Obesity is one of the most demanding medical, financial and public health epidemics of our modern day. Worldwide, obesity statistics are shocking causing researchers, pharmaceutical brands and global companies to invest millions into establishing a cure.

The main cause of obesity and related metabolic disorders like type 2 diabetes has been associated with lifestyle changes, including an increase in the consumption of nutrient deprived foods and a decrease in exercise. And while the answer to the epidemic may be eat less junk and exercise more, it’s not that simple. For people to voluntarily change their habits permanently appears extremely difficult and even those who do, they’re still struggling to lose the required weight and maintain weight loss long-term. Thus, obesity is now defined as a disease, not a deliberate choice.

This has promoted greater research to be focused on pathophysiological pathways, particularly our gut microbiomes and their effect on weight gain.

What is the gut microbiome?

The gut is a term used to refer to our digestive system or in medical terminology, our gastrointestinal system which begins in the mouth and ends at the anus. The nine-metre-long tube is the primary route our food travels through the body and involves several organs.

There are two major components of the gut that greatly determine its health and to a large extent, the overall health of the gut’s owner. These include the microbiome and the gut wall.

We share our bodies with microbes. In fact, there are more of these minuscule, living organisms we’ve termed bacteria than there are human cells; ten times more! You can think of it like a mini-ecosystem or rainforest with bacteria, fungi and viruses all calling our body “home”.

These microbes contribute to various metabolic functions in the body, they protect us from pathogens and influence the immune system. In the gut, the microbiota are integral for the digestion of our food and we need them in order to generate as much nutrients as possible.

It was previously thought that the human microbiome was established during birth with the foetus living in a completely sterile environment until they were born. However, now we understand that first exposure to microbiomes occurs in utero.

The microbiome further develops during birth as the baby passes through the vaginal canal and ingests the mother’s microbiota. Skin-to-skin contact and breastfeeding will also help form the baby’s gut flora. As the child grows, consumption of a wholesome diet and contact with our natural environment will provide the building blocks necessary to form a healthy gut microbiome.

The key to a healthy gut microbiome is having the right quantity and diversity of beneficial bacteria. While pathogenic and beneficial microbiota can live harmoniously within our gut, its vital the good bacteria outweighs the non-beneficial, otherwise poor health and disease will manifest.

Influence of diet on our gut microbiome

Our diet from infancy to adulthood has an incredible influence on our inner ecosystem.

Breastmilk plays a large role in colonising the infant gastrointestinal tract with distinct components including human milk microbiome, prebiotics which stimulate the growth of beneficial bacteria and antimicrobials which prevent pathogenic bacterial growth.

The human milk microbiome alters with time and is greatly dependent on the mother’s weight. It has been found strains such as Staphylococcus, Streptococcus, and Lactococcus, which are predominant in breastmilk immediately after birth, are less diverse in obese mothers than non-obese women. This will impact the development and diversity of gut microbiome of infants, thus impacting their overall health.

Fast forward to adulthood and numerous studies have found eating the standard Western diet, which consists of high fat and refined carbohydrates and low fibre intake, disrupts the balance of our gut microbiome. This disruption favours weight gain and fat accumulation, in turn encouraging obesity.

According Amanda Cox, immunologist of Griffith University, during digestion of food our gut microbiome produce metabolites that feed our body and then enter the bloodstream. Some bacteria are great at making short-chain fatty acid (SCFA) butyrate, which is beneficial for providing the gut energy and improving the intestinal barrier so it’s able to prevent pathogens and toxins from leaking into the bloodstream.

However, other SCFA’s produced by the microbiota can be harmful. Those SCFA’s subjected to a high-fat diet are seen to weaken the gut wall. Not only that, the high-fat diet itself also weakens the gut lining by increasing its permeability and encouraging the transportation of gut bacterial components into the bloodstream.

The overall effect is systemic, low-grade inflammation which are two characteristics of obesity. Incredibly, changes in microbiome can occur within 24 hours of eating a Western diet promoting a pro-inflammatory state and instantly effecting our health.

Reduced gut microbiome diversity and weight gain

In multiple studies, researchers have identified a reduced microbiome diversity leads to weight gain and inevitably, obesity. One of the earliest signs of the connection between microbiome diversity and obesity came through a study by Washington University in St. Louis which compared the intestinal bacteria of twins who were lean or obese.

The lean twins were found to have a diverse gut community brimming with different species of microbes. The gut microbiome of obese twins however was less diverse with very few species dominating the environment.

Inspired by this discovery, the researchers conducted a series of well-controlled experiments using “humanised” mice. Raising genetically identical mice in an entirely germ-free environment, their bodies were free of any bacteria.

Using gut microbes collected from the lean twins and their obese sisters, the team then populated the mice guts with the human bacteria. Throughout the study, the mice were fed the same diet of equal amounts and calories, yet their weight status later became noticeably different.

