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Dear Doctor,
Do you have any patients who are worried about osteoporosis? Are
there any women under your care who are considering estrogen
replacement therapy as protection against osteoporosis? Then, here is
one important study you will want to look into.
Kassem M., et al. Potential mechanism of estrogen-mediated decrease
in bone formation. Proc Assoc Am Physicians 1996, Mar;
108(2):155-64.
Yes, you read that correctly ... "Estrogen-mediated decrease in bone
formation." "What exactly is going on here?" you may be wondering.
Everyone "knows" that the one beneficial effect of estrogen is that it
prevents post menopausal bone loss. The fact is (as is clearly shown in
the scientific literature) that the truth is not only different than we are
led to believe, but the exact opposite of the propaganda we have been
fed. Here is another study which shows that estrogen is a causative
factor in osteoporosis:
Bauer, et al. Skin thickness, estrogen use and bone mass in older
women. Menopause 1(3), 131-136, 1991.
This study found that estrogen was associated both with thinning skin
and with decreased bone mass in older women.
Here is more evidence implicating estrogen as a destroyer of bone
mass:
Schlechte, et al. Bone density in amenorrheic women with and without
hyper prolactinemia. J Clin Endocrin & Metab 56,1120, 1983.
This study demonstrated a direct damaging affect of prolactin on bone.
And then this next study ...
Dannies. "Control of prolactin production by estrogen," Chapter 9 in
Biochemical Actions of Hormones I Academic Press, 1985.
... showed that estrogen is a primary stimulus to prolactin production.
Prolactin is a stress hormone produced by the pituitary which many
studies have shown causes osteoporosis. Furthermore, many studies
also show that estrogen promotes the secretion of prolactin. These
studies make it clear that something that increases something that
causes osteoporosis can not possibly prevent osteoporosis.
How can the pharmaceutical establishment get away with promoting
estrogen as protection against osteoporosis when research clearly
shows that the opposite is true? They have spent zillions of dollars in a
propaganda campaign that is entirely based on a half truth (evidence
which was subsequently proved to be false, showing a damaging, not a
protective role of estrogen -- but which was then quickly replaced by
another half truth on which they still base their dishonest claim).
The original half truth employed by the estrogen propaganda machine
was the discovery forty or more years ago that estrogen can cause a
positive calcium balance -- in other words, retaining some of a calcium
test dose, rather than dumping it all into the bowel and kidneys for
excretion. The estrogen promoters argued that this fact showed that the
retained calcium was being stored in bone. But very quickly endocrine
physiologists showed that estrogen causes the retention of calcium by
soft tissues, not by bone. The accumulation of calcium in soft tissues
is, of course, an accurate marker of stress and aging. (In other words
estrogen just makes you old -- as expressed in sclerotic calcium
deposits all through the body.)
This, of course, set the estrogen promoters scrambling to suppress the
nasty little details about calcium retention, and frantically look for
another excuse to peddle estrogen as a protector against osteoporosis.
They seized upon another discovery -- namely, that estrogen can reduce
the activity of osteoclasts, the cells that continuously break down bone
in their complimentary and cooperative role to osteoblasts, the cells
that then rebuild the bone.
Be certain you understand this so that you can explain it clearly to your
patients. There are two types of cells continuously at work in bones,
making bone a dynamic, continuously evolving living tissue. There is
one type of cell that continuously breaks down bone structure, while
the other type of cell continuously rebuilds it, and the two are in
constant balance. In reading the last two issues of this Letter you have
come to know that estrogen is a destructive stress hormone that
interferes with the normal function of many types of cells. One of the
cell types whose function estrogen particularly destroys is the
osteoclasts -- the cells that tear down bone. And, as it turns out,
estrogen is more destructive to the osteoclasts than it is to the
osteoblasts.
