Several million patients in Germany are treated with statins. In 2004, the consumption of lipid-lowering drugs throughout Germany amounted to around 856 million defined daily doses (DDD). In 2011 the amount increased to: 1.718 million DDD.

With the target  to lower cholesterol levels, this doubtful strategy is still being mistakenly promoted to reduce heart disease risk. As a side effect, doctors and patients are accepting a possible cognitive decline.

These are the results of a study published in 2018 in the journal Frontiers in Neurology, which looked into the relationship between cholesterol and cognitive function [1]. While cholesterol is still largely vilified, and statin use still heavily promoted, the study found that having lower levels of low-density lipoprotein (LDL) cholesterol is linked to a higher risk of dementia.

High LDL Cholesterol: a Protective Factor Against Cognitive Decline

The study involved data from nearly 4,000 residents aged 50 years or over in an urban community in China. A high level of LDL cholesterol was found to be inversely associated with dementia in the study participants, even after controlling for other factors that might increase risk, including demographic characteristics, health behavior, mood assessment and medical history.

What’s more, the researchers noted, “There was a significantly higher proportion of participants with low levels of total cholesterol (TC) and [LDL] cholesterol in the dementia group than in groups without dementia.” The association was so strong that they concluded a high level of LDL cholesterol may be considered as a “potential protective factor against cognitive decline.”

This may come as a surprise for those who have been told that cholesterol is more of a burden than an asset, but other studies have also found cholesterol to be protective to the brain. For instance, cholesterol levels in the high-normal range were associated with better cognitive performance in people aged 65 years and older.

Those researchers concluded, “Low cholesterol may serve as a clinical indicator of risk for cognitive impairment in the elderly.”

An earlier U.S. study of more than 4,300 Medicare recipients aged 65 and over also revealed that higher levels of total cholesterol were associated with a decreased risk of Alzheimer’s disease, even after adjusting for cardiovascular risk factors and other related variables [2].

Other studies have found higher HDL cholesterol to be associated with better cognitive function, with researchers suggesting, “Further exploration of the protective effect of HDL-C [HDL cholesterol] on cognitive function in aging is warranted through follow-up, longitudinal studies.”

Why Higher Cholesterol Levels May Be Good for Your Brain

The brain contains up to 30 percent cholesterol, which is an essential component of neurons and of great importance to develop and maintain neuronal plasticity and function. Cholesterol is critical for synapse formation, i.e., the connections between the neurons, which allow you to think, learn new things and form memories.

Beyond this, it’s been suggested that high cholesterol could be an indicator of overall good nutritional status and health, whereas low cholesterol has been linked to a higher risk of mortality and is often seen alongside malnutrition and chronic diseases, including cancer.

The Frontiers in Neurology study authors [1] also suggest that, as a major component of the brain, decreasing cholesterol levels could be associated with cerebral atrophy, “a typical anatomic sign of dementia,” and other factors more directly related to your brain health. They continued:

“Another speculation is that high LDL-C could reduce neurons’ impairments or facilitate compensatory repair of injured neurons. The inhibitions of dendrite outgrowth and synaptogenesis, and the acceleration of neurodegeneration have been observed when neurons was a short of cellular cholesterol or cholesterol supply.

Besides, cholesterol plays an important role in the synthesis, transportation and metabolism of steroid hormones as well as lipid-soluble vitamins, both of which have an impact on synaptic integrity and neurotransmission.”

Therefore it is wise to be careful before taking statins!

Aside from an increased risk of dementia, statins deplete your body of Coenzyme Q10 (CoQ10), which accounts for many of their devastating results.

CoQ10 is used for energy production by every cell in your body. Its reduced form, ubiquinol, is a critical component of cellular respiration and production of adenosine triphosphate (ATP). ATP is a coenzyme used as an energy carrier in every cell of your body. The depletion of CoQ10 caused by statins can actually increase your risk of acute heart failure.

While this can be somewhat offset by taking a Coenzyme Q10 supplement, statins still come with a risk of other serious side effects, including:

  • Diabetes, Cancer, Cataracts, Musculoskeletal disorders, including myalgia, muscle weakness, muscle cramps, rhabdomyolysis and autoimmune muscle disease and depression.

Statins also inhibit the synthesis of vitamin K2, which can make your heart health worse instead of better, and reduce ketone production. Ketones are crucial nutrients to feed your mitochondria especially in the brain and are important regulators of metabolic health and longevity.


