What is cholesterol?
Cholesterol is a fat-like substance that belongs to the group of steroids. It is an essential component of the cell membranes of animals and humans and is crucial for their stability and fluidity. In addition, cholesterol fulfills many other important functions in the body.
Different transport forms of cholesterol
Because cholesterol is fat-soluble and cannot be transported on its own in the aqueous bloodstream, it is bound to special protein complexes known as lipoproteins.
The two best-known forms are:
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LDL (low-density lipoprotein): Often referred to as “bad” cholesterol. It transports cholesterol from the liver to the body’s cells, where it is needed.
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HDL (high-density lipoprotein): Considered “good” cholesterol. It helps remove excess cholesterol and transport it back to the liver, where it is recycled.
In addition, there are other transport forms such as VLDL (very low-density lipoprotein) and IDL (intermediate-density lipoprotein), which also transport cholesterol from the liver to the cells. So-called chylomicrons transport cholesterol and fats absorbed from food from the intestine into the body.
It is important to note that all of these transport forms fulfill essential functions in the body. None of them is inherently “good” or “bad.”
Functions of cholesterol in the body
Without cholesterol, humans cannot survive. It fulfills the following essential functions:
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Formation and repair of cell membranes
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Formation of myelin sheaths (nerve insulation), particularly important for the brain
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Basis for the synthesis of all steroid hormones (pregnenolone, progesterone, testosterone, estradiol, cortisol)
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Precursor for the formation of vitamin D3
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Formation of bile acids, which are necessary for fat digestion and the absorption of fat-soluble vitamins
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Transport of carotenoids and fat-soluble vitamins in the blood
The body produces most cholesterol itself
Approximately 80–90% of cholesterol is produced by the body itself, primarily in the liver, but also in the intestine and the brain. Dietary cholesterol therefore plays only a minor role and has little influence on blood cholesterol levels (1). The consumption of eggs is therefore not a cause of elevated cholesterol levels, as is often claimed.
Production process and influence of statins
Cholesterol is synthesized via the so-called mevalonate pathway. Acetyl-CoA serves as the starting substrate. However, this metabolic pathway produces not only cholesterol, but also a wide range of other important substances.
These include the downstream products of cholesterol mentioned above, such as steroid hormones and vitamin D3, as well as additional compounds that share a common precursor with cholesterol. One important example is coenzyme Q10, which is essential for energy production in the mitochondria.
When statins (cholesterol-lowering drugs) are used to reduce elevated cholesterol levels, they inhibit not only cholesterol synthesis but also the production of many other substances formed along this pathway. This can have far-reaching consequences for health. The impact on steroid hormones illustrates this particularly clearly: these hormones influence the entire organism and are important, for example, for bone metabolism, metabolic health, sexual function, mental well-being, and immune function.
Is an elevated cholesterol level harmful?
Reference values for cholesterol have been lowered steadily over recent decades, with the result that more than 50% of adults in Germany and other industrialized countries are now classified as having elevated levels.
The following reference values currently apply (as of December 2025):
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Total cholesterol: < 200 mg/dl
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LDL cholesterol: < 160 mg/dl
Based on these reference values, many patients are prescribed statins. However, current research clearly shows that assessing an individual’s risk for cardiovascular disease is far more complex. Statin therapy based solely on these values is therefore no longer considered up to date.
Below, we present several relevant studies that question the use of cholesterol as a risk parameter or even demonstrate beneficial health effects of higher cholesterol levels:
A meta-analysis published in 2016 evaluated the results of 19 studies involving more than 68,000 individuals over the age of 60. It concluded that in 14 of the 19 studies (covering 92% of participants), higher LDL cholesterol levels were associated with lower mortality. In the remaining five studies, no association between cholesterol and mortality was observed (2).
A large Norwegian study also examined the use of total cholesterol as a risk parameter. The study followed more than 52,000 participants aged 20 to 74 over a period of ten years (3):
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In women, a linear relationship was observed: the higher the cholesterol levels, the lower the risk of death from cardiovascular disease and overall mortality.
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In men, a U-shaped curve emerged: the lowest mortality was observed at total cholesterol levels between 193 and 228 mg/dl. At levels below 193 mg/dl, mortality was particularly high—higher even than at values up to 270 mg/dl.
Studies in older adults also show improved cognitive performance in individuals with higher total and LDL cholesterol levels (4), as well as a reduced risk of dementia associated with higher total cholesterol (5).
When does cholesterol become dangerous?
The studies presented clearly show that cholesterol alone does not provide information about the actual risk of cardiovascular disease. Nevertheless, the image of “too much cholesterol” accumulating in the blood vessels is still widespread. In reality, atherosclerosis does not develop simply as a result of high cholesterol levels, but rather through a combination of unfavourable factors. What matters most is the conditions under which LDL circulates in the body.
Inflammation: the true risk factor
As long as the body is in balance – with well-regulated inflammatory processes, adequate oxygen supply, and sufficient nutrients – cholesterol can fulfill its functions without causing harm.
Problems arise when chronic inflammation is present, as is common in many people due to an unfavourable lifestyle:
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Unhealthy diet: excessive carbohydrate intake with high amounts of sugar, refined flour, and fructose; excessive caloric intake; many processed foods and “unhealthy” fats; insufficient intake of dietary fibre and secondary plant compounds
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Additional factors: lack of physical activity; sleep deprivation; chronic stress; exposure to pollutants from food, the environment, cosmetics, etc.
Under these conditions, increased amounts of free radicals are generated in the body. While free radicals are constantly produced as part of normal metabolism, excessive levels lead to oxidative stress and promote inflammatory processes, as important molecules such as proteins, fats, or DNA are damaged (oxidized) and can no longer perform their functions properly.
