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Writer's pictureMary Reilly

The Invisible Threat: Visceral Fat and Your Metabolic Health


I have decided to write a more technical (and longer!) post today about how differences in fat deposition lead to chronic disease. This is a crucial topic to understand if you want to take control of your health. So, buckle in, here we go…


When the body has excess energy to store, it has two depots or reservoirs to choose from in which to store the excess energy. The first place is in the subcutaneous space, which is the space underneath our skin. That is the place in which our bodies would prefer to store excess energy. However, once our bodies think that that reservoir is getting full, they will overflow fat storage into our visceral space. When our bodies store fat in the visceral space, they are storing it in and around our organs, including our muscles, liver, pancreas, and heart.


Fat stored in our subcutaneous space is not metabolically active—it just sits there. People often prefer not to have it, but it only causes disease by way of fat mass. Diseases of fat mass include reflux (heartburn), sleep apnea, and joint pain, but not metabolic or other chronic diseases.   Conversely, the fat stored in the visceral space is metabolically active and is proinflammatory, producing proinflammatory chemicals. These chemicals impact your metabolism and change the way your organs function, as well as lead to chronic diseases like diabetes, heart disease, dementia and cancer.


Fat stored in the visceral space leads to a cascade of metabolic problems starting with insulin resistance and metabolic dysfunction-associated steatotic liver disease (MASLD—this used to be called nonalcoholic fatty liver disease or NAFLD and NASH or nonalcoholic steatohepatitis). Insulin resistance is initiated by fat deposition in muscle tissue.  MASLD is driven by fat deposition in the liver, which leads to liver inflammation.


The liver inflammation of MASLD is sometimes identified because of elevation in the liver enzymes of ALT and AST (though less in AST than ALT).  Insulin resistance is identified by an elevation in your fasting insulin level.  Insulin resistance means that your pancreas must produce a higher amount of insulin to keep your blood sugar in a normal range because your cells are not responding to “normal” levels of insulin. 


Insulin is the “key” that unlocks the transporter in your cells’ membranes that allows glucose (sugar) to be transported from the serum (bloodstream) into the cell.  When someone has insulin resistance, that lock is “resistant” or unresponsive to normal levels of insulin and won’t work.  This is the harbinger for prediabetes and ultimately diabetes.  You can have a “normal” hemoglobin A1C level (which reflects your average blood sugar over 12 weeks) but have high fasting insulin and that means that your pancreas is working extra hard to keep your blood sugar in normal range.  Eventually, your pancreas won’t be able to keep up (it won’t be able to produce enough insulin to overcome the insulin resistance of your cells) and your blood sugar will start to rise.  Once that happens, you have crossed into the realm of prediabetes.  Continuing down this pathway without making changes will lead to diabetes and other metabolic disease.


The tipping point at which your body decides that it doesn’t want to store excess fat in the subcutaneous space and starts to store in the visceral space is different for every person.  There are people who become prediabetic due to visceral fat storage at a BMI of 27 (in the overweight but not obese range) and people who don’t become prediabetic until their BMI is >40. 


The diseases caused by fat stored in the visceral space are all initiated by insulin resistance.  Insulin resistance is the first consequence of visceral fat deposition (probably driven by fat deposited in the muscle) along with fatty liver disease (MASLD).  Unchecked, MASLD will lead to liver failure and in fact, is the number one cause of liver transplant in the US (not drugs, not viral hepatitis, not alcohol, but the disease of obesity). 


Insulin resistance also leads to prediabetes and then ultimately diabetes, if left unchecked. The other diseases of obesity and overweight that are driven by visceral fat include cancer (12  cancers are linked to visceral fat and the disease of obesity), cardiovascular disease (heart disease and stroke), as well as neurodegenerative diseases (Alzheimer’s and other forms of dementia, etc).


The good news is that all of this (up to liver failure) is REVERSIBLE.  We can reverse MASLD and insulin resistance, prediabetes and even diabetes and mitigate the risk of developing cancer, heart disease and dementia.  We have many tools in our toolbox to treat metabolic disease, including pharmacotherapy, nutrition, and exercise.  Even losing 5% of your body weight will improve metabolic disease. And exercise mitigates metabolic disease even when not losing weight!


More than three-fourths of Americans are overweight or obese—these diseases are the basis of so much chronic illness. We can and should do better to treat Americans with overweight or obesity.  Americans with obesity and overweight deserve the same treatment we afford those with high blood pressure or heart disease or cancer or high cholesterol.

Want to learn more? Come and see me! Make a meet ‘n greet appointment at www.renewalhealth.us.


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2. Bhaskaran K, et al. Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5.24 million UK adults.


3. Kasen S, et al. Obesity and psychopathology in women: a three decade prospective study.


4. Luppino FS, et al. Overweight, obesity, and depression: a systematic review and meta-analysis of longitudinal studies.


5. Field AE, et al. Impact of overweight on the risk of developing common chronic diseases during a 10-year period[8].


6. Neeland IJ, et al. Visceral and ectopic fat, atherosclerosis, and cardiometabolic disease: a position statement.


7. Després JP, Lemieux I. Abdominal obesity and metabolic syndrome.


8. Fox CS, et al. Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study.


9. Ouchi N, et al. Adipokines in inflammation and metabolic disease.


10. Tchernof A, Després JP. Pathophysiology of human visceral obesity: an update[4].


11. Fontana L, et al. Visceral fat adipokine secretion is associated with systemic inflammation in obese humans[4].


12. Després JP. Body fat distribution and risk of cardiovascular disease: an update.



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