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  • Writer's pictureDr. Randi Brown, ND

Are Your Gut Bugs Making You Fat?

The hidden role of the intestinal microbiome in regulating your metabolism, glucose control, hunger, and weight.

Anyone that has struggled with weight issues knows what it feels like to hear the words “just exercise more and eat less”. It basically makes your fists curl. This is our oldest, most basic understanding of energy balance - In order to lose weight, we must burn more calories than we consume. While not inaccurate, per se, this over-simplification of weight loss can leave many with feelings of helplessness, frustration, or worse yet, shame and worthlessness.

The truth is, it’s just not that simple, and while it can be helpful at times to simplify complex subjects, it is not helpful to oversimplify to the point of being misleading or deceiving. In reality, there are many factors at play that contribute to one’s weight including, of course, activity levels, dietary habits, genetics, socioeconomic status, stress levels, sleep quality and quantity, environmental exposures, and the list goes on.

How Gut Health Affects Our Body Weight

What is not considered in the "calories in, calories out" equation is what those calories are actually doing in your body in terms of blood sugar regulation, inflammation, and gut microbiome development. This commonly overlooked, yet vitally important aspect of health and weight maintenance is what I hope to shed some light on.

Now fair warning, this blog may be difficult to understand at times but I have put a “bottom line” sentence as a simplified takeaway for each paragraph. I still encourage you to read the full thing in order to make sense of it all – then just reference the take away from the bottom line.

Gut Health and Gut Microbiome Development as Risk factors for Overweight, Obesity, and Type 2 Diabetes

The first studies to look at whether our gut microbiota can affect our weight and obesity used models in mice.

Of the more compelling studies, one showed that mice that were given “obese gut flora” were significantly more overweight or obese that mice with “lean gut flora” despite being of the same gender, strain, genetic predisposition, and having identical diets (or even lower-calorie diets) (1,2).

It appears that colonizing a mouse with an “obese microbiota” can actually cause weight gain, while colonizing with “lean microflora” may improve weight loss (1,2). The idea of an “obese microbiota” is an interesting one, but is it true for humans? Research has found that “obese microbiota” have properties that tend to favor weight gain and fat deposition in the host by increasing dietary energy harvest (increasing energy extraction from foods), fueling inflammation, altering blood sugar and insulin levels, disturbing satiety and hunger levels, disrupting the gut-brain axis of communication and by altering fat cell responses to caloric intake, ultimately promoting fat mass gain and obesity (3,4).

Observational studies in humans have suggested that caesarian section children have microbiomes that closely match obese children, and that antibiotic administration in infancy may be a risk factor for developing obesity (1,8). These examples highlight the importance of one, developing a microbiome from a young age (through vaginal birth, breastfeeding, and minimizing early antibiotic exposure), and two, that the microbiome can have a profound effect on how we extract energy from foods, regulate metabolism, influence inflammation, and ultimately whether or not we are likely to become overweight or obese.

While the research in this area is still in its infancy, there are some promising clinical trials on the subject. One interventional study in particular showed that the transfer of intestinal microbiota from lean donors increased insulin sensitivity in individuals with metabolic syndrome (9).

Let’s now dive into the mechanism or “how” or gut microbiota can have such an influence on our weight. Because I get it… it does sound rather far-fetched.

Gut-Derived Metabolic Endotoxemia (Inflammation) and Obesity

Systemic inflammation that comes from the gut is primarily a result of gut-derived endotoxins. Endo, meaning within or absorbing, toxin, meaning a type of dangerous or poisonous material usually from microorganisms.

Thus, endotoxemia is having greater amounts of these toxins in your blood as a result of intestinal microbiota. The main endotoxin is called Lipopolysaccharide or LSP for short, which is commonly associated with gram-negative bacteria. When LPS enters the bloodstream from the gut it can cause a heightened pro-inflammatory state and oxidative environment (5,6,7). In short, metabolic endotoxemia dysregulates the inflammatory tone and triggers body weight gain and diabetes. Therefore, being able to lower LPS may be a reasonable target for type 2 diabetes and obesity treatment. After all, obesity itself is characterized by a chronic state of low-grade inflammation. One study did in fact show a positive correlation between serum lipopolysaccharides and body mass (BMI), triglycerides (fats in the blood) as well as waist circumference, with this effect being more evident in young obese females. i.e., higher LPS levels correlated with greater weight gain and larger weight circumferences (6).

Bottom Line #1: LPS may play a role in low-grade inflammation and insulin resistance, which can be commonly observed in obesity.

LSP Effects on Hunger and Satiety Signals

Another potential mechanism by which excessive intestinal inflammation (metabolic endotoxemia) may affect our weight is by altering important hunger and satiety hormones in the body. Leptin and ghrelin are the yin and yang, the tug of war between being ravenous, and being happily satiated.

