Longevity 10 MIN READ

Your Visceral Fat May Affect How Long You Live

Visceral fat refers to the fat that surrounds our visceral organs (heart, liver, pancreas, kidneys, intestines) located in the abdominal region. Unlike subcutaneous fat, which lies under our skin, visceral fat  cannot be seen from the outside as it lies deep within the body

Written by Team Ultrahuman

Oct 14, 2022
Visceral Fat Affect

Visceral fat refers to the fat that surrounds our visceral organs (heart, liver, pancreas, kidneys, intestines) located in the abdominal region. Unlike subcutaneous fat, which lies under our skin, visceral fat  cannot be seen from the outside as it lies deep within the body. This type of fat is highly metabolically active, which means that it is constantly releasing free fatty acids (or FFA) into the bloodstream. 

VisceralFat Affect Live


  • Significant factors that affect longevity or life expectancy include gender, genetics, nutrition, physical activity and lifestyle,
  • A growing body of evidence and a number of studies have implicated visceral fat as a major factor for type 2 diabetes, insulin resistance, metabolic syndrome, oxidative stress, endothelial dysfunction and cardiovascular disease, which are ultimately threats to longevity.

Visceral fat and proinflammatory cytokines

Visceral fat also releases proinflammatory cytokines that stimulate the hypothalamic–pituitary–adrenal (HPA) axis, which plays a significant role in the body’s response to stress.

These cytokines (adipokines, such as interleukin-1, interleukin-6, tumour necrosis factor-α, resistin) and a reduction in the hormone adiponectin (referred to as the “fat hormone”) have been seen to be associated with reduced insulin resistance. According to research, a protein called retinol-binding protein 4 (RBP4), which has been seen to increase resistance to insulin, is secreted by visceral fat. 

The location of visceral fat deep inside the body, between our organs, also enables it to affect these organs. Ultimately, these inflammatory compounds in visceral fat drain into the liver and 

can cause fatty liver and pancreas, which then further affects insulin regulation. This can ultimately lead to type 2 diabetes and metabolic disease due to excess glucose in our bloodstream.

It has been established that abdominal visceral fat may play a more important pathogenetic role or better reflect an underlying metabolic disorder than subcutaneous fat in the development of diabetes mellitus or hyperlipidemia (high level of fats or lipids in the blood). The accumulation of visceral fat in obesity is associated with metabolic syndrome and an increased risk for clinical cardiovascular disease.

Visceral fat and ageing

One  study demonstrates that caloric restriction can delay many age-related diseases and extend lifespan, while an increase in adiposity is associated with enhanced disease risk and accelerated ageing. Among the various fat depots, the accumulation of visceral fat is a common feature of ageing, and has been shown to be the most detrimental on the metabolic syndrome of ageing in humans. 

Visceral fat increases with age in both women and men. Apart from the dietary causes of visceral fat, such as arising from the consumption of highly refined carbohydrates and sugar which leads to excess calories, other potential contributors to visceral adiposity include chronic stress, lack of physical exercise and inadequate sleep.

Visceral fat stress

Visceral fat and stress

It has been seen that stress also leads to excess amounts of visceral fat being stored. One study looks at how visceral adiposity may be a physiological adaptation to stress. Under chronic stress, our body releases cortisol which in turn activates the HPA axis, which has been shown to exert hyperphagic (related to overeating) and anti-thermogenic (no-heat-producing) effects. Glucocorticoids (‘a group of corticosteroids, such as cortisol, that are involved especially in carbohydrate, protein, and fat metabolism, and are anti-inflammatory and immunosuppressive’) affect abdominal fat to a greater extent than subcutaneous adipose tissue, since  abdominal adipose tissue has more cells per mass unit, higher blood flow and more glucocorticoid receptors (one of two types of receptors to which glucocorticoids bind (the other being the mineralocorticoid receptor).

Cushing’s syndrome refers to a condition of an excess of cortisol over time and shows the correlation between hypercortisolemia (a prolonged excess of serum levels of cortisol) and the accumulation of central adiposity.

