How Gut Bacteria Increase The Chance You’ll Suffer From Metabolic Syndrome And A Simple Solution (Part 2/2)
New research suggests a powerful interplay between your gut microbiota and inflammation, which can dramatically increase the risk factors contributing to metabolic syndrome, such as obesity, cholesterol and triglycerides. The good news — there’s a simple solution.
IN PART 1, I reviewed the latest research that hypothesizes that although leptin and insulin play insidious roles in making us fat and sick (potentially leading to metabolic syndrome), persistent inflammation along with our microbiota may be malicious co-conspirators.
The summary of what we learned in Part 1 can boil down to this:
- Inflammation is caused by — and the immune system is thereby activated in response to — eating sugary carbs and certain unhealthy fats –>
- Which causes both a spike of white blood cell production in response to the inflammation and insulin/leptin resistance –>
- Which then allows sugar (glucose) to build up in the blood –>
- Causing the liver and pancreas to overwork in their attempt to shuttle the sugar into cells for energy as they compete with the white blood cells for the energy they both need–>
- Leading to impaired liver, pancreas, immune system function and inflammation–>
- And, potentially, to diabesity (= diabetes + obesity, two of the three conditions required for metabolic syndrome).
Metabolic syndrome is a nasty condition that you want to avoid. When this happens, there’s little that remains normal or good in life. Aging accelerates. Diabetes knocks on the door. Heart attacks lurk. The brain degenerates.
Could be that you can thank chronic inflammation for all this wreckage.
If so, a natural question would be: Where does all that inflammation come from?
Yes, some ingested fats are directly inflammatory, and shoveling copious calories into the bloodstream from fat or sugar can overwhelm and inflame cells. By now, having read Part 1, you know there’s another culprit — the 100 trillion microbes, give or take, yucking it up in your gut.
It appears that junk food — a new phenomena for humanity — disrupts an ancient symbiotic, healthy relationship between man and buggies.
One clear example of this disrupted dynamic is tooth decay.
In the days before plentiful sugar, teeth enamel battled with plaque microbes, but it was an even match. Now there’s a different outcome.
Now there’s sugar, sugar everywhere. And when those plaque microbes feed on sugar, well, they get strong and large in number, and the by-product they produce—acid—which, in normal amounts, protects you from foreign bacteria—now corrodes your teeth.
A once cooperative relationship becomes antagonistic.
What The Mice Tell Us
Given that mice are more amenable than we humans when it comes to participation in poking and prodding scientific experimentation, they have been used to study the potential cause and effect links between food, microbiota disposition, insulin resistance and obesity.
Patrice Cani at the Catholic University of Louvain in Brussels, Belgium studied these experiments and began to suspect that a major contributor to the mice’s insulin resistance and obesity was inflammation that emanated from their native microbes.
His was a learned guess, which is not convincing to the scientific community, so Mr Cani conducted his own experiment.
If you read Part 1 of this two part series, you may recall a brief look at “endotoxin”, which are molecules that reside in the outer walls of certain bacteria. To test his hypothesis that inflammation emanated from native microbes, Patrice Cani gave a low dose of endotoxin to one group of mice on a regular diet, and put the other group on a high-fat diet.
As he expected, both groups of mice developed insulin-resistant livers, became obese and got diabetes.
It appears that endotoxins are at the root of it. Endotoxins directly cause inflammation, and a high fat diet increases the endotoxin load into the blood stream, which then leads to inflammation and then obesity and diabetes — a microscopic domino effect.
The Soluble Hero
All is not lost, for those poor mice — and by extension — us, because there’s a hero in the story, one that made everything OK.
The hero is called, “oligosaccharides”.
Oligosaccharides are soluble prebiotic plant fibers that get to the colon without being fully digested, and thus can feed the bacteria (microbiota) in the colon. In the process, feeding on and thereby digesting these fibers, we get to use their healthy byproducts, such as acetic acid, butyric acid, B vitamins, and vitamin K.
At this point, we come full circle to Dr. Dandona’s discovery of how freshly squeezed orange juice disabled the ability of endotoxins to cause inflammation, as discussed in Part 1, Can The Right Gut Bacteria Fight Obesity And Slay Metabolic Syndrome?
Cani’s mice experiments suggest that orange juice inhibited the endotoxin’s ability to create inflammation and start a cascade of effects, from insulin de-sensitivity to obesity to diabetes, because orange juice has oligosaccharides. And they’re the heroes that feed the beneficial bacteria that overwhelm their harmful brethren.
Cani’s work showed the causality and effects:
- Junk food promotes the growth of harmful microbes, and the decline of friendly ones.
- Gut permeability increases thus enabling endotoxins to move from the gut into circulation.
- Endotoxins in the bloodstream spur inflammation.
- Consuming prebiotics containing certain gut-sealing microbes, like Bifidobacteria, keep the gut tightly sealed, thus preventing the cascade.
- In addition, the beneficial bacteria, now fortified by feeding on the prebiotics, muscle out the harmful microbial mob.
From Mice To Men
OK, sound good for mice… what about we human-types?
For this we go to China, where, as described on page 3 on a Mother Jone’s article about gut bacteria, a microbiologist named Liping Zhao decided that he either change his diet or drop dead. Given his high blood pressure, high LDL (“bad” cholesterol) and 44 extra pounds, he had three of the five risk factors for metabolic syndrome.
