Population aging, not margarine or a low-cholesterol diet, is behind the rise in Alzheimer’s

In October 2024, a Facebook reel with almost 250,000 views claimed that “Alzheimer’s never existed until 1979”. It argued that the brain is mainly formed from a substance called myelin, which is 100% cholesterol, and that in the 1970s, the animal fats initially used to produce margarine were replaced by vegetable oils to offer “a lower cholesterol alternative”.

The video was originally published on TikTok in March 2024, and received more than 11 million views. The account that published it, @ecotopia_s.a.f.e, has more than 350,000 followers. The video also circulated on other platforms including YouTube.

Although the reel said that these were all “separate and completely unrelated” subjects, by juxtaposing these statements, the reel implied that margarine, or a low-cholesterol diet in general, leads to Alzheimer’s by depleting the brain of cholesterol.

The claim that a low-cholesterol diet or statins, a cholesterol-lowering medication, is linked to Alzheimer’s isn’t new, as Science Feedback and LeadStories documented in 2023. The claim that a low-cholesterol diet or statins, a cholesterol-lowering medication, is linked to Alzheimer’s isn’t new, as Science Feedback and LeadStories documented in 2023. But this claim and the claim made in the reel are incorrect for multiple reasons that we will explain below.

Alzheimer’s disease was described in 1906

Alzheimer’s disease is the leading cause of dementia, a general term that describes the progressive loss of memory and the ability to think and reason. In its early stages, the disease causes confusion and impairs the person’s ability to handle emotions and concentrate. As the disease progresses, the person eventually depends on others to carry out simple daily tasks.

It is false that Alzheimer’s first emerged in the 1970s. Symptoms of dementia have been documented since early civilizations^[1]. Dementia has also been proposed as a possible explanation for the symptoms displayed by King Lear, the main character in William Shakespeare’s eponymous play, first printed in 1608.

Alzheimer’s disease, as we understand it today, was first described by German pathologist Alois Alzheimer in 1906^[2]. At the 37th Meeting of South-West German Psychiatrists, Alzheimer reported the case of Auguste D., a 51-year-old woman with an “Unusual Illness of the Cerebral Cortex” who had memory loss, aggressiveness, disorientation, and delusions until she died five years later.

The autopsy revealed that Auguste had an unusually thin brain cortex, the brain’s outer layer. In addition, Alzheimer found abnormal deposits outside the neurons called senile plaques, which had been described in older people, and bundles of twisted filaments (tangles) inside the neurons that had never been observed before.

The discovery elicited little interest at the time. But after Alzheimer and other physicians continued reporting similar cases in the following years, psychiatrist Emil Kraepelin introduced the term “Alzheimer’s disease” in the third edition of his Compendium of Psychiatry in 1910.

The plaques and tangles that Alzheimer described are still today the pathological hallmarks of Alzheimer’s. Now we know that they result from an abnormal accumulation of the proteins amyloid-beta (amyloid plaques) and tau (neurofibrillary tangles) in the brain. Researchers haven’t yet identified the underlying causes of this accumulation, but agree that the disease most likely results from the interaction of multiple factors, including genetics, environment, and lifestyle habits.

Data shows that population aging is the primary cause of the rise in Alzheimer’s

According to data from the Global Burden of Disease, Injuries, and Risk Factor Study by the Institute For Health Metrics and Evaluation (IHME), the number of people affected by dementia more than doubled globally between 1990 and 2016^[3]. But the implied link between this increase and the consumption of vegetable margarine is contradicted by scientific evidence.

Among the various risk factors known to contribute to Alzheimer’s and other dementias, aging is the most important one. This doesn’t mean that dementia is a normal part of aging. It is not. Instead, it means that dementia is more common as people grow older. The risk increases after the age of 65, and above the age of 85, Alzheimer’s occurs in one in three people. The effect of aging explains at least in part why women, who tend to live longer than men, have a greater risk of developing Alzheimer’s during their lifetime.

In the last century, the average life expectancy has increased globally from 32 to 71 years (Figure 1). While a reduction in child mortality has largely contributed to this effect, older people also live longer than they did in the past. A direct consequence of this increase in lifespan is that there is a greater proportion of older people, who are the population at the highest risk of dementia.

