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How Your Gut Microbiota Can Make You Fat (or thin)

Written by Joe Cohen, BS | Last updated:

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This post will explain how the gut microbiota can affect your weight.

What Are Short Chain Fatty Acids (SCFA)?

Short-chain fatty acids (SCFAs; acetic, propionic and butyric acid) are formed during bacterial fermentation of carbohydrates in the colon.

SCFAs cause low intestinal pH from the ileum (end of the small intestine) to the cecum (beginning of large intestine), which prevent the overgrowth of bad bacteria (like Enterobacteriaceae and Clostridia) [1].

SCFAs help fix ‘leaky gut’, strengthening the intestinal wall by increasing the secretion of mucin-2 (MUC-2), which then prevents LPS from crossing the barrier [2].

The composition of SCFAs In Our Gut

Out of the total SCFAs present in the colon, 90%-95% are acetate, propionate, and butyrate in healthy people.

  • Acetate=60%,
  • Propionate=25%,
  • Butyrate=15%,

Most of the SCFAs are absorbed in the colon, being exchanged with bicarbonate [1].

SCFAs are acidic, while bicarbonate is alkaline.

Short Chain Fatty Acids (SCFA) and Obesity

There is some conflicting information on SCFAs and weight.

On the one hand, they increase caloric utilization, which means you absorb more calories. On the other hand, they have some anti-obesity effects.

Overall, however, butyrate is antiobesity, propionate has mixed effects, and acetate seems to promote weight gain [1].

The fecal concentration of SCFAs is 20% higher in obese individuals than their lean counterparts. But this may reflect a compensatory protective mechanism against obesity, in which a greater amount is eliminated from the stool [2].

This would prevent the increased accumulation of SCFA in the intestines, which may cause weight gain (mainly from acetate) [2].

SCFAs, like butyrate and propionate, increase the formation of the gut hormones glucagon-like peptide-1 (GLP-1) and polypeptide YY (PYY). It reduces food intake by decreasing appetite [3].

PYY increases gut flow.


Butyrate reduces food intake and causes weight loss.

Butyrate has so many benefits. It combats autoimmunity, cancer, and psychological disorders. It also changes the epigenetics in our brain [4].

Butyrate is mainly produced by Firmicutes [1].

Butyrate is mostly not absorbed because it is primarily used by colon cells, where it serves as a major source of energy for them [1].

Butyrate production is determined by the level of bacteria that produce butyrate, and the pH of the large intestine [1].

Butyrate-producing bacteria seem to thrive in a more acidic environment (lower pH), whereas acetate and propionate bacteria seem to thrive in a more alkaline environment (higher pH) [1].

In the mitochondria of colon cells, 70% to 90% of butyrate is oxidized into acetyl-CoA, which is subsequently processed through the tricarboxylic acid cycle to generate a large quantity of ATP [5].

Butyrate (in summary):

  • Is a major energy source for colon cells
  • Has anti-cancer effects
  • Increases mitochondrial activity
  • Prevents toxins from crossing gut barrier
  • Prevents activation of intestinal glucose production
  • Improves insulin sensitivity
  • Increases energy expenditure by improving mitochondrial function, reducing obesity
  • Increases intestinal barrier function – an anti-inflammatory potential
  • Protects against diet-induced obesity without necessarily causing a reduction in caloric intake (mediated through gut hormones).
  • Increases the synthesis of leptin (which reduces appetite)


Propionate also reaches the liver via portal circulation and produces glucose (in the liver) [1].

Propionate possesses both pro- and anti-obesity effects, but overall it seems to be protective against obesity.

Acetate and propionate are the main products of Bacteroidetes [1].

Proprionate (in summary):

  • Increases the synthesis of leptin (which reduces appetite).
  • Protects against diet-induced obesity without causing a reduction in caloric intake (mediated through gut hormones).
  • Decreases cholesterol synthesis (by inhibiting acetyl-CoA synthetase, the enzyme that converts acetate to acetyl-CoA).
  • Is a precursor for glucose generation by the liver, which decreases the synthesis of cholesterol.
  • Inhibits resistin in human fat tissue.


Of all the three SCFAs, acetate seems to cause the most weight gain. However, it also has some properties that protect against obesity.

Acetate causes obesity outside of the brain. But it has been shown that it can also control weight gain in the hypothalamus (arcuate nucleus) by increasing GABA [6].

A substantial part of acetate is readily absorbed and reaches the liver (via portal circulation), where it’s used to create cholesterol [73].

Human studies have shown that when lactulose (metabolized by microbiota to produce high amounts of acetate) was administered to the diets of six volunteers for two weeks, there was a significant increase in both total and LDL cholesterol, ApoB, and blood levels of acetate [7].

Acetate and propionate are the main products of Bacteroidetes [1].

Acetate (in summary):

  • Acts as fuel for fat creation and cholesterol synthesis in the liver and other tissues
  • Protects against diet-induced obesity without causing a reduction in caloric intake

Bacterial Species and Obesity

Obese animals and people have a lower microbiome diversity, a lower percentage of Bacteroides, Verrucomicrobia, Faecalibacterium prausnitzii and a higher percentage of Firmicutes and Actinobacteria. Some of these results were not reproduced [1].

