No Increase in Breast Cancer Risk in BRCA1 Carriers on HT

Can you tell I'm catching up on my journal reading? I've got several patients with the "breast cancer gene" or have a high risk for it (2 or more relatives with breast cancer), so this latest data showing no increased risk of breast cancer in BRCA1 carriers on Hormone Therapy is GOOD NEWS.

Also from North American Menopause Society.


Eisen A, Lubinski J, Gronwald J, et al, and the Hereditary
Breast Cancer Clinical Study Group. Hormone therapy and
the risk of breast cancer in BRCA1 mutation carriers. J Natl
Cancer Inst 2008;100:1361-1367. Level of evidence: II-2.

Using hormone therapy (HT) is not associated
with an increased risk for breast cancer in
postmenopausal women with a BRCA1 mutation,
this study suggests. In fact, researchers found a
decreased risk with HT use among this small
cohort with the mutation. Participants were
drawn from the larger cohort of the Hereditary
Breast Cancer Clinical Study, a prospective study
to evaluate nongenetic modifiers of cancer risk in
BRCA1 and BRCA2 mutation carriers. Cases
were diagnosed with invasive breast cancer after
reaching menopause. Controls had experienced
menopause and did not have breast cancer. Cases
and controls were matched for year of birth, age
at menopause, and type of menopause; 236
matched sets with the BRCA1 mutation were
generated. A questionnaire administered to each
woman garnered information on medical and
reproductive history and past and current HT use
(average age, 58.2 y; range, 32-85 y). The study
analyzed whether HT use after surgical or natural
menopause is associated with subsequent risk for
breast cancer in women with BRCA1 mutation.

More controls than cases had used HT (29% vs.
20%); the average duration was 3.7 years for
controls and 4.0 years for cases. Compared with
never use, women who had used HT had a
lower risk of breast cancer (odds ratio [OR],
0.58; 95% confidence interval [CI], 0.35-0.96;
P = 0.03). There was no modification of the OR
for duration of use, and the association was
similar for current and past users. Results were
also similar for women who had undergone
surgical as opposed to natural menopause. For
women who used estrogen only, there was an
inverse association with breast cancer risk (OR,
0.51; 95% CI, 0.27-0.98; P = 0.04). Results
were similar with combined estrogen and
progestogen (OR, 0.66; 95% CI, 0.34-1.27; P =
0.21). Surprisingly, HT use was reported for
12% of patients with estrogen-receptor positive
(ER+) tumors but only 23% of women with
estrogen-receptor negative (ER-) tumors. ER
status was available in 44% of cases.

Comment. There is a growing body of
evidence suggesting that the premature loss of
ovarian function caused by bilateral
oophorectomy performed before natural
menopause is associated with several negative
outcomes including an increased risk of
premature death, cardiovascular disease,
cognitive impairment or dementia,
parkinsonism, osteoporosis and bone fractures,
decline in psychological well-being, and
decline in sexual function. HT use may prevent
some but not all of these negative outcomes.
After receiving a positive genetic test result,
68% of women in the United States and 54% of
women in Canada with a BRCA1 or BRCA2
mutation undergo oophorectomy.1 The surgery
has been associated with risk reductions of 50%
or more for breast cancer and of 80% for
ovarian or peritoneal cancer. Some women
might be reluctant to undergo premenopausal
oophorectomy because of the adverse effects of
surgical menopause and are concerned that if
HT were taken to alleviate symptoms, then
their risk of breast cancer might rise.

The majority of BRCA1-associated breast
cancers in the current study (68%) were ER-. If
the adverse effect of HT were limited to ER+
cancers, then we would not expect to see an
acute effect of similar magnitude in mutation
carriers. It may be also that HT use protects
against the early stages of cancer development,
which results in a decline in the incidence of
breast cancer later in life. Published studies show
that in the noncarrier population, the increased
breast cancer risk associated with HT appears to
be stronger for ER+ cancers than ER-.2 If HT
were a risk factor for ER+ breast cancer in
BRCA1 mutation carriers as well, one would
expect that a greater proportion of women with
ER+ breast cancers had used HT than women
with ER- breast cancers. This was not seen, and
these findings suggest that the use of menopausal
HT is not associated with an increase in the risk
of breast cancer among women with a BRCA1
mutation, but the numbers of cases known to be
ER+ are too small to draw a definite conclusion.