Hervey’s hypothesis, which suggests that fat cells take up and catabolize glucocorticoids, is one of the possible regulatory effects that supports the adaptive role of visceral fat in response to stress. There is also other evidence which shows that abdominal obesity is linked to increased cortisol clearance.

Both cortisol and insulin, on the one hand, tend to cause an increase in visceral fat, while growth hormones and sex hormones may prevent it.

Visceral fat and fat accumulation

An excess of visceral fat also inhibits the hormone adiponectin, which is referred to as the “fat hormone”. Adiponectin is a fat regulator, and if we do not have enough of it circulating in our systems, it could cause our body to accumulate more fat than necessary. Studies have demonstrated that visceral fat and adiponectin were independently associated with the clustering of metabolic risk factors such as high cholesterol, higher triglycerides and lower LDL (low-density lipoprotein) and HDL (high-density lipoprotein).

Visceral fat and cognition

Yet another effect of accumulated and increased visceral fat seems to be on cognition. One study demonstrated how visceral fat is harmful to the brain because it allows the inflammatory cytokine interleukin-1 beta to heavily infiltrate the brain The interleukin-1 beta cytokine is produced by visceral fat, which then travels through the bloodstream, passes through the blood–brain barrier and enters the brain, where it causes the microglia to become dysfunctional and hampers cognition. Microglia are the immune cells in the brain which regulate neuronal function indirectly by clearing dead cells and extracellular debris, and directly by releasing signalling molecules that support or suppress neuroplasticity. 


Inflammation is our immune response to a threat, injury or infection. During the process of inflammation, inflammatory cells and cytokines are released. 

Acute and chronic inflammation

Inflammation can be of two types: acute and chronic.

Acute or temporary inflammation occurs when there is a sudden body change, or damage or injury to our system. For example, if we cut ourselves, if we have an infection or if we work out. In response to this, our body’s immune system sends out proinflammatory cells to the area and then sends anti-inflammatory cells called prostaglandins to repair it.

Chronic inflammation, on the other hand, is when the body continues to send out inflammatory cells and there is a continuous inflammatory response. Major sources of inflammation also include environmental stressors, environmental toxins as well as psychological stress. Shifts in the inflammatory response from short- to long-lived can cause a breakdown of immune tolerance, which leads to oxidative stress and damage to tissues and cells.

Chronic inflammation and inflammaging

It has been seen that chronic inflammation also contributes to the pathophysiology of a number of metabolic diseases. Systemic chronic inflammation can lead to a number of conditions such as metabolic syndrome (a triad of hypertension, hyperglycemia and dyslipidemia), cancer, diabetes, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders.

A new term—inflammaging—has been used to describe the “up-regulation of certain proinflammatory cytokines at older ages, and associated chronic diseases”. One study also describes it as: “Human ageing [which] is characterised by a chronic, low-grade inflammation termed ‘inflammaging’.”

It is established that the levels of cortisol in the blood increase with age. This is mainly considered to be on account of the HPA axis getting activated by many non-specific stressors. Over time, the phenomenon of anti-inflammaging, mainly exerted by cortisol, gives rise to a tangible decrease in immunological functions. The coexistence of anti-inflammaging alongside the increased levels of proinflammatory cytokines of inflammaging ultimately negatively impact metabolism, bone density, strength, exercise tolerance, the vascular system, cognitive function as well as mood. This is how inflammaging and anti-inflammaging “together have a hand in controlling many of the progressive pathophysiological changes that characterise the ‘aged-phenotype’, and the struggle to maintain robustness finally results in frailty.”

Inflammation and insulin resistance

Inflammation plays a critical role in the development of insulin resistance. There are various established mechanisms that play a part in this process. When we eat highly processed, high-sugar foods, it can trigger inflammation and the release of proinflammatory compounds. High-sugar foods cause a spike in insulin and, over time, these types of diets could also lead to insulin resistance. 

Dietary fat might play a role in the production of inflammatory molecules by way of modifying the intestinal microbiota, which might result in an inappropriate immune reaction, through processes like leaky gut, and can also lead to autoimmune conditions like rheumatoid arthritis, lupus, psoriasis, etc. 

