Ketogenic diet

How insulin resistance affects PCOS:

• In insulin resistance, cells respond poorly to insulin, and the pancreas compensatorily increases its production.
• High insulin levels stimulate the ovaries to produce excess androgens (testosterone, androstenedione).
• Excess androgens disrupt follicle maturation and lead to anovulation, resulting in the formation of multiple immature follicles (visually - “polycystic” ovaries).
• Insulin also lowers the level of sex hormone-binding globulin (SHBG), which further increases the free fraction of androgens.

Why the ketogenic diet may help:

• Reduction of carbohydrate load → blood glucose levels stabilize, and insulin secretion decreases.
• Increased insulin sensitivity due to the shift to using fats and ketones as the primary energy source.
• Reduction of hyperandrogenism: with normalization of insulin, the ovaries start to produce less androgens.
• Restoration of ovulation: many women with PCOS experience improved cycles, ovulatory cycles, and the possibility of conception on a ketogenic diet.
• Reduction of chronic inflammation (ketones have anti-inflammatory effects, reducing systemic levels of pro-inflammatory cytokines).

The ketogenic diet in the case of PCOS works not as a “magic pill,” but as a tool to eliminate the key pathogenic factor - hyperinsulinemia. However, its effectiveness is maximized when combined with other measures: adequate protein intake, physical activity (especially strength training that increases insulin sensitivity), normalization of sleep, and stress management.

The ketogenic diet creates metabolic conditions in the body where detoxification organs (liver, kidneys, intestines) work more efficiently, and the level of systemic inflammation and oxidative stress decreases. This explains why people on a keto diet objectively cope more easily with various forms of toxicosis—from food intoxication to the consequences of inflammatory diseases.

Ketones as Clean Fuel

In a state of ketosis, the body uses ketone bodies (beta-hydroxybutyrate, acetoacetate) instead of glucose. This "clean" fuel produces fewer free radicals upon oxidation compared to glucose. This reduces oxidative stress—one of the key factors in the development of toxicosis and inflammatory conditions.

Increased Activity of the Glutathione Pathway

The ketogenic diet promotes the activation of the NRF2 pathway—the main regulator of antioxidant defense. This increases the synthesis of glutathione, which is the primary intracellular antioxidant and participates in the neutralization of xenobiotics (drugs, chemicals, toxins).

Reduction of Inflammatory Processes

Ketosis lowers the levels of pro-inflammatory cytokines (such as TNF-α and IL-6), which often increase during intoxication. Thus, systemic inflammation, which exacerbates toxicosis, is reduced.

Optimization of Liver Function

The liver is the main detoxification organ. With ketogenic nutrition, its function improves due to:

• reduced fat infiltration (especially in non-alcoholic fatty liver disease),
• lower levels of insulin and leptin (which reduces the burden on the liver),
• activation of autophagy—a process in which cells recycle damaged structures and toxins.

Provision of Amino Acids and Cofactors

The ketogenic diet is rich in proteins and fats that contain important amino acids (such as cysteine, glycine), necessary for glutathione synthesis.

Fats also provide phospholipids and fat-soluble vitamins (A, D, E, K), which participate in protecting cell membranes from toxins.

Stabilization of Blood Sugar

High levels of glucose enhance the glycation of proteins and the formation of advanced glycation end products (AGEs), which are toxic in themselves. Keto stabilizes blood sugar levels, reducing this type of endogenous intoxication.

When a person switches to a keto or low-carbohydrate diet, a whole range of metabolic changes occurs in their body, which directly affects the quality and duration of sleep.

Reduction of glucose and insulin fluctuations. With a traditional high-carbohydrate diet, there are often nighttime "sugar swings": after dinner, glucose rises, then falls, sometimes below normal, causing micro-awakenings and restless sleep.

On keto, blood glucose levels become stable, eliminating nighttime "swings" and reducing the number of awakenings.

Increase in ketone bodies. Ketones (beta-hydroxybutyrate and acetoacetate) cross the blood-brain barrier and serve as "clean" fuel for neurons. They reduce oxidative stress and increase mitochondrial efficiency. This makes sleep more effective: the brain recovers as well in less time as it does with longer sleep on a carbohydrate diet.

Influence on neurotransmitters:

• The ketogenic diet increases the level of GABA (gamma-aminobutyric acid) — the main inhibitory neurotransmitter. This makes sleep deeper, reduces nighttime anxiety, and the number of awakenings.
• The level of glutamate decreases, the excess of which is associated with excitation and insomnia.
• The levels of serotonin and melatonin normalize as tryptophan metabolism stabilizes.

Reduction of cortisol levels at night. High carbohydrates in the evening → insulin spike → nighttime drop in sugar → cortisol release to maintain glucose levels. This interferes with deep sleep.

On keto, this chain is disrupted, and cortisol interferes less with recovery at night.

