In a previous article in this series on diabesity I briefly mentioned the role of gut health in obesity and diabetes. I’d like to go into more detail on that subject here, especially since it’s not a very well known relationship.

Our gut is home to approximately 100,000,000,000,000 (100 trillion) microorganisms. That’s such a big number our human brains can’t really comprehend it. One trillion dollar bills laid end-to-end would stretch from the earth to the sun – and back – with a lot of miles to spare. Do that 100 times and you start to get at least a vague idea of how much 100 trillion is.

The human gut contains 10 times more bacteria than all the human cells in the entire body, with over 400 known diverse bacterial species. In fact, you could say that we’re more bacterial than we are human. Think about that one for a minute.

We’ve only recently begun to understand the extent of the gut flora’s role in human health and disease. Among other things, the gut flora promotes normal gastrointestinal function, provides protection from infection, regulates metabolism and comprises more than 75% of our immune system. Dysregulated gut flora has been linked to diseases ranging from autism and depression to autoimmune conditions like Hashimoto’s, inflammatory bowel disease and type 1 diabetes.

Recent research has shown that the gut flora, and the health of the gut in general, also play a significant role in both obesity and diabetes. I’ve seen this anecdotally in my practice as well. Nearly every patient I treat with a blood sugar issue also has a leaky gut, a gut infection, or some other chronic inflammatory gut condition.

We now know that the composition of the organisms living in your gut determines – to some extent, at least – how your body stores the food you eat, how easy (or hard) it is for you to lose weight, and how well your metabolism functions. Let’s take a closer look at the mechanisms involved.

Intestinal bacteria drive obesity and metabolic disease

A study published this year in Science magazine found that mice without a protein known as toll-like receptor 5 (TLR5) in their gut gain excessive weight and develop full-blown diabetes and fatty liver disease when fed a high-fat diet. If we think of the gut flora as a community, TLR5 is like a neighborhood police force that can keep the houligans in check. Without TLR5, bad bacteria can get out of control.

The study authors found that these bad bacteria caused a low-grade inflammation in the mice, which caused them to eat more and develop insulin resistance. They also found that treating these mice with strong antibiotics (enough to kill most of the bacteria in the gut) reduced their metabolic abnormalities.

But the most interesting part of this study is what happened when the researchers transferred the gut flora from the TLR5-deficient overweight mice into the guts of skinny mice: the skinny mice immediately started eating more and eventually developed the same metabolic abnormalities the overweight mice had. In other words, obesity and diabetes were “transferred” from one group of mice to the other simply by changing their gut flora (as shown in the image below).

Other studies have shown that the composition of the gut flora differs in people who are obese and diabetic, and people who are normal weight with no metabolic irregularities.

One possible mechanism for how changes in the gut flora cause diabesity is that different species of bacteria seem to have different effects on appetite and metabolism. In the study on TLR5 deficient mice I mentioned above, the mice with too much bad bacteria in their guts experienced an increase in appetite and ate about 10 percent more food than their regular relatives. But it wasn’t just that these mice were hungrier and eating more; their metabolisms were damaged. When their food was restricted, they lost weight – but still had insulin resistance.

Other studies have shown that changes in the gut flora can increase the rate at which we absorb fatty acids and carbohydrates, and increase the storage of calories as fat. This means that someone with bad gut flora could eat the same amount of food as someone with a healthy gut, but extract more calories from it and gain more weight.

Bad bugs in the gut can even directly contribute to the metabolic syndrome by increasing the production of insulin (leading to insulin resistance), and by causing inflammation of the hypothalamus (leading to leptin resistance).

How modern life screws up our gut and makes us fat and diabetic

What all of this research suggests is that healthy gut bacteria is crucial to maintaining normal weight and metabolism. Unfortunately, several features of the modern lifestyle directly contribute to unhealthy gut flora:

• Antibiotics and other medications like birth control and NSAIDs
• Diets high in refined carbohydrates, sugar and processed foods
• Diets low in fermentable fibers
• Dietary toxins like wheat and industrial seed oils that cause leaky gut
• Chronic stress
• Chronic infections

We also know that infants that aren’t breast-fed and are born to mothers with bad gut flora are more likely to develop unhealthy gut bacteria, and that these early differences in gut flora may predict overweight and obesity in the future.

It’s interesting to note that the diabesity epidemic has neatly coincided with the increasing prevalence of factors that disrupt the gut flora. I’m not suggesting that poor gut health is the single cause of obesity and diabetes, but I am suggesting that it likely plays a much larger role than most people think.

How to maintain and restore healthy gut flora

The most obvious first step in maintaining a healthy gut is to avoid all of the things I listed above. But of course that’s not always possible, especially in the case of chronic stress and infections, and whether we were breast-fed or our mothers had healthy guts.