Leptin is largely responsible for prolonged feelings of fullness, whereas ghrelin makes you feel hungry and tells your brain to seek food. We need both to tell us when to eat and how much, but when these two hormones get thrown out of balance this can lead to increased appetite and overeating. One potential modulator of this leptin and ghrelin balance in LPS. Certain gut-microbiome metabolites have shown to blunt the brain's response to satiety signals from leptin, therefore ignoring signs of fullness (4,5). The same can be true for ghrelin in that more intestinal inflammation (LPS) seems to correlate with more ghrelin (hunger).

The overall effect of our microbiome on hunger, cravings, and overeating can be 2-fold then; first by blunting our leptin "fullness" signals, and second, by accentuating ghrelins "hunger" response (5,6).

The good part is that we may be able to alter our gut microbiota, improve our gut health and therefore improve our energy balance. One study showed that after improving metabolic endotoxemia, as evaluated by LPS and inflammatory cytokines in the blood, there was a positive trend towards improved ghrelin levels, thus potentially improving satiety (11).

Bottom Line #2: less gut inflammation (LPS) may improve your satiety levels, helping you reduce excessive hunger and cravings, aiding in weight loss.

Gut Microbiota and the Gut-Brain Axis

The gut-brain axis is a form of bidirectional communication between the brain and the gut, which is largely mediated by the vagus nerve. The brain can send signals to the gut about hunger, needs for food intake, etc. but the gut can also send messages back to the brain about current food intake, calories, nutrients, etc. This communication is aided by gut bacteria. The gut microbiota (gut bugs) can either create metabolites (waste by-products) that are helpful or harmful in terms of weight regulation and health. One main bacterial metabolite is SCFA’s (Short-chain fatty acids) (3, 4, 10). These bacterial by-products form as a result of the fermentation process of bacteria consuming indigestible nutrients.

These SCFA’s provide intestinal cells with an important food source, but also serve as a means of regulating hunger and satiety. Research has suggested that obese individuals have altered SCFA production by bacteria in their intestine, thus causing disruption in their hunger and energy balance signals leading to overeating and weight gain(3).

In fact, one study showed that improving SCFA levels, specifically butyrate may improve fasting glucose levels as well as insulin sensitivity, both of which are factors in developing obesity and type 2 diabetes (3).

Bottom Line #3: Ultimately, the gut microbiota can influence gut-brain signaling, thus modulating the food intake/energy expenditure balance.

Gut-Microbiome and Gut-Hormone Regulation in Energy Balance

Some bacteria can directly regulate incretin secretion (gut hormones) by the metabolic compounds they produce. Incretins are essentially the chemical massagers that go from the intestines to other digestive organs in order to prepare them for what is to come. Incretins are largely responsible for regulating insulin secretion and affecting glucose control and hunger levels during meals. Incretins such as glucagon-like peptide-1 (GLP-1), and gastric inhibitory polypeptide (GIP), are secreted by specialized cells in the intestinal tract (enteroendocrine cells) and are released into the bloodstream where they can alter pancreatic and liver functions to optimize responses to foods. Research has suggested that certain intestinal bacteria may be able to either enhance this effect, leading to a healthy response after food consumption or inhibit or block this process, leading to altered responses to food intake (7,8,10). This altered incretin response that is disturbed by intestinal bacteria can be a potential contributor to metabolic syndrome, type two diabetes, weight gain, increased hunger levels, and over-eating, and ultimately obesity.

Bottom Line #4: Gut microbes can alter the chemical messaging signals from our intestines to other digestive organs causing aberrant responses to food intake that may promote weight gain.

Gut-Microbiota Metabolites and Adipose Tissue Regulation

Several gut microbiota-derived compounds have been described to link the intestines with the regulation of overall energy metabolism through adipose (fat) tissue remodeling. Adipose tissue used to be considered inert (functionally irrelevant), however, we now know that collectively fat cells (adipose tissue) are an active organ, releasing key metabolic and endocrine functions and playing a critical role in metabolism. Adipose tissue, when in abundance, can contribute to chronic low-grade inflammation by secreting inflammatory cytokines (immune-related molecules), perpetuating insulin resistance, increased blood sugars, diabetes, and cardiovascular disease. So, what do fat cells have to do with gut bugs?

Several gut microbiota-derived compounds have been described to link the intestines with the regulation of the host energy metabolism through adipose tissue remodeling. For example, compounds such as KetoA, a metabolite produced by gut bacteria, has been shown to up-regulate genes involved in brown adipocyte functions, which further enhances energy expenditure (increasing energy expenditure i.e., burning more calories is ideal when trying to lose weight) (3, 10).

“Brown fat” burns more calories than white fat at a resting state, thereby increasing the overall metabolic rate, protecting from obesity, and improving overall metabolic health.

Bottom Line #5: Healthy gut bugs may produce compounds that improve our fat cell health and help us increase our metabolism, making it easier to lose or maintain our weight.

SIBO and Type 2 Diabetes

One final gut-microbiome connection with metabolic health comes from a clinical observation study of SIBO positive (small intestinal bacterial overgrowth) patients and elevated glucose levels in type 2 diabetics. This study found an independent association with SIBO and lower levels of insulin secretion (lower pancreatic beta-cell function), and higher levels of glucose after an oral glucose tolerance test (12).