Figure 1 – Period life expectancy at birth from 1770 to 2021. This metric represents the average lifespan of a person born in a given year if they experienced the same age-specific mortality rates of that specific region and year for the rest of their life. Source: Our World in Data.

When we adjust the share of the population with Alzheimer’s disease and other dementias for this change in the age structure of the population, we can see that dementia was as common in 2021 as it was in 1990 (Figure 2).

Figure 2 – Comparison between the estimated share of the global population with Alzheimer’s and other dementias (blue line) and the share adjusted to the proportion of people in different age groups (age-standardized). Source: Our World in Data, from the IHME Global Burden of Disease Study 2021.

In other words, the data shows that the rise in Alzheimer’s is primarily due to the population aging^[3], a trend that is estimated to continue in the following decades^[4].

Margarines marketed in the 1970s contained trans fats, which increase cholesterol levels

The reel presented vegetable margarine as a low-cholesterol substitute to butter and other animal fats. However, this isn’t entirely accurate.

In 1869, French chemist Hippolyte Mege-Mouries invented margarine in response to Napoleon III’s demand for “a suitable substance to replace butter for the navy and less prosperous classes”. This early substitute consisted of chopped beef tallow cooked with water and was presented as beads.

The product became a commercial success in Europe and in the U.S. in the early 1870s, as it was about half the price of butter. A few years later, U.S. manufacturers developed a spreadable version of the product by emulsifying beef tallow with water or milk.

In the late 19th century, animal fat in margarine was replaced with vegetable oils, which in general, contain less saturated fats. Because saturated fats cause cholesterol to accumulate in the blood vessels, increasing the risk of cardiovascular disease, these vegetable margarines were considered a healthier option than animal fats.

However, vegetable oils are liquid at room temperature. To convert them into a solid form, manufacturers used hydrogenation, a chemical process that generates trans fats as a side product. Trans fats are considered the worst type of dietary fat because they have no known benefits and have a double effect of increasing “bad” (low-density lipoprotein or LDL) cholesterol while decreasing “good” (high-density lipoprotein or HDL) cholesterol. This increases the risk of heart attack and stroke even more than saturated fats, which increase LDL but also HDL cholesterol.

Therefore, presenting margarine marketed in the 1970s as a low-cholesterol food is at the very least arguable.

In fact, the U.S. Food and Drug Administration (FDA) determined in 2015 that artificial trans fats were no longer generally recognized as safe (GRAS) and banned them from food products such as margarine in 2018. Currently, margarines are manufactured using a different solidification process called interesterification, which produces a spreadable product without trans fats. Evidence suggests that margarines produced in this way may be a healthier option than butter^[5].

A potential role of dietary cholesterol, brain cholesterol, and myelin damage in Alzheimer’s is still under investigation

The general claim that a low cholesterol intake causes a loss of myelin in the brain that ultimately leads to Alzheimer’s is incorrect, as Science Feedback explained before. The reason is that this argument is based on multiple inaccuracies and premises that are unsupported by current scientific evidence.

First, it is false that myelin is 100% cholesterol as the reel claimed. Myelin contains 70% to 85% of fats, of which approximately 40% is cholesterol^[6]. The remaining 15% to 30% of myelin components are proteins. Therefore, while cholesterol is the most abundant component of myelin, it only accounts for about one-third of myelin components.

Second, Alzheimer’s is a neurodegenerative disease affecting neurons, not a demyelinating disease, a term that refers to conditions like multiple sclerosis that are caused by myelin destruction.

Myelin is a protective fatty sheath that wraps around nerves in the brain and the spinal cord. This sheath is crucial for efficiently transmitting electrical impulses along the nerve, and therefore, it plays an essential role in cognition and memory.

People with Alzheimer’s show damage in myelin and the cells responsible for producing it, the oligodendrocytes^[7,8]. However, this isn’t a characteristic feature of the disease, and it is unclear whether myelin damage is involved in the development of Alzheimer’s or is just a consequence of it^[9].

Third, while there is evidence that changes in brain cholesterol metabolism might impact brain myelin in people with Alzheimer’s^[9], researchers still don’t know whether and to what extent dietary cholesterol may influence this process. This is because cholesterol itself can’t cross the blood-brain barrier (BBB) that surrounds the brain. Instead, the brain produces and recycles its own cholesterol^[10], and therefore it doesn’t depend on dietary cholesterol to produce myelin.

