It should surprise none of you that I consider weight dysregulation one of the many manifestations of gut dysbiosis. Obesity is associated with a whole host of disorders, including type 2 diabetes, cardiovascular disease and non-alcoholic fatty liver. Much of what I’ve written about endotoxemia also applies to obesity.

This isn’t to say that weight is not determined by the difference between caloric intake and expenditure, it most certainly is. You may have the healthiest gut in the world and eat nothing but the purest and freshest food. However, if you eat more than you expend you’ll still gain weight. Conversely, if you eat less due to choice or famine, you will lose weight. That said, in healthy humans the deviations from a lean or relatively lean body set point are typically short-term.

There exist hormonal and neuronal networks within us that control body weight. In extreme cases of weight dysfunction as in anorexia or obesity, these systems are no longer operating as they should. I’d like to tell you I know the entire reason why this is so but I don’t. No one does. Nevertheless, a big part of the explanation lies in the health and microbial ecology of our second brain otherwise known as the gut. This makes perfect sense, after all, since this is the organ designed to digest and absorb our food.

I’m struck by how often those battling weight issues, either trying to lose it or gain it, have gastrointestinal issues. I receive many emails from people detailing gut issues and when I ask them if they are happy with their current weight the answer is inevitably no. Many have a history of weight struggle, often extending back decades to early childhood.

Now it would be easy to dismiss this common association by saying the excess caloric intake brought about the GI issues, and once they lose weight, this will all clear up. I certainly agree with the first part of this statement. Bad dietary choices eaten or drunk in sufficient quantities can most certainly cause a case of gut dysbiosis. Otherwise, I wouldn’t bother warning my readers about gluten grains, plant lectins, binge drinking, refined fructose or omega-6 vegetable oils.

However, in a subgroup of people diet change isn’t enough to resolve the dysbiosis once it takes hold. I receive emails from people who still struggle with their weight or gut even after transitioning to a more healthful diet. Some experience even worse GI issues than before. Why? I suspect it’s because once they give up or cut back their intake of dietary opioids and alcohol, their brain finally registers the distress signals emanating from an inflamed gut that have been there all along. Nothing dampens nerve signals like opiates and alcohol!

Gut dysbiosis, however it was originally caused, can make proper weight regulation a difficult proposition. The reason is because sickness, and folks that’s what gut dysbiosis is, interferes with all sorts of bodily systems including those regulating weight. If my series on cardiovascular disease didn’t convince you of this, then it’s time to move on to another blog.

A small intestine with an overgrowth of bacteria, yeast or parasites is a gut incapable of properly digesting and absorbing food and nutrients. It’s also, by definition, a gut that is inflamed due to chronic infection. Malnutrition always leads to hunger and cravings while inflammation results in lowered metabolic rate or in more severe cases, body wasting.

Is it possible to lose weight if you have gut dysbiosis? Sure it is. Through sheer willpower you can ignore insistent hunger pangs and bike or run past feelings of chronic fatigue. The participants of the 1944 Minnesota starvation experiment are proof of that. If you have time, I encourage you to read up on this experiment to learn what severe caloric restriction can do to a person. You can find a nice article about it here.

I too have “starved” myself in the past and lost a bit of weight. Nevertheless, it was always a miserable experience akin to what the young men in Minnesota experienced. I remember obsessing continually about food and living for my “cheat day” when I would gorge myself only to feel depressed about what I’d eaten afterwards. Unfortunately, I was never able to sustain the weight loss. Within a brief period I would gain everything back and then some. My experience is the norm, not the exception. Even the strongest among us are no match for the powerful biological signals that regulate hunger.

My focus in this series is how small intestinal dysfunction can make weight loss a challenge even in the presence of a food scale, a room full of exercise equipment and steel-like willpower.

However, let me get something out of the way first. There are many studies in the scientific literature that have looked at differences in gut bacterial populations between the obese and lean both in rodents and humans. While I think these finding are of some interest, I really don’t think they tell us much about why someone gains lots of weight or has trouble losing it.

