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Probiotics: Why Blood Type Matters
by Peter D'Adamo, ND and Gregory Kelly, ND

The term "Probiotic" means "in favor of life". It was coined in 1910, by a Russian physician named Metchnikoff, who promoted a theory of longevity that associated prolonged life and improved health with decreased gastrointestinal toxicity. He suggested that aging is a process mediated by chronic exposure to putrefactive intoxication caused by imbalances in intestinal bacteria and that this process could be halted by the routine ingestion of lactic acid bacteria and their "fermented" ("cultured") food products. Almost 90 years have passed since he introduced these radical ideas; however, in many respects his ideas have been proven to be true. Consumption of lactic acid bacteria, or food cultured or fermented with these friendly microorganisms does extend life in animal experiments and does dramatically reduce a wide range of intestinal metabolites, such as indoles, polyamines, cresols, nitrates/nitrites, and carcinogens which we now know are counterproductive to good health.

The Microbiome and Obesity

The human intestine represents an organic bioreactor programmed with an enormous population of bacteria (microbiota). This microbiota and its collective genomes (microbiome) provide us with genetic and metabolic attributes we have not been required to evolve on our own, including the ability to harvest otherwise inaccessible nutrients. New studies are revealing how the gut microbiota has coevolved with us and how it manipulates and complements our biology in ways that are mutually beneficial.We are also starting to understand how certain keystone members of the microbiota operate to maintain the stability and functional adaptability of this microbial organ. It is estimated that the human digestive tract may contain up to 100 trillion microorganisms (2) and the human gut may host up to 500-1000 different species of bacteria, of which as little as 7% have been successfully cultured in the laboratory. (3)

The comparison of the fecal microbial profile of obese subjects and their relatives could allow the identification of a familial-specific core microbiota that could represent a simple tool for the evaluation of predisposition to obesity. Obesity appears in fact as the result of a complicated mix of factors such as genetics, environment, diet, and lifestyle, resulting in an alteration of the equilibrium between energy expenditure and storage. Gut microflora are increasingly being seen as a potential factor in human obesity. By using germ-free mice, transplanted with human fecal microbiota, scientists have shown that a high-fat, high-sugar diet durably changes the transplanted microbiome and that this diet-altered microbiome promotes obesity. The gastrointestinal microbiota have been shown to impact insulin resistance, inflammation, and adiposity via interactions with epithelial and endocrine cells. (9)

Gut microbiota, profoundly involved in the utilization of ingested nutrients, is thought to be more efficient in energy extraction from nutrients in obese people than in lean ones. This effect has been demonstrated indirectly by the fact that the inoculation of germ-free mice with a conventional 'obese' flora led to a significant weight gain and that genetically obese mice harbored a fecal microflora much more efficient in sugar fermentation and therefore promoting fat deposition.

What's your type?

The human GI tract is predominantly a bacterial ecosystem. Cell densities in the colon (1011-1012/ml contents) are the highest recorded for any known ecosystem. The vast majority of the bacteria belong to two divisions (superkingdoms): the Bacteroidetes (48%) and the Firmicutes (51%). Gut bacteria can have direct effects on gene activation that may be essential for proper gut development. Bacteria induced expression of mammalian genes has been known since the 1980’s when Japanese researchers were able to show that a fucosyltransferase enzyme (fucosyl-asialo GM1) was induced by bacteria but was absent from germ-free strains. (4) This is especially interesting in light of the fact that many of the fucosyltransferase enzymes convey blood group and/or secretor status. (5)

Your blood type antigens are actually prominent in your digestive tract and, in about 80% of individuals (secretors), are also prominent in the mucus that lines your digestive tract. Because of this, many of the bacteria in your digestive tract actually use your blood type as a preferred food supply. In fact, blood group specificity is common among intestinal bacteria with almost 1/2 of strains tested showing some blood type A, B, or O specificity. To give you an idea of the magnitude of the blood type influence on intestinal microflora, it has been estimated that someone with blood type B will have up to 50,000X more of some strains of friendly bacteria than either blood type A or O individuals.

Human feces contain enzymes produced by enteric bacteria that degrade the A, B, and H blood group antigens of gut mucin glycoproteins. The secretor gene together with the ABO blood group gene controls the presence and specificity of A, B, and H blood group antigens in musocus liningof the gut . There is evidence that the host’s ABO blood group and secretor status affects the specificity of blood group-degrading enzymes produced by his fecal bacteria in vitro. (6)In essence, bacteria ‘eat right for their type’ even if we sometimes don’t. Comparatively small populations of fecal bacteria produce blood group-degrading enzymes but their presence is highly correlated with the ABO /secretor phenotype of the host: Fecal populations of blood type B-degrading bacteria were stable over time, and their population density averaged 50,000-fold greater in blood group B secretors than in other blood types. In fact, the large populations of fecal anaerobes may be an additional source of blood group antigen substrate for blood group antigen degrading bacteria: antigens crossreacting with blood group antigens were detected on cell walls of anaerobic bacteria from three of 10 cultures inoculated. (7,8)

Should You Take a Probiotic?

