Gabor Szendi:
The solution to the Alzheimer's crisis is in our hands

I have both good and bad news. The good news is that we know what causes Alzheimer's, the bad news is that medicine is ignoring it.

 

 

Alzheimer's disease and other dementias, which represent complete mental decline from the age of 40 to 60, are the new epidemic of Western civilization. It begins with forgetfulness and difficulty in finding words, then later the person does not know any of their relatives. The complete inability to speak and administer self-care is the final state, which can be accompanied by toddler-like stubbornness and aggression. According to modern medicine, bad genes and bad luck decide who gets this fate. In fact, the disease can be easily avoided, or even reversed.

If we didn't know anything about our evolutionary past, we should still be suspicious of the fact that the first patient was described by Alois Alzheimer in 1906, while today we estimate that 12% of men over 65 and 20% of women over 65 are expected to have Alzheimer's. Of course, we can't say that the case described in 1906 was the world's first example of a confused man, since the symptoms of dementia were known in earlier times; but the incidence of Alzheimer's dementia has increased rapidly during the 20th century. This is not explained by the increased lifespan of the Western world, as the majority of indigenous populations reach an age of 70-75 years, but we do not find Alzheimer's sufferers among them.

The genetic explanations are also very flimsy. In the human body, the so-called apolipoproteins transport fats and cholesterol. APOEε genes are responsible for a group of transport proteins. The APOEε4 variant of this gene group carries a high risk for Alzheimer's disease, as 40-65% of patients are known to carry this gene. Agriculture and the spread of the associated lifestyle from south to north could mean a strong selection for this gene type. Today in Sardinia, 5% of the population is characterized by this gene variant, while in Norway, where farming was adopted much later, the gene is already present in 31% (Crean et al., 2014). At the same time, APOEε4 is 20-40% prevalent in indigenous people, but Alzheimer's patients are not found there (Henderson, 2004). So the common correlation that genes only cause disease through interaction with lifestyle is confirmed by this.

There are many components to our lifestyle, but what do we need to consider?

Our starting point can be the difference between indigenous people's and contemporary people's food. In the diet of our ancestors and the indigenous people who still live our ancestors' way of life, we find no fast-absorbing carbohydrates other than the rare delicacy of honey, while carbs form 50-60% of the Western diet. At least if you follow the advice of dietitians. Opposition to fast-absorbing carbohydrates is not at all arbitrary when you consider that diseases that afflict Western people, such as cardiovascular disease, cancer, or diabetes, are closely linked to high blood sugar and insulin levels. Studies have shown that middle-aged obese people are 3-5 times more likely to have Alzheimer's disease (Whitmer et al., 2005), while diabetics have four times the risk of Alzheimer's (Luchsinger, 2008) in old age. Numerous studies have confirmed that Alzheimer's disease is related to insulin resistance, and in Alzheimer's patients and diabetics, alpha-amyloid protein plaques, called specifically for Alzheimer's, are present in the brain as well as in the pancreas. As a summary of the data, researchers have suggested that Alzheimer's disease should be named type 3 diabetes (Kroner, 2009). So dementia is caused by brain insulin resistance, and as a result brain cells are unable to get nutrients and therefore die over time.

The results of the research were put into practice by the American neurologist Dale Bredesen. He banned his patients from fast-absorbing carbohydrates and prescribed them all kinds of vitamins to improve brain function. Alzheimer's patients with serious conditions who were certified to carry the APOEε4 gene, and had Alzheimer's lesions in their brains were also healed. It seems even more incredible, but was confirmed by MRI, that the size of the hippocampus shrank due to the disease significantly increasing, this being one of the most important brain substrates for memory (Bredesen, 2017).

In the light of all this, what does medicine do? It sits with arms folded and waits for the pharmaceutical industry to develop the right medicine or vaccine to cure the disease. Over the past twenty years, 400 clinical trials have tested a variety of trial drugs, totalling100, and the failure in every case was 100%. So many good things cannot be expected. The old truth is that lifestyle-related illnesses can be prevented or reversed by lifestyle changes. If the pharmaceutical industry doesn't heal with lifestyle advice, it should at least have been expected from medicine, but it does not do so.

 

References

Bredesen, DE: The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline. Vermilion, London, 2017.

Crean, S; Ward, A; Mercaldi; CJ; Collins, JM; Cook; MN; Baker, NL; Arrighi, HM: Apolipoprotein E 4 Prevalence in Alzheimer's Disease Patients Varies across Global Populations:A Systematic Literature Review and Meta-Analysis. Dement Geriatr Cogn Disord. 2011;31(1):20-30.

Henderson, S. T. 2004. High carbohydrate diets and Alzheimer's disease, Med Hypotheses, 62(5):689-700.

Kroner, Z. 2009. The relationship between Alzheimer's disease and diabetes: Type 3 diabetes?, Altern Med Rev, 14(4):373-379.

Luchsinger, J. A. 2008. Adiposity, hyperinsulinemia, diabetes and Alzheimer's disease: an epidemiological perspective, Eur J Pharmacol, 585(1):119-129.

Whitmer, R. A. et al. 2005. Obesity in middle age and future risk of dementia: A 27 year longitudinal population based study, BMJ, 330(7504):1360.