It may be also that HT use protects against the
early stages of cancer development, which results
in a decline in the incidence of breast cancer later
in life. If HT promotes the growth of existing
ER+ breast cancers but protects against the early
stages of development of new breast cancers
(ER+ and ER-), then we would expect HT to
protect against breast cancer in BRCA1 mutation
carriers (who are mostly ER-).

Editorial writers have argued that the results
presented by Eisen et al regarding HT use in
postmenopausal BRCA1 mutation carriers
provide some evidence for safety but are
insufficient to reliably inform routine clinical
practice.3 Decision making regarding menopausal
HT in women at increased risk of breast cancer is
complex. The current HT package insert
identifies climacteric symptoms as the main
indication of HT use at the lowest dose and
shortest duration consistent with therapeutic
goals. We do not know how many post-
menopausal women with BRCA1 mutations have
limiting symptoms of hot flashes, vaginal/vulvar
problems, and/or sexual dysfunction that
cannot be addressed using nonhormonal
approaches, nor do we know how to define the
term “limiting” as a threshold for HT use.

Eisen et al say that it is not possible to
recommend an optimal duration of HT, but some
experts (eg, the National Comprehensive
Cancer Network) have suggested that “short-
term hormone replacement therapy” be
prescribed until the time of natural menopause
(ie, age 50-54).4 After that age, consideration
should be given to the use of tamoxifen for
breast cancer risk reduction. In mathematical
models, prophylactic oophorectomy lengthens
life expectancy in women with BRCA1/2
mutations, irrespective of whether HT is used
after oophorectomy. Women with BRCA1/2
mutations who undergo prophylactic
oophorectomy after completion of childbearing
should decide about short-term HT based
largely on quality-of-life issues rather than life
expectancy, and consider discontinuing
treatment at the time of expected natural
menopause, approximately age 51.

Victor G. Vogel, MD, MHS
Associate Investigator
Magee-Womens Research Institute
Professor, Medicine and Epidemiology
University of Pittsburgh
Co-Director, University of Pittsburgh Cancer
Institute Biochemoprevention Program
Director, UPCI/Magee-Womens Hospital Breast
Cancer Prevention Program

References
1. Metcalfe KA, Birenbaum-Carmeli D, Lubinski J, et al.
International variation in rates of uptake of preventive
options in BRCA1 and BRCA2 mutation carriers. Int J
Cancer 2008;122:2017-2022.
2. Ravdin PM, Cronin KA, Howlader N, et al. The
decrease in breast-cancer incidence in 2003 in the
United States. N Engl J Med 2007;356:1670-1674.
3. Chlebowski RT, Prentice RL. Menopausal hormone
therapy in BRCA1 mutation carriers: uncertainty and
caution. J Natl Cancer Inst 2008;100:1341-1343.
4. National Comprehensive Cancer Network. NCCN
Clinical Practice Guidelines in Oncology. Genetic/
Familial High-Risk Assessment: Breast and Ovarian.
Available at http://www.nccn.org/professionals/
physician_gls/PDF/genetics_screening.pdf. Accessed
December 10, 2008.

Hormone Therapy Lowers Colon Cancer 25-36%

Here's another post from North American Menopause Society. Seems cyclic progesterone was associated with the greatest risk reduction of colon cancer. Check it out.

Does hormone therapy decrease colorectal cancer risk?

Johnson JR, Lacey JV Jr, Lazovich D, et al. Menopausal
hormone therapy and risk of colorectal cancer. Cancer
Epidemiol Biomarkers Prev 2009;18:196-203.

