this is done, many of these food allergies disappear.
Remedying or alleviating allergic reactions requires the introduction of beneficial bacteria via viable probiotics, adding fermented foods to the diet, ingesting prebiotics to encourage growth of friendly colonic gut flora, eliminating gluten grains and other allergy provoking foods, treating bacterial and yeast overgrowth, and adding foods rich in fat-soluble vitamins A and D. Anything less is likely to result in disappointment.
Harris H.W., Grunfeld C., Feingold K.R., Rapp J.H. (1990) Human Very Low Density Lipoproteins and Chylomicrons Can Protect against Endotoxin-induced Death in Mice. The Journal of Clinical Investigation, (86): 696-702.
Hormannsperger G, Clavel T., Haller D. (2011) Gut matters: Microbe-host interactions in allergic diseases. Journal of Allergy and Clinical Immunology, 129: 1452-1459.
Ly N.P., Litonjua A., Gold D. G., Celedon J. C. (2011). Gut microbiota, probiotics, and vitamin D: Interrelated exposures influencing allergy, asthma, and obesity? Journal of Allergy and Clinical Immunology, 127: 1087-1094.
McLoughlin R. and Mills K. H. G. (2011) Influence of gastrointestinal commensal bacteria on the immune response that mediate allergy and asthma. Journal of Allergy and Clinical Immunology, 127: 1097-1107.
Vreugdenhil A.C.E., Snoek A.M.P., van ‘t Veer C., Greve J.W.M., Buurman W.A. (2000). LPS-binding protein circulates in association with apoB-containing lipoproteins and enhances endotoxin-LDL/VLDL interaction. The Journal of Clinical Investigation, 107:225–234.