{"id":2144,"date":"2023-02-21T00:06:56","date_gmt":"2023-02-21T05:06:56","guid":{"rendered":"http:\/\/haidut.me\/?p=2144"},"modified":"2023-05-17T13:13:52","modified_gmt":"2023-05-17T17:13:52","slug":"the-cancer-metabolism-drives-aging-in-humans","status":"publish","type":"post","link":"https:\/\/haidut.me\/?p=2144","title":{"rendered":"The “cancer metabolism” drives aging in humans"},"content":{"rendered":"

A truly monumental study, as it is perhaps the first one to demonstrate that “aging” in human cells is entirely under metabolic control. What can I say – Ray Peat right again! Unfortunately, the way the actual study has been worded has been, once again, criminally mis-represented by mainstream media to state the exact opposite of what the study findings were. Namely, the study identified that a deficiency of OXPHOS and, compensatorily, elevation of glycolysis – i.e. the “cancer metabolism” – drives the aging process. For some strange reason, the study chose the word “hypermetabolism<\/strong><\/span>” to refer to the hyperlycolytic state, though it makes it quite clear numerous times that the “hypermetabolism” discussed hereby is actually a state of low OXPHOS and high glycolysis<\/strong><\/span>. Whether that choice of words was an unfortunate mistake or deliberate manipulation, time will tell. What matters is that the press picked up that poor choice of words and ran with the story that “overactive cell metabolism<\/em><\/span>” drives aging. That press claim is not only in contradiction to the gist of what the study found, but it will invariably be seen by all sorts of public health agencies as a confirmation of the (in)famous “rate of living<\/a>” theory. I included the popular press article (first link below) for reference, but due to the garbage “journalism” it contains I decided to quote directly from the study, unlike other posts of mine. Perhaps the most revealing finding from the study was that in healthy, non-senescent cells the ATP production is derived from an OXPHOS:glycolysis metabolic ratio of about 2:1. Namely, in a healthy, non-aged cell, about 2\/3 of the ATP is derived from OXPHOS and the other 1\/3 from glycolysis. In contrast, in aged (and sick) cells, this OXPHOS:glycolysis ratio for ATP synthesis changes over to 1:4 – i.e. more than completely reversed, in favor of glycolysis. Thus, just as in cancer, the aged cells ramp up their glycolysis to produce the same amount of ATP as healthy cells. So in a way, in cancer and in aging, a cell has to “run” twice as fast just to keep up<\/a>. As the study shows, this inefficient, glycolytic metabolism directly results in mitochondrial (and possibly nuclear) DNA instability, which can, of course, directly cause cancer. In addition, the study demonstrated that the deranged metabolism also resulted in massive release of inflammatory cytokines, increase in (wasteful) energy-consuming pathways, and telomere shortening. In fact, the Hayflick limit<\/a> (HL) of the hyperglycolytic cells was 53% lower than the healthy ones! Now, as Dr. Peat has mentioned in the past, the HL is likely a fake limit on cellular division, but it does have its uses when comparing aging with healthy cells, and such a drastic shortening is likely to result in much higher risk of a number of degenerative diseases, especially ones of the brain and muscles (Alzheimer’s Parkinson’s, Huntington’s, ALS, etc).<\/p>\n

Assuming the study findings are replicated by other scientists the path to retarding, or even reversing, aging seems rather simple. Namely, increase mitochondrial activity while suppressing excessive glycolysis. Thyroid, aspirin, methylene blue and various other quinones such as vitamin K, progesterone, saturated fats, vitamins B1\/B3, androgens, etc all have a sizeable pile of evidence in regards to promoting OXPHOS and\/or suppressing excessive glycolysis. Moreover, most of these substances have already been demonstrated to extend maximum lifespan in-vivo.<\/p>\n

Study Finds Mechanism That Resembles Ageing And Cancer In A Finnish Mitochondrial Disease<\/a><\/p><\/blockquote>\n