We evaluated colorectal cancer risk associated
with the duration and recency of specific
menopausal hormone therapy formulations (ie,
unopposed estrogen versus estrogen plus
progestin) and regimens (ie, sequential versus
continuous estrogen plus progestin use) among
56,733 postmenopausal women participating in
the Breast Cancer Detection Demonstration
Project follow-up study. Hormone therapy use
and other risk factors were ascertained through
telephone interviews and mailed questionnaires
from 1979 to 1998. The final cancer group
included 960 women who were identified from
self-report, medical records, state registry data,
and the National Death Index. Poisson regression
was used to generate multivariable rate ratios
(RR) and 95% confidence intervals (95% CI).
We observed a decreased risk of colorectal
cancer among ever users of unopposed estrogen
therapy (RR, 0.83; 95% CI, 0.70-0.99). Among
estrogen users, the largest reduced risk was
observed for current users (RR, 0.75; 95% CI,
0.54-1.05) and users of ≥ten years duration
(RR, 0.74; 95% CI, 0.56-0.96). We found a
reduced risk among users of estrogen plus
progestin therapy (RR, 0.78; 95% CI, 0.60-
1.02), with sequential regimen users (progestin
<15 days per cycle) having the largest risk
reduction (RR, 0.64; 95% CI, 0.43-0.95). Past
users of ≥5 years ago (RR, 0.55; 95% CI, 0.32-
0.98) had the largest risk reduction. In this
study, estrogen plus progestin use, especially
sequential regimen use, was associated with the
largest overall reduction of colorectal cancer
risk.

Comment. This is a retrospective study, the
stated purpose of which was to identify
separate risk estimates for colon cancer
according to menopausal hormone form-
ulations. A paper published 9 years earlier1
from the same database found a suggested
inverse relationship between the use of HT and
colon cancer. The current paper analyzed
postmenopausal women divided into groups of
never users, those who had ever used estrogen,
and those who had ever used estrogen plus
progestogen (EPT), and then further divided
them by sequential hormone use and length of
time exposed to HT. What the current authors
found was that those who had ever used
unopposed estrogen had a decreased risk of
colon cancer. Those who had used sequential
EPT had the largest risk reduction. What does
this information add to our knowledge of this
topic?

Estrogen receptors have been detected on colonic
cells, with estrogen-receptor β being over-
expressed in healthy colon cells and reduced in
colon cancer cells. This overexpression, coupled
with negligible expression of estrogen-receptor α,
is thought to provide protection by HT against
colon cancer. What is also known is that
prescribing patterns for HT vary among race,
with African-American, Asian, and Latina
women receiving less treatment than Caucasian
women. An evaluation of how many women
were represented in each group rather than a
designation of “nonwhite” and a designation of
“person-years” only would have been
informative. It would also have been beneficial if
the groups had been matched by age, ethnicity,
and HT use (perhaps this is a paper that will be
published later).

African-American women have the highest risk
for colon cancer, higher even than white males;
and colon cancer in these women is often
detected at a more advanced stage. If HT really
does reduce the risk of colon cancer, all women
should have a discussion with their healthcare
provider about the potential benefits of HT for
them. A prospective study of matched groups of
women would be very informative regarding risk
reduction across ethnic groups in which there is a
dearth of comparative information available.
Women who use HT are more likely to have
mammograms, as well as Pap smears and
colonoscopies. Colonoscopy, however, is still at
the bottom of the list even for women who
regularly undergo other types of health screening.
It would be helpful if healthcare providers
encouraged women to have a colonoscopy. It has
been shown that if a healthcare provider strongly
recommends a test, a patient will often agree.

As March is National Colon Cancer Awareness
Month, this might be a good time to consider a
large-scale prospective randomized trial of HT
use with timed colon cancer screening across
ethnic groups by those in this field.
Michelle Inkster, MD, PhD
Department of Gastroenterology and Hepatology
Cleveland Clinic
Cleveland, OH

Reference:
1. Troisi R, Schairer C, Chow WH, et al. A prospective
study of menopausal hormones and risk of colorectal
cancer (United States). Cancer Causes Control 1997;

Your Bones: Role of Bone Turnover Markers

Here's a post from the latest North American Menopause Society's First to Know site. Bruce Ettinger is an osteoporosis expert. See what you think of his comments about this recent article. -- SG

BTMs to predict BMD response

Burnett-Bowie SA, Saag K, Sebba A, et al. Prediction of

changes in bone mineral density in postmenopausal

women treated with once-weekly bisphosphonates. 

