Visceral Fat: the Devil You Don't Know
Better the devil you know than the devil you don’t
Traditional proverb
Deep within us lies an éminence grise.
When given the opportunity, an otherwise innocuous tissue holds an outsized influence over our health, degrading metabolic function and hastening the development of diabetes, liver disease, kidney disease, and atherosclerosis. Unlike more conventional metrics like blood pressure and cholesterol levels, this threat does not make itself easily known.
Menace, thy name is visceral fat.
Cutting the Fat
When we think of “fat,” we mainly call to mind the subcutaneous adipose tissue that lies just below the skin around our mid-section, hips, thighs, and buttocks.
Accumulating too much visible mass in these areas is deemed anathema by modern culture. Being thin or slender instead typifies beauty, leading subcutaneous fat to be roundly vilified.
Not only is being obese regarded by society as unsightly; it is now increasingly classified as a disease, determined by arbitrary cut-offs for body mass index (BMI).
These trends belie key facts of our underlying physiology. The growth of subcutaneous adipose tissue is a normal process refined over millions of years of evolution and should not be thought of as pathologic in itself.
Adipose tissue is an exceptional arsenal of energy. A single pound (0.45 kg) of fat cells contains about 3500 calories, nearly 30 per cent more than all glycogen reserves in the liver and skeletal muscle. The whole of adipose tissue stores about 135,000 calories in a metabolically healthy adult, enough to last for roughly 200 meals.
Our ability to easily store vast amounts of energy as fat is unique in nature. Whereas other primates have body fat levels below 9 per cent, a healthy human body is usually composed of 14 to 21 per cent fat. These fat depots likely enabled the survival of our ancestors, helping generations weather starvation, fluctuations in energy intake, and cold environments.
The “thrifty genes” that promote adiposity were likely selected several millennia ago when energy sources were rarely abundant. The human body adapted to capitalize on sporadic windfalls by swiftly building up energy reserves in adipose tissue. During periods of scarcity and famine, our physiology slows our metabolism and economizes these stores, expending as little as possible to preclude an earlier death.
The propensity to store fat when access to calories was plentiful meant a larger body type could indicate social status and maternal potential, both in carrying and caring for offspring. Aesthetic preferences towards thinness are at once fundamentally unattainable, particularly for women, and a marked reversal of historic trends.
Characteristics of surviving Paleolithic artifacts suggest ideals for female beauty long emphasized increased body mass in the abdomen, hips, buttocks, and thighs. “In ancient times,” records one history of obesity, “the rotund female body was considered healthy, fertile, and prosperous in affairs of the heart.”
In short, we are designed to gain weight quickly and lose it slowly. Given contemporary predilections, this once vital feature is now seen as a bug.
The fixation of culture and clinicians alike on visible body fat and BMI obscures what should be among the dominant concerns in health— visceral adipose tissue, the fat deposits around the stomach, intestines, and liver that cannot be seen at surface level.
Below the Surface
For most healthy individuals, about 10 per cent of total body fat is stored viscerally. The vast majority of adipose tissue resides subcutaneously, and very small amounts are found around the kidneys, heart, and skeletal muscle.
While subcutaneous fat is a capacious sink for energy, the storage area of these cells eventually reaches a limit when faced with a sustained caloric surplus.
If new subcutaneous adipose tissue cannot be generated quickly enough, lipids in the bloodstream search for a home elsewhere and easily find one in visceral adipose tissue.
A previous piece comprehensively explores the pathogenesis of visceral fat:
With excessive growth, visceral fat makes its pathologic capacity known, contributing to fatty liver disease, atherosclerotic disease, cancer progression, and insulin resistance through at least three key mechanisms:
Due to its proximity, visceral fat exposes the liver to high amounts of free fatty acids and glycerol, which promote insulin resistance and produce atherogenic molecules called VLDL (very low-density lipoproteins).
Visceral fat contains immune cells that release pro-inflammatory signals that reduce insulin sensitivity, generate oxidative stress, and damage blood vessels.