The mice who received the gut microbes from the obese twins grew larger and had more body fat than those with the lean twin’s bacteria. The fatter mice also had less diversity of gut microbes, than the thin mice.

Taking the experiment one step further, the researchers studied the effect this had on mice living in a shared cage environment. This time, both groups of mice remained thin regardless of whether they were populated with the obese or lean twin’s bacteria. The mice with the obese human microbes picked up the gut bacteria from their lean roommate.

In the next stage of the experiment, 54 varieties of the microbiota found in the lean mice was transferred into the animals who were destined to be obese. With the increased diversity, these mice maintained a healthy weight instead of getting fat. “Taken together, these experiments provide pretty compelling proof that there is a cause-and-effect relationship and that it was possible to prevent the development of obesity,” says the study’s lead researcher Professor Jeff Gordon.

Regular antibiotic use in childhood causing gut dysbiosis

New research has found strong correlations between the use of antibiotics, changes in the gut bacteria and the occurrence of disease in adulthood. Antibiotics are the most prevalent drug prescribed by doctors for children, with around 30% of the prescriptions considered unnecessary.

Researchers from the University of Minnesota warn antibiotics prescribed to infants and newborns are likely to alter the gut bacteria which are tied to numerous conditions ranging from allergies and obesity to infectious diseases.

In obesity-related infant dysbiosis, the microbiome biodiversity is altered with any antibiotic treatment given during the first 2 years of life. These changes in the gut microbiota can result in functional changes that affect the metabolism. The more antibiotic exposure during infancy, the greater the predisposition to obesity and other health conditions such as allergies, autoimmune disorders, and diabetes.

It’s not just medical prescriptions of antibiotics that are further strengthening the link between the use of these pharmaceuticals and obesity. Dr. Cho and Blaser have been researching the association of antibiotics in animal meats and weight gain. A study of mice found those that were injected with low-dose antibiotics over time became fat. This was the same amount humans consume eating the meat of animals given antibiotics and was despite eating the exact same number of calories as the control mice.

It’s believed the weight gain is due to gut dysbiosis where the microbiome becomes more efficient at drawing energy from the food. Essentially the microbiota doesn’t consume more calories, but absorbs more of them causing weight gain.

The gut brain connection

It’s easy to see why many people are calling the gut the second brain. Recently there has been an explosion of research into the gut brain connection (known as the Brain-Gut Axis) and its influence on weight and general health.

Using enteroendocrine cells, the gut microbes transmit information to the brain via the hypothalamic pituitary-adrenal (HPA) axis. The microbes communicate information to direct the body’s insulin response and improve insulin resistance. They send messages to promote satiety, to delay gastric emptying and to reduce the gut wall permeability.

These messages allow us control over our weight and provide protection against obesity. However, disrupt the microbiota, and this protection is compromised.

Like in the brain, neurons are found in gut including those that produce neurotransmitters which act as communication molecules, such as serotonin and dopamine. Dopamine is said to be responsible for the pleasure and reward centres.

Serotonin on the other hand is responsible for appetite and digestion, as well as the control of our mood, memory, sleep and social behaviour. What’s fascinating is that about 95% of this neurotransmitter is found in the lining of the gut, not our brain. This could be the reason why improving our nutrition may be an effective treatment for depression, as opposed to antidepressants which act to raise the levels of serotonin in the brain.

When it comes to gut and mental health, it’s a two-way street. Poor gut microbiome diversity and quantity contributes to mood problems. High amounts of stress has the potential to damage our gut microbiome and disrupt the hormonal balance.

According to researchers of the Department of Psychiatry, Leiden University Medical Center there is an increased risk of developing depression in those who are obese. Depression has also been found to be a key predictive factor of developing obesity.

Understanding this connection between the gut microbiome and brain could have a profound impact in effective treatment and prevention of not only common mental disorders, but also obesity.

Is your gut microbiome community unhealthy?

An upset stomach isn’t the only indication of an imbalance in the gut microbiome. The signs and symptoms of an unhealthy gut can be diverse and present both physically and psychologically.

Some of the most common indications of a unhealthy gut microbiome include:

  1. Food allergies or intolerances
  2. Digestive upsets including bloating, gas, diarrhoea and constipation
  3. Acid reflux
  4. Poor immunity with the occurrence of frequent infections
  5. Skin issues like acne, eczema, psoriasis and rosacea
  6. Trouble maintaining a healthy weight
  7. Autoimmune disease like irritable bowel disease, Hashimoto’s or Graves disease
  8. Type 2 diabetes
  9. Anxiety
  10. Depression
  11. Irritability and mood swings
  12. Behavioural disorders like ADD or ADHA
  13. Poor concentration and memory

We share our bodies with microbes and the play an integral role in our overall health from our emotional and mental to our physical wellbeing. The composition of our gut microbiome is largely dictated by our lifestyle and environment and how well we look after our bodies. Maintaining diversity and keeping the gut microbes happy may well be the elusive secret to weight control and curing obesity.