J Clin Endocrinol Metab 2009 Jan 13 [Epub ahead of

print] Level of evidence: II-2.

 

Abstract copyright © 2009 The Endocrine Society. All

rights reserved. Used with permission.

 

BACKGROUND: In clinical practice, bone

mineral density (BMD) determined by DXA is

used to monitor response to osteoporosis

therapy. However, 1 to 2 years are usually

required to assess patients’ BMD responses.

The possibility of earlier indicators of a

response or non-response to treatment, such as

changes in bone turnover markers (BTMs), is

of interest to physicians and patients.

METHODS: In this post-hoc analysis of

women treated with once-weekly bis-

phosphonates, we examined the association of

tertile percent change from baseline in BTMs at

3 or 6 months, and association of several

baseline clinical characteristics, with 24-month

percent change from baseline in BMD, and

with percentage of patients showing BMD non-

response (defined as BMD loss at 2 or more of

4 sites) at 24 months. Multivariable analysis

was performed to determine which factors were

associated with BMD non-response.

RESULTS: Patients in the tertile with the

greatest decrease in each of the BTMs had the

greatest mean increase in BMD and the lowest

percentage of BMD nonresponders at 24

months. Several characteristics were

independently associated with BMD non-

response including smaller 3-month reductions from baseline in CTX, bone ALP, and PINP,

younger age of menopause, a family history of

osteoporosis, and higher baseline trochanteric

BMD. Baseline BTMs were not predictive of 24-

month BMD response to therapy. The strongest

associations were for changes in BTMs with

treatment. CONCLUSION: In groups of patients,

short term changes in markers of bone turnover

appear to be predictors of longer term BMD

response and non-response to bisphosphonate

therapy.

 

Comment. It has been over 15 years that BTMs

have been commercially available—yet few

practitioners ever use these tests in management

of osteoporosis. There was high hope that BTMs

would be useful for individual patients in several

ways including: 1) determining fracture risk and

need for treatment; 2) determining what kind of

drug to use; and 3) encouraging adherence and

persistence with therapy. 

 

This report adds to our general skepticism about

application of BTMs to individual patients. Even

using group data (with more power to find

associations), the authors failed to find that

baseline BTM values predicted response to

bisphosphonate (BP) treatment among compliant

users after 2 years. Furthermore, change between

baseline and 3-6 month BTM values showed only

weak associations with 2-year bone density

changes.

 

Typically, studies of BMD in clinical trials of BP

indicate a 90% response rate; in this paper,

alendronate users had an 88% BMD response

rate. Thus, the number of poor responders that

could ideally be found by a perfect BTM test

 

would be about 1 in 10. But, as the current article

shows, BTM tests have poor specificity and

sensitivity when applied to patients starting BPs.

This is not new. Delmas et al,1 using NTx, found

that about one third of patients starting on BP did

not decrease NTx the expected 30%—a lot of

false positives.

 

BTMs have been useful in research, but for

several reasons are not worth the trouble in

practice. First, the cost: in the range of $140 to

$150 per test (double this when getting baseline

and 3-6 month follow-up). Second, the

inconvenience for patients: requiring morning

12-hour fasting blood sampling. Third, the low

predictive value: in this paper, the correlation

coefficient between BTM and BMD was only 

-0.25, meaning that only 6% of the variance in

the BMD increase could be predicted from the

BTM decrease. Finally, investigators who have

examined feedback of BTM results on patients’

drug persistence have found no difference

between giving BTM results and simply

contacting and supporting those patients newly

starting.1

 

It is no wonder that NAMS and other expert

societies have not recommended to clinicians

that they use BTMs to make early treatment

decisions in individual patients.