Liping Zhao did two simple things:
- He changed his diet to whole grains, rich in those prebiotic fibers important for beneficial bacteria; and
- He began regularly consuming two traditional medicinal foods thought to have such properties: bitter melon and Chinese yam.
Three important things happened:
- Zhao’s blood pressure normalized.
- He lost 44 pounds in two years.
- His methodical sampling of his microbes revealed that as his metabolism normalized, quantities of a bacterium called Faecalibacterium prausnitzii increased in his gut.
What occurred to Zhao was that inflammation, always observed to be a part of the risk factors for metabolic syndrome, may actually be a casual agent, one influenced, in part, by our microbiota.
Zhao was just one data point.
Could what he did to reverse his metabolic syndrome work for others as well?
A patient of his gave him an opportunity to test his protocol on someone other than himself. Tipping the scales at 385 pounds, he was morbidly obese, diabetic, inflamed, had high bad cholesterol, and more blood sugar.
Naturally, Zhao examined his patient’s microbes, and discovered that 35% belonged to a single, endotoxin-producing species called Enterobacter cloacae. Zhao put the man on a version of his own regimen — whole grains supplemented with other prebiotics.
Soon, the Enterobacter cloacae declined, as did circulating endotoxin and markers of inflammation.
After 23 weeks, the patient had lost 113 pounds, an amazing 4.9 pounds per week! Harmful endotoxin bacteria became nearly undetectable as counts of anti-inflammatory bacteria (microbes that specialize in fermenting non-digestible fibers) increased.
What this did not prove, however, was that these specific microbial changes caused the dramatic weight loss. It’s possible that is was simply a matter of consuming far fewer calories than before.
As mentioned, there’s only so much experimentation you can do with humans, as they tend to resist living in cages and having everything in their life controlled. So, back to the mice.
The Mother Jone’s article from which the Zhao story was reported is unclear about how he conducted the experiment, but it seems that he had at least two groups of mice with clearly spelled out results. Each were fed a high fat diet, but:
- Group One was given Enterobacter, the endotoxin-producing species of bacteria; and
- Group Two was given Enterobacter plus Bifdobacteria, the beneficial prebiotic.
Here’s what happened to these mice…
The first group developed endotoxemia, got chubby and became diabetic — but only when eating a high fat diet. The mice colonized with good ole Bifidobacteria, and also fed a high fat diet, remained lean.
Zhao surmised that the enterobacter was uniquely opportunistic. Aided by a high fat diet, the microbe appeared able to hijack the metabolism of both mice and man, unless aided by a prebiotic.
This experiment is far from conclusive, but when added to the others, these results suggest that consuming prebiotics and probiotics is an important step toward controlling inflammation and obesity, and the other risk factors related to metabolic syndrome.
Does Everyone Agree That Inflammation Drives Metabolic Syndrome And Obesity?
In a word, no.
There’s a bunch of reasons why there’s dissent among scientists who study these things, among them, these:
- They’re scientists, so of course they’re congenitally disposed to disagree.
- It’s a stretch to think that all inflammation originates from the micobiota, something even proponents of this microbe/inflammation theory agree with.
- Given that everyone agrees that inflammation is caused by more than microbiota, then the question becomes, what other inflammation inciters might also contribute to metabolic syndrome, such as environmental toxins.
- Chronic stress in known to cause chronic inflammation, but does that have the same metabolic effects as does endotoxin-caused inflammation? (Stress sure does mess with your telomeres.)
So, you can see that there’s more research work to be done before consensus can be reached about certain particulars about the relationships between microbiota, inflammation and the various risk markers for metabolic syndrome.
But we don’t need to wait for consensus. We can act on what has so far been revealed.
Just a few days short of a year ago, I wrote a post about Dr. Andrew Weil’s Anti-inflammation Diet. I called it, Why Dr. Weil’s Anti-Inflammation Pyramid May Be The Best Diet. Here’s what it looks like:
Note that the base of this anti-inflammation diet is loaded with fruits and veggies, the very foods that contain the wonderful, endotoxin ass-kickers, the prebiotic Oligosaccharides.
You might wish to check the pyramid and see what food categories are absent from your diet. I wouldn’t worry much if you’re not eating grains and pasta — they don’t have much nutritional value and some nutritionists believe that the gluten contained in them is responsible for various autoimmune diseases.
Specific foods you can begin to add to your diet that are inflammation fighters include:
- Broccoli sprouts
- Kimchi, and a steady supply of probiotic supplements, such as New Chapter.
Another worthwhile thing to do is to read my post, Six Simple Solutions To Rid Yourself of Inflammation, which recommends some pretty powerful supplements.
Some Parting Thoughts
It takes a long time and much experimentation for something to be scientifically proven, and then become widely known to we plebeians. Such it will be with this dance between microbiota, inflammation and metabolic syndrome.
You dear reader are, however, lucky.
You’ve now been exposed to some leading edge research that suggest that with some simple tweaks to your diet, you can improve your chances of not succumbing to the leading causes of death in the developed world — heart disease, stroke, certain cancers, and even dementia.
I’ve thrown a lot of information at you, but thanks to the work of Sarah Zhang, much of it can be distilled down to her flowchart of the inflammation/obesity cascade shown below.
Study it well and add some inflammation fighting foods to your diet.
Ciao for now.
—By Sarah Zhang
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