The Cure For Aging Might Be The Cure For Alzheimer’s


Mar 18, 2013
USA / Europe
Almost 25 years ago, Dr. Peat himself wrote a 2-article series in which he outlined arguments in favor of the hypothesis that aging and Alzheimer Disease (AD) are just examples of a more and less systemic sign respectively of declining energy production, and that curing one would lead to a cure of the other.

The problem of Alzheimer's disease as a clue to immortality Part 1
The problem of Alzheimer's disease as a clue to immortality Part 2

Now, after decades of 99.6% failure to make even a dent in the formidable wall that AD is, the article below outlines the exact same arguments presented in Dr. Peat's articles. It's almost as if somebody read his articles and decided to use the ideas there to craft an apologetic essay about medicine's abysmal failure and feebly suggest a "different" (but does not dare call it better) course of future work in curing chronic diseases such as AD, cancer, CVD, etc. Well, I guess better later than never but the troubling part is that even though medicine seems to be realizing the futility of the current highly-specialized approach, the systemic approach to diseases/aging mentioned in the article still seems to be based on the same discredited ideas - i.e. deleting "bad genes" as a "promising" approach to addressing the systemic nature of all chronic diseases. Not a single mention of that other thing that is common among ALL diseases and aging - low metabolism. Let's just hope that the utter failure of techniques like CRISPR to produce anything of note so far will be a strong deterrent to base the next 50 years of medical developments on the same obsolete ideas that dominated the world of medicine for the last century.

The Cure for Aging Might be the Cure for Alzheimer’s - Andreessen Horowitz

"...There’s been a lot of talk lately about possibilities for treating aging—from blood transfusions from old mice to young, to eradicating “zombie” cells, to taking daily rapamycin and metformin pills to extend your healthspan. Some of it sounds like science fiction; some of it is. But what is very real is what is underlying all the talk: the creation of a very substantial new field of science, and a new area of biology, focused on the aging process. Aging doesn’t kill people—diseases kill people. Right? In today’s world, and in a country like the United States, most people die of diseases such as heart attack and stroke, cancer, and Alzheimer’s. These diseases tend to be complex, challenging, difficult, and extremely ugly to experience. And they are by nature chronic, caused by multifactorial triggers and predispositions and lifestyle choices. What we are only now beginning to understand is that the diseases that ultimately kill us are inseparable from the aging process itself. Aging is the root cause. This means that studying these diseases without taking aging into account could be dangerously misleading… and worst of all, impede real progress."

"...The biggest risk factor for Alzheimer’s isn’t your APOE status; it’s your age. People in their twenties don’t get Alzheimer’s. But after you hit the age of 65, your risk of Alzheimer’s doubles every five years, with your risk reaching nearly one out of three by the time you’re 85. What if going after this one biggest risk factor is the best vector of attack? Maybe even the only way to truly address it? This isn’t about the vanity of staying younger, about holding on to your good looks or your ability to run an 8 minute mile. It’s about the only concrete possibility we have to cure these diseases. Instead of choosing targets for a single specific disease, i.e. a specific condition that arises in conjunction with aging, we can get out in front of disease by choosing targets that promote health. And we can identify these by looking at disease through the lens of the biology of aging. Take the example of senescent cells. These “zombie” cells that accumulate with aging were long postulated to be actively toxic. In 2016 scientists discovered that simply deleting these cells in middle-aged mice could dramatically increase lifespan and delay the onset of age-related disease. While the first clinical skirmish against this toxic cell type was not successful (for a particular target, and a particular indication, osteoarthritis), today there is a whole new crop of biotech companies actively targeting this cell population with different small molecules addressing multiple different biological pathways, and planning human clinical trials in a broad range of different indications: Alzheimer’s, COPD, macular degeneration, frailty… the list goes on. The one common risk factor underlying all these different diseases? Aging."

"...Even with our best efforts, best technologies, and best science for each of these major diseases, curing age related diseases one at a time is ultimately low impact. Let’s say we completely cured cancer; that would add a paltry 4yrs to average lifespan, because another major killer like stroke would be just around the corner. Only by targeting aging itself can we make significant impact on improving quality of life and healthspan. Understanding how we age is a way into a new era of medicine, into identifying new targets for diseases we’ve never truly understood (let alone known how to treat). The cure for aging just might be the cure for disease."


Jun 25, 2017
Alzheimer's is associated with undermethylation. Same with many degenerative diseases. Another way of saying it: associated with lower IGF-1.

IGF-1 helps maintain insulin sensitivity and opposes glycation. IGF-1 does many more things: slows thymus shrinking, opposes wrinkles and sagging, opposes estrogen via 5-alpha reductase, maintains bone and muscle, etc.

IGF-1 steadily rises until the end of puberty, then begins to decline. It's said resistance builds to IGF-1. Perhaps there's receptor downregulation and the initial rise with age was to overcome such a state. That is, maybe there's a need for restoration/maintenance of levels and also cycling to maintain sensitivity.

The main thing associated with higher IGF-1: cancer. On the other hand, most things that naturally raise/maintain IGF-1 are anticancer: magnesium, DHEA, vitamin D3, melatonin priming before sleep, etc.

Keeping IGF-1 near the middle of the pubertal peak range while maintaining receptor sensitivity (just may involve fasting) is likely a big step. With IGF-1 levels set; DHEA, hGH, and melatonin would be adjusted to match the associated age.


Sep 24, 2016
I no longer discard the "genetic" idea out of hand so carelessly.

Cell energy from good metabolims is not a cure all. Cancer cells can use this energy as well as can senescent cells. There is a switch somewhere independent of metabolic energ that drives decline and entropy. Poor metabolism at an early stag in life would haten that decline, but good metabolism does not prevent it either. Is that genetic? Not entirely in the scholarly sense, and we all here are aware that epigenetic modulations are important and highly subject to metabolism. Still, there is something resembling to the paadigma of "genetic" that determines lot of whats going on physilogically in the human organism


Oct 29, 2015
Only by targeting aging itself can we make significant impact on improving quality of life and healthspan. Understanding how we age is a way into a new era of medicine, into identifying new targets for diseases we’ve never truly understood (let alone known how to treat). The cure for aging just might be the cure for disease."

Yes Bro....I believe this...I am fighting aging..not disease...I have overcome all my health disasters of recent years but I have not figured out how to stop the clock...I feel it is a natural process that I can not stop.
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