If chronic inflammation is present in the body, the blood vessel walls are also damaged. Cholesterol is increasingly deposited for repair purposes – something that would not be problematic in a healthy internal environment.
However, under the conditions described above, there is increased formation of small, particularly dense LDL particles, known as “small dense LDL.” These particles can easily penetrate inflamed vessel walls and are especially susceptible to free radicals. As a result, oxidized (“rancid”) LDL accumulates within the vessel walls.
This marks the beginning of an inflammatory cascade:
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The immune system recognizes that oxidized LDL particles do not belong in the vessel wall and sends scavenger cells (macrophages).
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These scavenger cells absorb the particles, become so-called foam cells, effectively “burst,” and accumulate within the vessel wall.
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This leads to the formation of a soft, unstable plaque that narrows the vessel lumen.
The body then attempts to stabilize this unstable plaque by depositing calcium and hardening it. Although a hard plaque is undesirable, it is less dangerous because it is less likely to rupture and suddenly block a blood vessel.
We can therefore conclude that the risk of cardiovascular disease does not increase per se due to elevated cholesterol levels, but rather due to increased levels of small dense LDL and oxidized LDL, which arise more frequently in the presence of chronic inflammatory processes. How these factors can be assessed in the laboratory will be explained in Part 2 of our series.
Is statin therapy therefore not useful?
For individuals who merely have mildly elevated cholesterol levels, without evidence of atherosclerosis and without additional risk factors, there is generally no reason to lower cholesterol levels pharmacologically.
However, the use of statins can be important in cases of:
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existing heart or vascular disease
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inherited disorders of lipid metabolism
In these situations, lowering LDL levels may be appropriate because affected individuals have a significantly increased risk of atherosclerosis due to their genetic background or pre-existing conditions. Nevertheless, even in these cases, lifestyle modifications are essential in order to reduce the overall inflammatory burden in the body.
Genetically elevated cholesterol levels
Elevated cholesterol levels can be inherited. Various genetic and epigenetic factors play a role. Genetic testing can help determine whether an individual is affected by such a lipid metabolism disorder.
Familial hypercholesterolemia
Familial hypercholesterolemia (FH) is an autosomal-dominant inherited disorder of lipid metabolism in which elevated LDL levels can often be detected as early as childhood. The cause is a gene mutation affecting the LDL receptor on the surface of cells. As a result, LDL cannot be taken up efficiently by cells, leading to markedly elevated blood levels.
In homozygous FH (inheritance of the unfavourable gene from both parents), there is an approximately 20-fold increased risk of atherosclerosis and thus of heart attack and stroke. Affected individuals often have LDL levels ranging from 400 to 1,000 mg/dl. The prevalence of this condition is approximately 1 in 1,000,000. Heterozygous FH (one unfavourable gene and one healthy gene) is much more common, affecting about 1 in 500 people. LDL cholesterol levels typically range between 190 and 450 mg/dl. These individuals should receive pharmacological treatment, as their risk of cardiovascular disease is significantly increased (6).
APOE gene
The APOE gene is another important risk factor, as it influences how fats and cholesterol are processed. In particular, the APOE4 variant (inherited once or twice) is associated with higher LDL levels, increased sensitivity to saturated fats, and a higher cardiovascular risk.
The presence of this gene variant does not automatically require cholesterol-lowering medication. However, it is especially important to adhere strictly to an anti-inflammatory lifestyle, maintain moderate fat intake, and ensure optimal omega-3 fatty acid supply.
Individuals with the APOE4 variant should use krill oil rather than algae oil or fish oil, as krill oil provides omega-3 fatty acids in a form that is more bioavailable for these individuals (phospholipid form rather than triglycerides).
Additional genetic influences
There are numerous other genetic and epigenetic factors that can influence cholesterol levels and LDL quality. In many cases, a healthy lifestyle combined with adequate micronutrient intake can help compensate for an increased genetic risk.
Outlook
In the second part of our series, you will receive information on important laboratory tests and learn how you can positively influence your risk of cardiovascular disease through a healthy lifestyle.
Sources
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Fernandez ML, Calle M. Revisiting dietary cholesterol recommendations: does the evidence support a limit of 300 mg/d? Curr Atheroscler Rep. 2010 Nov;12(6):377-83.
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Ravnskov U, Diamond DM, Hama R, Hamazaki T, Hammarskjöld B, Hynes N, Kendrick M, Langsjoen PH, Malhotra A, Mascitelli L, McCully KS, Ogushi Y, Okuyama H, Rosch PJ, Schersten T, Sultan S, Sundberg R. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open. 2016 Jun 12;6(6):e010401.
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Petursson, Halfdan, et al. „Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study.“ Journal of evaluation in clinical practice 18.1 (2012): 159-168.
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West R, Beeri MS, Schmeidler J, Hannigan CM, Angelo G, Grossman HT, Rosendorff C, Silverman JM. Better memory functioning associated with higher total and low-density lipoprotein cholesterol levels in very elderly subjects without the apolipoprotein e4 allele. Am J Geriatr Psychiatry. 2008 Sep;16(9):781-5.
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Mielke MM, Zandi PP, Sjögren M, Gustafson D, Ostling S, Steen B, Skoog I. High total cholesterol levels in late life associated with a reduced risk of dementia. Neurology. 2005 May 24;64(10):1689-95.
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Familiäre Hypercholesterinämie – wenn hohe Cholesterinwerte vererbt werden. Cholesterin neu verstehen [Internet]. [aufgerufen am 26.11.25].