At winter solstice, the two moments during the year when the path of the Sun in the sky is farthest south in the Northern Hemisphere (December 21 or 22) and farthest north in the Southern Hemisphere (June 20 or 21).  When it is the summer solstice at one Pole, it is the winter solstice on the other.   At the winter solstice, in the Northern hemisphere, the Sun travels the shortest path through the sky, and that day therefore has the least daylight and the longest night.

I think of solstice as a passage and one that is connected with the season.  For those of us in the Northern Hemisphere, December 21^st is the passage time to a return of the light and the time of the Sun returning to the Northern Hemisphere.

You might find it interesting to read how different cultures throughout history celebrate this winter solstice.  Various holidays and celebrations are associated with or an outcome of the solstice.  Cultures of all kinds including Christian, Hinduism, Greeks, South African, paganism and others, all have celebrations and feasts and traditions recognizing the importance of this time of year.

I’m drawn to a nature-based approach to the Winter Solstice.  One that includes thoughts and moments and celebrations that focus on rebirth, renewal and the return of the light.  This can be a simple time to reflect on the cycles of nature with a meditative walk in the woods, nighttime candles and a fire in the wood stove.  They all represent the return of the light for me.  And maybe I’ll add a glass of freshly squeezed cold lemon water, an organic Cara Cara orange, a cup of freshly brewed rose hips from my winter harvest or some sips of Pinot Noir from a nearby grape harvest.  We shall see.

What’s the best way to recognize and attend to this transition and return of the light for you?

In the spirit of the autumn earth’s harvest, the earth, and extending gratitude……. here are two poems to reflect upon.

The Way In- by Linda Hogan

Sometimes the way to milk and honey is through the body.
Sometimes the way in is a song.
But there are three ways in the world: dangerous, wounding,
and beauty.
To enter stone, be water.
To rise through hard earth, be plant
desiring sunlight, believing in water.
To enter fire, be dry.
To enter life, be food.

What If – by Ganga White

What if?

What if our religion was each other?

If our practice was our life?

If prayer was our words?

What if the temple was the earth?

If forests were our church?

If holy water- the views, lakes and oceans?

What if meditation was our relationship?

If the teacher was life?

If wisdom was self-knowledge?

If love was the center of our being?

Data bases were searched to provide information to see if there was a dose-response relationship between alcohol intake and bone mineral density (BMD) and risk of osteoporotic fractures.  A total of 11 studies including 46,916 individuals with BMD assessment and 8 studies including 240,871 individuals with risk of fracture analysis were included.

Compared to non-drinkers, the consumption of up to two standard alcohol drinks per day was correlated with higher lumbar spine (low back) and femoral neck (a part of the hip) BMD values, while up to one standard drink of alcohol was correlated with higher hip compared to no alcohol consumption.  A higher risk of hip fractures was found starting from three standard drinks of alcohol per day and more so if 4 drinks per day.  The risk steadily increased with higher intake of alcohol.

Commentary:

Firstly, you might be confused.  Higher alcohol consumption is definitely associated with a higher risk of osteoporotic fractures.  But 1-2 drinks per day, or what is considered lower doses, the role of alcohol gets fuzzy, given that BMD was higher in these drinkers compared to non-drinkers.  The study has some problems: Firstly, this is an observational design of the original studies which does not allow us to really conclude a cause and effect relationship.  Secondly, since the alcohol intake was assessed during interviews, this may not reflect early intake or lifelong exposure.  In addition, the interview and assessment of alcohol consumed did not identify drinking patterns.  The study also failed to make clear the differences in men and women or women pre vs. post menopause.  Lastly, the increase in BMD values in the light drinkers compared to non-drinkers was not clinically relevant.  While it is tempting to conclude that there is clinical improvement in BMD values in lighter drinkers, the more accurate conclusion is no effect – positive or negative. compared to non-drinkers.

There are several mechanisms that provide the rationale for the negative effects of excessive intake of alcohol on bone health.  We know that chronic alcohol consumption negatively alters bone remodeling, the process of bone formation and bone resorption.  To be specific, alcohol impairs the bone microarchitecture and affects the thickness of the bone that is 50% of the hip, as well as trabecular bone, which makes up 90% of the kind of bone in the lumbar spine.  Another indirect mechanism has to do with how alcohol overconsumption affects hormone regulation including leptin, vitamin D and parathyroid hormone all of which influence bone metabolism.  Excess alcohol intake may also impair nutrient absorption, including the malabsorption of calcium from the intestines, which then leads to lower levels of serum calcium and calcium deficiency.  In women, over consumption of alcohol can decrease estrogens and/or alter estrogen metabolism.  Less estrogen stimulation of bone, especially after menopause, can lead to more bone loss due to a faster pace of bone turnover in favor of resorption (bone loss) vs. formation.