One study published in Neurology in 2023 found an association between large rises or drops in cholesterol and triglyceride levels and a slightly increased risk of developing dementia^[11]. However, the risk increase was very small and it is uncertain whether it would translate into a meaningful clinical effect.

So far, the clearest association identified between cholesterol and dementia is exactly the opposite of what the reel implied. Health conditions associated with cardiovascular disease, such as overweight, diabetes, and high blood pressure, are in general also associated with an increased risk of developing Alzheimer’s. The same happens with cholesterol.

High cholesterol levels have been shown to trigger the accumulation of amyloid and tau proteins in laboratory cells and in the brains of experimental animals^[12]. Conversely, treatment with cholesterol-lowering medication (statins) reduces this abnormal protein accumulation. Population studies also show an association between high levels of cholesterol in the blood and a higher risk of developing Alzheimer’s, which is reduced in people treated with statins^[12].

It is impossible to modify our genetics or stop aging. However, by reducing cardiovascular-related risk factors like blood cholesterol levels, we can minimize our risk of developing dementia^[13]. Healthy lifestyle habits including physical activity, a balanced diet, and mental stimulation, along with not smoking and moderating alcohol consumption, also promote brain health and can help further reduce the risk.

Conclusion

The claim that Alzheimer’s is a new disease that appeared in 1979 linked to margarine consumption is incorrect and contradicts scientific evidence. Symptoms of dementia have been documented since ancient times. The specific type of dementia known as Alzheimer’s was formally described more than a century ago.

Cases of Alzheimer’s have greatly increased in recent decades. However, data shows that population aging, not margarine or low-cholesterol diets, is behind this increase. Suggesting that low-cholesterol products like margarine cause Alzheimer’s reflects a misunderstanding of the disease and of how cholesterol is regulated in the brain. Although the specific role of dietary cholesterol, brain cholesterol, and myelin damage in Alzheimer’s is still not well understood, high cholesterol levels in the blood are associated with an increased risk of developing Alzheimer’s and other dementias.

REFERENCES

• 1 – Finch and Burstein (2024) Dementia in the Ancient Greco-Roman World Was Minimally Mentioned. Journal of Alzheimer’s Disease.
• 2 – Stelzmann et al. (1995) An English Translation of Alzheimer’s 1907 Paper, “Über eine eigenartige Erlranliung der Hirnrinde”. Clinical Anatomy.
• 3 – GBD 2016 Dementia Collaborators (2019) Global, regional, and national burden of Alzheimer’s disease and other dementias, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet Neurology.
• 4 – GBD 2019 Dementia Forecasting Collaborators (2022) Estimation of the global prevalence of dementia in 2019 and forecasted prevalence in 2050: an analysis for the Global Burden of Disease Study 2019. The Lancet Public Health.
• 5 – Weber et al. (2021) Nutrient comparisons of margarine/margarine-like products, butter blend products and butter in the US marketplace in 2020 post-FDA ban on partially hydrogenated oils. Public Health Nutrition.
• 6 – Kister and Kister (2023) Overview of myelin, major myelin lipids, and myelin-associated proteins. Frontiers in Chemistry.
• 7 – Nasrabady et al. (2018) White matter changes in Alzheimer’s disease: a focus on myelin and oligodendrocytes. Acta Neuropathologica Communications.
• 8 – Huang et al. (2024) Myelin Pathology in Alzheimer’s Disease: Potential Therapeutic Opportunities. Aging and Disease.
• 9 – Blanchard et al. (2022) APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes. Nature.
• 10 – Zhang and Liu (2015) Cholesterol metabolism and homeostasis in the brain. Protein and Cell.
• 11 – Moser et al. (2023) Association Between Fluctuations in Blood Lipid Levels Over Time With Incident Alzheimer Disease and Alzheimer Disease–Related Dementias. Neurology.
• 12 – Björkhem and Meaney (2021) Brain Cholesterol: Long Secret Life Behind a Barrier. Arteriosclerosis, Thrombosis, and Vascular Biology.
• 13 – Wolters et al. (2020) Twenty-seven-year time trends in dementia incidence in Europe and the United States: The Alzheimer Cohorts Consortium. Neurology.