The estrogen peddlers seized on this fact and began to promote it as
proof that estrogen was good for the bones because it inhibited
osteoclastic activity. Of course it is never mentioned that estrogen does
nothing to help rebuild the bone. It merely slows down and destroys
the balance of the normal remolding process of bone.
But at any rate, the estrogen promoters now had their half truth on
which they could base their case for estrogen. Now that they could say
(with tongue in cheek) that estrogen "prevents bone loss," never again
was mentioned the original half truth about estrogen promoting a
positive calcium balance. Positive calcium balance had been the
essence of the first argument for using estrogen to prevent osteoporosis
-- but when it was recognized by everyone that calcium wasn't being
stored in the bones as a result of estrogen, it was convenient for the
estrogen industry to forget all about the positive calcium balance
produced by estrogen since it really meant that estrogen was causing
aging, tissue damage, and degeneration. The second half truth enabled
them to tidy up their fraudulent case for estrogen replacement therapy.
"Surely," I can hear you wondering, "There must have been some
evidence in support of estrogen rebuilding bone for the pharmaceutical
establishment to contrive such a huge campaign in support of the bone
protecting benefits of estrogen." No. Again, there is only scant
research showing that estrogen slows bone loss, and none that it
rebuilds bone. Furthermore, the studies purporting to show benefits
resulting from estrogen were done using the Dexa method of measuring
bone density. Here is an interesting study which shows the poor
validity of Dexa:
Schneider and Reiners. Dual-energy x-ray absorptiometry for bone
density can lead to false conclusions about bone mineral content,
because of alterations in tissue fat or water content. JAMA 277(1), 23,
1997.
This study showed that the influence of fat distribution on bone mass
measurements with DEXA can be of considerable magnitude and
ranges up to 10% error per two centimeters of fat. It also showed
tremendous variability in bone mass measurement due to changes in
fluid retention.
Now, ask yourself, what are the most immediate effects on a woman's
body of estrogen replacement therapy? There is an immediate and
steadily progressing increase in body fat, and, there is a tremendous
increase in fluid retention. As described in the study noted above, both
increased fat and fluid retention give a false increased bone density
reading using Dexa. So, after a woman has been on estrogen for six
months, she has gained five pounds of fat and five pounds of water.
She puts her now squishy body in front of the Dexa and, presto! -- her
bone density number is improved.
What we are saying is that it has never been demonstrated that estrogen
helps rebuild or remineralize bone. At best, it slows bone loss.
Furthermore, even the rate of slowing the bone loss is over- estimated
by bone scans because the increase in fat and particularly fluid
retention due to the estrogen gives a false increase in the density
measurement.
If falling estrogen at menopause does not cause osteoporosis, then what
does? There are some hormonal factors involved, and there are many
nutrition and other lifestyle factors involved. In the hormonal category
consider this study:
Johnston, et al. "Age-related bone loss," in osteoporosis II, Grune and
Stratton, NY, 1979, pp 91-100.
In this study it was found that progesterone, but not estrone, estradiol,
testosterone, or androstedione, was significantly lower in those losing
bone mass most rapidly.
Progesterone actually promotes bone rebuilding, rather than just
slowing its loss. One mechanism by which progesterone protects bones
is that it is an antagonist to catabolic stress hormones such as
glucocorticoids which destroy bone (as well as skin, brain, etc.) tissue,
and which increase with aging.
The other hormones supporting bone density maintenance in old age
are DHEA, testosterone, pregnenolone, and thyroid. Now, you may
still be wondering, "But if the drop in estrogen at menopause doesn't
cause osteoporosis, then why does it begin with the onset of
menopause?"
It doesn't. And that is the greatest lie of all. Bone density actually
begins decreasing during early adulthood and progresses steadily until a
woman reaches her mid 40's, when progesterone levels typically start to
drop, at which point the rate of mineral loss accelerates. Here are the
facts:
Between the ages of 21 and 40 there is a considerable increase in
women's estrogen production. However, bone loss has been shown to
actually begin around the age of 23, and progresses through the years
when estrogen levels are actually rising. In fact, most women lose two
thirds of the bone loss that they are ultimately going to lose in their life
before they even reach menopause. Do you begin to see how absurd it
is to blame menopause-related hormone changes for osteoporosis?