In terms of the big picture, alcohol consumption can be a cause or risk factor for depression, breast cancer, heart disease, stroke, hypertension, heart attacks, liver disease and osteoporosis.

Reference: Godos J, Giampieri F, Chisari E, et al.  Alcohol consumption, bone mineral density, and risk of osteoporotic fractures: A dose-response meta-analysis.  Int J Envciron. Res. Public Health 2022, 19:1515

Myth: Women who take MHT should stop by the age of 60.

There is no such guideline from the main menopause expert organizations.  There is no general rule for stopping systemic hormone therapy in a woman aged 60, or even 65 years.  The Beers criteria from the American Geriatrics Society does list a warning for the use of MHT in women 65 and older.  However, any routine discontinuation of systemic MHT is not cited by evidence nor supported by the American College of OB/Gyns (ACOG)  or the North American Menopause Society (NAMS).  However, the continued use of MHT in a healthy woman older than 65 and at low risk of breast cancer and cardiovascular disease is limited by insufficient evidence for safety, risks and benefits but is now supported by a significant study published in April 2024.

This study aimed to assess the use of menopausal hormone therapy beyond age 65 years and its health implications by types of estrogen/progestogen, routes of administration, and dose strengths. Using prescription drug and encounter records of 10 million senior Medicare women from 2007-2020 and Cox regression analyses adjusted for time-varying characteristics of the women, the researchers examined the effects of different preparations of menopausal hormone therapy on all-cause mortality, five cancers, six cardiovascular diseases, and dementia. Results: Compared with never use or discontinuation of menopausal hormone therapy after age 65 years, the use of estrogen monotherapy beyond age 65 years was associated with significant risk reductions in mortality (19% ), breast cancer (16%), lung cancer (13%), colorectal cancer (12%), congestive heart failure (CHF) (5%), venous thromboembolism (3%), atrial fibrillation (4%), acute myocardial infarction (11%), and dementia (2%). For the use of estrogen and progestogen combo-therapy, both E+ progestin and E+ progesterone were associated with increased risk of breast cancer by 10%-19%, but such risk can be mitigated using low dose of transdermal or vaginal E+ progestin. Moreover, E+ progestin exhibited significant risk reductions in endometrial cancer (45%), ovarian cancer (21%), ischemic heart disease (5%), CHF (5%), and venous thromboembolism (5%), whereas E+ progesterone exhibited risk reduction only in CHF (4%).

Conclusions: Among senior Medicare women, the implications of menopausal hormone therapy use beyond age 65 years vary by types, routes, and strengths. In general, risk reductions appear to be greater with low rather than medium or high doses, vaginal or transdermal rather than oral preparations, and with estradiol rather than conjugated estrogen.

If a woman is considered healthy and has persistent vasomotor symptoms, continuing MHT is a reasonable option with evaluation or risk and benefit yearly.  MHT is also a treatment option for osteoporosis and prevention of hip and spine fractures.  MHT would need to be continued in order to get that fracture risk reduction.   Long term MHT is not indicated or considered appropriate for reduction of dementia or CHD.  However, there is an increasing amount of biologic plausibility and data on the benefits of systemic estrogen to the brain, if started in perimenopause or within the first 10 years of last menstrual period and perhaps even within the last 5 years or before age 60.  If a woman has a family history of Alzheimer’s  disease (AD)  and has initiated MHT within the optimal window of before age 60 and before 10 years postmenopause, it is this practitioner’s opinion and recommendation that she continue on MHT long term, in order to reduce her risk of AD. This is not yet an FDA approved use of MHT nor is it a standard of care guideline from the advisory organizations.   However, given we have a terrible disease, with no cure, and my patient is at increased risk, this is a topic I’m going to discuss.  However, if she is > 60 or past 10 years postmenopause, I will not initiate it, even with her family history, because initiating outside of the window, may actually increase her risk.  See the next myth for more.

Women should be evaluated at minimum, once per year, to weigh the benefits and risks with their health care provider.  Women can continue if there are appropriate indications including severe vasomotor symptoms, and/or as a treatment option for osteoporosis of the lumbar spine.

