SCIENTIFIC AMERICAN ARTICLE
CRITICAL OF MEDIA CONFUSION
RESEARCH STATES: "I think that it borders
on a tragedy that Premarin and Provera were chosen as the only HRT treatments." {AS JK STATED ABOVE IT IS THE
PROSTOGLANDIN in Provera & Premarin that caused the serious side effects Another researcher finds that hat
Provera--and no other progestin--blocks the mechanisms that allow estrogen to fight the brain's immune response to Alzheimer's.
This immune response wears away at brain cells and causes them to leak neurotransmitters such as glutamate, which
overloads and kills neurons. "It's basically as if someone were to open your mouth and shove down gallons" of soft drink,
Brinton explains. "It's caustic, and you can't metabolize it enough."
After the usual journalistic waffling, the Scientific
American articles gets to the issue:
For many scientists, a critical question yet remains:
To what extent do the results of the initiative study apply to other forms of hormone replacement? "We cannot be sure whether
other hormone combinations will have the same effects," Rossouw cautions, "but in my opinion we should assume they do until
proven otherwise." But neuroendocrinologist Bruce S. McEwen of the Rockefeller University is unequivocally critical of the
study: "I think that it borders on a tragedy that Premarin and Provera were chosen as the only HRT treatments."
A growing number of researchers believe that Provera is
a poor substitute for progesterone. For example, medroxyprogesterone will bind in the breasts to progesterone receptors, which
causes breast cells to divide after puberty and during the menstrual cycle, and also to glucocorticoid receptors, which causes
cell division during pregnancy. This double-barreled assault on breast cells, explains C. Dominique Toran-Allerand, a developmental
neurobiologist at Columbia University, probably led to the high rates of breast cancer in the study. "With Provera you are
activating two receptors involved with cell division in the breast," she says, "and that's the culprit, not estrogen."
Hormone Hysteria?
In addition, recent research shows
that Provera interferes with estrogen's ability to prevent memory loss and dementia. "Estrogen is able to protect neurons
against toxic assaults that are associated with Alzheimer's disease," notes Roberta Diaz Brinton, a neuroscientist at the
University of Southern California. Using in vitro studies of several types of progestin, she found that Provera--and
no other progestin--blocks the mechanisms that allow estrogen to fight the brain's immune response to Alzheimer's.
This immune response wears away at brain cells and causes them to leak neurotransmitters such as glutamate, which overloads
and kills neurons. "It's basically as if someone were to open your mouth and shove down gallons" of soft drink, Brinton explains.
"It's caustic, and you can't metabolize it enough."
Scientific News
In this section, The North American Menopause Society features the latest
research news, along with expert commentary that places the news into perspective.
The North American Menopause Society requests commentary from experts in the clinical
practice and research communities on subjects of interest to its constituents. Unless
specifically stated otherwise, the comments contained on this Web site are opinions or information of the authors and not
necessarily the opinions or information of The North American Menopause Society, its officers, agents, or trustees.
Past estrogen use decreases Alzheimers disease
in older women
December 2002 report of
NAMS
Zandi PP, Carlson MC, Plassman BL, et al,
for the Cache County Memory Study Investigators. Hormone replacement therapy and incidence of Alzheimer disease in older women:
the Cache County study. JAMA 2002;288:2123-2129.
Use of hormone therapy is associated with
a reduced risk of Alzheimers disease (AD), especially use for longer than 10 years, according to results from this prospective
observation al study conducted in Cache County (Logan, Utah). A total of 1,889 women (mean age, 74.5 years) were enrolled.
