LE: Life Extension Update 2001.03.09

From: Technotranscendence (neptune@mars.superlink.net)
Date: Sun Mar 11 2001 - 22:44:09 MST

Next message: Zahir Alpaslan: "muslim extropian"
Previous message: Damien Broderick: "Re: CLONING: "Human Being, or Human Folly?""
Messages sorted by: [ date ] [ thread ] [ subject ] [ author ]

LIFE EXTENSION UPDATE MARCH 9 2001

IN THIS ISSUE, MARCH 9, 2001:

LIFE EXTENSION UPDATE EXCLUSIVE: Gene involved in aging in both yeast and
worms;

WHAT'S HOT: Calorie restriction does not effect bone mineral metabolism or
hormones in female primates;

PROTOCOL: Osteoporosis;

FEATURED PRODUCTS OF THE WEEK: Bone Assure,Chronoforte;

MARCH LIFE EXTENSION MAGAZINE NOW ONLINE;

ICONTACT RETURNS TO WWW.LEF.ORG

LIFE EXTENSION UPDATE EXCLUSIVE
Gene involved in aging in both yeast and worms

In an article published in the March 8 issue of the journal Nature, MIT
researchers discovered that the SIR-2 gene, previously discovered to be
involved in the control of lifespan in yeast, is also involved in the
aging process of the nematode worm C elegans. The control of the gene over
lifespan evidently reduces the activity of a signaling pathway
corresponding to insulin or insulin-like growth factor in mammals. This
sheds light on a possible mechanism of calorie restriction in lifespan
extension.

Gerontologist George Martin has differentiated between "private" aging
mechanisms, unique to a species, and "public" ones common to all species.
Calorie, or energy restriction, involves the intake of a lower amount of
calories without malnutrtion, and is the only proven method of lifespan
extension in every species in which it has been tested, therefore
categorized as a public method. Gerontologists studying the yeast S
cerevisiae had previously discovered that the gene SIR-2 effects aging
through its control of gene silencing by altering the chromatin: the DNA,
RNA and protein that makes up the chromosomes. SIR-2 silences genes at
various DNA sites, and in a mechanism specific to S cerevisiae, reduces
extrachromosomal circles of ribosomal DNA that reduce yeast cell lifespan.
However, the method by which calorie restriction extends lifespan in yeast
involves a different mechanism of SIR-2, one that may be present in other
species. Worms bred with an extra copy of sir-2.1, the gene closest to
SIR-2 in yeast, live 50% longer than worms with the normal single copy.

The MIT researchers found that sir-2.1 antagonizes the insulin/IGF-1
pathway. This pathway, which is likely activated in the presence of food,
inhibits the gene daf-16, which is responsible for encoding a
transcription factor. When genes in this pathway are mutated, lifespan is
extended. Sir-2.1 appears to mutate genes in this pathway. Conversely,
when daf-16 is mutated, the lifespan extension created in worms with the
extra copy of sir-2.1 is blocked.

This experiment sheds light on one possible "public" aging mechanism and
provides a possible explanation of calorie restriction's mechanism of
action in delaying aging.

WHAT'S HOT
Calorie restriction does not effect bone mineral metabolism or hormones in
female primates

Calorie, or energy restriction is a remarkable method of delaying aging
and death through a reduction in caloric intake which has shown success
across species in extending maximum lifespan and preventing many diseases
associated with aging. In exploring energy restriction's effects in male
rhesus monkeys, it had previously been found to delay sexual and skeletal
maturity and lower bone mass, despite the numerous benefits it confers.

Similar effects have been seen in rats. In a study published in the March
2001 issue of the Journal of Nutrition, researchers from the National
Institute of Aging attempted to determine if energy restriction has
similar effects on female rhesus monkeys. Female rhesus monkeys undergo
menopause and changes in reproductive hormones similar to that of human
females.

Forty female rhesus monkeys ranging in age from one to twenty-one were fed
either a standard diet or a diet consisting of 30% less calories than the
control diet for six years prior to data collection. The restricted diet
was formulated to exceed the National Research Council's standards for
vitamin and mineral status by 30-40% to compensate for the loss of
vitamins created by lower food intake. No monkeys were postmenopausal at
the time of the collection of the data.

While body fat was lowered in the monkeys receiving the restricted
diet,lean body mass was not. Although bone mineral density tended to be
lower with age in the restricted group, bone mass controlled for age and
weight measured at several sites was not effected by energy restriction,
and correlated with lean body mass, a correlation that has been observed
in human females. Concentrations of the reproductive hormones estradiol,
follicle-stimulating hormone (FSH), progesterone and luteinizing hormone
were not affected by calorie restriction, nor was menstrual cycling,
although estradiol and FSH declined with age and menstrual cycling began
to become less frequent in older animals. Parathyroid hormone and vitamin
D levels were also unaffected. The researchers speculated that females may
have a different response to calorie restriction than males. Ongoing
longitudinal studies at the NIA will further elucidate this area.
http://www.lef.org/cgi-local/welcome.cgi/id=151062318/sgroup_id=699/welcome.
html

PROTOCOL
Osteoporosis

The primary cause of osteoporosis is hormonal imbalances that interfere
with the bone-forming cells. The osteoblasts are specialized bone cells
that function to pull calcium, magnesium, and phosphorus from the blood in
order to build bone mass. Osteoblasts require the hormone progesterone to
maintain youthful bone-forming capability during and after menopause.

For bone mineral maintenance and replacement, the Life Extension
Foundation recommends that women take between 1000 and 2000 mg of
elemental calcium along with 600 to 1000 mg of elemental magnesium every
day. The addition of between 400 and 1000 IU of vitamin D3 is mandatory to
ensure optimal calcium absorption. The inability to absorb calcium is a
major reason that calcium therapy fails to prevent or slow the progression
of osteoporosis. Vitamin D3 taken with calcium will normally promote
absorption and assimilation of calcium into the bone matrix. Vitamin D3
has also been shown to promote the production of IGF-1 and other growth
factors in osteoporotic patients, which improves osteoblast
(bone-building) function. Other minerals that are important for healthy
bone metabolism include at least 30 mg a day of elemental zinc, 3 mg a day
of elemental manganese, and 2 mg of elemental boron a day.
http://www.lef.org/cgi-local/welcome.cgi/id=151062319/sgroup_id=699/welcome.
html