Arteriosclerosis describes a chronic change in the arteries, in which deposits form in the vessel wall over an extended period, thereby narrowing the vessels and reducing their elasticity.
These deposits – known as plaques – consist of various components. These include lipids (fats, especially cholesterol), inflammatory cells of the immune system, which respond to stimuli or damage in the vessel wall, as well as connective tissue, which the body forms to stabilise the affected area. As it progresses, calcium deposits can also form, increasingly hardening the vessel wall and reducing its elasticity.
As they become more pronounced, these plaques can narrow the vessels and reduce their elasticity. This restricts blood flow.
Arteriosclerosis is considered one of the most important causes of conditions such as:
- heart attack
- stroke
- peripheral arterial disease
The disease usually develops over many years or decades and goes unnoticed for a long time.
How does arteriosclerosis develop?
Today, arteriosclerosis is no longer regarded as a mere “fat deposit” in the vessels. Rather, it is a complex biological process involving several mechanisms. A central factor is chronic inflammatory processes in the vessel wall.
When the inner layer of the vessel – the so-called endothelium – is irritated or damaged, the body responds with an immune reaction. Immune cells migrate into the vessel wall and trigger inflammatory processes there. These reactions are part of a biological repair and defence mechanism of the body.
Over time, lipids, cellular components and connective tissue can accumulate in the vessel wall. These changes gradually lead to the formation of plaques, which can narrow the vessels and impair their function.
The classic cholesterol hypothesis
For many decades, arteriosclerosis was explained above all by the so-called lipid or cholesterol hypothesis.
This hypothesis emerged in the 1950s and assumed that:
- a high intake of fat and cholesterol through the diet raises cholesterol levels in the blood
- elevated cholesterol levels lead to the deposition of cholesterol in the arteries
- these deposits ultimately cause arteriosclerosis.
On the basis of these assumptions, many dietary recommendations arose, advocating in particular a reduction of fat and saturated fatty acids.
In modern cardiology, it is still assumed that elevated LDL cholesterol levels are an important risk factor for arteriosclerosis.
At the same time, however, the understanding of the disease has expanded considerably over the past decades.
What cholesterol actually is
To better understand the debate, it is worth taking a brief look at the role of cholesterol in the body.
Cholesterol is not a “toxic substance”, but a vital substance that the body produces itself. Among other things, it is needed for:
- cell membranes
- hormones
- vitamin D production
- bile acids for digestion
Because cholesterol – like all fats – is not water-soluble, it cannot be transported freely in the blood. That is why cholesterol is transported in the body within so-called lipoproteins – small transport particles made of fats and proteins.
The most important of these are:
LDL (Low Density Lipoprotein) transports cholesterol from the liver to the cells.
HDL (High Density Lipoprotein) transports excess cholesterol back to the liver.
This simplified representation, together with statistical correlations between LDL levels in the blood and arteriosclerosis, led to the popular terms “bad” and “good” cholesterol. In reality, the system is considerably more complex.
When “cholesterol levels” in the blood are referred to in everyday life, this usually means the cholesterol contained in these lipoprotein transport particles. As a rule, what is measured is the amount of cholesterol transported in the blood by LDL or HDL particles.
The interpretation of these values – for example the assumption that certain lipoprotein levels directly reflect the risk of arteriosclerosis – draws on various scientific observations, including epidemiological studies, genetic analyses and clinical intervention trials. At the same time, the exact role of these factors in the development of the disease continues to be debated.
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New perspectives in arteriosclerosis research
In recent years, researchers have begun to take a more nuanced view of the development of arteriosclerosis.
Standard blood tests usually do not measure the number of lipoprotein transport particles themselves, but the amount of cholesterol they contain. More recent research indicates, however, that the number of these lipoprotein particles could also play a role. Two people can, for example, have the same LDL cholesterol level but a different number of LDL particles in the blood.
In addition, some studies show that LDL cholesterol is not uniform, but consists of particles of different size, density and structure.
A marker that can approximately reflect this particle number is apolipoprotein B (ApoB). Since each of these so-called atherogenic lipoprotein particles – such as LDL or VLDL – contains one ApoB molecule, the ApoB value can provide indications of the total number of these particles in the blood. These particles are described as “atherogenic” because many studies associate them with the development of arteriosclerosis. It is observed, for example, that such particles enter the vessel wall under certain conditions and can be involved in inflammatory processes there.