Re-read that last paragraph, and memorize it. You are going to recite it
over and over again with patient after patient for years and years until
the estrogen hoax is fully exposed. Each time a post-menopausal
patient comes to you explaining how she just had a bone scan which
showed, "the beginnings of osteoporosis," you must make her
understand that that loss of bone density has been going on since she
was 23 years old, and had nothing to do with low estrogen (and
probably much to do with too much estrogen and too little progesterone
throughout her 20's, 30's and 40's). If she shows osteoporosis today it is
because of lifestyle choices she made over a period of several decades
including: insufficient exercise, insufficient sunlight, insufficient trace
minerals, along with excess stress hormones such as glucocorticoids,
cathecolamines, and estrogen, whose excess is generally associated
with various metabolic imbalances.
Notice, I didn't say anything about a calcium deficiency. Here is
another critical piece of info. It has been clearly shown that many of
the aging, tissue damaging and degeneration effects caused by estrogen
are exacerbated by calcium, and opposed by magnesium. In this light it
is seen that excessive calcium supplementation actually potentiates the
damaging effect of estrogen - including the damaging effect of estrogen
on bone - while magnesium has a protective effect against excess
estrogen, including a protective effect against osteoporosis. The two
studies you want to check in support of this are:
Abraham and Grewal. A total dietary program emphasizing
magnesium instead of calcium. Effect on the mineral density of
calcanius bone in post menopausal women on hormonal therapy. J
Reprod Med 1990, May; 35(5):503-7.
Muneyyirci-Delale, et al. Serum ionized magnesium and calcium in
women after menopause: Inverse relation of estrogen with ionized
magnesium. Fertil Steril 1999, May; 71(5):869-72.
It is interesting to note that both men and women lose minerals from
their bones at a rate of about 1% per year. Men have lower estrogen in
youth than women do, and their bones are much heavier. During aging,
however, as their bones get thinner, men's estrogen levels (unlike
women's) keep rising. After about age 54 the average man actually has
higher estrogen than the average woman. Similarly, muscle loss occurs
at about the rate of one percent per year. Women's muscles, like their
bones, are normally smaller than men's during youth, and estrogen,
which inhibits muscular development, explains much of this difference.
With aging, as men's estrogen levels rise, they begin to lose their
muscular advantage over women.
Reiterating our comments from the last two issues of this Letter,
estrogen is a damaging stress hormone to both men and women.
Accelerating the loss of bone and muscle strength is just one of its
many devastating effects. As regards the proper treatment for your
patients with osteoporosis consider the following:
Hochberg. Preventing fractures in post-menopausal women with
osteoporosis. A review of recent controlled trials of anti-resorptive
agents. Drugs Aging 2000 Oct; 17(4):317-30.
This study was a review of all the recent work done on treatments for
post-menopausal osteoporosis and reached several conclusions,
including that, "there is insufficient published evidenced from
randomized controlled trials to convincingly support the anti-fracture
efficacy of ... agents ... including ... estrogen ... at this time."
Interestingly, this study did show clear objective evidence supporting
calcium plus vitamin D in reducing fractures.
In other words, your patients are not likely to benefit from either
estrogen replacement or any other form of medical intervention for
osteoporosis. The answer is certainly not in estrogen replacement,
nor in mega dose calcium supplementation. The
only adjunct you need to each patient's protocol is
the judicious use of progesterone or DHEA or pregnenolone or thyroid,
along with some extra vitamin D. We will give you protocol for the
proper use of these therapeutic agents in our next Letter. Meanwhile,
do everything you can to keep your patients off any form of estrogen.
ESTROGEN MAKES YOU FAT, DEPRESSED, AND OLD!