 

Bruce Ettinger, MD

Clinical Professor of Medicine and Radiology

University of California, San Francisco

San Francisco, CA

Certified NAMS Menopause Practitioner

 

Reference:

Delmas PD, Vrijens B, Eastell R, et al. Effect of

monitoring bone turnover markers on persistence with

risedronate treatment of postmenopausal osteoporosis. 

J Clin Endocrinol 2007;92:1296-1304. 

My Yoga Gurus

One of my favorite aspects of vacation is having the time and space to invigorate my personal yoga practice. Thought I'd reflect here on some of the teachers for whom I have the most gratitude.


Ana Forrest has been my greatest influence recently. Since the birth of my second child, I've found her work to be the most deep, transformative and challenging. There is something about her original insights into emotional holding, opening the back and shoulders, and surfing gravity that really worked for me post-partum. Unfortunately, Ana is not in the Bay Area much this year, but perhaps she is near you somewhere.

Something about Ana reminds me of Madonna. Can't quite put my finger on it... both fierce and narcissistic? Original and cunning? Totally hot at 50?


Another fave is Shiva Rea. She is such a kind person and actually embodies many of the precepts we yogis are supposed to live by.


I'd love to house swap with someone in Venice and go to her studio daily for classes. But what to do with the kids? And the husband?


For those looking for a local teacher here in Berkeley, check out Michelle Cordero. She is a great friend, and an awesome teacher. She is teaching a great upcoming workshop with Dr. Derek Abbassi on June 20, 2009 at Mountain Yoga, entitled "Yoga for Restoring Energy & Libido."

Osteoporosis: Beyond Boniva to Integration

What is bone? It’s a living, active tissue composed of vitamins, minerals and other substances, from calcium, magnesium, boron, strontium, to a protein matrix that attracts calcium and other minerals. We build bone density (or amount of mineral) until age 35 and then it gradually decreases with age with some acceleration in women at the time of menopause due to decreased hormones.

The purpose of this blog entry is to review an integrative approach to the health of your bones, drawing upon nutritional healing and the benefits of movement, the role of pollutants and xenohormones, as well as new information, made available just in the past couple of years, about the benefits of minerals such as strontium and “quarter-dose” natural estrogen in improving bone density and reducing fracture.

Osteoporosis, or porous bone, is a disease of low bone density and structural deterioration of bone tissue, leading to bone fragility and an increased risk of fractures, particularly of the hip, spine and wrist. In most cases, calcium and other minerals leeches out of our system, leading to bones getting thinner and more porous, like Swiss cheese. Women are more affected than men by a 6:1 ratio. Half of Americans over 50 have osteoporosis, which became an epidemic in 1950. Yet since 1950, the rate of fracture has doubled in the U.S. and now millions of fractures occur annually. Why? Some postulate that something has happened in our environment, and the leading suspect is the depleted soil used for most farming. As we’ve used less composting and manure in soil, there is less trace minerals available in our food supply such as zinc, copper, strontium, manganese and silicon. Reinvigorate your commitment to composting, and use it in your garden, as a way of improving your bones!
What are some of the modifiable and non-modifiable risk factors? The main risk factors are Caucasian race, female gender, menopause (especially early), weight less than 127 (fat makes hormones, and thinner women have less); smoking, family history and personal history of fracture. Most of these risk factors you cannot change. Others you can, including low bone density and sedentary lifestyle. Caffeine drinkers and high-glycemic carbohydrate addicts also have an increased risk, and after 2 cups of coffee or sugar, increased calcium is lost through the urine for several hours.

One other risk factor that is not well-known is endogenous estradiol level, or the level of estrogen made naturally by your body. We know in post-menopausal women from a study at UCSF that if you are in the lowest quartile, you have the highest risk of osteoporosis. This makes intuitive sense. On the flip side, women with the highest quartile of endogenous estradiol have the highest risk of breast cancer. This is in women not on hormone therapy, synthetic nor bioidenticals. It seems as usual that the middle road might be best in terms of reducing risk of either osteoporosis or breast cancer, which is where the new quarter-dose estrogen comes in. 

