BHT supplements were big for a while, until the dangers became evident.
Powerful antioxidants, such as rosemary herb, can inhibit normal
biochemistry. There is a price to be paid for too much antioxidant
activity. The funny thing is that critics like this MattLB character
will make a claim in one post that the body needs to oxidize, then turn
around and make the opposite claim in another thread. Why don't you
tell us everything we need to know, MattLB, since you clearly thin you
know everything?
For those who want to read about the scientific reality, instead of the
usual "associational markers," "surrogate endpoints," "dependent risk
factors," "tentative correlations," and "postulated models," you can
read some of biochemist Ray Peat's free essays on the internet. Here
is one that is not too technical:
Estrogen and Osteoporosis
by Raymond Peat, PhD
Excerpts from Ray Peat's Newsletter: Estrogen and Osteoporosis
The government declared victory in the war on cancer, though the
age-specific death rate from caner keeps increasing. In the equally
well publicized effort to prevent disability and death from
osteoporosis, no one is declaring victory, because the only trend in
its incidence that has been reported is an increase. The
estrogen-promoting culture tells us that this is because of the aging
of the population, but the age corrected numbers still show a great
increase-for example, in Finland between 1970 and 1995, the number of
women (for a given population of women older than 60) breaking their
forearm because of osteoporosis more than doubled (Palvannen, et al.,
1998). That this happened during a time when the use of estrogen had
become much more common doesn't present a good argument for the
protective effects of estrogen treatment. (And during this period there
was a large increase in the consumption of estrogenic soy products.)
Recently our local newspaper had a story at the bottom of the front
page reporting that lean women who used estrogen and synthetic
progestins had a 80% higher rate of breast cancer. Several days later,
across the top of the front page, there was a rebuttal article, quoting
some doctors including a "world class expert on hormone replacement
therapy" and as woman who has taken Premarin for forty years and
urges everyone to take it. The "protection against osteoporosis"
and against heart disease, they said, must be weighed against a trifle
such as the 80% increase in cancer. It appeared that the newspaper was
apologizing for reporting a fact that could make millions of women
nervous. (Jan 26, Register-Guard).
Medical magazines, like the mass media, don't like to miss any
opportunity to inform the public about the importance of using estrogen
to prevent osteoporosis. Their attention to the bone-protective effect
of progesterone has been noticeably less than their mad campaign to
sell estrogen, despite the evidence that progesterone can promote bone
rebuilding, rather than just slow its loss...
A former editor of Yearbook of Endocrinology had reviewed a series of
studies showing that excess prolactin can cause osteoporosis. Then, he
presented a group of studies showing how estrogen promotes the
secretion of prolactin, and can cause hyperprolactinemia. In that
review, he wryly wondered how something that increases something that
causes osteoporosis could prevent osteoporosis.
Women have a higher incidence of osteoporosis than men do. Young women
have thinner more delicate bones than young men. The women who break
bones in old age are generally the women who had the thinnest bones in
youth. Menstrual irregularities, and luteal defects, that involve
relatively high estrogen and low progesterone, increase bone loss.
Fatter women are less likely to break bones than thinner women.
Insulin, which causes the formation of fat, also stimulates bone
growth. Estrogen however, increases the level of free fatty acids in
the blood, indicating that it antagonizes insulin (insulin decreases
the level of free fatty acids), and the fatty acids themselves strongly
oppose the effects of insulin. Estrogen dominance is widely thought to
predispose women to diabetes.
Between the ages of 20 and 40, there is a very considerable increase in
the blood level of estrogen in women. However, bone loss begins around
the age of 23, and progresses through the years when estrogen levels
are rising.
Osteoarthritis, which involves degeneration of the bones around joints,
is strongly associated with high levels of estrogen, and can be
produced in animals with estrogen treatment.
Thirty years ago, when people were already claiming that estrogen would
prevent or cure osteoporosis, endocrinologists pointed out that there
was no x-ray evidence to support the claim. Estrogen can cause a
positive calcium balance, the retention of more calcium than is
excreted, and the estrogen promoters argued that this showed it was
being stored in the bones, but the endocrine physiologists showed that
estrogen causes the retention of calcium by soft tissues. There are
many reasons for not wanting calcium to accumulate in the soft tissues;
this occurs normally in aging and stress.
....The toxic effects of excessive intracellular calcium (decreased
respiration and increased excitation) are opposed by magnesium. Both
thyroid and progesterone improve magnesium retention. Estrogen
dominance is often associated with magnesium deficiency, which can be
an important factor in osteoporosis (Abraham and Grewal, 1990;
Muneyyirci-Delale, et all., 1999).
As part of the campaign to get women to use estrogen, an x-ray (bone
density) test was devised which can supposedly measure changes in the
mineral content of bone. However, it happens that fat and water
interfere with the measurements. Estrogen changes the fat and water
content of tissues. By chance, the distortion produce by fat and water
happen to be such that estrogen could appear to be increasing the
density of a bone, when it is really just altering the soft tissues.
Ultrasound measurements can provide very accurate measurements of bone
density, without the fat and water artifacts that can produce
misleading results in the x-ray procedure, and don't expose the
patient to radiation, but the ultrasound method is seldom used.
....Recent studies have found that both men and women lose minerals from
their bones at the rate of about 1% a year. Although men have lower
estrogen in youth than women do, their bones are much heavier. During
aging, as their bones get thinner, men's estrogen levels keep rising.
Besides having weaker bones, old people have weaker muscle, and are
more likely to injure themselves in a fall because their muscles
don't react as well. Muscle loss occurs at about the rate of 1% per
year.
Women's muscles, like their bones, are normally smaller than men's,
and estrogen contributes significantly to these differences.
In the case of osteoporosis (A. Murrillo-Uribe, 1999) as in
Alzheimer's disease, the incidence is two to three times as high in
women as in men. In both Alzheimer's disease and osteoporosis, the
estrogen industry is arguing that the problems are caused by a suddenly
developing estrogen deficiency, rather than by prolonged exposure to
estrogen.
Similar arguments were made fifty years ago regarding the nature of the
menopause itself-that it was caused by a sudden decrease in estrogen
production. The evidence that has accumulated in the last forty years
has decisively settled that argument: Menopause is the result of
prolonged exposure to estrogen. (Even one large dose destroys certain
areas in the brain, and chronic, natural levels damage the nerves that
regulate the pituitary. Overactivity of the pituitary leads to many
other features of aging.)
....Unsaturated fats, iron, and lactic acid are closely related to the
actions and regulation of TNF (Tumor Necrosis Factor), and therefore
they strongly influence the nature of stress and the rate of aging.
The fact that cancer depends on the presence of polyunsaturated fats
probably relates to the constructive and destructive effects such as
multiple organ failure/congestive heart failure/shock-lung, etc.
metabolites, which are based on the so-called essential fatty acids.
When oxygen and the correct nutrients are available, the
hypermetabolism produced by TNF could be reparative (K. [censored], et
al., 1999) rather than destructive. Stimulation in the presence of
oxygen produces carbon dioxide, allowing cells to excrete calcium and
to deposit it in bones, but stimulation in the absence of oxygen
produces lactic aid and causes cellular calcium uptake.
It is in this context that the therapeutic effects of saturated fats,
carbon dioxide, progesterone, and thyroid can be understood. They
restore stability to a system that has been stimulated beyond its
capacity to adapt without injury.
Ray Peat's Newsletter(s) can be purchased by writing to: Ray Peat,
PhD, PO Box 5764, Eugene, Oregon 97405
Source:
http://www.moonlighthealth.com/library2.asp?A=60
