Hey! – Rob here 👋🏼
Your Daily Health Fix today is about …
Alzheimers Prevention (for young and old)
Alzheimers disease, observed and named after Alois Alzheimer in 1906, is the most common form of dementia. Typically we think of this disease as affecting just old people. However, rates of early onset Alzheimers are are growing, affecting people in their 30’s and 40’s more frequently than ever.
Fabricated data
Whilst there are many theories as to the cause of Alzheimers disease, the most common one, the βAmyloid Plaque Hypothesis (where β-proteins accumulate in the brain), has been the most prevalent.
But as per this 2022 exposé, fabricated data and imaging was presented in the highly influential research that has been relied upon to guide treatment plans.
The motive for fabricating the data is not entirely clear, or if there were external corporate interests involved, but we do know that the author Sylvain Lesne was listed as the inventor on a patent filing involving Amyloid β-56.
The Damage
In these situations, everyone loses.
The NIH and other funding bodies have invested millions into further studies off the back of Sylvain Lesne’s claims – not only wasting millions in research dollars, but also wasting decades of researchers time.
Multiple drugs have been produced to target βAmyloid Plaque accumulation. Yet despite their proliferation world wide, none have managed to achieve their desired outcome of preventing or reversing Alzheimers dementia.
The patients suffer from ongoing progression of this debilitating condition, often perpetuated by the damage caused by the medications themselves. This is before recognising the immense financial burden of long term medication and care that patients and their families endure.
What we do know
Progression of dementia is strongly linked to the ApoE gene, meaning that carriers of this gene are 4 times more likely to develop Alzheimers disease.
But as we know, the actions of many genes are triggered by environmental conditions. More recently this has been recognised for dementia and specifically Alzheimers disease. Those in the know are now likely to refer to Alzheimers as Type 3 Diabetes.
As with type 2 Diabetes, in type 3 Diabetes insulin levels and insulin resistance play a critical role. Insulin resistance of the brain prevents the proper clearance of βAmyloid plaques, and also leads to problems with the transfer of nutrients and energy from the blood into the brain, along with brain inflammation (hence the rapid cognitive decline).
What CAN I do though?
Reduce your chances of developing this condition early, and effectively reverse many of the symptoms (for anyone who’s loved ones are suffering), by doing all the same things you would do to optimise your health for avoiding and reversing type 2 diabetes.
Eat a clean, unprocessed, low carbohydrate diet.
Prioritise animal fats for their nutrient and energy density without spiking insulin levels.
Exercise, not only for maximising your metabolic health, but also as exercise boosts cognitive function in the short and long term.
Start young, and continue into later life.
. . . That’s it for this dose,
Until the next time – Stay Motivated!💪🏼
Rob
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References . . .
History and progress of hypotheses and clinical trials for Alzheimer’s disease
Early-Onset Dementia and Alzheimer’s Rates Grow for Younger American Adults
Amyloid biomarkers in Alzheimer’s disease
Alzheimer’s Disease: The Link Between Amyloid-β and Neurovascular Dysfunction
The amyloid hypothesis on trial
How Is Alzheimer’s Disease Treated?
Apolipoprotein E and Alzheimer disease: risk, mechanisms, and therapy
Alzheimer’s Dementia LIVE with AMY BERGER, CNS and Dr Berry
UC study: Decreased proteins, not amyloid plaques, tied to Alzheimer’s disease
Alzheimer’s Disease Is Type 3 Diabetes–Evidence Reviewed
Type 3 Diabetes and Its Role Implications in Alzheimer’s Disease
Is Alzheimer’s disease a Type 3 Diabetes? A critical appraisal