Increased visceral adiposity is an indication of ectopic fat storage within organs not designed to hold large volumes of lipids, including the liver, spleen, pancreas, kidneys, skeletal muscle, and heart.
This deposition impedes organ function—for instance, increased fat accumulation in the pancreas may reduce secretion of insulin and digestive enzymes as well as promote cancerous growth.
Despite its significance, most readers likely have not heard of visceral fat, whether on social media or in a doctor’s office.
We know of BMI because of its ubiquity in healthcare. Calculated from height and weight, BMI allows individuals to be quickly classified as underweight, healthy, overweight, or obese, spurring an immediate inference—if someone’s BMI diverges from “healthy,” they should probably change their weight.
BMI can never tell the full story of a person’s health. Evidence from cross-sectional representative population studies (1, 2) suggests that 51-53% of individuals with overweight BMI and 26-32% with obese BMI may remain metabolically healthy. Between 24-31% of the participants with “healthy” BMI were meanwhile found to have poor metabolic health. (See the Appendix for the exact parameters of this definition of metabolic health.)
This observation is sometimes referred to as metabolically healthy obesity (MHO): a subpopulation of individuals with obesity who maintain normal markers of cardiometabolic health.
Such discordance between BMI and metabolic disease risk may be especially pronounced in Asian and black populations. A prospective cohort study following 1.5 million participants for an average of 6.5 years found the same incidence of type two diabetes for white patients at a BMI of 30 was seen at a BMI of 28.1 for black, 26.9 for Chinese, 26.6 for Arab, and 23.9 for South Asian adults.
Compared to white patients, individuals of Chinese and South Asian descent have higher amounts of visceral fat across a wide spectrum of body weight, accounting for the higher prevalence of metabolic dysfunction found at “normal” BMI.
Indeed, conditions associated with obesity, like type two diabetes, fatty liver disease, and high cholesterol levels, are regularly found in individuals of all ethnic backgrounds at “healthy” BMI, and are likely under-diagnosed.
What accounts for the broad discrepancy in these findings? That deep-seated terror, visceral fat.
Visceral fat burden, physical activity levels, lower extremity subcutaneous fat content, and inflammatory markers largely account for the phenomenon of MHO. Given its role in inflammation and the ability of exercise to reduce visceral adiposity, a lower proportion of visceral fat is likely the key etiological factor behind MHO.
Similarly, the apparent survival benefit of elevated BMI in acute cardiovascular disease (e.g., heart attacks), sometimes called the “obesity paradox,” is extinguished when accounting for measures of visceral fat.
In certain groups, visceral fat may be more accurate than BMI in predicting risk of heart disease, heart attacks, high cholesterol levels, colorectal cancer survival, prostate cancer, progression of kidney disease, diabetes, and fatty liver disease, as well as all-cause mortality.
Similarly, visceral fat is found to be an independent risk factor for major sources of morbidity including asthma severity, heartburn severity, severity of pancreatitis, gallstones, sleep apnea in adults and children, osteoarthritis, low back pain, and depression.
Measuring Visceral Fat
If we collectively aim to optimize the length and quality of life for the greatest number of individuals, we must dispense with the devils we know, BMI and subcutaneous fat.
In their stead, we can utilize more accurate predictors of morbidity and mortality—namely, visceral fat. (VO2 max also makes the cut. Together, visceral fat and VO2 max form the “Double-V” strategy I explore in A Simpler Approach to Health.)
Here is the snag: because visceral fat resides deep within the body, its measurement does not come easily.
MRI and CT scans are required to directly quantify different forms of adipose tissue and are the gold standards for measuring visceral fat. DEXA scans, often used to assess bone mineral density in older age, can also measure visceral fat but are less accurate in certain populations, including children.
Many modern weight scales claim to measure body fat levels through bioelectrical impedance analysis (BIA). Small pads on the surface of the scale send a painless electrical current throughout the body. The pads then measure resistance to the current to compute relative levels of muscle, water, and fat in the body using proprietary algorithms.