Do you have any patients who are worried about osteoporosis? Are
there any women under your care who are considering estrogen
replacement therapy as protection against osteoporosis? Then, here is
one important study you will want to look into.
Kassem M., et al. Potential mechanism of estrogen-mediated decrease
in bone formation. Proc Assoc Am Physicians 1996, Mar;
108(2):155-64.
Yes, you read that correctly ... "Estrogen-mediated decrease in bone
formation." "What exactly is going on here?" you may be wondering.
Everyone "knows" that the one beneficial effect of estrogen is that it
prevents post menopausal bone loss. The fact is (as is clearly shown in
the scientific literature) that the truth is not only different than we are
led to believe, but the exact opposite of the propaganda we have been
fed. Here is another study which shows that estrogen is a causative
factor in osteoporosis:
Bauer, et al. Skin thickness, estrogen use and bone mass in older
women. Menopause 1(3), 131-136, 1991.
This study found that estrogen was associated both with thinning skin
and with decreased bone mass in older women.
Here is more evidence implicating estrogen as a destroyer of bone
mass:
Schlechte, et al. Bone density in amenorrheic women with and without
hyper prolactinemia. J Clin Endocrin & Metab 56,1120, 1983.
This study demonstrated a direct damaging affect of prolactin on bone.
And then this next study ...
Dannies. "Control of prolactin production by estrogen," Chapter 9 in
Biochemical Actions of Hormones I Academic Press, 1985.
... showed that estrogen is a primary stimulus to prolactin production.
Prolactin is a stress hormone produced by the pituitary which many
studies have shown causes osteoporosis. Furthermore, many studies
also show that estrogen promotes the secretion of prolactin. These
studies make it clear that something that increases something that
causes osteoporosis can not possibly prevent osteoporosis.
How can the pharmaceutical establishment get away with promoting
estrogen as protection against osteoporosis when research clearly
shows that the opposite is true? They have spent zillions of dollars in a
propaganda campaign that is entirely based on a half truth (evidence
which was subsequently proved to be false, showing a damaging, not a
protective role of estrogen -- but which was then quickly replaced by
another half truth on which they still base their dishonest claim).
The original half truth employed by the estrogen propaganda machine
was the discovery forty or more years ago that estrogen can cause a
positive calcium balance -- in other words, retaining some of a calcium
test dose, rather than dumping it all into the bowel and kidneys for
excretion. The estrogen promoters argued that this fact showed that the
retained calcium was being stored in bone. But very quickly endocrine
physiologists showed that estrogen causes the retention of calcium by
soft tissues, not by bone. The accumulation of calcium in soft tissues
is, of course, an accurate marker of stress and aging. (In other words
estrogen just makes you old -- as expressed in sclerotic calcium
deposits all through the body.)
This, of course, set the estrogen promoters scrambling to suppress the
nasty little details about calcium retention, and frantically look for
another excuse to peddle estrogen as a protector against osteoporosis.
They seized upon another discovery -- namely, that estrogen can reduce
the activity of osteoclasts, the cells that continuously break down bone
in their complimentary and cooperative role to osteoblasts, the cells
that then rebuild the bone.
Be certain you understand this so that you can explain it clearly to your
patients. There are two types of cells continuously at work in bones,
making bone a dynamic, continuously evolving living tissue. There is
one type of cell that continuously breaks down bone structure, while
the other type of cell continuously rebuilds it, and the two are in
constant balance. In reading the last two issues of this Letter you have
come to know that estrogen is a destructive stress hormone that
interferes with the normal function of many types of cells. One of the
cell types whose function estrogen particularly destroys is the
osteoclasts -- the cells that tear down bone. And, as it turns out,
estrogen is more destructive to the osteoclasts than it is to the
osteoblasts.
The estrogen peddlers seized on this fact and began to promote it as
proof that estrogen was good for the bones because it inhibited
osteoclastic activity. Of course it is never mentioned that estrogen does
nothing to help rebuild the bone. It merely slows down and destroys
the balance of the normal remolding process of bone.