A similarly aged group of men (n = 1,357) served as controls. History of hormone therapy use (either estrogen alone or estrogen
plus a progestogen), as well as intakes of calcium and multivitamin supplements, were assessed at baseline. After 3 years
of follow-up, 88 women (4.7%) and 35 men (2.6%) had developed AD. Women aged 80 and older had more than twice the rate of
AD as men of that age (hazard ratio [HR], 2.11; 95% CI, 1.22-3.86). Overall, hormone therapy significantly reduced the risk
of AD by 41% compared with nonusers (95% CI, 0.36-0.96). Hormone use for at least 10 years resulted in a 69% reduction in
risk (95% CI, 0.17-0.86), which was statistically the same as the risk for matched males. When the results were assessed by
current and former hormone use, current use (72% unopposed estrogen) was not associated with decreased AD risk unless the
duration of treatment exceeded 10 years. For former users, 3 or more years of use significantly reduced the AD risk, with
more than 10 years use reducing the risk by 83% (95% CI, 0.01-0.80). No similar effects were seen with either calcium or multivitamin
use.
Hormone therapys effect on atherosclerosis associated with presence of apolipeprotein
A gene.November 2002 report of NAMS
Lehtimaki T, Dastidar P, Jokela H, et al.
Effects of long-term hormone replacement therapy on atherosclerosis progression in postmenopausal women relates to functional
apolipoprotein E genotype. J Clin Endocrinol Metab 2002;87:4147-4153.
Postmenopausal hormone therapy appears to
have a beneficial effect on atherosclerosis progression in women who do not have the apolipoprotein E (apoE) genotype, based
on results from this prospective, cohort study conducted in Finland. The study enrolled 141 postmenopausal women aged 45 to
71 with no clinically evident cardiovascular disease or hypertension. Women were classified into three groups: estrogen plus
progestogen, estrogen alone, and no hormone use (control). Estradiol valerate (2 mg/day) was used, with either levonorgestrel
(0.25 mg/day) or medroxyprogesterone acetate (10 mg/day) administered cyclically to women with a uterus. In all, 93 women
completed the 5-year follow-up study. Sonography was used to determine atherosclerosis severity. In apoE-negative women, hormone
therapy significantly slowed the progression of atherosclerosis when compared with the control group. In apoE-positive women,
no significant between-group differences were seen.
In the commentary it was pointed out that
compared with apoE-positive women. Since
apoE genetic polymorphism may affect plasma lipids and the severity of atherogenesis, it is possible that the hormone-related
adverse effects in the WHI and HERS studies manifested themselves specifically in apoE-positive women, therefore reflecting
a biased study population.
NAMS, North American Menopause Society.
In Patient Care June 15, 1999,
p. 144:
at patientcareonline.com
"Numerous studies have demonstrated an inverse relationship
between estrogen replacement therapy and the relative risk of developing A.D. In a recent meta-analysis of postmenopausal
etrogen therapy and risk of dementia, cumulative data from 10 studies suggested that there was a 29% risk reduction with estrogen
replacement. [Yaffe K., Sawaya G, Lieberg I, et a. Estrogen therapy in postmenoopausal women, effects in cognitive
function and dementia. l JAMA 1998; 279:688-695.]
Kristine Yaffe, MD; George Sawaya, MD; Ivan Lieberburg, PhD, MD; Deborah Grady,
MD, MPH
JAMA. 1998;279:688-695.
Context.— Several studies have suggested that estrogen replacement therapy in postmenopausal women improves cognition,
prevents development of dementia, and improves the severity of dementia, while other studies have not found
a benefit of estrogen use.
Objective.— To determine whether postmenopausal estrogen therapy improves cognition, prevents development of dementia,
or improves dementia severity.
Data Sources.— We performed a literature search of studies published from January 1966 through June 1997, using MEDLINE,
manually searched bibliographies of articles identified, and consulted experts.
Study Selection.— Studies that evaluated biological mechanisms of estrogen's effect on the central nervous system and studies
that addressed the effect of estrogen on cognitive function or on dementia.
Data Extraction.— We reviewed studies for methods, sources of bias, and outcomes and performed a meta-analysis of the 10
studies of postmenopausal estrogen use and risk of dementia using standard meta-analytic methods.