  • Having lower levels of low-density lipoprotein (LDL) cholesterol is linked to a higher risk of dementia, according to a study of nearly 4,000 people aged 50 and over
  • A high level of LDL cholesterol was found to be inversely associated with dementia in the study participants, even after controlling for other factors that might increase risk, including demographic characteristics, lifestyle, mood factors and medical history
  • The association is so strong, that a high level of LDL cholesterol may be considered as a “potential protective factor against cognitive decline”
  • The human brain contains up to 30 percent cholesterol, which is an essential component of neurons and necessary to develop and maintain neuronal plasticity and function
In the end, a nutrition scheme rich on healthy fats and low refined sugars is a promising strategy against dementia. The use of statins to lower cholesterol may end in a fast cognitive decline.

Statistik: Arzneimittelverbrauch von lipidsenkenden Mitteln* in Deutschland in den Jahren 2003 bis 2011 (in Millionen DDD**) | Statista
Mehr Statistiken finden Sie bei Statista


[1] Zhou, F. et al. (2018) ‘High low-density lipoprotein cholesterol inversely relates to dementia in community-dwelling older adults: The Shanghai aging study’, Frontiers in Neurology, 9(NOV), pp. 1–8. doi: 10.3389/fneur.2018.00952.

[2] Reitz, C., Tang, M. X., Luchsinger, J., & Mayeux, R. (2004). Relation of plasma lipids to Alzheimer disease and vascular dementia. Archives of neurology, 61(5), 705–714. doi:10.1001/archneur.61.5.705

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The focus of Alzheimer’s research has been, so far, the molecular process which leads to a change in the brain structure, above all and first in the hippocampus. Here, an increased formation of  amyloid beta (Aß) plaques is observed in the brains of Alzheimer patients. These protein adhesions impair the communication between nerve cells. Such alterations are attributed to ageing and genetic predisposition. As a result, Alzheimer’s research has been searching for years (but without any success) for a drug therapy to eliminate or at least reduce plaque formation. A very monocausal view of the problem.

Thus there are also studies suggesting that plaque formation cannot be the only underlying problem, since there are certainly old people with strongly increased plaque formation who are mentally extremely fit. 

Dementia researcher David Snowdon at the University of Minnesota made an impressive study questioning plaque formation as a monocausal cause in the so-called nun study, in which a total of 678 nuns aged between 76 and 106 participated.

Since 1986 Snowden was allowed to test the mental abilities of the nuns and after their death to examine the brains for signs of dementia. The astonishing result: Some brains of nuns who were mentally fit and active up to old age and had an excellent memory, all had “plaques” like in a severe Alzheimer’s dementia. 

Subsequently and in parallel, other influencing factors were intensively investigated. These included viral and bacterial infections, but most of all chronic inflammations.  In addition, there is the problem of insulin resistance caused by excessive sugar consumption by the population in industrialized countries. Today, it is very likely that Alzheimer’s disease is based not only on genetic factors but also on negative lifestyle factors that promote chronic inflammation and insulin resistance of brain cells. Some doctors even refer to Alzheimer’s disease as type 3 diabetes. Amyloid-ß plaques, on the other hand, are a natural protective mechanism that intents to ensure that no more brain cells perish! They are therefore a warning signal, but not a cause.

You can find detailed considerations on the scientific basics and the cause research here….

At the same time, however, this is a bridge to meaningful Alzheimer’s prevention and treatment. A reduction and avoidance of insulin resistance as well as an anti-inflammatory diet and way of life, among other things by:

If you implement these points widely, your Alzheimer’s risk will drop drastically.

In a study conducted by the University of Leipzig, scientists have identified the potential for preventing Alzheimer’s dementia in Germany. Based on internationally available study results, seven risk factors were specifically investigated: High blood pressure, obesity in middle age, depression, physical inactivity, smoking and low education.  The result: about 50% of dementia cases could be avoided by preventive measures alone regarding these risk factors!

Conclusion: Even if the available numbers correspond to theoretical projections, the vast potential for prevention can still be presumed. Especially in the context of demographic change and the corresponding ageing of the German population, preventive measures and educational programmes on Alzheimer’s dementia such as the KsD project are becoming increasingly important.


[1]  Luck, T. & Riedel-Heller, S.G. Nervenarzt (2016) 87: 1194.

Photo: Maria Teneva

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