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This is the latest medical consensus for delaying the onset or worsening of Alzeimer's:

https://www.amazon.com/Alzheimers-Solution-Breakthrough-Symptoms-Cognitive-ebook/dp/B01N5PY7CU




"Based on the largest clinical and observational study to date, neurologists and codirectors of the Brain Health and Alzheimer’s Prevention Program at Loma Linda University Medical Center, Drs. Dean and Ayesha Sherzai, offer in The Alzheimer’s Solution the first comprehensive program for preventing Alzheimer’s disease and improving cognitive function. Alzheimer’s disease isn’t a genetic inevitability, and a diagnosis doesn’t need to come with a death sentence. Ninety percent of grandparents, parents, husbands, and wives can be spared. Ninety percent of us can avoid ever getting Alzheimer’s, and for the 10 percent with strong genetic risk for cognitive decline, the disease can be delayed by ten to fifteen years. This isn’t an estimate or wishful thinking; it’s a percentage based on rigorous science and the remarkable results the Sherzais have seen firsthand in their clinic. "

Yes, presence of the E4 allele is associated with substantial increased risk of AD, with highest risk linked to being homozygous for E4 (E4/E4). However, even among E4/E4 carriers, only about half who reach the age of 90 show any evidence of AD. That could be taken as some kind of reassurance, as most folks will never see their 90th birthday.

APOE4 is also associated with increased risk of CVD, and again with highest risk increase among those who are E4/E4. The product of APOE4, the Apoe4 lipoprotein, is less effective at delivery of cholesterol/fatty acids than the lipoproteins coded by the other APOE alleles. Apoe4 is also more susceptible to a form of biochemical damage known as "glycation". Glycation is the attachment of a sugar molecule to a protein, sometimes intentional, sometimes random and uncontrolled. Diabetics are especially prone to the damage caused by uncontrolled glycation resulting from hyperglycemia. Diabetics also have higher risk of AD.

APOE4 is considered to be the ancestral allele, based upon research in comparative genetics between Homo sapiens and our nearest living relatives. It's not known to be a corruption of an earlier "healthy" allele.

APOE4 is relatively less common among regional populations with a longer history of agriculture (e.g. peoples of the Levant). APOE4 presence trends upward among populations who persisted longest with diets closer to "hunter-gather".

A higher incidence of APOE4 is observed in Nigerians, yet they are also known for a distinctly low rate of AD.

You can see that the overall picture is rather complex, as is the norm in human biology. Presence of APOE4 is no guarantor of eventual AD, even in the "worst case" of E4/E4. We all live in a personal stew of lifestyle, environment, genetic inheritance, and epigenetic influences, all of which drive outcomes. Genetics alone is often not enough.

A few starter papers from the literature:

Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a ‘thrifty’ allele?

Epidemiology of Dementia among the Elderly in Sub-Saharan Africa

Incidence of Dementia and Alzheimer Disease in 2 Communities

High carbohydrate diets and Alzheimer’s disease

Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet

The above are just a tiny sampling from the ever-growing literature.

For easier, lay person-friendly reading, consider these as a beginning in your research:

The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline

The Alzheimer's Antidote: Using a Low-Carb, High-Fat Diet to Fight Alzheimer’s Disease, Memory Loss, and Cognitive Decline