BIA can measure total body fat with a similar accuracy to DEXA scans but may fail to properly assess visceral fat compared to CT scans.
Absent special equipment, visceral fat can be approximated by several low-cost methods:
Waist circumference (WC): while standing up, wrap a flexible tape measure around your abdomen, just above your hip bones and likely just below your belly button. Measure your waist only after you breathe out; do not “suck” your gut in. Record the value.
Waist-to-hip ratio (WHR): after measuring your waist circumference, wrap a flexible tape measure around the widest part of your hips and buttocks while standing. Record the value.
Divide your waist circumference by your hip circumference.
Sagittal abdominal diameter (SAD): lie flat on your back with your knees bent at a 90° angle. On either side of your body, place a rigid meter stick pointing vertically against the top of your hip bone. Lay a flat, rigid object (e.g., another meter stick) perpendicular to the vertical meter stick over your abdomen. Measure the value on the vertical meter stick after breathing out; do not “suck” your gut in.
This method might be particularly difficult to replicate at home.
At present, there are only preliminary guidelines based on sex and ethnic background to stratify risk based on waist circumference (another example is found here). As noted, South Asian populations routinely have higher levels of visceral fat at a given waist circumference compared to European populations, so a “healthy” value for these patients is lower.
Other guidelines provide WC thresholds based on BMI for white and black patients, which may better account for a variety of body sizes. Thresholds for optimal waist circumference likely increase as BMI increases and are usually higher in men compared to women at the same BMI. This inclusion is not meant to be a ringing endorsement of BMI.
Given the primacy of visceral fat, developing rigorous guidelines based on age, sex, and other demographic characteristics for routine use in both clinical and at-home settings needs to be a core research priority in population health. There are several emerging modalities (examples 1 and 2) that require validation and standardization for a diverse range of patients.
Unfortunately, based on objectives outlined in the U.S. Department of Health and Human Services’s Healthy People 2030, BMI will continue to define obesity and function as a principal marker of health risk. No mention whatsoever is made of visceral fat.
Until further research is conducted, the above guidelines for waist circumference are likely the best tools we have at our disposal for identifying individual risk and monitoring changes in visceral fat over time.
Reducing Visceral Fat
There are two main strategies that reduce levels of visceral fat—weight loss and physical activity.
The suggestion to lose weight is not made in service to any particular aesthetic appearance or BMI. Reducing visceral fat burden requires specific triggers, some of which may also promote weight loss.
Weight Loss
Loss of body mass inherently requires an energy deficit, which occurs when the energy required by the body to perform movement and various biological processes exceeds caloric intake.
This shortfall requires stores of energy to be mobilized to meet physiologic needs. Visceral fat serves as a major energy reservoir and might be preferentially metabolized before stores of subcutaneous fat during an energy deficit.
An energy deficit occurs with reducing caloric intake, augmenting overall energy expenditure (e.g., increased physical activity), or a combination of both.
When caloric restriction is used in isolation to achieve an energy deficit, loss of visceral fat usually corresponds to weight loss. When physical activity is instead utilized alone, reductions in visceral fat may occur in the absence of weight loss as exercise drives formation of fat-free mass such as muscle.
Established guidelines suggest a deficit of 500 to 1000 calories per day below habitual caloric intake contributes to sustainable weight loss, about two to three pounds (0.9-1.4 kg) per week. Alternatively, daily caloric intake could be reduced to 70-80% of habitual levels. Women might aim for a target of 1200 to 1500 calories per day, and men, for 1500 to 1800 calories/day.
For some, time-restricted eating, also known as “intermittent fasting,” might be an effective strategy to reach these goals. In this approach, one only eats within a pre-determined “window,” usually about eight hours, and fasts for the remainder of the day. For instance, one might consume food between 10am and 6pm.
