Here is a troubling fact: Australia is fat. More than 65% of Australian adults and nearly 25% of our children are overweight or obese. There are many factors at play behind these figures, but an important factor resides in our gut. Gut microbes influence how our body’s metabolism function and maybe a driving factor in our propensity to gain weight.
Obesity – The Basics:
Gut microbes and obesity – In a classic study from 20051, researchers studied genetically obese and lean mice, looking for differences in the composition of their gut microbes. One of their key findings was that obese mice had a striking difference in the composition of their gut microbes, compared to lean mice. Obese mice had 50% fewer Bacteroidetes, a broad group of gut bacteria, than lean mice. Also, these obese mice had a significantly higher proportion of Firmicutes, another group of gut bacteria, compared to lean mice. These results strongly suggest that obesity affects the bacterial composition of the gut.
In recent years, studies in mice and humans have reported further links between weight gain, obesity and gut microbes, involving different yet interconnected pathways. For example, gut microbes can affect energy harvest and storage. They can also influence metabolic functions such as fermentation of undigested carbohydrates and proteins, which lead to the production of chemicals like butyrate, acetate, and other short-chain fatty acids (SCFAs). These chemicals, collectively known as bacterial metabolites, can affect the function of different processes linked to obesity3. For example, they can regulate the secretion of some hormones or affect intestinal barrier function2. Tweaking with these systems can influence different processes that link back to obesity, such as the way food is processed, gut motility, appetite regulation, and how efficiently our body uses nutrients and energy4.
How strong is the obesity evidence?
Multiple studies confirm that gut microbes can influence the harvest, storage, and expenditure of energy5. Our body stores energy in the form of fat and studies have found that obese people have different microbial makeup in their gut, compared to healthy people. Specific groups of “bad bacteria” are over-represented in an obese gut6. These “bad bacteria” send chemical signals that increase the amount of energy extracted from food and stored in your body as fat.
A key mechanism used by these bacteria involves SCFAs. In one study, for example, SCFAs were shown to have a protective effect against obesity, inducing cells to switch from storing to utilising fats. This helped counteract the effects of a diet rich in bad fats, such as those found in processed and fast foods7.
Implications for your health
Obesity is influenced by many factors, including diet, genetics, and lifestyle. Among these, diet is one of the most important factors you can control. An unhealthy diet, high in sugar and bad fats, will significantly change the makeup of your gut microbiota, increasing the proportion of “bad bacteria” and decreasing the number of beneficial microbes. This is on top of all the other problems associated with a poor diet, like clogged arteries, cardiovascular disease and a myriad of other problems. You should aim for a diet not only low in sugar and bad fats; but rich in fibre and resistant starch – think soluble and insoluble fibre from fruits and vegetables, for example.
On this line of thought, you should know that using artificial sweeteners is not a silver bullet that will let you satiate your cravings for sweets and remain healthy. In a recent study, sugar alternatives such as sucralose, saccharin or aspartame, were shown to have detrimental effects on glucose tolerance in mice and humans. This effect, the study showed, could be traced back to the effect these sweeteners had on the abundance of specific groups of gut bacteria8-9.
At our centre, we develop patient-centred diets that are customised to meet your personal needs. Following our health plan will give you tangible results that will improve your wellbeing.
- Ley, R.E., Bäckhed, F., Turnbaugh, P., Lozupone, C.A., Knight, R.D. and Gordon, J.I., 2005. Obesity alters gut microbial ecology. Proceedings of the National Academy of Sciences, 102(31), pp.11070-11075. Read it!
- Heiss, C.N. and Olofsson, L.E., 2018. Gut microbiota-dependent modulation of energy metabolism. Journal of innate immunity, 10(3), pp.163-171.Read it!
- Vajro, P., Paolella, G. and Fasano, A., 2013. Microbiota and gut-liver axis: a mini-review on their influences on obesity and obesity related liver disease. Journal of pediatric gastroenterology and nutrition, 56(5), p.461. Read it!
- Lazar, V., Ditu, L.M., Pircalabioru, G.G., Picu, A., Petcu, L., Cucu, N. and Chifiriuc, M.C., 2019. Gut Microbiota, Host Organism, and Diet Trialogue in Diabetes and Obesity. Frontiers in Nutrition, 6. Read it!
- Krajmalnik‐Brown, R., Ilhan, Z.E., Kang, D.W. and DiBaise, J.K., 2012. Effects of gut microbes on nutrient absorption and energy regulation. Nutrition in Clinical Practice, 27(2), pp.201-214. Read it!
- Turnbaugh, P.J., Ridaura, V.K., Faith, J.J., Rey, F.E., Knight, R. and Gordon, J.I., 2009. The effect of diet on the human gut microbiome: a metagenomic analysis in humanized gnotobiotic mice. Science translational medicine, 1(6), pp.6ra14-6ra14. Read it!
- den Besten, G., Bleeker, A., Gerding, A., van Eunen, K., Havinga, R., van Dijk, T.H., Oosterveer, M.H., Jonker, J.W., Groen, A.K., Reijngoud, D.J. and Bakker, B.M., 2015. Short-chain fatty acids protect against high-fat diet–induced obesity via a PPARγ-dependent switch from lipogenesis to fat oxidation. Diabetes, 64(7), pp.2398-2408. Read it!
- Suez, J., Korem, T., Zeevi, D., Zilberman-Schapira, G., Thaiss, C.A., Maza, O., Israeli, D., Zmora, N., Gilad, S., Weinberger, A. and Kuperman, Y., 2014. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 514(7521), p.181. Read it!
- Suez, J., Korem, T., Zilberman-Schapira, G., Segal, E. and Elinav, E., 2015. Non-caloric artificial sweeteners and the microbiome: findings and challenges. Gut microbes, 6(2), pp.149-155. Read it!