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  • Resveratrol Normalizes Gut Bacteria, Indirectly Increases Bile Production And Bile Flow In The Liver To Facilitate Excretion Of Cholesterol And Reduce Fatty Plaque In Arteries

    April 11, 2016: by Bill Sardi

    The ability of the red wine molecule resveratrol (res-vair-ah-trol) to favorably alter the family of bacteria in the human digestive tract known as the microbiome is just now beginning to be appreciated. [ January 7, 2016]  A new revelation is that resveratrol inhibits a chemical in the gut that is implicated in arterial disease (atherosclerosis). [American Society Microbiology]

    Investigators used lab mice that were genetically altered to be prone to atherosclerosis (fatty plaque buildup in arteries) to make it easier to prove their point.

    More than 90% of the bacteria in the human gut come from two groups – Bacteroidetes and Firmicutes. Mice fed a choline-rich diet (example: eggs) that markedly increases the bacterial concentrations of Bacteroides and decreases the concentrations of Firmicutes compared to mice given normal animal chow. Choline decreases Bacteroides — Lactobacillus acidophilus and Bifidobactium, considered to be “good bacteria.”

    Choline is metabolized by intestinal bacteria to produce a noxious molecule trimethylamine-N-oxide (TMAO).  TMAO reduces bile production in the liver that then indirectly results in a marked increase in arterial fatty plaque (see graphic).

    The population of Bacteroides increased from 20.6% to 34.0% at the expense of Firmicutes (60-1% to 50.1%) in choline-fed animals.  The abundance of Bacteroides is associated with greater TMAO levels.  This undesirable effect is reversed by resveratrol!

    Under normal healthy circumstances the liver makes bile from cholesterol, which is then excreted. This is the human body’s way of inhibiting fatty plaque (cholesterol) buildup in arterial walls.   In other words, as bile is excreted normally, cholesterol is also excreted and arteries remain clear of plaque buildup.

    TMAO interferes with bile production that results in fatty plaque buildup in arteries.  Feeding lab mice choline or TMAO resulted in the same atherosclerotic effect.

    This deleterious effect was demonstrated in the aorta (the first blood vessel outside the heart) of laboratory mice (see graphic).

    Of note, antibiotics killed off all bacteria in the gut of these lab animals and interfered with the enhancement of bile production by resveratrol (see graphic).

    Researchers said (paraphrased): “This study demonstrates resveratrol improves the dysregulation of the gut microbiota induced by a high-fat diet, increases Bacteroides-to-Firmicutes ratios, and increases the growth of Lactobacillus acidophilus and Bifidobacterium in mice.”  [mBio April 2016]

    This study also suggests that the artificial and toxic method of inhibiting cholesterol production in the liver is inappropriate.  The problem is in the gut, not the liver.


    Additional note: like choline, artificial sweeteners may adversely alter the microbiome, the community of bacteria in the intestines.  [Nature 2014]  Despite being calorie-less, artificial sweeteners like saccharin, sucralose and aspartame induce glucose intolerance.   Artificial sweeteners may promote obesity and diabetes.  This adverse effect is also mediated by disturbance of the normal composition of bacteria in the human intestines.

    Genetically obese mice (animals that cannot make leptin, the hormone that limits appetite) have 50% fewer Bacteroidetes bacteria and 50 percent more Firmicutes bacteria than normal mice.  This results in mice storing fat rather than using it for energy.

    At least in lab animals, artificial sweeteners result in high blood sugar (glucose) levels, meaning sugar was not being utilized and converted to energy.  But lab animals given table sugar (sucrose) had normal blood sugar levels!

    When laboratory mice were given antibiotics to kill off (sterilize) all their gut bacteria the microbial population returned to its original makeup and blood sugar was controlled.  This biological phenomenon doesn’t appear to be restricted just to laboratory mice.  A study of 381 humans confirms that users of artificial sweeteners are more likely to be overweight.  [Scientific American 2015]

    Of interest, artificial sweeteners run opposite to the natural sweetener stevia and its fractions (steviosides and rebaudiosides).  Stevia-based sweeteners, 300 times as sweet as table sugar, do not appear to significantly alter gut bacteria.  When compared to an anti-diabetic drug (Gilbenclamide, aka Micronase, DiaBeta, Glynase), the natural sweetener stevia actually outperformed the drug in its ability to control blood sugar and favorably altered circulating blood cholesterol levels.  []

    This information then begs the question: do artificial sweeteners by their alteration of the normal composition of gut bacteria also accelerate the buildup of fatty plaques in arteries just as choline does?

    The answer to that question appears to be yes, artificial sweeteners strikingly increase atherosclerotic plaque in arteries. [Molecules & Cells 2011]

    We now know these deleterious effects induced by artificial sweeteners may be mediated the disruption of bacterial colonies in the human gut.   The Food & Drug Administration needs to convene an immediate meeting of public health officials to reconsider the use of artificial sweeteners.  ©2016 Bill Sardi,

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