What is true relative to stopping systemic estrogen is that by age 65, if women are on oral or sublingual, they need to switch to transdermal delivery of that estrogen.  Her aging vessels and metabolism of estrogen are now more subject to higher effects of oral/sublingual estrogen on atherosclerosis and risk for DVT and stroke.  The pharmacokinetics of estrogen metabolism (and of many drugs), in the liver, changes with age and warrants transdermal delivery of that estrogen to mitigate the stimulation of clotting factors by oral estrogen, and to mitigate more variable absorption issues.

References and Resources:

“The 2022 Hormone Therapy Position Statement of The North American Menopause Society” Advisory Panel.  The 2022 hormone therapy position statement of The North American Menopause Society. Menopause 2022 Jul 1;29(7):767-794.

Baik S, et al. Use of menopausal hormone therapy beyond age 65 years and its effects on women’s health outcomes by types, routes, and doses. Menopause 2024 May 1;31(5):363-371.

In this episode Dr. Smeaton and I discuss menopausal hormone therapy (MHT) and its resurgence in recent years. Dr. Hudson explains that MHT may be recommended for women experiencing significant quality of life symptoms related to perimenopause or menopause, such as hot flashes, night sweats, mood swings, fatigue, and low libido.

Dr. Hudson and Dr. Smeaton also discuss:

• The initial concerns raised by the 2002 Women’s Health Initiative (WHI) study
• The re-examination of the WHI study, which found that the risks associated with MHT are relatively small and comparable to other lifestyle factors
• Bioidentical hormones versus synthetic hormones
• The significance of finding providers with expertise in menopause management
• The importance of individualized treatment plans

I hope you learn and enjoy.

Click Here to watch the Podcast – There is an Audio Only option as well, on the same page.

Green tea consumption and supplementation has been the subject of many research studies in areas of cardiovascular health, cancers and metabolic health and some studies now demonstrate that it has antidepressant effects.

The hypothesis for the mechanism of action of green tea’s antidepressant effects may be in its ability to reduce oxidative stress and/or inflammation.  Another possibility might be an influence on hormones and the gut microbiota.  The current study evaluated the lifestyle habit of long-term green tea consumption on hormones, inflammation, and depression in postmenopausal women.

A total of 386 participants met the inclusion criteria for this study with 221 women assigned to the green tea group and 165 in the control group.  The tea drinking group was characterized as having at least one cup (500 mL) of green tea daily at least six days per week for over 20 years.

Depression was determined using the patient health questionnaire (PHQ-9). Blood samples were collected following an overnight fast. Estradiol, testosterone, thyrotropin (TSH), free triiodothyronine (FT3), thyroxine (FT4), and inflammatory markers were measured. The systemic immune inflammation index (SII) was used to measure inflammation.

Both groups were similar in demographic parameters and there were no significant differences between the two groups for sleep duration, blood pressure, thyroid stimulating hormone (TSH), free T3 (FT3), free T 4 (FT4), and testosterone. Green tea drinkers had lower degrees of insomnia and depression compared to non-tea drinkers. Body mass index (BMI) and SII were significantly lower in the green tea group and estradiol was significantly higher in the tea drinking group. SII and estradiol were  correlated with degree of depression.

The analysis showed significant indirect effects of SII (10.3%) , estradiol (6.7%), and degree of insomnia(28.2%)  on the relationship between tea drinking and degree of depression.  The indirect effect of tea drinking on depression accounted for 45.2% of the total effect.

Commentary: Relying on the memory of how much green tea you have accumulated in the last 20 years seems like a big ask.  In addition, not all women consumed the same amount.  Questions I have: how much did each woman consume per day/per week?  How concentrated was the product?  What was the quality of the green tea?

While this study was of postmenopausal women, I think a more ideal group would have been perimenopausal women, since that is a vulnerable time for recurrence, worsening of chronic depression and new onset depression.

One oddity is that serum estradiol was not even tested, so it is unclear to me that they could make any association with green tea affecting estradiol levels.  Mechanistically, green tea actually increases sex hormone binding globulin – and this results in a slight lowering of estradiol. The effect of green tea on depression, hormones, metabolic activity, gut microbiota, neurotransmitters and inflammation would be desirable areas of research for the future.  One other thought is that green tea contains caffeine, unless it has been decaffeinated, and caffeine as we know can improve mood.  Coffee companies figured that out long ago.