Data Synthesis.— Biochemical and neurophysiologic studies suggest several mechanisms by which estrogen may affect cognition:
promotion of cholinergic and serotonergic activity in specific brain regions, maintenance of neural circuitry,
favorable lipoprotein alterations, and prevention of cerebral ischemia. Five observational studies and
8 trials have addressed the effect of estrogen on cognitive function in nondemented postmenopausal women. Cognition
seems to improve in perimenopausal women, possibly because menopausal symptoms improve, but there is no clear
benefit in asymptomatic women. Ten observational studies have measured the effect of postmenopausal
estrogen use on risk of developing dementia. Meta-analysis of these studies suggests a 29% decreased risk
of developing dementia among estrogen users, but the findings of the studies are heterogeneous. Four trials
of estrogen therapy in women with Alzheimer disease have been conducted and have had primarily positive
results, but most have been small, of short duration, nonrandomized, and uncontrolled.
Conclusions.— There are plausible biological mechanisms by which estrogen might lead to improved cognition, reduced
risk for dementia, or improvement in the severity of dementia. Studies conducted in women, however, have
substantial methodologic problems and have produced conflicting results. Large placebo-controlled trials
are required to address estrogen's role in prevention and treatment of Alzheimer disease and other dementias. Given
the known risks of estrogen therapy, we do not recommend estrogen for the prevention or treatment of Alzheimer
disease or other dementias until adequate trials have been completed.
From the Departments of Psychiatry
(Dr Yaffe), Medicine (Drs Lieberburg and Grady), Epidemiology and Biostatistics (Drs Sawaya and Grady), and Obstetrics and
Gynecology (Dr Sawaya), University of California, San Francisco, and Athena Neurosciences, South San Francisco, Calif (Dr
Lieberburg).
Endocrinology, doi:10.1210/en.2006-0495, Endocrinology Vol 147, No. 11 5303-5313, 2006 copyright by the Endocrine
Society
Dose and Temporal Pattern of Estrogen Exposure Determines Neuroprotective Outcome
in Hippocampal Neurons: Therapeutic Implications
To address controversies
of estrogen therapy, in vitro models of perimenopause and prevention vs. treatment modes of 17ß-estradiol
(E2) exposure were developed and used to assess the neuroprotective efficacy of E2
against ß-amyloid-1–42 (Aß1–42)-induced neurodegeneration in rat primary hippocampal neurons.
Low E2 (10 ng/ml) exposure exerted neuroprotection in each of the perimenopausal temporal
patterns, acute, continuous, and intermittent. In contrast, high E2 (200 ng/ml) was ineffective at inducing
neuroprotection regardless of temporal pattern of exposure. Although high E2 alone was not
toxic, neurons treated with high-dose E2 resulted in greater Aß1–42-induced neurodegeneration.
In prevention vs. treatment simulations, E2 was most effective when present before and
during Aß1–42 insult. In contrast, E2 treatment after Aß1–42 exposure
was ineffective in reversing Aß-induced degeneration, and exacerbated Aß1–42-induced cell
death when administered after Aß1–42 insult. We sought to determine the mechanism by
which high E2 exacerbated Aß1–42-induced neurodegeneration by investigating the impact
of low vs. high E2 on Aß1–42-induced dysregulation of calcium homeostasis.
Results of these analyses indicated that low E2 significantly prevented Aß1–42-induced
rise in intracellular calcium, whereas high E2 significantly increased intracellular calcium
and did not prevent Aß1–42-induced calcium dysregulation. Therapeutic benefit resulted only from
low-dose E2 exposure before, but not after, Aß1–42-induced neurodegeneration. These data are relevant to impact of perimenopausal E2
exposure on protection against neurodegenerative insults and the use of estrogen therapy to prevent vs.
treat Alzheimer’s disease. Furthermore, these data are consistent with a healthy cell bias of
estrogen benefit.
Unfortunately the literature does not present easy clear answers. For examples some studies found that women with dementia did worse with HRT, while those without benefited. Other studies using the same formulation as the combination with medroxyprogesterone
(Provera & Premarin) faired worse, while those using a different formulation benefited.
The Scientific American study zeroes in on this error—while most others mist this important distinction--jk.