We know from the Women’s Health Initiative that you can reduce your risk of hip and vertebral fracture by taking hormone therapy for 5 years. Yet many women do not want to accept the small risk of other problems such as breast cancer in 1.9% (versus 1.5% in women on placebo pills), stroke in 1.5% (versus 1.1%) and heart attack in 1.9% (versus 1.5%).
Since WHI, millions of women have stopped hormone therapy since the synthetic hormones do more harm than good. Many women found they could not tolerate the poor quality of life associated with the increased hot flashes, night sweats, joint aches and poor mood, and restarted at half-doses. 

The half dose has fewer risks and is almost as effective at reducing symptoms. How low can we go? There is a new natural estrogen patch being tested now that is a quarter of the standard dose, and it has been shown in the best quality study design (randomized controlled trials) to improve the hip bone density by 1% and the spine bone density by 2-3% in just 2 years, with very few risks. We should be hearing more about this in the future, but it may be a great option for thinner women with low endogenous estradiol levels. Other women find that the quarter dose isn’t enough when they’re suffering from hot flashes, poor sleep and mood, and choose a more physiological dose of bioidentical hormones, which are hormones identical to what your body made in your 20s and 30s.

I was trained in OB/GYN residency to hand out Fosamax like Halloween candy to my postmenopausal women with low bone density. Now we have Sally Field telling us to take Boniva instead, since it’s just once/month. Unfortunately bis-phosphonates, like Boniva, Actinel and Fosamax, are toxic and have serious risks from hurting your gastrointestinal system to the more serious osteonecrosis of the jaw. Wouldn’t it be better to approach osteoporosis more from a nutritional perspective, with the idea of using therapies that occur naturally in the body such as mineral therapy?

There are several nutritional deficiencies that increase your risk of osteoporosis. We all know that calcium deficiency is one risk. Yet many women do not realize that their gluten sensitivity, or other cause of bowel inflammation such as food allergies, is interfering with their ability to absorb calcium from their diet.

Women with Celiac disease have an increased risk of osteoporosis and need special care to get sufficient calcium. Vitamin D deficiency is another common cause, especially with our more religious use of sunblock. Magnesium deficiency is also very common and can be associated with fatigue, anxiety, insomnia, migraines, muscle aches as well as osteoporosis. In one study, 84% of women with osteoporosis had magnesium deficiency and most of us don’t get enough from our diet. We have seen in some research studies increased bone density of up to 8% in women supplemented with magnesium. Manganese deficiency is another risk factor and affected famed NBA player Bill Walton until a holistic physician figured out it was the cause of his repetitive fractures that threatened his career. You can get your levels checked for all of these minerals. Another important issue is something Dr. Alan Gaby calls the “homocysteine connection,” which is the increased homocysteine levels we see if some people who have excessive animal protein consumption. Homocysteine levels can also be correlated with heart disease and it is important to know your level.

Heavy metals can also be associated with osteoporosis, including the ubiquitous toxin aluminum. Aluminum is added to some municipal water supplies as a way of reducing particulate matter. Aluminum cans containing beer have three times the amount of aluminum as glass bottles, and for cola, it’s six times! Other risky heavy metals are lead and tin, especially from water pipes and tin cans containing food. Consider getting your levels checked also for heavy metal toxicity if you find yourself with low bone mass.

One promising new approach is to supplement with strontium, which is a natural therapy. Strontium is licensed in Europe but has not yet been approved in the U. S. by the FDA. There are several studies showing that it increases bone density and reduces fracture in women, even in older women over aged 74. One study in particular, published in the New England Journal of Medicine in 2004 showed that in 1649 women aged 50+ who had at least one vertebral fracture, strontium ranelate led to fewer vertebral fractures and increased bone density. Women in the placebo group lost bone density. The dose used in Europe is 2 grams taken at bedtime more than 2 hours after eating or drinking anything other than water. Stontium ranelate is not yet approved for use in the U.S. as it is still under investigation.
Exercise is another important strategy. All exercise is good,e.g. swimming is better than no exercise in terms of your bones and muscles, but some forms are better than other. Most research shows that a combination of impact aerobic exercise such as walking or running, along with resistance training and/or yoga can increase bone density up to 1% per year. 

