Are Love Handles Caused by Stress and Cortisol?

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Are Love Handles Caused by Stress and Cortisol? - Thomas DeLauer

Repeated, or constant, elevation of cortisol can lead to weight gain, so cortisol can affect fat storage and weight gain in stressed individuals:

Tissue cortisol concentrations are controlled by a specific enzyme (11-hydroxysteroid dehydrogenase) that converts inactive cortisone to active cortisol

This particular enzyme is located in adipose tissues - the gene for this enzyme is expressed more by obese conditions and has also been demonstrated in research that human visceral fat cells have more of these enzymes compared to subcutaneous fat cells

Thus, higher levels of these enzymes in these deep fat cells surrounding the abdomen may lead to obesity due to greater amounts of cortisol being produced at the tissue level

Additionally, deep abdominal fat has four times more cortisol receptors compared to subcutaneous fat

So increased cortisol activity increases LPL activity among fat cells

This (generally) becomes a problem in the context of high insulin

Cortisol & Insulin

It stores fat by increasing the activity of lipoprotein lipase (LPL) a fat storing enzyme - conversely, it helps burn fat by increasing the release of hormone sensitive lipase (HSL)

So technically speaking, cortisol is both a fat storing and fat burning hormone - this is because it increases the activity of lipoprotein lipase (LPL), the body’s major fat storing enzyme

But it also increases the activity of hormone sensitive lipase (HSL), the body’s chief fat releasing enzyme

Growth hormone and catecholamines, which are higher during exercise and fasting periods, accentuate cortisol’s fat burning potential while suppressing its fat storing potential

In the fed state, when insulin is around in high amounts, HSL activity is turned way down while LPL activity is cranked up - in this way, insulin magnifies cortisol’s fat storing properties while blocking its fat burning activity

Cortisol and insulin also block the action of each other by decreasing the sensitivity of their respective receptors - this means that eating is not the only way to become insulin resistant; stress can do it too.

Cortisol is not inherently fat-storing, but insulin and cortisol together, with a high-calorie diet, are the real cause of belly fat.

Cortisol & GH

Cortisol exerts major effects on adipose tissue metabolism, both on lipid accumulation and mobilization - it’s really the hormone with the strongest relation to fat distribution in both genders

In the presence of insulin, lipoprotein lipase (LPL) is markedly expressed - in relation to lipid mobilization, the addition of cortisol in the presence of insulin exerts slightly inhibitory effects

When GH is also added, activity is shifted dramatically to a lipid mobilizing effect (since GH stimulates fat metabolism)

Cortisol acts via the glucocorticoid receptor to stimulate lipoprotein lipase (LPL) - in other words, cortisol’s effects are mediated via a specific glucocorticoid receptor (GR), with a variable density in different regions of adipose tissue, in a ranking order of visceral, abdominal subcutaneous, and femoral subcutaneous fat

LPL

Simply put, LPL is an enzyme that makes fat cells ready for storage - the fat in between the organs in your abdomen consists mainly of fat
cells called visceral adipocytes

Visceral adipocytes have more glucocorticoid receptors than other fat cells - Fat cells in the torso have fewer glucocorticoid receptors and subcutaneous fat cells found on the rest of your body have even fewer

The fat cells on your hips and upper legs have the least glucocorticoid receptors

This means cortisol causes fat storage primarily on your abdomen, followed by the rest of your torso and only minimally on your lower body
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In summary, cortisol in the presence of insulin exerts powerful lipid accumulating effects, and these are abolished by GH which inhibits lipid accumulation and also activates lipid mobilization

These effects are probably most pronounced in visceral adipose tissue due to its high density of glucocorticoid receptors

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