Understanding Blood Lipids Properly

Good Fats vs. Bad Fats?

Cholesterol is an essential building material for cell membranes throughout the body. In the brain alone, with its approximately 86 billion nerve cells, about one quarter of the body’s total cholesterol is incorporated.

Nerve cell signals are transmitted via action potentials along their cell membranes. Many metabolic processes—as well as the production of bile acids and hormones—are not possible without cholesterol.

The liver is the body’s main producer of cholesterol. Only a small portion is directly obtained through food.

Because fats are needed throughout the body but are neither water- nor blood-soluble, nature has developed a highly efficient transport system. Packed into small, spherical particles and bound to proteins, fats (lipids) are transported as lipoproteins through the bloodstream to even the most distant parts of the body—for example, to the tip of a finger.

Low-density lipoprotein (LDL) acts as a delivery system, transporting cholesterol from the liver (production site) to the body’s cells, where it is needed.

Its counterpart, high-density lipoprotein (HDL), is responsible for reverse transport, carrying excess cholesterol from the body’s tissues back to the liver, where it is partially broken down or re-released into circulation. In doing so, HDL also helps remove excess lipids deposited along blood vessel walls.

Both LDL and HDL are essential partners in lipid transport and are vital for normal bodily function.

Triglycerides are blood fats that are primarily absorbed through food but can also be produced by the body. LDL transports them to adipose (fat) tissue, where they can be stored and accessed when needed, or to muscle tissue, where they serve as a short-term energy source.

What happens in atherosclerosis?

It often begins as small inflammatory foci in the inner lining of the arterial wall, sometimes as early as between the ages of 20 and 40. White blood cells, LDL (“bad”) cholesterol, cellular waste products, and calcium particles accumulate in these areas, triggering an immune response.

Some immune cells begin to engulf this accumulated “debris.” In doing so, they transform into so-called foam cells, which further amplify the inflammatory process within the vessel wall. Over time, a plaque develops.

Due to the buildup of fat and calcium deposits, the plaque appears as a yellowish thickening. Over the years, this pathological deposit grows and gradually protrudes into the bloodstream.

Similar to a groyne in a river, the plaque disrupts and slows blood flow at its edges. Reduced flow velocity in turn promotes further deposition along the vessel wall, causing the plaque to enlarge further.

Muscle cells from the middle layer of the arterial wall migrate over the plaque, forming a kind of fibrous “cap.” If this cap ruptures due to blood flow stress, platelets adhere to the exposed area and form a clot. This leads to a mural thrombosis.

Eventually, blood flow may be severely restricted or even completely blocked. The affected tissue is then deprived of oxygen and nutrients and can no longer function properly. As a result, the patient may suffer a heart attack or stroke, for example.

Who is at increased risk of atherosclerosis?

Some risk factors cannot be influenced. These include male sex. Until approximately the age of 70, men have a significantly higher risk than women. With increasing age, the risk of arterial narrowing rises in both sexes.

If arterial changes, heart attacks, or strokes occur at a young age, a genetic predisposition is very likely. Statistically, about 1 in 500 people is affected by such an inherited condition.

In addition to these non-modifiable risk factors—such as age, sex, and genetic predisposition—several other factors can promote the development of arterial plaques.

These include:

  • Elevated LDL cholesterol levels due to an unhealthy lifestyle
  • Diabetes mellitus
  • Overweight and obesity
  • Lack of physical activity
  • High blood pressure
  • Smoking
  • Excessive alcohol consumption

Diabetes and the Risk of Atherosclerosis

People with diabetes therefore belong to a high-risk group for complications caused by progressive atherosclerosis.

In addition to an adapted diet and regular physical activity, treatment with medications that effectively lower LDL cholesterol—so-called statins—has proven particularly beneficial.

In people with diabetes, statins can prevent a proportion of heart attacks and strokes and reduce overall mortality.

For example, if 1,000 people with diabetes but without existing cardiovascular disease take a statin for four years, there are approximately:

  • 8 fewer deaths
  • 9 fewer strokes
  • 12 fewer heart attacks prevented

If coronary artery disease is already present, the benefit of statin therapy is even more pronounced. Among 1,000 patients treated with statins over four years, there are approximately:

  • 15 fewer deaths
  • 22 non-fatal heart attacks prevented

How safe are statins?

The normal range for LDL cholesterol in the serum of healthy individuals is approximately 100–129 mg/dl. In patients with a high baseline cardiovascular risk due to atherosclerosis, current specialist guidelines recommend a substantial reduction of LDL cholesterol to around 50% of the normal range.

Side effects of statins, such as muscle pain or elevated liver enzymes, are rare and usually resolve after discontinuation of the medication.

More concerning for some patients is the concern that a strong reduction in LDL cholesterol could impair brain function by affecting neuronal cell membranes. However, a 2023 statement by an expert panel of the American Heart Association, based on extensive research, concluded that this concern is unfounded.

Occasionally reported mild memory or orientation difficulties during statin therapy have been shown to resolve completely after dose reduction or discontinuation.

I am happy to provide individual consultation and advice.

— Reza Falsafi