Reference: Wan Z, Qin X, Tian Y, Ouyang F, Wang G, Wan Q. Long-term consumption of green tea can reduce the degree of depression in postmenopausal women by increasing estradiol. Nutrients. October 2023;15(21):4514.

I’d like to focus this blog on a top myth… that estrogen causes breast cancer.  In the next few blogs,  I’ll address a few other classic myths that can lead to depriving women of hormones they may in fact need, prescribing insufficient doses of progesterone  in combination with systemic estrogen, the timing of initiation of MHT and  myths on discontinuation.

Myth #1:  Estrogen causes breast cancer

The primary fear that most women have about menopause hormone therapy (MHT) is that it will cause breast cancer.  Not only does most data show that recommended menopausal estrogen doses alone do not cause breast cancer, but even recommended estrogen plus a progestin for 4 years or more appears to increase the risk ever so slightly; Not even quite one extra breast cancer per 1,000 women per year with estrogen and progestin.  Estrogen and bio-identical progesterone, according to three observational French studies, and a recent population-based study, does not increase the risk at all.  The systemic estrogen alone studies range from 1) a slight decreased risk (the original RCT from the Women’s Health Initiative=WHI);  2) slight decreased risk from the 20-year WHI f/u; 3) slight increased risk in the Nurses Health Study; 4) the recent population-based study in the next paragraph from the UK; 5) to others with a null effect. 

The recent  population-based case control study of women aged 50 years or older using data from the UK also highlights no increased risk with estrogen alone and  different risk dependent on type of progestogen with estrogen as in the 3 observational French studies.  Over a course of almost 20 years, there were 43,183 cases of breast cancer identified and matched to 431,830 women in a control group.  Compared with women who never used MHT, it’s use was associated with a very slight increased risk of breast cancer.  Compared with never users, estrogens alone were not associated with breast cancer  (bio identical estrogens 1.04); animal derived estrogens 1.01 or both 0.96.  Progestogens appeared to be differentially associated with breast cancer; (micronized progesterone OR 0.99) (synthetic progestin OR 1.28 )

References and Resources: (for those of you who want more!)

Book: Estrogen Matters: Why Taking Hormones in Menopause Can Improve Women’s Well-Being and Lengthen Their Lives — Without Raising the Risk of Breast Cancer. Avrum Bluming MD, Carol Travis PhD.

“The 2022 Hormone Therapy Position Statement of The North American Menopause Society” Advisory Panel.  The 2022 hormone therapy position statement of The North American Menopause Society. Menopause 2022 Jul 1;29(7):767-794.

Abenhaim H, Suissa S, Azoulay L, et al.  Menopausal Hormone Therapy Formulation and Breast Cancer Risk.  Obstet Gynecol 2022;139(6):1103

Fournier A, Berrino F, Riboli E, et al. Breast cancer risk in relation to different types of hormone  replacement therapy in the E3N-EPIC cohort.   Int J Cancer; 2005 Apr 10;114(3):448-54.

 Fournier A, Berrineo F, Clavel-Chapelin F. Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study.  Breast Cancer Res Treat;  2008;107(1):103-111.

Cordina-Duverger, E, Truong T, Anger A, et al. Risk of breast cancer by type of menopausal hormone therapy: a case-control study among post-menopausal women in France. PLoS One; 2013 Nov 1;8(11)

Brinton L, Hoover R, Fraumeni J.  Menopausal oestrogens and breast cancer risk: An expanded case-control study.  Br J Cancer. 1986;54:825-32.

 Armstrong B.  Estrogen therapy after the menopause: Boom or bane?  Med J Aust. 1988; 148: 213-14.

 Dupont W, Page D, Rogers L, et al.  Influence of exogenous estrogens, proliferative breast disease, and other variables on breast cancer risk.  Cancer. 1989;63:948-57

 Palmer J, Rosenberg L, Clark E, et al.  Breast cancer risk after estrogen replacement therapy: Results from the Toronto breast cancer study.  Am J Epidemiol. 1991;134:1386-95.

 Dupont W, Page D.  Menopausal estrogen replacement therapy and breast cancer.  Arch Intern Med. 1991;151:67-72.

 Nachtigall M, Smilen S, Nachtigal R, et al.  Incidence of progestin replacement therapy.  Obstet Gynecol. 1992;80:827-30.

 Colditz G, Hankinson S, Hunter D, et al.  The use of estrogens and progestins and the risk of breast cancer in postmenopausal women.   NEJM 1995; 332:1589-93.