Increase in adenosine. When using fats and ketones as fuel, adenosine — a molecule that induces drowsiness and regulates sleep depth — accumulates more actively in the brain. This leads to a quicker onset of the "full recovery" state.

Thus, on keto, the body experiences deeper, higher quality sleep with more phases of slow-wave sleep (stages 3–4). Therefore, total sleep time may decrease by 1–2 hours, but the feeling of alertness and recovery remains even higher than with longer sleep on a carbohydrate diet.

This is not "sleep deprivation," but rather sleep optimization: the brain and body perform restorative processes more efficiently in less time.

Insulin and the Brain

For the normal functioning of neurons in the brain, glucose is essential. However, for glucose to enter the cell, insulin and sensitive receptors are needed. In the brain, insulin resistance develops in Alzheimer's disease: receptors stop responding to insulin signals, and neurons gradually lose the ability to absorb glucose.

This "energy starvation" leads to mitochondrial damage, accumulation of amyloid and tau proteins, and neuronal death. Essentially, brain cells slowly "starve to death," even when there is enough sugar in the blood.

Why is it called "type three diabetes"?

In classic type II diabetes, body tissues (muscles, liver, adipose tissue) do not respond to insulin. In "type three diabetes," a similar situation occurs in the brain.

There is evidence that carbohydrate metabolism disorders, metabolic syndrome, and chronically high blood sugar levels increase the risk of dementia and accelerate the development of Alzheimer's disease.

How Ketones Help

When carbohydrates are restricted and the body switches to a ketogenic diet, it begins to use ketone bodies (beta-hydroxybutyrate, acetoacetate) formed from fats.

Ketones can penetrate the brain and provide neurons with energy without the involvement of insulin. That is, they "bypass the broken lock" of glucose metabolism and supply nutrients to cells that can no longer absorb sugar.

Research has shown that ketones improve cognitive functions, reduce the accumulation of toxic proteins, decrease inflammation in the brain, and support mitochondrial function.

Ketogenic Diet and Alzheimer's Remission

Patients on a ketogenic diet report improvements in memory, concentration, and behavior. This is not a "magical cure," but a relief from the brain's energy starvation and a slowdown in neuronal degeneration.

In combination with antioxidants, omega-3s, B vitamins (especially B1, B12, folate), and correction of insulin resistance, this offers a chance for stabilization and remission.

The predominant macronutrient in the diet affects respiration, tissue oxygen saturation, lung function, and even the subjective feeling of vitality.

Carbohydrates

During the complete oxidation of glucose (the main carbohydrate), the following reaction occurs:

C₆H₁₂O₆ + 6 O₂ → 6 CO₂ + 6 H₂O + energy (ATP)

This means:

• 6 molecules of oxygen (O₂) are consumed,
• 6 molecules of carbon dioxide (CO₂) are released,
• The ratio CO₂ / O₂ = 1.0 — this is called the respiratory quotient (RQ).

The lungs receive oxygen exactly in the volume that is then released as carbon dioxide. This does not create an excess of oxygen in the tissues.

Fats

During the oxidation of, for example, palmitic acid (one of the common fatty acids), the reaction looks like this:

C₁₆H₃₂O₂ + 23 O₂ → 16 CO₂ + 16 H₂O + energy (ATP)

What we see:

• 23 molecules of oxygen are consumed,
• only 16 molecules of CO₂ are released,
• The respiratory quotient RQ ≈ 0.7.

For each molecule of oxygen, there is less carbon dioxide produced — in other words, oxygen "remains" in the body longer or is used differently than just for the formation of CO₂.

What happens to this "excess" oxygen?

The body does not produce oxygen, but during fat metabolism, more oxygen is consumed than CO₂ is released. This excess:

• Is used in the mitochondria to form water (H₂O) in the final phase of the respiratory chain;
• Dissolves in blood plasma and tissues, increasing saturation;
• Increases the partial pressure of oxygen in the alveoli;
• Improves ventilation and perfusion of the lungs, especially in the lower regions.

Impact on the lung surfactant complex

Surfactant is a lipid-protein film produced by alveolar type II pneumocytes. Its main function is to reduce surface tension in the alveoli, preventing their collapse during exhalation.

A diet focused on fats supports and stimulates the surfactant system:

• Fatty acids and choline are raw materials for surfactant;
• Increased oxygen content in the alveoli improves its distribution across the lung surface;
• Deep breathing during fat metabolism contributes to the mechanical expansion of alveoli and activation of pneumocytes.

Thus, fat metabolism improves the conditions for stable lung function, making breathing more economical and efficient.

Conclusion

The oxidation of fats is not just "another source of energy." It is a holistic metabolic mode that:

• reduces carbon dioxide release,
• improves lung ventilation,
• activates the surfactant complex,
• and supports a stable, oxygen-saturated energy supply for the body.