But at any rate, the estrogen promoters now had their half truth on
which they could base their case for estrogen. Now that they could say
(with tongue in cheek) that estrogen "prevents bone loss," never again
was mentioned the original half truth about estrogen promoting a
positive calcium balance. Positive calcium balance had been the
essence of the first argument for using estrogen to prevent osteoporosis
-- but when it was recognized by everyone that calcium wasn't being
stored in the bones as a result of estrogen, it was convenient for the
estrogen industry to forget all about the positive calcium balance
produced by estrogen since it really meant that estrogen was causing
aging, tissue damage, and degeneration. The second half truth enabled
them to tidy up their fraudulent case for estrogen replacement therapy.
"Surely," I can hear you wondering, "There must have been some
evidence in support of estrogen rebuilding bone for the pharmaceutical
establishment to contrive such a huge campaign in support of the bone
protecting benefits of estrogen." No. Again, there is only scant
research showing that estrogen slows bone loss, and none that it
rebuilds bone. Furthermore, the studies purporting to show benefits
resulting from estrogen were done using the Dexa method of measuring
bone density. Here is an interesting study which shows the poor
validity of Dexa:
Schneider and Reiners. Dual-energy x-ray absorptiometry for bone
density can lead to false conclusions about bone mineral content,
because of alterations in tissue fat or water content. JAMA 277(1), 23,
1997.
This study showed that the influence of fat distribution on bone mass
measurements with DEXA can be of considerable magnitude and
ranges up to 10% error per two centimeters of fat. It also showed
tremendous variability in bone mass measurement due to changes in
fluid retention.
Now, ask yourself, what are the most immediate effects on a woman's
body of estrogen replacement therapy? There is an immediate and
steadily progressing increase in body fat, and, there is a tremendous
increase in fluid retention. As described in the study noted above, both
increased fat and fluid retention give a false increased bone density
reading using Dexa. So, after a woman has been on estrogen for six
months, she has gained five pounds of fat and five pounds of water.
She puts her now squishy body in front of the Dexa and, presto! -- her
bone density number is improved.
What we are saying is that it has never been demonstrated that estrogen
helps rebuild or remineralize bone. At best, it slows bone loss.
Furthermore, even the rate of slowing the bone loss is over- estimated
by bone scans because the increase in fat and particularly fluid
retention due to the estrogen gives a false increase in the density
measurement.
If falling estrogen at menopause does not cause osteoporosis, then what
does? There are some hormonal factors involved, and there are many
nutrition and other lifestyle factors involved. In the hormonal category
consider this study:
Johnston, et al. "Age-related bone loss," in osteoporosis II, Grune and
Stratton, NY, 1979, pp 91-100.
In this study it was found that progesterone, but not estrone, estradiol,
testosterone, or androstedione, was significantly lower in those losing
bone mass most rapidly.
Progesterone actually promotes bone rebuilding, rather than just
slowing its loss. One mechanism by which progesterone protects bones
is that it is an antagonist to catabolic stress hormones such as
glucocorticoids which destroy bone (as well as skin, brain, etc.) tissue,
and which increase with aging.
The other hormones supporting bone density maintenance in old age
are DHEA, testosterone, pregnenolone, and thyroid. Now, you may
still be wondering, "But if the drop in estrogen at menopause doesn't
cause osteoporosis, then why does it begin with the onset of
menopause?"
It doesn't. And that is the greatest lie of all. Bone density actually
begins decreasing during early adulthood and progresses steadily until a
woman reaches her mid 40's, when progesterone levels typically start to
drop, at which point the rate of mineral loss accelerates. Here are the
facts:
Between the ages of 21 and 40 there is a considerable increase in
women's estrogen production. However, bone loss has been shown to
actually begin around the age of 23, and progresses through the years
when estrogen levels are actually rising. In fact, most women lose two
thirds of the bone loss that they are ultimately going to lose in their life
before they even reach menopause. Do you begin to see how absurd it
is to blame menopause-related hormone changes for osteoporosis?