Seemingly, the interaction between immune cells and metabolic cells has a major role to play in the disturbance of metabolic homeostasis. High levels of dietary saturated fatty acids or of their metabolites can be detected by immune sensors, leading to the synthesis of inflammatory cytokines in different metabolic tissues. Intestinal microbiota, which produce different inflammatory molecules, can also be modified by dietary fat, which can lead to an inappropriate immune reaction. The inflammatory cytokines, saturated fatty acids and lipopolysaccharides activate a network of signalling pathways that impinges on insulin signalling, leading to alterations in metabolic cell functions. 

There is evidence to show that physical exercise and activity has an anti-inflammatory effect, where exercise-induced cytokines may impact cardiometabolic diseases. Interleukin (IL)-1β is involved in pancreatic β-cell damage, whereas TNF-α is a key molecule in peripheral insulin resistance. According to a study, “TNF-α appears to be involved in the pathogenesis of atherosclerosis and heart failure. A marked increase in IL-6 and IL-10 is provoked by exercise and exerts direct anti-inflammatory effects by an inhibition of TNF-α and by stimulating IL-1ra, thereby limiting IL-1β signalling. Moreover, muscle-derived IL-6 appears to have direct anti-inflammatory effects and serves as a mechanism to improve glucose tolerance.” In addition, the indirect anti-inflammatory effects of long-term exercise are brought about via improvements in body composition and reduction in visceral adipose tissue.


Ageing is often associated with the deterioration of metabolic health. Increased adiposity, insulin resistance and dyslipidemia are all the causes and effects of visceral adiposity and inflammation.

A common feature of metabolic syndrome is chronic inflammation. As the visceral adipose tissue expands in response to chronic positive energy balance, it is possible that inflammatory signals may originate within this fat depot. “Both adipocytes and macrophages within fat secrete numerous hormones and cytokines that may contribute to the characteristic pathophysiologic changes seen in the metabolic syndrome and local inflammation within adipose” tissue may be the sentinel event that causes systemic insulin resistance and systemic inflammation, two of the cardinal features of the metabolic syndrome. 

Research suggests that: “The metabolic alterations triggered by acute inflammation mimic the metabolic syndrome in many ways suggests that circulating cytokines, whether they are derived from adipose tissue or peripheral blood immune cells”, which “may have similar metabolic effects on muscle, liver, and endothelium while potentially having differential effects on immune function.” Recognition of the interaction between adipocytes and macrophages within fat exposes a new paradigm, whereby adipocyte-derived factors modulate local immune responses and macrophage-derived cytokines alter adipocyte differentiation and metabolic responses.

A meta-analysis published in the British Medical Journal, where researchers screened 98,745 papers and focused on 72 co­hort studies from around the world, involving a combined 2.5 million participants, found that central adiposity was consistently associated with a higher risk of premature mortality from all types of illnesses. Existing evidence suggests that central fatness might be more strongly associated with the risk of mortality than overall obesity. In the case of fat tissue, this could involve preventing the development of new fat cells or the enlargement of existing ones in favour of acquiring cells capable of facilitating repair. According to research in fat tissue, it is possible to envisage that: “ [C]cellular senescence could be an alternative cell fate involving [the] activation of proinflammatory responses owing to intra- or extracellular injury signals” at any stage of life. 

Disclaimer: The contents of this article are for general information and educational purposes only. It neither provides any medical advice nor intends to substitute professional medical opinion on the treatment, diagnosis, prevention or alleviation of any disease, disorder or disability. Always consult with your doctor or qualified healthcare professional about your health condition and/or concerns and before undertaking a new healthcare regimen including making any dietary or lifestyle changes.


  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4419494/.   
  2. https://www.express.co.uk/life-style/health/1471742/how-to-get-rid-of-visceral-fat-high-quality-protein-insulin-resistance-burn-belly-fat
  3. https://www.sciencedirect.com/science/article/abs/pii/0026049587900631.  
  4. https://www.sciencedirect.com/science/article/pii/S0735109709007463?via%3Dihub
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2504027/.     

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