It is important to note, however: these connections are based mainly on observations and statistical relationships. They show a link between certain lipoproteins and cardiovascular disease, but do not necessarily prove a direct cause.
The role of cholesterol from the diet is also viewed in a more nuanced way today. Some studies show that the intake of cholesterol through food often has only a limited influence on cholesterol levels in the blood, because the body can partly regulate its own cholesterol production.
In addition, further factors are moving more strongly into the focus of research, as they too can be linked to inflammatory processes in the vessel wall and to plaque formation, including:
- chronic inflammation and immune reactions
- metabolic disorders
- blood sugar and insulin regulation
- oxidative stress
- lifestyle factors
These findings have led to arteriosclerosis increasingly being understood today as a multifactorial disease.
Such a view can also explain why people with similar cholesterol levels can have very different risks of cardiovascular disease.
Critical perspectives on the cholesterol hypothesis
Alongside the classic cholesterol hypothesis, there are also researchers and scientists who critically question individual aspects of this theory or discuss alternative explanatory models.
One of the best-known voices in this debate is Dr Zoë Harcombe, who has examined in several analyses the historical development of dietary recommendations and the role of fat and cholesterol in the diet.
Harcombe examined, among other things, the studies on which early dietary recommendations in the USA and Great Britain were based. In her analyses, she argues that these recommendations were largely based on epidemiological observational studies and on the cholesterol hypothesis prevailing at the time. Randomised controlled trials – which are regarded in medicine as particularly meaningful – were only available to a limited extent at that point and showed no clear effect on overall mortality.
In her analyses, Harcombe also points out that some early study results were later interpreted very far-reachingly. She and other critics of this interpretation argue that stronger conclusions were sometimes drawn from the available data than the statistical evidence originally suggested.
A further point of discussion concerns the question of what role lipoproteins actually play in the formation of plaques. While some models assume that certain lipoprotein particles can contribute directly to plaque formation, other researchers argue that first damage to or inflammation of the vessel wall must occur before lipoproteins can even be deposited in the vessel wall at all. In this perspective, lipoprotein deposits are in part regarded rather as a consequence of already existing inflammatory processes.
In connection with the cholesterol topic, there is also discussion of what effects very low cholesterol levels could have on other bodily functions, since cholesterol plays, among other things, an important role in the formation of cell membranes, hormones and certain metabolic processes.
Some of these perspectives more strongly question the role of cholesterol in the development of cardiovascular disease, while other researchers continue to assume a connection, but emphasise that the context – in particular inflammatory processes, metabolic health and lifestyle factors – could play an important role.
Proponents of the first perspective argue that other factors may play a more central role in the development of vascular damage. Frequently mentioned in this context are, among other things, persistently elevated blood sugar levels, which through various mechanisms – such as oxidative stress or glycation processes – can promote inflammatory changes in the vessel wall. Toxic influences such as tobacco smoke are also regarded as well-documented triggers of endothelial damage and chronic inflammatory processes. Furthermore, industrially produced trans fats are regarded by many specialist organisations as a clear risk factor for cardiovascular disease and discussed by some researchers as a possible additional influencing factor on the development of arteriosclerosis.
The discussion about these different models remains part of scientific research and shows that the understanding of arteriosclerosis is still being further developed in many areas.
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What we can learn from this for prevention
Regardless of the exact weighting of individual mechanisms, research shows an important common denominator:
Many factors that influence arteriosclerosis are connected with lifestyle.
Among the frequently mentioned preventive factors are:
- regular exercise
- a balanced diet
- stable blood sugar levels
- sufficient sleep
- stress regulation
- refraining from smoking
These factors can positively influence both inflammatory processes and metabolic health – two aspects that are increasingly in focus in modern arteriosclerosis research.
Conclusion
Arteriosclerosis is a complex disease, the development of which has been studied over many decades.
While the classic cholesterol hypothesis was long the dominant model, more recent findings show that inflammation, metabolic processes and lifestyle factors can also play an important role.
The scientific discussion on this topic continues to develop – and shows how dynamic medical knowledge can be.
It is encouraging, however, that many of the known risk factors can be influenced through lifestyle and prevention.