Re-read that last paragraph, and memorize it. You are going to recite it
over and over again with patient after patient for years and years until
the estrogen hoax is fully exposed. Each time a post-menopausal
patient comes to you explaining how she just had a bone scan which
showed, "the beginnings of osteoporosis," you must make her
understand that that loss of bone density has been going on since she
was 23 years old, and had nothing to do with low estrogen (and
probably much to do with too much estrogen and too little progesterone
throughout her 20's, 30's and 40's). If she shows osteoporosis today it is
because of lifestyle choices she made over a period of several decades
including: insufficient exercise, insufficient sunlight, insufficient trace
minerals, along with excess stress hormones such as glucocorticoids,
cathecolamines, and estrogen, whose excess is generally associated
with various metabolic imbalances.
Notice, I didn't say anything about a calcium deficiency. Here is
another critical piece of info. It has been clearly shown that many of
the aging, tissue damaging and degeneration effects caused by estrogen
are exacerbated by calcium, and opposed by magnesium. In this light it
is seen that excessive calcium supplementation actually potentiates the
damaging effect of estrogen - including the damaging effect of estrogen
on bone - while magnesium has a protective effect against excess
estrogen, including a protective effect against osteoporosis. The two
studies you want to check in support of this are:
Abraham and Grewal. A total dietary program emphasizing
magnesium instead of calcium. Effect on the mineral density of
calcanius bone in post menopausal women on hormonal therapy. J
Reprod Med 1990, May; 35(5):503-7.
Muneyyirci-Delale, et al. Serum ionized magnesium and calcium in
women after menopause: Inverse relation of estrogen with ionized
magnesium. Fertil Steril 1999, May; 71(5):869-72.
It is interesting to note that both men and women lose minerals from
their bones at a rate of about 1% per year. Men have lower estrogen in
youth than women do, and their bones are much heavier. During aging,
however, as their bones get thinner, men's estrogen levels (unlike
women's) keep rising. After about age 54 the average man actually has
higher estrogen than the average woman. Similarly, muscle loss occurs
at about the rate of one percent per year. Women's muscles, like their
bones, are normally smaller than men's during youth, and estrogen,
which inhibits muscular development, explains much of this difference.
With aging, as men's estrogen levels rise, they begin to lose their
muscular advantage over women.
Reiterating our comments from the last two issues of this Letter,
estrogen is a damaging stress hormone to both men and women.
Accelerating the loss of bone and muscle strength is just one of its
many devastating effects. As regards the proper treatment for your
patients with osteoporosis consider the following:
Hochberg. Preventing fractures in post-menopausal women with
osteoporosis. A review of recent controlled trials of anti-resorptive
agents. Drugs Aging 2000 Oct; 17(4):317-30.
This study was a review of all the recent work done on treatments for
post-menopausal osteoporosis and reached several conclusions,
including that, "there is insufficient published evidenced from
randomized controlled trials to convincingly support the anti-fracture
efficacy of ... agents ... including ... estrogen ... at this time."
Interestingly, this study did show clear objective evidence supporting
calcium plus vitamin D in reducing fractures.
In other words, your patients are not likely to benefit from either
estrogen replacement or any other form of medical intervention for
osteoporosis. The answer is certainly not in estrogen replacement,
nor in mega dose calcium supplementation. The
only adjunct you need to each patient's protocol is
the judicious use of progesterone or DHEA or pregnenolone or thyroid,
along with some extra vitamin D. We will give you protocol for the
proper use of these therapeutic agents in our next Letter. Meanwhile,
do everything you can to keep your patients off any form of estrogen.
ESTROGEN MAKES YOU FAT, DEPRESSED, AND OLD!
