Atherosclerosis

Atherosclerosis is largely related to mineral and protein metabolism, and this connection is explained by the physiology of the vascular wall and lipid metabolism.

Protein Factor

Blood vessels consist not only of endothelium and lipids but also of protein structures — collagen and elastin. In the case of protein deficiency, the synthesis of these structures decreases, making the vessels brittle and permeable. In response to endothelial damage, the body "patches" them with lipids (primarily low-density lipoproteins), which initiates the atherosclerotic process.

Moreover, low levels of albumin in plasma disrupt the transport of minerals (calcium, magnesium, iron), exacerbating their imbalance.

Calcium Metabolism

Atherosclerosis is accompanied by pathological calcification of blood vessels. Here, the important factor is not the quantity of calcium but its proper distribution:

• With a deficiency of vitamin K2, calcium is not retained in the bones and "leaves" for the vascular wall, where it deposits in plaques.
• A lack of magnesium worsens the situation: magnesium is a natural antagonist of calcium, relaxing blood vessels and preventing calcium deposition in soft tissues.
• Disruption of stomach acidity (hypoacidity) hinders the absorption of calcium in ionic form and further disturbs the balance.

Iron and Its Role

Iron metabolism also directly affects:

• An excess of iron accelerates lipid peroxidation (LPO), damaging the endothelium through free radicals.
• A deficiency of iron reduces the synthesis of antioxidant defense enzymes (e.g., catalase), which also increases oxidative stress.
• Thus, both excess and deficiency of iron can enhance the progression of atherosclerosis.

General Pathogenesis Scheme:

1. Endothelial damage (stress, toxins, protein deficiency).
2. Disruption of calcium and iron transport → destabilization of the vascular wall.
3. The body "repairs" the vessel with lipids, gradually forming a plaque.
4. If protein and magnesium deficiency persists, calcium becomes fixed in the plaque, making it hard and dangerous.

Correction:

• Sufficient intake of animal protein (collagen amino acids, albumins).
• Control of calcium + magnesium + vitamin K2 + vitamin D3 for proper calcium distribution.
• Maintenance of normal levels of iron and ferritin, avoiding both overload and deficiency.
• Support of the antioxidant system (selenium, zinc, vitamins C and E) to reduce lipid oxidation.

A diet that limits cholesterol intake but contains a large amount of vegetable oils rich in omega-6 fatty acids creates conditions for the development of inflammatory and atherosclerotic processes.

The Role of Cholesterol and Its Protective Function

Cholesterol is not an enemy, but a vital molecule. It is necessary for:

• synthesis of sex and steroid hormones (testosterone, cortisol, estrogens);
• formation of bile acids (without them, there is no normal digestion of fats);
• building cell membranes — cholesterol makes them strong and elastic;
• protection of blood vessels: when the endothelium is damaged, cholesterol "seals" microcracks, acting as a natural "band-aid".

When cholesterol is restricted in the diet, the liver begins to synthesize it in larger quantities to compensate for the deficiency. However, if the diet is high in omega-6, oxidative stress occurs, making cholesterol "sticky" and inflamed.

Omega-6 and Inflammation of Blood Vessels

The main component of vegetable oils (sunflower, corn, soybean) is linoleic acid (omega-6). In the body, it is converted into arachidonic acid, from which inflammatory mediators are synthesized:

• prostaglandins of series 2 (PGE2),
• thromboxanes (TXA2),
• leukotrienes (LTB4).

All these substances:

• increase blood clotting,
• contribute to vasospasm,
• activate immune cells and inflammation in the endothelium.

The result is endothelial dysfunction, lipid accumulation in the vessel wall, and the formation of an atherosclerotic plaque.

Imbalance of Omega-6 : Omega-3

For normal fat metabolism, the ratio of omega-6 to omega-3 should be approximately 3:1 or even 2:1. Modern anti-atherogenic diets based on vegetable oils give a ratio of 20:1 or higher.

Omega-3 (EPA and DHA) are antagonists of omega-6; they:

• reduce platelet aggregation,
• dilate blood vessels,
• lower triglyceride levels,
• suppress the synthesis of inflammatory prostaglandins.

When there is a deficiency of omega-3 and an excess of omega-6, the body enters a state of chronic low-grade inflammation, which is the trigger mechanism for atherosclerosis.

Why Blood Vessels Suffer Without Cholesterol

If cholesterol is removed but the damaging factor (oxidized omega-6 and inflammation) remains, the vessel is left without a protective mechanism. The endothelium continues to deteriorate, and even "low cholesterol" does not help — on the contrary, the risk increases:

• ruptures of the vessel wall,
• myocardial ischemia,
• stroke.

As a result, the paradox is that the less cholesterol there is in the diet, the more actively the liver synthesizes it, and the inflamed vessel wall makes this cholesterol atherogenic.

The key difference between «bad» and «good» lipoproteins lies not so much in the cholesterol itself, but in the amount of triglycerides they transport. To understand this physiologically, one needs to consider the pathway of lipoprotein transformation in the body.

How Lipoproteins Are Formed

All lipoproteins — are transport capsules that carry fat (triglycerides and cholesterol) through the blood, as fats are insoluble in water.

The liver secretes very low-density lipoproteins (VLDL) — these are large particles that contain:

• a lot of triglycerides (up to 50–60% of the mass),
• a little cholesterol,
• a protein shell (apolipoproteins, mainly ApoB100).

VLDL are directed to peripheral tissues — muscles and adipose tissue, where the enzyme lipoprotein lipase (LPL) breaks down triglycerides into fatty acids. These fatty acids are used by cells for energy or stored in fat depots.

Transformation of «Bad» into «Good»

When VLDL lose some triglycerides under the action of lipase, they become intermediate-density lipoproteins (IDL). If the process continues and triglyceride levels drop even further, IDL transform into low-density lipoproteins (LDL).

LDL contain:

• already few triglycerides,
• a lot of cholesterol,
• and perform an important function — delivering cholesterol to cells, where it is used for building membranes, synthesizing hormones, and vitamin D.

Thus, LDL — is not "bad cholesterol", but rather the result of «maturation» of VLDL, when the excess amount of triglycerides has been removed from the blood.

Why Excess Triglycerides Make Lipoproteins Dangerous

If a person consumes a lot of fast carbohydrates (sugar, bread, starch, fructose), the liver actively synthesizes triglycerides from them. This leads to:

• overproduction of VLDL,
• increased triglyceride levels in the blood,
• and reduced activity of lipoprotein lipase (especially in insulin resistance).

As a result, VLDL and IDL circulate longer, oxidize, and become atherogenic particles — they damage the vascular wall, trigger inflammation, and form plaques.

What Happens on a Keto Diet

On a ketogenic diet:

• insulin levels decrease,
• triglyceride synthesis in the liver drops,
• less VLDL is formed,
• lipolysis is activated, and fats are used as fuel.

The amount of triglycerides in the blood sharply decreases, while the share of dense LDL (large buoyant LDL) increases — these particles are considered safe and even beneficial for cholesterol metabolism.

Conclusion

What is referred to as «bad cholesterol» is actually a consequence of carbohydrate metabolism and excess triglycerides, rather than cholesterol itself.