Notably, no single diet or structure of macronutrient consumption is found to be superior for weight loss. Small-scale studies do suggest that consuming a higher proportion of whole foods relative to ultra-processed foods might encourage lower caloric intake in the absence of deliberate restriction.
Over a four- to six-month period, weight loss of 5 to 10% may correspond to a reduction in visceral fat burden by 15 to 20%. Another meta-analysis found that losing about 18 lbs. (8.2 kg) of fat mass could reduce visceral adipose tissue by as much as 31%.
That said, maintaining weight loss is considerably difficult. As few as 20% of individuals with overweight BMI are able to maintain weight loss of 10% of their initial body mass after one year. Over a five year span, more than 80% of lost weight might be regained.
Again, the human body is exceptional in gaining weight quickly and losing it slowly.
Factors implicated in long-term maintenance of weight loss (≥ 10% of initial body mass for ≥ 1 year) include low-calorie meals, a consistent eating pattern across weekdays and weekends, regular consumption of breakfast, self-monitoring weight, and about one hour per day of physical activity (> 250 minutes per week might be optimal).
The advent of GIP and GLP-1 receptor agonists form a new paradigm for weight loss that is outside the immediate scope of this piece, though emerging research does suggest these drugs significantly reduce visceral and ectopic fat.
Given that weight loss might be neither realistic nor sustainable for all-comers, the most practical approach to reducing visceral fat is likely increasing physical activity.
Physical Activity
In past writing, I refer to moderate-intensity, aerobic cardiovascular exercise as “Zone 2” and higher-intensity, anaerobic cardiovascular exercise as “Zone 5.” (Although these zones refer to discrete levels of blood lactate, a heart rate range is likely to be the most actionable and feasible to monitor.)
“Resistance training” is broadly referred to as lifting weights.
In the absence of an energy deficit, resistance training alone can significantly lower visceral fat levels. Some data suggest that Zone 2 training might be more efficacious than resistance training in driving these reductions. Again, these findings often occur without observed weight loss.
Additional studies (1, 2, 3) suggest that Zone 5 sessions have similar efficacy to Zone 2 training in reducing visceral fat with the added benefit of driving more significant improvements in VO2 max, cholesterol levels, and fasting blood glucose. The time investment for Zone 5 training also tends to be lower than Zone 2 sessions.
Following consensus guidelines (performing 150 to 300 minutes of Zone 2 training or 75 to 150 minutes of Zone 5 training in a typical week) over four to six months may reduce visceral fat by 15 to 20%.
For most, brisk walking, rucking, rowing, swimming, or cycling (whether upright or recumbent) will be among the safest forms of physical activity to reach a putative “Zone 2” heart rate range.
Given the exertion required for Zone 5 exercise, walking on a treadmill at a steep incline, cycling at a high resistance, or running may be necessary.
The Fat is in the Fire
As evidence continues to mount, the days of BMI as a central marker of health are numbered. Albeit unlikely, societal attitudes towards subcutaneous fat may also begin to shift.
Accurately monitoring and mitigating our risk for some of the most significant sources of mortality and morbidity—among them diabetes, kidney disease, liver disease, and atherosclerosis—requires we focus expressly on visceral fat.
It is time to confront the devil lurking within us.
Appendix
Wildman et al. 2008 and Tomiyama et al. 2016 define “metabolic health” as at least one of the following abnormalities:
Systolic/diastolic blood pressure ≥ 130/85 mm Hg or antihypertensive medication use;
Fasting triglyceride level ≥ 150 mg/dL (1.69 mmol/L);
High density lipoprotein-cholesterol level < 40 mg/dL (1.04 mmol /L) in men or < 50 mg /dL (1.29 mmol /L) in women or lipid-lowering medication use;
Fasting glucose level ≥ 100 mg/dL (5.55 mmol /L) or antidiabetic medication use;
Homeostasis model assessment-IR > 5.13;
High-sensitivity C-reactive protein level > 0.1 mg/L (0.95 nmol/L)