How you can improve your gut health and microbiota to help you with weight and energy balance:

The Problem with Probiotics

Now by this time, I’m sure you’re thinking “can I just take probiotics then to help me lose weight”. Well no, if that were true, probiotics would be flying off the shelves everywhere! Sadly, there is still no single bullet, magic weight loss pill. But here’s why it doesn't work quite as you'd think. Taking probiotics as a sole means to improve your gut health is essentially like putting a single drop of clean water in a large swampy bucket… It’s not going to do much in terms of long-term benefits or really have any significant impact on your overall gut microbiome composition. A good analogy to make sense of this concept is this: “if you had a garden that is absolutely full of weeds would you just go in there and start planting more vegetables and flowers amongst the heavy weeds? No that’s ridiculous you would weed the garden creating a better environment for fresh healthy growth of your new seeds, thus giving these new plants a greater opportunity to grow without having to compete with their neighbors for sunlight, energy, soil, and other nutrients and resources. You’re more likely to get a much better crop if you first create the proper environment to plant seeds in.

This is exactly like taking probiotics without first weeding out the excess competition.

To have proper colonization of bacteria you need to create an environment where they can thrive.

To do this takes more than popping a daily pill. It requires healthy food intake to provide good nutrition for the good gut bugs while deterring the not-so-good ones, it requires good immune system function, adequate vitamin D levels, the right amount of exercise, sleep and so on!

Not only are you creating a good environment for the good bugs, in your gut but you’re also creating a better environment and lifestyle for yourself. When you think about it, who would you rather live with? The friend who never cleans leaves their dirty dishes out and doesn't shower, or one that keeps a clean house, showers regularly and takes care of themselves, and you in the process. So why do you think your gut bugs would be any different? You have the power to attract the gut bugs you want to live with too!

Bottom Line #6: It takes more than just probiotic supplementation to cultivate a healthy intestinal microbiome. For noticeable improvements, an evidence-based naturally focused solution has the greatest likelihood of providing meaningful results.

Closing Thoughts

My point I want to get across is that your overall health including your gut health and intestinal microbiota play a role in how you will respond to diet and lifestyle changes for weight loss. This is why I always emphasize a holistic, multifaceted, personalized approach to care. One where we can create a plan that feels right for you.

If you are interested in how your gut and microbiota may be affecting your health, contact me here, or book an initial visit.

I offer both in-person visits in Victoria, BC as well as Telemedicine consultations to BC residence across the province. You can view more information on my website.


1.) Compare, D., Rocco, A., Zamparelli, M. S., & Nardone, G. (2016). The gut bacteria-driven obesity developmentDigestive Diseases34(3), 221-229.

2.) Davis, C. D. (2016). The gut microbiome and its role in obesityNutrition today51(4), 167.

3.) Gérard, C., & Vidal, H. (2019). Impact of gut microbiota on host glycemic controlFrontiers in Endocrinology10, 29.

4.) Heiss, C. N., & Olofsson, L. E. (2018). Gut microbiota-dependent modulation of energy metabolismJournal of innate immunity10(3), 163-171.

5.) Boutagy, N. E., McMillan, R. P., Frisard, M. I., & Hulver, M. W. (2016). Metabolic endotoxemia with obesity: Is it real and is it relevant?. Biochimie124, 11-20.

6.) Radilla-Vázquez, R. B., Parra-Rojas, I., Martínez-Hernández, N. E., Márquez-Sandoval, Y. F., Illades-Aguiar, B., & Castro-Alarcón, N. (2016). Gut microbiota and metabolic endotoxemia in young obese Mexican subjectsObesity facts9(1), 1-11.

7.) Davis, C. D. (2016). The gut microbiome and its role in obesity. Nutrition today51(4), 167.

8.) Luoto, R., Collado, M. C., Salminen, S., & Isolauri, E. (2013). Reshaping the gut microbiota at an early age: functional impact on obesity risk?. Annals of Nutrition and Metabolism63(Suppl. 2), 17-26.

9.) Vrieze, A., Van Nood, E., Holleman, F., Salojärvi, J., Kootte, R. S., Bartelsman, J. F., ... & Derrien, M. (2012). Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndromeGastroenterology143(4), 913-916.

10.) Suez, J., Shapiro, H., & Elinav, E. (2016). Role of the microbiome in the normal and aberrant glycemic response. Clinical Nutrition Experimental6, 59-73.

11.) McFarlin, B. K., Henning, A. L., Bowman, E. M., Gary, M. A., & Carbajal, K. M. (2017). Oral spore-based probiotic supplementation was associated with reduced incidence of post-prandial dietary endotoxin, triglycerides, and disease risk biomarkers. World Journal of Gastrointestinal Pathophysiology8(3), 117.

12.) Yan, L. H., Mu, B., Pan, D., Shi, Y. N., Yuan, J. H., Guan, Y., ... & Guo, L. (2020). Association between small intestinal bacterial overgrowth and beta-cell function of type 2 diabetes. Journal of International Medical Research48(7), 0300060520937866.

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