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Cholesterol, triglycerides and dementia: what is the connection?

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Cholesterol, triglycerides and dementia: what is the connection?

The relationship between cholesterol, lipids and cognitive decline is a complex one. And studies on the subject continue to provide conflicting results. In some, excess lipids in the body appear to represent a risk factor for the development of Alzheimer’s and other forms of dementia. In others, the effect seems even opposite: the last one was published on Neurology by researchers at the University of Melbourne and indicates that, in older adults, a high triglyceride level may be associated with a lower incidence of dementia and slower cognitive decline. Results that must be taken with caution, given the known negative effects of these fats on cardiovascular health, but which demonstrate, if nothing else, how, on a clinical level, the relationship between fats and brain health in old age is still to be deciphered.

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I study

The Australian research used data from 18,294 people with an average age of 75 and no diagnoses of Alzheimer’s or dementia. The participants were followed for an average of six years, and during this time 823 people developed some form of dementia. The researchers assessed levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) during each year of the study, then dividing participants into four groups based on their fasting triglyceride levels. and assessed the incidence of dementia and, more generally, symptoms of cognitive decline in each.

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After eliminating from the data the effects of variables such as education level or use of cholesterol treatments, which could have affected the results, the researchers found that each doubling of triglyceride levels was associated with an 18% lower risk % of developing dementia. More generally, participants with normal (150 mg/dl) or elevated triglyceride levels showed a much lower risk of developing dementia and a rate of cognitive decline than those with lower-than-normal triglyceride levels. Furthermore, the results were validated using data from 68,200 elderly people taken from the UK Biobank.

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Are fats good for the brain?

How to interpret the results? One possibility, which cannot be ruled out due to the way the (observational) study was conceived, is that the presence of high levels of triglycerides is not in itself protective, but is for some reason correlated with better general health (despite representing a known cardiovascular risk factor) or to habits and behaviors that have a protective effect on cognitive decline. On the other hand, it is possible that it is precisely the triglycerides that protect the brain from the onset of Alzheimer’s and other types of dementia, and it would not be so absurd given that – as some experts point out – the brain largely draws its energy precisely from the consumption of triglycerides.

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As we were saying, looking at the research of recent years one can easily find results that go in a completely different direction. A study from last October, published in this case on Lancet Regional Health Western Pacific and carried out on the same cohort of patients used by the University of Melbourne study, identified for example a link between high levels of HDL cholesterol (also called good cholesterol, because it is usually associated with a lower cardiovascular risk) and an increased risk of developing dementia: for participants with levels above 80 mg/dl, the odds rose by 27%. And since high triglyceride levels are usually associated with lower concentrations of HDL cholesterol, it is difficult to reconcile the results of the two studies.

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Where are we at?

One possibility, cited by Betsy Millsdeputy director of the Alzheimer’s Drug Discovery Foundation’s Aging and Alzheimer’s Prevention program, in an article by Medscape Urology, is that it is not the levels of individual lipids present in the blood that represent a risk or protective factor against cognitive decline, but rather the interaction between them. If around the age of 40-50, in fact, high levels of triglycerides and LDL cholesterol are almost always indicative of a greater cardiovascular risk, after 65/70 years of age things become more complicated. “In the elderly – explains the expert – it seems that the fluctuations in both directions are more indicative of a general imbalance in the system”. In this sense, Mills believes that today it is impossible to draw relevant clinical information on the risk of onset of dementia from the lipid levels that emerge from blood tests. But perhaps – you suggest – clinicians could consider monitoring the levels of triglycerides, HDL and LDL cholesterol over time, and the relationship between these values ​​as a possible indication that something, in the body and in the brain, is not going as we would like .

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Intervening with changes in lifestyle, or with drugs, in the case of abnormal cholesterol or triglyceride levels, is possible but, as definitive research results are not available, it is something that every doctor must evaluate for now based on each person’s history. single patient. For the future, however, this is an extremely interesting field, because for many specialists it is precisely in the relationship between lipids and the brain of the elderly that the explanation for the onset of Alzheimer’s and other forms of dementia may lie.

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The so-called amyloid hypothesis, which attributes the onset of the clinical symptoms of dementia to the accumulation of beta-amyloid protein in the brain, is now increasingly less solid, at least for the late-developing forms which represent 90% of Alzheimer’s diagnoses. This is demonstrated, among other things, by the very poor results that the drugs, although approved in recent years, which target this protein are obtaining. The clinical history of Alzheimer’s and dementia is therefore probably much more complex. And a growing number of experts now believe that it may start from an imbalance in the production of cholesterol and other lipids that promote inflammation of brain tissues that damage brain function. Having as a consequence, at least in some cases, the production and accumulation of beta-amyloid protein.

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