I could bore you with a very long list of these research articles showing that one bacterial family is prevalent in the obese only to present you with another study showing exactly the opposite result. For the sake of my sanity and yours, I’ll cut to the heart of the matter and report what reviews of the literature show in humans:

  • No difference was discovered in Bacteroidetes species between the obese and lean.
  • Obese people were shown to have less Firmicutes than the lean.
  • Obese people have less Methanobrevibacter species than normal-weight people
  • Obese people have less Bifidobacterium than lean people. Of all mentioned relationships, this appears to be the most consistent finding. (1)

However, meta-analysis are only as good as the studies they review. If the studies are flawed, the meta-analysis isn’t really of much use. Garbage in, garbage out so to speak. Many of these studies used specific genetic-sequencing techniques that would give entirely different results if another method were used. So while I don’t deny there are differences in gut flora populations between the obese and lean, I just don’t believe this line of research gets us very far in unraveling why hunger and metabolism vary between the two.

Of more interest to me is evidence that in the obese, the digestive tract is not functioning as it should because of dysbiosis. To that end, I want to talk about a common, yet paradoxical finding in the overweight: malnutrition.

Malnutrition can cause either weight loss or weight gain depending on its severity, the ready availability of food and the genetic makeup of the person experiencing it. For example, an undiagnosed celiac can suffer malabsorption of such severity that they become rail thin and nutrient deprived regardless of what and how often they eat; and unexplained weight loss is a sign many physicians look for when screening for this disease.

However, there are plenty of overweight celiacs out there who go undiagnosed by medical professionals because this is never considered a possible outcome of the disorder. This has changed somewhat in recent years as doctors now recognize that in some celiacs, eating enough food is sufficient to mask even the most severe form of malabsorption and resulting malnutrition.

So let’s review some of the common nutrient deficiencies found in the obese:


Magnesium is required for strong, healthy bones and teeth. It also helps muscles relax, improves cardiovascular function, reduces blood pressure and lessens the severity of menstrual symptoms. It is also vital for maintaining proper nerve functioning.

Sources of magnesium include dark, green leafy vegetables, legumes, fish, fresh meat, milk, yogurt, coffee, tea, cocoa, chocolate, molasses, corn, peas, carrots, brown rice, parsley, seeds, nuts, whole grains (especially oats and barley) and fruit.

While absorbed throughout the small intestine, it is mainly absorbed in the jejunum and ileum with the help of fat-soluble vitamin D. Magnesium is excreted in urine, and its reabsorption by the kidneys is the main way levels are regulated in the body. Parathyroid hormone increases its retention while excess calcium inhibits it.

Low magnesium levels are a common finding in the overweight and obese. Magnesium deficiency is also common in those experiencing insulin resistance, a hallmark symptom of metabolic syndrome. It’s also quite common in those suffering from Crohn’s, celiac disease, in those experiencing recurrent diarrhea or vitamin D deficiency, those who have undergone gastric-bypass surgery and in those with small intestinal bacterial overgrowth (SIBO).

In studies comparing both obese and non-obese youth, 27% in both groups had inadequate intake of magnesium. (2) No surprise as processed junk food is typically low in it. However, note that 73% of both groups were getting the recommended daily allowance suggesting that in the obese, at least, low serum levels were caused by either lack of absorption or increased excretion or both.


Selenium is an essential trace element. It is important as an antioxidant and anticancer mineral. It is an activating component for glutathione, the body’s main antioxidant. Deficiency in animals increases the incidence and rate of cancer growth.

Selenium content in food depends on the soil plants are grown in or the food farmed or wild animals eat. Meat, seafood, organ meats and Brazil nuts are high in selenium.

It is mainly absorbed in the duodenum, but some absorption occurs in the jejunum and ileum. Vitamins C, A and E enhance its absorption while heavy metals and phytates inhibit it.

Phytates or phytic acid, by the way, is the storage form of phosphorus in plants. As an antinutrient, it will prevent the absorption of minerals in foods that contain it. Phytic acid is especially rich in legumes, seeds, nuts and whole grains, which is why primitive cultures would never eat these foods unless they had soaked or sprouted or fermented them first. But us “moderns” are too “smart” to pay any attention to these long-forgotten practices. Plus, processed-food manufacturing is about reducing the time it takes to make the product as a means of lowering its cost of production, a goal at odds with neutralizing plant antinutrients and toxins.

