There are two types of fat: subcutaneous and visceral. Subcutaneous fat is found under the skin and is sometimes called “flab”. Visceral fat exists inside the abdominal cavity, either the connective tissue around organs (such as the intestine or liver) or on organs themselves (ectopic). Sometimes visceral fat is called “abdominal fat”.
The two different types of fat serve different functions. Subcutaneous fat stores extra lipids to be used as an energy reserve in case of food shortage or illness. The function of visceral fat is not so obvious.
A key difference is in the types of cells within each kind of fat. Subcutaneous fat contains mostly fat cells (adipocytes) but as many as 40% of the cells in visceral fat are pro-inflammatory immune cells. These immune cells release substances called adipokines, which are hormones that can cause or increase low-grade systemic inflammation (Grant 2015, Trim 2012). Adipokines are also called cytokines, when they are released by non-adipose tissue immune cells.
Why does visceral fat contain so many immune cells? One possibility is that the normal role of visceral fat is to support immune function of the gut and serve as a reservoir for immune cells in case of infection.
What are the health risks of visceral fat?
In contrast to subcutaneous fat, which just stores fats, visceral fat releases fats and very low-density lipoproteins (VLDL, a mix of fat and protein) into the bloodstream (Neeland 2020, Trim 2021, Uranga 2019).
Some of these lipids are pro-inflammatory, especially VLDL. This is why visceral fat is considered to be the fat compartment that mechanistically links together co-morbidities of obesity such as hyperlipidemia, atherosclerosis and metabolic syndrome. Low-grade inflammation can also drive chronic pain and mood problems, which are also common in obesity and metabolic syndrome (Milaneschi 2019).
The adipokine/cytokines released from visceral fat can induce inflammation in other tissues when released into the circulation. Such inflammation may occur in the pancreas, liver and gut. Visceral adipose tissue is closely linked to the development of non-alcoholic fatty liver disease, which is currently the most common liver condition in the United States. And another consequence of systemic inflammation is to induce resistance to the hormone insulin (Petersen 2018), which causes or worsens diabetes. Visceral fat is also a key factor in inflammatory bowel diseases (see below).
Dysregulation of the immune system is often seen with obesity and this can lead to serious, life-threatening responses to infections, such as the “cytokine storm” observed with severe COVID-19 infection. Visceral adipose tissue specifically has been linked to severe Covid-19 (Petersen 2018, Deng 2020). It is thought that the already elevated and probably dysregulated inflammation associated with visceral fat is a major contributor to this increased risk (Butler 2020).
How does overweight or obesity affect visceral fat?
The amount of visceral fat is correlated with the level of body fat overall. That is, the greater Body Mass Index (BMI) the more visceral fat (Agbim 2019). In the context of too many calories for the body to use, the liver converts the extra calories to fat and sends it via the blood to adipose tissue. When there are chronically too many calories in the diet, fat tissue becomes overgrown. This overgrowth may exceed the vasculature’s ability to supply it, and sections of the fat can become starved of oxygen (Grant 2015, Neeland 2020). This induces the fat to release damage signals, which further drives inflammation (Grant 2015).
How does visceral fat affect the gut?
Visceral fat plays an active role in the pathophysiology of Inflammatory Bowel Diseases (Drouet 2012), especially Crohn’s Disease (Islam 2022) and diverticulitis (Paeschke 2016).
Ectopic visceral fat, called “creeping fat”, occurs on the small and large intestines in Crohn’s Disease and is usually found where there is active inflammation (Drouet 2012, Paeschke 2016). Creeping fat releases pro-inflammatory cytokines/adipokines, and higher levels of inflammation in visceral fat is associated with more aggressive disease (Drouet 2012). It is not yet known what causes creeping fat but it may result from increased intestinal permeability (leaky gut) that allows pro-inflammatory microbes into the gut and visceral fat tissue, inducing inflammation (Drouet 2012, Islam 2022, Paeschke 2016).
Obesity is a risk factor for IBD (Islam 2022), and this may follow from the increased visceral fat that accompanies elevated weight. Crohn’s Disease develops in people with a genetic predisposition for poorly regulated responses to inflammation. That is- inflammation, once initiated, can be difficult to stop, leading to damage to gut tissue. The inflammatory mediators produced in visceral fat may induce or enhance this inflammation.
The Western Diet is a risk factor for both obesity and Inflammatory Bowel Diseases. The Western Diet is associated with a condition called microbial dysbiosis. Dysbiosis means that there is an imbalance in the populations of microbes in the gut which can lead to overgrowth of some species. In order to have a healthy balance of microbes, you need to have a lot of different species. The kinds of microbes you have in your gut are mostly dependent on what foods you eat. The Western Diet of high energy/low nutrition highly processed foods simply does not support a healthy microbe population. Dysbiosis can cause increased gut permeability (leaky gut) and inflammation.
Another problem with the Western Diet is that it does not support the microbes that provide short-chain fatty acids, especially butyrate, for the gut. These short-chain fatty acids provide energy for gut cells, and they also have the ability to calm inflammation in the gut by interacting with specific receptors on immune cells. Western Diet foods are associated with increased visceral fat (Odegaard 2022, Rodriguez Ortera 2019) as another way to increase inflammation in the gut.
Visceral fat, especially “creeping fat” also contributes to diverticulitis (Paeschke 2016). Diverticulae are little herniations in the wall of the gut, forming what look like little caves. They are common, affecting around 10% of people aged 40 years or younger, and the incidence increases with aging (Piscopo 2019). They do not usually cause symptoms. However, in 10-25% of people with diverticulae, inflammation can occur, causing diverticulitus. One of the main risks for diverticulitis is obesity and especially visceral fat. As with Crohn’s Disease, creeping fat is associated with the region of inflamed diverticulae (Paeschke 2016).
A key feature of diverticulitis is bacterial overgrowth (Piscopo 2020) and diverticulitis, thus another consequence of microbial dysbiosis.
Stress plays a role in visceral fat
People with chronic stress are more likely to have increased visceral fat (Lee 2018) and this may be one way that stress increases the risks of conditions associated with inflammation.
One link between stress and visceral fat is that chronic psychosocial stress can lead to dysregulation of the hormone cortisol. One of cortisol’s main functions is to regulate metabolism and excess cortisol and bias towards increasing fat deposition. This may explain the paradoxical relationship of food insecurity (lack of access to healthy food because of insufficient financial resources) to obesity, and that this relationship is not explained by eating behavior (Richardson 2016). The stress of being poor may encourage fuel storage as fat (possibly mediated by cortisol) as a way to protect against future adversity (Dhurandhar 2016).
Another factor linking stress, obesity, and visceral fat is that stress can cause overeating (Cotter 2018), especially of sugary foods and beverages that are more likely to be converted to fat (Rodriguez Mortera 2019), especially visceral fat.
Thus, chronic stress may increase to visceral adiposity by biasing the endocrine system to cause the increase in visceral fat, and stress-induced diet choices may lead to the expansion of visceral fat.