I've found a lot of good stuff on mercola's site, www.mercola.com but it
seems that at least of late, he is not doing his homework. For example, a
recent study found that calorie restriction enhances respiration, but
mercola says:
"A low metabolism is ideal for long life and good health. A high metabolism excites hormones in the
body that eventually cause age-related diseases."
mercola.comcarbohydrates age.htmOpen ↗
He also claims (at that web address) that fruit is not healthy because: "Fructose causes insulin
resistance as proven in scientific tests. Fructose is highly addictive and most people simply refuse
to give up fruit no matter how sick they become. This is identical to lung cancer patients who
continue to smoke cigarettes." Too silly to warrant a response.
Here is the reality, though scientists like Ray Peat have been saying similar things for years:
"Cold Spring Harbor Laboratory Date: 2004-01-01 MIT Helps Unlock Life-extending Secrets Of Calorie
Restriction CAMBRIDGE, Mass. -- Shedding light on why drastically restricting calorie intake
prolongs life span in some organisms, MIT researchers report in the Jan. 1 issue of Genes &
Development that lowering the level of a common coenzyme activates an anti-aging gene in yeast.
Calorie restriction extends life span in a wide spectrum of organisms, and has been shown to delay
the onset or reduce the incidence of many age-related diseases, including cancer and diabetes. No
one is sure why it works. MIT Biology Professor Leonard P. Guarente discovered in 2000 that calorie
restriction activates the silenced information regulator (SIR2) gene, which has the apparent ability
to slow aging during the low-calorie diet. This gene makes a protein called Sir2, which is normally
activated by the coenzyme molecule NAD. Guarente has shown that SIR2 is integrally tied to extending
life span in yeast and in the roundworm. Humans carry a similar gene. This latest study probes how
Sir2 is activated by calorie restriction. The authors report that a coenzyme related to NAD, called
NADH (nicotinamide adenine dinucleotide) inhibits Sir2 by blocking the action of NAD. During calorie
restriction, levels of NADH decline in cells. This decrease in NADH allows NAD to better activate
Sir2 and thereby extend life span. "These findings provide a simple model for activation of Sir2 and
extension of life span by calorie restriction," the authors write. "Our findings suggest that the
NAD/NADH ratio can serve a critical regulatory function, determining the life span of yeast mother
cells. A reduction in this nucleotide activates Sir2 to extend the life span in calorie
restriction." In previous research, Guarente found that rather than a slower metabolism leading to a
slower rate of respiration, it turns out that respiration in yeast cells under calorie restriction
goes up, not down. "A high respiration rate is intimately connected with calorie restriction in
yeast," he said. "A high respiration rate activates SIR2. When respiration goes up, NADH goes down
and SIR2 goes up. When SIR2 goes up, longevity happens." NADH, a coenzyme or enzyme helper, is
present in all living cells. (An enzyme is a protein that works like a catalyst in the body to
prompt chemical changes; for instance, turning food into energy.) NADH, an activated form of the B
vitamin niacin, helps produce energy through a series of chemical reactions in the cell. In cells,
NADH stimulates the production of ATP (adenosine triphosphate), a compound that represents chemical
energy in cells. The more NADH a cell has, the more stored energy it has. It remains to be seen
whether these findings about yeast and NADH will relate to the extension of life span in mammals by
calorie restriction. "