We all know by now that we should take care to get a total of 1200 mg of calcium from our diet and/or supplements combined with 600-800 IU Vitamin D. Many people reach for their Tums, but take care to get a calcium supplement without aluminum in it. In summary, there are nutritional and lifestyle interventions that can help you prevent and reverse osteoporosis.
If you have osteoporosis, I recommend that you get your Vitamin D, homocysteine, magnesium and manganese levels checked. Supplement if you are low. Optimize your exercise regimen and take care not to ingest heavy metals such as aluminum, lead and tin. Consider bioidentical hormone therapy if appropriate and in consultation with a trusted physician. Consider quarter dose estrogen if your endogenous estrogen is low. Keep an eye out for emerging data on strontium.

Bioidentical Homornes: Are They for You?

by Guest Editor 

Dr. Marsha Nunley, MD

Are you confused about bioidentical hormones and just hormones in general? Well, that is because it is a somewhat confusing story and there are many players in the game who stand to make or lose a lot of money. This, of course, always muddies the water and we have no long term randomized controlled trials (which is the gold standard in the medical literature but very difficult to do with natural substances and hormones) on bioidentical hormones. To further complicate matters, hormones such as estradiol and progesterone are natural substances and cannot be patented and sold as a drug unless they are altered in some way. Synthetic estrogens such as Premarin and progestins such as Provera are made by pharmaceutical companies. Vivelle and other patches are “natural and bioidentical” estradiol but can be sold as a drug because they are in a “special form” ie the patch delivery system. Prometrium is natural progesterone in “micronized form” that is sold as a drug. The drug companies have made billions of dollars and are still making billions of dollars from synthetic hormones and have a great stake in stopping the trend toward compounding “natural bioidentical hormones.” In fact, the Women’s Health Initiative, though flawed in many respects, clearly showed unacceptable risks with oral synthetic hormone therapy. However, the final conclusion was to continue to give synthetic hormones…just not for too long. If you search Pub Med you will find hundreds if not thousands of articles on hormonal therapy, all with their own biases and conclusions and if you search carefully you will frequently find a financial tie that helps explain the conclusions. Compounding pharmacies are not blameless and have rushed to cash in on the bonanza in bioidentical hormone treatment. There is very little regulation of compounded products (though one could argue that the FDA is more interested in protecting Wyeth than women).

A recent review published in Postgraduate Medicine, volume, 121, Issue 1, January 2009, p.73-85 by Dr. Kent Holtorf, MD from Torrance, CA is a meta analysis and literature review of 163 articles. He looked at all types of hormone therapy including synthetic therapies (i.e., The Women’s Health Initiative and Premarin and Prempro) as well as everything he could find on bioidentical hormones including in vitro studies.

Looking at the combined results of these studies, he concluded that “bioidentical hormones (meaning estradiol and progesterone) are associated with lower risks, including the risk of breast cancer and cardiovascular disease, and are more efficacious than their synthetic and animal derived counterparts…and of course that we need randomized controlled trials to delineate these differences.”

Bottom line:
1. If you think you may be a candidate for hormonal therapies, choose bioidentical and choose a physician that is knowledgeable in all fields of hormonal therapies including adrenal, thyroid, and insulin issues. The hormones of your body function in a complex network affecting each other and almost every bodily process. This requires a physician who is knowledgeable and experienced in utilizing bioidentical hormones. With the recent feature of hormonal therapy on Oprah, the interest has exploded and the search engines are hot. This is an area in which physicians are self taught. It is not a standard part of physician training, and I suggest you look for physicians that have received additional training in hormonal therapy such as that received through the Antiaging and Functional Medicine Fellowship offered through the A4M or talk to your friends. They may be your best resource in finding a physician
2. There is no conclusive data that bioidentical hormones are safe. Each woman should discuss her personal risks and symptoms with a knowledgeable physician and decide if it is the right decision for her. There is data that suggests that bioidentical hormone therapy may carry a somewhat less risk and does have a positive impact on quality of life.
3. The only FDA approved treatment for menopause is Premarin and Provera. Don’t rely on the government to protect you. Educate yourself, find a doctor that you trust and make informed choices.
4. Medical research is currently funded primarily by pharmaceutical companies. Many prominent physicians and researchers rely on them for the money to do their research and are on their payroll as speakers. It was recently disclosed that a prominent physician who was paid thousands of dollars by a drug company was instrumental in recommending and greatly expanding the role of using powerful antipsychotic medications in the treatment of psychiatric illness and the use of these drugs in children had interpreted his data in favor of the drugs when in fact, the benefit was minimal at best and dangerous at worst. The research is only as good as the researchers. Money corrupts the process.