Microbiota in normal gutMicrobiota in obesity [1].
Firmicutes phylumIncrease in Firmicutes phylum
Bacteriodetes phylumReduced abundance of Bacteroidetes
Actinobacteria phylumA higher level of Actinobacteria phylum
Verrucomicrobia phylumA lower proportion of Verrucomicrobia
Faecalibacterium prausnitzii speciesReduced abundance of Faecalibacterium prausnitzii species

My Ubiome Results:

As a whole, I was pretty happy with the results. According to Ubiome, my gut sample is more diverse than 74 percent of the population, which is in accordance with being fit. But there’s always room for improvement.


I have 1.29X higher Firmicutes compared to all of their samples.

Firmicutes help us to digest fat that our bodies need for energy. An oversupply of Firmicutes has been linked to a higher risk of obesity, as a result of increased calorie absorption.

The increased population of Firmicutes has been found to raise the number of lipid droplets, thereby proportionately intensifying fatty acid absorption [8].

The first settlers of Europe needed to be able to better digest fat so they would have enough energy to survive brutal winters.


I have 34% fewer Bacteroides.

Bacteroidetes are thought to help protect against obesity because they do not digest fat well.


I have 1.17X higher Actinobacteria.

Actinobacteria are important to a healthy microbiome.

People with psoriasis have less of these bugs but people with ulcerative colitis tend to have more. 


I have 91% fewer proteobacteria than other people.

People with inflammatory bowel disease seem to have more Proteobacteria and fewer varieties of other bacteria.

Other Bacterial Species and Obesity

The following bacteria have less evidence in causing obesity:

Methane-producing Archaea have been found to be present in greater abundance in obese mice and humans compared with lean subjects [1].

Cocolonization of M. smithii with B. thetaiotaomicron led to the fermentation of dietary fructans to acetate, resulting in a significant increase in fat creation [9].

M. smithii is found in 70% of human beings. It generates methane. It has been found to enhance the fermentation of polysaccharides and other carbohydrates by removing hydrogen atoms, leading to greater production of SCFAs and hence, their increased absorption. These SCFAs function as an extra source of energy which contributes towards weight gain and subsequent obesity [10].

The numbers of hydrogen-producing Prevotellaceae (a Bacteroidetes) and Methanobacteriales (Archaea, which are hydrogen-oxidizing methanogens), were at a higher level in obese individuals compared with lean subjects and with those after gastric bypass. The investigators hypothesized that hydrogen was reduced, which allowed greater production of SCFAs.  This leads to more energy that is absorbed across the intestines (was not reproduced) [9].

Prevotellaceae is a source of LPS [2], which causes inflammation.

C. ramosum in the mucosa of the small intestine of mice increase body fat as a result of an increase in intestinal absorption of glucose and lipids [11].

The intestines of obese humans and mice have been found to contain [1]:

  • Low relative proportions of Bacteroides vulgatus
  • High Erysipelotrichi (Firmicutes)
  • High Clostridium ramosum (part of Erysipelotrichi)
  • High Lactobacillus spp. – was positively correlated with hs-CRP
  • High Lactobacillus reuteri
  • High Staphylococcus species (linked with increased caloric intake in children) [12]
  • Oscillibacter and Clostridium cluster XIVa and IV (found in obese-prone mice and were totally absent from their obese-resistant counterparts).
  • High Ruminococcus (most of its species fall under several Clostridium clusters, including Clostridium clusters IV and XIVa).
  • Clostridium leptum (cluster IV) has been found to be associated with both obesity and weight loss.
  • F. prausnitzii – linked with alteration in the inflammatory state and diabetes [13]. The presence of F. prausnitzii species is directly associated with the reduction in low-grade inflammation state in obesity and diabetes (independent of calorie intake) [14, 13].

How to Increase Butyrate

I use all 3 of these sources for butyrate.

You’ll need the Hi-Maize for butyrate in your large intestine, and the butyrate pills for your stomach and small intestine.

The pills provide calcium and magnesium.

I use HMB mainly for its synergistic effects with Resveratrol in activating SIRT1.

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About the Author

Joe Cohen, BS

Joe Cohen won the genetic lottery of bad genes. As a kid, he suffered from inflammation, brain fog, fatigue, digestive problems, anxiety, depression, and other issues that were poorly understood in both conventional and alternative medicine.Frustrated by the lack of good information and tools, Joe decided to embark on a journey of self-experimentation and self-learning to improve his health--something that has since become known as “biohacking”. With thousands of experiments and pubmed articles under his belt, Joe founded SelfHacked, the resource that was missing when he needed it. SelfHacked now gets millions of monthly readers.Joe is a thriving entrepreneur, author and speaker. He is the CEO of SelfHacked, SelfDecode and LabTestAnalyzer.His mission is to help people gain access to the most up-to-date, unbiased, and science-based ways to optimize their health.
Joe has been studying health sciences for 17 years and has read over 30,000 PubMed articles. He's given consultations to over 1000 people who have sought his health advice. After completing the pre-med requirements at university, he founded SelfHacked because he wanted to make a big impact in improving global health. He's written hundreds of science posts, multiple books on improving health, and speaks at various health conferences. He's keen on building a brain-trust of top scientists who will improve the level of accuracy of health content on the web. He's also founded SelfDecode and LabTestAnalyzer, popular genetic and lab software tools to improve health.

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