Abnormally low levels of selenium have been found in up to 58% of morbidly obese patients before gastric-bypass surgery. One year after surgery, only 3% of these same subjects had low levels. (3) Among premenopausal women, higher body mass index is significantly associated with low selenium levels. (4)

This is amazing considering how little selenium we need and how prodigious the caloric intake of the obese. I don’t care how nutrient starved your diet is, malabsorption is playing a role here.


This important mineral is needed for healthy red blood cells where 75% of the body’s iron stores are found in the form of hemoglobin. Hemoglobin is responsible for transporting oxygen from the lungs to all parts of the body. Another form of iron is myoglobin found in muscles and is used to carry oxygen within these tissues. Iron is also important in proper immune system function.

Dietary iron is found in two forms: heme and nonheme. Heme iron is found mainly in organ meat, meat, fish, shellfish and poultry and comprises about 50% to 60% of the iron found in these foods with the rest composed of nonheme iron. Nonheme iron is found primarily in plant foods and dairy. Breads, pasta, cereals, grits and flour are also fortified with nonheme iron.

The heme iron molecule is not bound to other components of food. All that’s required for proper digestion are enzymes in the stomach and small intestine that act on proteins to make it digestible. Once this happens, the iron enters the absorptive cell readily. Nonheme iron, however, comes bound with other food components and comes in two different forms necessitating a bit more digestion in order to be absorbed.

Iron is absorbed throughout the small intestine, but the majority is taken up in the duodenum. Factors that promote iron absorption are vitamin C, fructose, sorbitol, lactic acid (which is produced by beneficial lactobacillus bacteria), and mucin produced by intestinal cells.

Inhibitors of iron absorption include polyphenols from tea and coffee, oxalic acid (from spinach for example), phytic acid, phosvitin found in egg yolks, and nutrients like calcium, zinc, manganese and nickel.

Iron deficiency is the most common mineral deficiency in the world. In a study of 321 children and adolescents, low iron levels were found in 38.8% of obese and 12.1% of overweight children compared to just 4.4% of normal-weight kids. (5) The lower iron levels went, the more likely a higher body mass index. A significant number of obese children have anemia.

In morbidly obese adults examined prior to gastric-bypass surgery, abnormally low levels of iron and high rates of anemia were common. Another study showed that obese men were at significantly higher risk of developing anemia than obese women. (6)

Other common deficiencies are zinc (7), folate, vitamin C and fat-soluble vitamins D, A, and E. (4) Deficiencies in fat-soluble vitamins isn’t surprising to me. As you may recall from my SIBO series, a common finding in those with small gut dysbiosis is fat malabsorption which manifests as fatty stools or steatorrhea.

There is no possible way a person can control hunger or cravings if their body lacks essential nutrients either because these nutrients are being used by pathogens to fuel their growth, or they have an inability to absorb them in their digestive tract. As I’m fond of telling friends and family, it’s not what you eat, but what you absorb.

Food intake is always visible and measurable, absorption isn’t. Both, however, are of equal importance. Unfortunately, the absorption side of the equation usually gets short shrift in discussions concerning this or that weight loss method or mode of eating.

The unspoken assumption in all these debates is that everyone’s digestive tract is healthy and working at maximum efficiency. So if there is a weight problem, the reasoning goes, it’s obviously because the person is too gluttonous or lazy to do anything about it.

Nevertheless, the fact remains that a lot can go wrong from the time food or drink enters the mouth and its residue leaves the other end. Pretending otherwise might be a great way to sell diet books, generate blog visits or feel superior to someone heavier, but it’s a disservice to the millions of people who have an unrecognized medical condition.

And yes, there are people who could care less what they eat and willfully remain clueless about how their dietary choices perpetuate their weight issues and ill health. I know because some of them are family members or friends.

However, there are also many others who do care deeply about their health and longevity and are totally baffled about why they can’t lose weight or sustain weight loss after having eaten less and moved more.

You can’t fix something unless you know how it’s supposed to work. To that end, I’ll be covering some of the basics of proper digestion in the next post.



Gropper, S. R., Smith, J. L., Groff, J. L. (2009). Advanced Nutrition and Human Metabolism. Belmont, CA: Wadsworth Cengage Learning.

Liebermann, S., Bruning, N. (2007). The Real Vitamin and Mineral Book, 4th edition: The Definitive Guide to Designing Your Personal Supplement Program. New York: Avery.


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