Omega 3s: Are You Getting Enough?

"Oh, I have flax oil in my breakfast - I get enough."

I often hear this from my patients. Girlfriend, you have to eat about 1½ cup of flax seed oil or salmon daily to get a sufficient amount. 

Take a supplement -- this is one of those very few situations where the food sources probably aren't as good for you as the pill. We have new data showing dramatic benefits of omega 3s in the prevention of depression, cancer, heart disease, inflammation, pain and more. 

You also need to be careful to get a fish oil supplement without contaminants like mercury. Ask your doctor to test your AA/ EPA ratio to find out how low your ratio is. More on this in a moment. 

Good vs bad fats. We eat different types of fat: saturated, monounsaturated, polyunsaturated and partially hydrogenated or transfats. While you have a limited budget of saturated fats daily for a healthy diet, they are not your worst enemy. 

Saturated fats are solid at room temperature, i.e., animal fats in meat and cheese contain saturated fats. Monounsaturated fat such as the fat in olive oil is liquid at room temperature but cloudy in the fridge. Your salad dressing should contain extra virgin olive oil.

Polyunsaturated fats are liquid in the refrigerator. They have more double bonds -- the chemical structures that make them fluid. Trans fats are artificial chemically produced fats such as margarine or "partially hydrogenated" fats, which are bad to your health and should not be eaten. Transfats are the worst offenders. Omega 3 and omega 6 are polyunsaturated fats. Both are essential fatty acids, meaning we can't make them in our bodies. Omega 3 refers to the position of the double bond in the molecule itself. There are two types: short chain and long chain. 

When my patients tell me they eat plenty of flaxseed oil, I have to break the bad news: flax won't do it because we need long-chain omegas for the benefits, not short chain. We only convert about 5% of short-chain omega 3s to long chain. So you need to take fish oil. If you're vegan, you can take krill oil as an alternative. We need long-chain omega 3s, and you also need to limit omega 6s. Omega 3s will favor fewer blood clots, kill cancer cells, improve your immune system and mental acuity, and prevent heart disease. 

How is it that Eskimos can eat half their calories from fat yet have low risk of heart disease? Researchers think it's because of their omega 3s. I tend to focus my learning on research in women, and in 2002 we learned that 84,688 nurses who took fish oil had a 45% lower risk of heart disease. Omega 3s don't just help the heart: they also have been shown to benefit cancer risk, ADHD, bipolar disorder, depression, dementia, multiple sclerosis, asthma and rheumatoid arthritis. 

How much omega 3 do you need? 

Goal Grams/day 

Maintaining good health 2 

Improved CV health 2-5 

Improved Brain function 5-10 

Inflammation Reduction 5-10 

Optimal health 5-10 

What to look for in your Omega 3 supplement. Try to find pharmaceutical-grade long-chain essential fatty acids. It should be cholesterol-free and molecularly distilled for the safest grade possible. We now have a new blood test to measure your omega 3 to omega 6 ratio, called the AA/EFA (arachidonic acid to essential fatty acid ratio). Eskimos have a ratio of 0.7; the Japanese 1.5. Americans typically have a ratio of 10, and among kids with ADHD, the ratio is 20. Start your supplement today, and check your ratio. It will help you age optimally and prevent heart disease, depression and inflammation.