Cortisol

Cortisol is often referred to as the "stress hormone," but in the context of nutrition, it can also be called the "hunger hormone" — especially in the sense that its release signals the body to mobilize energy.

How it works at the physiological level

The primary task of cortisol is to provide the body with fuel. It raises blood glucose levels by stimulating gluconeogenesis — the process of synthesizing glucose from non-carbohydrate sources, primarily from amino acids.

If amino acids are not obtained from food (for example, in cases of protein deficiency), cortisol activates the catabolism of muscle tissue: muscles are broken down so that glucose can be synthesized in the liver from the amino acids contained in them.

Cortisol regulates lipolysis — the breakdown of fats. If the body does not receive enough fats from food, cortisol activates the breakdown of fat reserves to provide energy to the brain and organs.

However, this process is unstable and is accompanied by other hormonal shifts, including increased production of free fatty acids, which can lead to insulin resistance with chronic elevation of cortisol.

Cortisol increases not from the number of meals but from nutrient deficiency. Even if you eat 4–5 times a day, if the diet is predominantly carbohydrates and fats and proteins are deficient, the body does not receive the necessary amino acids and fatty acids. This is perceived as stress, and cortisol begins to perform a compensatory function: "harvesting" the needed elements from the body's tissues.

Consequences of chronically elevated cortisol

• Loss of muscle mass
• Increased anxiety and irritability
• Sleep disturbances (cortisol suppresses melatonin production)
• Insulin resistance
• Accumulation of visceral fat (especially in the abdominal area)

Conclusion

Cortisol is not just a reaction to hunger as a lack of food; it is a reaction to internal deficiency of necessary substances.

Proteins and fats are key macronutrients without which the body perceives the situation as a threat to survival, thus triggering the stress cascade.

Therefore, a balanced diet with sufficient amounts of proteins and fats is one of the main ways to keep cortisol under control.

With chronically elevated cortisol levels (for example, due to stress, hypercortisolism, or the intake of glucocorticoids), changes in lipid metabolism are observed in the body, particularly an increase in very low-density lipoproteins (VLDL). This occurs through the following mechanisms:

Activation of lipogenesis in the liver

Cortisol stimulates gluconeogenesis — the synthesis of glucose from non-carbohydrate sources, especially amino acids and glycerol. However, it also indirectly increases fatty acid synthesis in the liver:

• There is an increased mobilization of free fatty acids from adipose tissue (through the activation of hormone-sensitive lipase).
• The liver "takes in" these fatty acids and processes them into triglycerides.
• Triglycerides are packaged into VLDL and released into the bloodstream.

As a result: an increase in VLDL concentration and hypertriglyceridemia.

Insulin resistance and suppression of lipoprotein lipase (LPL)

Cortisol disrupts tissue sensitivity to insulin. Insulin resistance leads to the following consequences:

• The activity of lipoprotein lipase (LPL) — a key enzyme that breaks down VLDL in tissues — decreases.
• VLDL remain in the bloodstream longer and in greater quantities.
• Additionally, the uptake of lipids by tissues is impaired, exacerbating hyperlipidemia.

Transition from VLDL to LDL

When VLDL circulate longer than usual, they gradually lose triglycerides (under the action of LPL and hepatic triglyceride lipase) and transform into low-density lipoproteins (LDL), which increases the atherogenicity of the blood. Thus, high cortisol is a factor in increasing not only VLDL but also, in the long term, LDL.

Additional changes caused by cortisol:

• Increased blood glucose → glycation of lipoproteins → worsened recognition by receptors.
• Increased acute phase proteins of inflammation, including CRP, which enhances atherogenesis.
• Decreased HDL (high-density lipoproteins), especially during chronic stress.

Conclusion

High cortisol triggers a cascade of metabolic shifts leading to increased levels of VLDL due to enhanced triglyceride synthesis in the liver, decreased utilization, and insulin resistance. This condition is highly atherogenic and increases the risk of cardiovascular diseases.

Correction of cortisol levels, stress management, adequate sleep, and metabolic support (for example, through omega-3, magnesium, B vitamins, and adaptogens) are important elements in the prevention of stress-induced hyperlipidemia.