[ExI] Autophagy and Aging
Rafal Smigrodzki
rafal.smigrodzki at gmail.com
Sat May 4 23:53:06 UTC 2019
On Fri, May 3, 2019 at 10:00 PM Stuart LaForge <avant at sollegro.com> wrote:
>
> Anyways, water only fasting every other day is working for me so I
> thought I would share
>
### I never got fat in my life but over the years there was some creeping
up of my weight. About two years ago I started intermittent fasting and now
I am only 2 lb above my high school/college weight. I am definitely a fan
of this habit.
I found that fasting for 36 hours was rather taxing, I would cheat and end
up eating lots of snacks before the "official" end of the fast. Now I eat
one meal a day on weekdays, and this happens to be a breakfast, with
absolutely no snacks in between. I find it is quite easy, I don't have to
exert much self-control to keep it going. On weekends I pig out, eating
huge ribeyes smothered in butter and blue cheese. Of course, the quality of
your one meal of the day is still very important - it should have low
glycemic index, low average caloric density, be high in nutrients including
animal protein and fat. I am finding that a very large green salad
(arugula, kale, spinach) with fresh tomatoes, avocado and various
combinations of sardines, other meats, aged cheeses, nuts, olive oil,
balsamic vinegar, fresh herbs, berries and other goodies (about 800 - 900
calories) followed by a Panera pastry keep me satisfied until the next
breakfast.
Regarding the role of autophagy - this is indeed a crucial maintenance
process which becomes suppressed by the continuous ad lib feeding typical
of modern lifestyles. Humans have not evolved under conditions of
continuous food availability and our metabolism is not adapted to it.
However, I doubt that recycling of proteins is really what matters in
autophagy - my guess is that the real mechanism responsible for aging
retardation by fasting is actually mitophagy, or the disposal of
mitochondria. This process selectively removes metabolically defective
mitochondria and their mutated genomes that are responsible for metabolic
defects, thus slowing down the long-term accumulation of mitochondrial
mutations, which is one of the key mediators of aging.
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