Even using strains of friendly bacteria that have a great ability to survive digestion and colonize your digestive tract, there is a tendency for a gradual decline in the quantity of these bacteria over time. This decline is substantially worsened with stress, poor dietary choices, antibiotics and other drugs. In today's world, with all of it's modern pressures, the ability to maintain an optimal intestinal microbial balance is almost always taxed. It has also actually been estimated that we consume 1 million times less healthy bacteria in our diet today than are ancient ancestors consumed.

Friendly bacteria work better when more of them are combined together. There are actually hundreds of strains of bacteria in your digestive system and the friendly bacteria actually operate as a team, promoting the beneficialeffects of each other. The term "Synergism" best describes the interrelationshipof friendly bacteria. They mutually support each other by producing bacteriocidins and organic acids that they are resistant to, but which decrease pathogenic (harmful) bacteria. In fact, these bacteriocidins are up to 1000X more active when combined then when they are isolated. But even more importantly, health effects of one strain of friendly bacteria are often not duplicated by other strains. So a more complex mixture, combining more friendly strains of bacteria, translates into more profound long-term health benefits.

Polyflora Probiotics

Polyflora Blood Type Specific Probiotic Formulas are unique in that they blend blood type specific prebiotics --foods which provide special growth factors for probiotic bacteria-- right into the probiotic formula. In many respects, friendly bacteria can be thought of as having "adaptogenic" effects on your immune system. They appear to modulate the nonspecific immune response differently in healthy and hypersensitive subjects. This is seen as an immuno-stimulatory effect in healthy subjects, and as a down-regulation of immuno-inflammatory responses in hypersensitive subjects.

Second, some strains of beneficial bacteria actually can have lectin-like hemagglutinin activity directed against your blood type, so avoiding those is a good idea.

Friendly bacteria restore intestinal balance:
  • the prevention of adherence of unwanted microorganisms
  • the production of a wide array of antibacterial and antifungal compounds
  • improved resistance against bacteria like E. coli, Salmonella, and H. pylori

Friendly bacteria enhance immunity by:
  • promoting improved anti-viral immune system function
  • increasing NK cell activity
  • increasing S-IgA
  • producing nitric oxide
  • modulating cell mediated immune response
  • activating the reticuloendothelial system
  • promoting a more balanced production of cytokines
  • promoting resistance against some autoimmune processes
  • evoking anti-Tn antibodies
  • decreasing IgE-mediated responses
  • enhancing immune system response to administered vaccines
  • mediating against radiation-induced depression in white blood cells

Friendly bacteria promote detoxification by:
  • inactivating and eliminating carcinogens
  • decreasing mutagenic compounds
  • decreasing activity of nitroreductase and azoreductase
  • decreasing activity of B-Glucuronidase
  • decreasing activity of B-Glucosidase
  • decreasing activity of ornithine decarboxylase
  • decreasing activity of tryptophanase
  • decreasing activity of neuraminidase and mucinase
  • decreasing levels of polyamines, cresols and indoles
  • decreasing ammonia
  • decreasing levels of nitrates and nitrites
  • enhancing liver function and promoting elimination of bile acids
  • enhancing cholesterol metabolism

For more information on Polyflora Probiotics:

  1. D'Adamo P, Whitney C. Live Right For Your Type. 2001. GP Putnam and Sons, NYC
  2. Backhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Host-bacterial mutualism in the human intestine. Science. Mar 25; 307(5717):1915-20. (2005)
  4. Eckburg, P. B., Bik, E. M., Bernstein, C. N., Purdom, E., Dethlefsen, L., Sargent, M., Gill, S. R., Nelson, K. E. & Relman, D. A. Diversity of the human intestinal microbial flora. Science 308, 1635-38. (2005)
  5. Umesaki Y. Immunohistochemical and biochemical demonstration of the change in glycolipid composition of the intestinal epithelial cell surface in mice in relation to epithelial cell differentiation and bacterial association. J Histochem Cytochem. 1984 Mar; 32(3):299-304.
  6. D'Adamo PJ, Kelly GS. Metabolic and immunologic consequences of ABH secretor and Lewis subtype status. Altern Med Rev. Aug;6(4):390-405; 2001
  7. Hoskins LC, Boulding ET. Degradation of blood group antigens in human colon ecosystems. I. In vitro production of ABH blood group-degrading enzymes by enteric bacteria. J Clin Invest Jan;57(1):63-73;1976
  8. Hoskins LC, Boulding ET. Degradation of blood group antigens in human colon ecosystems. II. A gene interaction in man that affects the fecal population density of certain enteric bacteria. J Clin Invest Jan;57(1):74-82; 1976
  9. Elli M, Colombo O, Tagliabue A. A common core microbiota between obese individuals and their lean relatives? Evaluation of the predisposition to obesity on the basis of the fecal microflora profile. Med Hypotheses. 2010 Apr 8

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