The Melatonin DHEA Cycle and Calorie Restriction
James Michael Howard
Fayetteville, Arkansas, U.S.A.
I have written about the connection of melatonin and DHEA in the past. In
fact, I have developed what I call the melatonin DHEA cycle. It is my
hypothesis that melatonin and DHEA are directly involved in controlling the
other, hence, the melatonin DHEA cycle. (To read about this in more
detail, please read my explanation of sleep at
http://www.naples.net/~nfn03605/.) In my explanation of sleep, you will
find that when one is low, the other is high. Anyway, a short time back I
posted an article here entitled DHEA and Calorie Restriction, which was
intended to demonstrate that calorie restriction works because calorie
restriction reduces the daily production of DHEA, and, therefore, extends
the life-span production of DHEA. Extending the availability of DHEA
extends its use for an organism, hence, extending the life-span of the
The following citation has just come to hand: The production of melatonin
declines with increasing age, and circulating melatonin levels are affected
by certain pharmacological or physiological manipulations, notably food
restriction which increases melatonin levels and prevents its age-related
decline. (Gerontology 1996;42(2):87-96). This effect of calorie
restriction on melatonin production is supported by Acta Endocrinol (Copenh)
1987 Aug;115(4):507-13, J Endocrinol Invest 1989 Feb;12(2):103-10 and Brain
Res 1991 Apr 5;545(1-2):66-72. So, this produces a mechanism involving
melatonin and DHEA which directly explains the extension in life-span
produced by calorie restriction. That is, food restriction increases
melatonin which inhibits the production of DHEA. Reducing the production of
DHEA extends the usable life-span of production of DHEA by the adrenals.
Hence, the mechanism of life-extension due to calorie extension results from
an increase in melatonin, which reduces the daily production of DHEA.
Hence, the production of DHEA is extended.
Here is my original post:
DHEA and Calorie Restriction
Since I developed my hypothesis that every cell utilizes DHEA for optimal
function, I have thought that DHEA is also necessary for optimal function of
all tissues. I think DHEA optimizes transcription and duplication of DNA.
With that in mind, I decided that loss of DHEA results in reduced
transcription and duplication of DNA. Therefore, I define aging as loss of
transcription and duplication of DNA, as a result of the natural loss of
DHEA. Therefore, anything that reduces the loss of DHEA, or use thereof,
will extend the lifetime of DHEA and, therefore, reduce aging. Now, since
fasting reduces DHEA production, eating should cause its increased use. In
the following citation, which directly connects calorie restriction and
DHEA, it is shown that calorie restriction reduces DHEA the
postmaturational decline in serum DHEAS levels. Therefore, it could be
that the life-extending qualities of calorie restriction may actually result
from an extension of the production of DHEA.
J Clin Endocrinol Metab 1997 Jul;82(7):2093-6
Dehydroepiandrosterone sulfate: a biomarker of primate aging slowed by
Lane MA, Ingram DK, Ball SS, Roth GS
The adrenal steroids, dehydroepiandrosterone (DHEA) and its sulfate
(DHEAS), have attracted attention for their possible antiaging effects.
DHEAS levels in humans decline markedly with age, suggesting the potential
importance of this parameter as a biomarker of aging. Here we report that,
as seen in humans, male and female rhesus monkeys exhibit a steady,
age-related decline in serum DHEAS. This decline meets several criteria for
a biomarker of aging, including cross-sectional and longitudinal linear
decreases with age and significant stability of individual differences over
time. In addition, the proportional age-related loss of DHEAS in rhesus
monkeys is over twice the rate of decline observed in humans. Most important
is the finding that, in rhesus monkeys, calorie restriction, which extends
life span and retards aging in laboratory rodents, slows the
postmaturational decline in serum DHEAS levels. This represents the first
evidence that this nutritional intervention has the potential to alter
aspects of postmaturational aging in a long-lived species.