If you’ve been exposed to some of these factors, there are still steps you can take to restore your gut flora:

• Remove all food toxins from your diet
• Eat plenty of fermentable fibers (starches like sweet potato, yam, yucca, etc.)
• Take a high-quality probiotic, or consider more radical methods of restoring healthy gut flora
• Treat any intestinal pathogens (such as parasites) that may be present
• Take steps to manage your stress

Hippocrates said: “All disease begins in the gut.” 2,500 years later we’re just beginning to understand how right he was. And, as I’ll explain in this article, hypothyroidism is no exception. Poor gut health can suppress thyroid function and trigger Hashimoto’s disease, and low thyroid function can lead to an inflamed and leaky gut – as illustrated in the following diagram:

The gut-thyroid-immune connection

Have you ever considered the fact that the contents of the gut are outside the body? The gut is a hollow tube that passes from the mouth to the anus. Anything that goes in the mouth and isn’t digested will pass right out the other end. This is, in fact, one of the most important functions of the gut: to prevent foreign substances from entering the body.

Another important function of the gut is to host 70% of the immune tissue in the body. This portion of the immune system is collectively referred to as GALT, or gut-associated lymphoid tissue. The GALT comprises several types of lymphoid tissues that store immune cells, such as T & B lymphocytes, that carry out attacks and produce antibodies against antigens, molecules recognized by the immune system as potential threats.

Problems occur when either of these protective functions of the gut are compromised. When the intestinal barrier becomes permeable (i.e. “leaky gut syndrome”), large protein molecules escape into the bloodstream. Since these proteins don’t belong outside of the gut, the body mounts an immune response and attacks them. Studies show that these attacks play a role in the development of autoimmune diseases like Hashimoto’s.

We also know that thyroid hormones strongly influence the tight junctions in the stomach and small intestine. These tight junctions are closely associated areas of two cells whose membranes join together to form the impermeable barrier of the gut. T3 and T4 have been shown to protect gut mucosal lining from stress induced ulcer formation. In another study, endoscopic examination of gastric ulcers found low T3, low T4 and abnormal levels of reverse T3.

Likewise, thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH) both influence the development of the GALT. T4 prevents over-expression of intestinal intraepithelial lymphocytes (IEL), which in turn causes inflammation in the gut.

The gut-bacteria-thyroid connection

One little known role of the gut bacteria is to assist in converting inactive T4 into the active form of thyroid hormone, T3. About 20 percent of T4 is converted to T3 in the GI tract, in the forms of T3 sulfate (T3S) and triidothyroacetic acid (T3AC). The conversion of T3S and T3AC into active T3 requires an enzyme called intestinal sulfatase.

Where does intestinal sulfatase come from? You guessed it: healthy gut bacteria. Intestinal dysbiosis, an imbalance between pathogenic and beneficial bacteria in the gut, significantly reduces the conversion of T3S and T3AC to T3. This is one reason why people with poor gut function may have thyroid symptoms but normal lab results.

Inflammation in the gut also reduces T3 by raising cortisol. Cortisol decreases active T3 levels while increasing levels of inactive T3. ¹

Studies have also shown that cell walls of intestinal bacteria, called lipopolysaccharides (LPS), negatively effect thyroid metabolism in several ways. LPS:

• reduce thyroid hormone levels;
• dull thyroid hormone receptor sites;
• increase amounts of inactive T3;
• decrease TSH; and
• promote autoimmune thyroid disease (AITD).

Other gut-thyroid connections

Hypochlorhydria, or low stomach acid, increases intestinal permeability, inflammation and infection (for more on this, see my series on acid reflux & GERD). Studies have shown a strong association between atrophic body gastritis, a condition related to hypochlorhydria, and autoimmune thyroid disease.

Constipation can impair hormone clearance and cause elevations in estrogen, which in turn raises thyroid-binding globulin (TBG) levels and decreases the amount of free thyroid hormones available to the body. On the other hand, low thyroid function slows transit time, causing constipation and increasing inflammation, infections and malabsorption.

Finally, a sluggish gall bladder interferes with proper liver detoxification and prevents hormones from being cleared from the body, and hypothyroidism impairs GB function by reducing bile flow.

Healing the gut-thyroid axis

All of these connections make it clear that you can’t have a healthy gut without a healthy thyroid, and you can’t have a healthy thyroid without a healthy gut. To restore proper function of the gut-thyroid axis, both must be addressed simultaneously.

Healing the gut is a huge topic that can’t be covered adequately in a few short sentences. But I will say this: the first step is always to figure out what’s causing the gut dysfunction. As we’ve reviewed in this article, low thyroid is one possible cause, but often hypochlorhydria, infections, dysbiosis, food intolerances (especially gluten), stress and other factors play an even more significant role. The second step is to address these factors and remove any potential triggers. The third step is to restore the integrity of the gut barrier. My preferred approach for this last step is the GAPS diet.

The influence of thyroid hormones on the gut is one of many reasons why I recommend that people with persistently high TSH and low T4 and T3 take replacement hormones. Low thyroid hormones make it difficult to heal the gut, and an inflamed and leaky gut contributes to just about every disease there is, including hypothyroidism. Fixing the gut is often the first – and most important – step I take with my patients.