 Willis D, Calle E, Miracle-McMahill H, et al.  Estrogen replacement therapy and risk of fatal breast cancer in a prospective cohort of postmenopausal women in the U.S.  Cancer xauses Control.  1996;7:449-57.

While cyclic mastalgia is prevalent and not related to breast cancer, the cause remains poorly understood and includes multifactorial mechanisms that likely contribute.  Hormonal fluctuations, breast tissue sensitivity, inflammation, cyclic changes in breast anatomy, iodine insufficiency,  psychological factors, nerve sensitivity and fibrocystic changes have all been explored in the research.  Normal variations in hormonal fluctuations, particularly estrogen and progesterone levels during the menstrual cycle, are thought to play a central role in the development of cyclical breast pain.  These hormonal changes can induce cyclic changes in breast tissue, including epithelial proliferation, fluid retention, and inflammation, leading to the cyclic breast pain symptoms. Some women’s breast tissue is  then more sensitive to these normal hormonal changes.

Evening primrose oil (EPO) is derived from the seeds of evening primrose plant.  It is rich in gamma-linolenic acid (GLA), an omega-6 fatty acid with anti-inflammatory properties.  It is thought that GLA modulates prostaglandin synthesis and promotes a balance of hormonal influence in the breasts, thus alleviating breast pain.  Vitamin E may mitigate oxidative stress-induced inflammation in breast tissue.

Previous studies have explored the efficacy of EPO and vitamin E in cyclical mastalgia, although the results are mixed.  There has been little research exploring the combination of the two in treating cyclic mastalgia.  The current study aimed to address this and was a randomized controlled trial evaluating the efficacy of EPO, vitamin E and the combination in alleviating cyclic breast pain.

Participants were at least 18 years, experienced cyclical mastalgia within the two weeks of onset of menses and relieved by menses, and present for at least two consecutive menstrual cycles.  They had to have a pain score of at least 3 or greater.  They were randomly assigned to one of four groups for a 6 month period.  Group 1) Placebo  Group 2) Vitamin E 400 mg (600 IU)  once daily Group 3) EPO 1,000 mg bid  Group 4) Combination EPO 1,000 mg bid and vitamin E 400 mg once daily.

The primary outcome measure was the change in breast pain, assessed using the modified McGill Pain Questionnaire at enrollment and at the end of the 6 months.

A total of 126 participants were randomized with a mean age of 38.  A notable decrease in both the worst and average pain scores across all treatment groups was observed.  The combined EPO/E group had the most substantial reduction in pain scores with changes of -4.0 those with the worst pain and

-3.7 for average pain. There were statistically significant differences among the treatment groups, confirming the superior effects of the combination EPO/E.

Commentary: Previous research on cyclical mastalgia with vitamin E, EPO or the combination has been inconsistent.  The results of this study confirm the researcher’s hypothesis that a synergistic action of EPO and vitamin E may enhance the therapeutic effects.  Their rationale seems plausible in that EPO, rich in GLA, exerts anti-inflammatory effects, whereas vitamin E functions as a potent antioxidant, reducing oxidative stress and inflammation in breast tissue.  No testing of hormones or altering of hormones levels is needed to assess and treat cyclic mastalgia. The current study, along with any previous positive studies on EPO and vitamin E as single agents for this condition, demonstrate short term efficacy.  What we don’t know from research, is if this can offer a sustainable effect after stopping the treatment after 6 months.  In my clinical experience, using doses of EPO at 3,000-4,000 mg/day, or vitamin E at 400 mg/day or greater, most women can reduce the dose after 6 months and still have satisfactory results.  Some women can discontinue altogether.  So far, it has been a very individualized response, and strategy for long term relief.  I always look at potential influential issues, such as other PMS/PMDD symptoms with a more comprehensive plan for those symptoms and their breast symptoms.  Other influencers could be diets too high in fats, especially saturated fats, overweight/obesity, caffeine and sugar intake.  Perimenopause women  with newly acquired cyclic breast pain can also respond to addressing the broader perimenopause symptom picture.  If perimenopause or menopause women acquire mastalgia due to taking systemic estrogen, this is not cyclic mastalgia, and the usual solution is lowering their dose of estrogen.

Reference: Kumari J, et al.  Effectiveness of Evening Primrose and Vitamin E for Cyclical Mastalgia: A Prospective Study.  Cureus. 2024 Apr; 16(4): e58055.