Two UCLA Studies Show Menopause Accelerates Aging
A new study by Dr Morgan E. Levine from UCLA in PNAS shows that menopause accelerates aging. (1) A second study by Dr Judith Carroll from UCLA reported in Biological Psychiatry that “insomnia symptoms are implicated in accelerated aging”.(2) Insomnia is a frequent menopausal symptom, along with other typical symptoms of hot flashes, night sweats, vaginal dryness, and loss of libido, etc.(3) Left Image Girl Before A Mirror courtesy of PabloPicasso.org
Menopause Accelerates Early Mortality
These two studies also show that menopause is associated with increased aging-related diseases and early mortality.(4,5,6) Acceleration of mortality after menopause had been reported 20 years ago. Dr Shiro Horiuchi reported in 1997 that “mortality data from seven industrialized countries have shown postmenopausal mortality acceleration clearly”. (6)
Menopause and Skin Aging
According to Dr Julie Thornton in her 2013 article, menopause causes estrogen deficiency, and accelerated aging, or deterioration of the skin, all of which are delayed or prevented by estrogen administration.(14) Many other doctors have reported similar opinions.(15-18)
Longer Telomere Length in Women on Estrogen HRT
The telomere theory of aging states that the telomeres on the ends of our chromosomes shorten as we age. Aging can be prevented or reverse by lengthening telomeres. Dr Lee reported in 2005 that “post-menopausal long-term estrogen therapy lengthened telomeres” thus slowing and reversing the aging process.(9) Left Image Aging Woman in mirror courtesy of Mirror UK.
Estrogen HRT Prevents Bone Loss
Dr David Felson reported in NEJM 1993, estrogen therapy prevents bone loss in post menopausal women.(10) For this reason, estrogen therapy was recommended.(10)
Estrogen Prevents Coronary Artery Disease in Postmenopausal Women
Dr Grodstein et al reported in 2006 that estrogen hormone replacement, early after menopause prevented coronary artery disease.(11)
Estrogen HRT Prevents Menopausal Arthritis
Dr Russell Cecil reported in 1925 fifty cases of Arthritis after menopause (12) In 2013 Dr Rowan Chlebowski confirmed these findings with his report on “Estrogen alone and joint symptoms in the Women’s Health Initiative randomized trial.” Post menopausal women on estrogen replacement had significantly less joint pain than the placebo group.(13)
Estrogen Protects the Brain
A large body of studies show that estrogen is protective of the brain in the context of aging, cognitive function, cerebrovascular insult, and head trauma. (19-21)
Conclusion: Bioidentical Hormones Prevent Aging and Reduce Mortality:
Estrogen deficiency related to Menopause is associated with accelerated aging and early mortality, findings which can be prevented and reversed with bioidentical hormone therapy. Our program includes a robust cocktail of all female hormones including estrogen, progesterone, testosterone, all with identical chemical structures to those that occur naturally in the female body.
Articles with Related Interest
Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Fl 33314
References and Links
Morgan E. Levine, Ake T. Lu, Brian H. Chen, Dena G. Hernandez, Andrew B. Singleton, Luigi Ferrucci, Stefania Bandinelli, Elias Salfati, JoAnn E. Manson, Austin Quach, Cynthia D. J. Kusters, Diana Kuh, Andrew Wong, Andrew E. Teschendorff, Martin Widschwendter, Beate R. Ritz, Devin Absher, Themistocles L. Assimes, and Steve Horvath. Menopause accelerates biological aging. PNAS, July 2016 DOI: 10.1073/pnas.1604558113
Although epigenetic processes have been linked to aging and disease in other systems, it is not yet known whether they relate to reproductive aging. Recently, we developed a highly accurate epigenetic biomarker of age (known as the “epigenetic clock”), which is based on DNA methylation levels. Here we carry out an epigenetic clock analysis of blood, saliva, and buccal epithelium using data from four large studies: the Women’s Health Initiative (n = 1,864); Invecchiare nel Chianti (n = 200); Parkinson’s disease, Environment, and Genes (n = 256); and the United Kingdom Medical Research Council National Survey of Health and Development (n = 790). We find that increased epigenetic age acceleration in blood is significantly associated with earlier menopause (P = 0.00091), bilateral oophorectomy (P = 0.0018), and a longer time since menopause (P = 0.017). Conversely, epigenetic age acceleration in buccal epithelium and saliva do not relate to age at menopause; however, a higher epigenetic age in saliva is exhibited in women who undergo bilateral oophorectomy (P = 0.0079), while a lower epigenetic age in buccal epithelium was found for women who underwent menopausal hormone therapy (P = 0.00078). Using genetic data, we find evidence of coheritability between age at menopause and epigenetic age acceleration in blood. Using Mendelian randomization analysis, we find that two SNPs that are highly associated with age at menopause exhibit a significant association with epigenetic age acceleration. Overall, our Mendelian randomization approach and other lines of evidence suggest that menopause accelerates epigenetic aging of blood, but mechanistic studies will be needed to dissect cause-and-effect relationships further.
Insomnia and Menopause
2) Carroll, Judith E., et al. “Epigenetic aging and immune senescence in women with insomnia symptoms: Findings from the Women’s Health Initiative Study.” Biological Psychiatry (2016).
In this large population based study of women in the United States, insomnia symptoms are implicated in accelerated aging.
A prospective population-based study of menopausal symptoms.
Obstet Gynecol. 2000 Sep;96(3):351-8. Dennerstein L1, Dudley EC, Hopper JL, Guthrie JR, Burger HG.
To identify symptoms that change in prevalence and severity during midlife and evaluate their relationships to menopausal status, hormonal levels, and other factors.
METHODS: In a longitudinal, population-based study of 438 Australian-born women observed for 7 years with an 89% retention rate, 172 advanced from premenopause to perimenopause or postmenopause. Annual measures included a 33-item symptom check list; psychosocial, lifestyle, and health-related factors; menstrual status; hormone usage; and blood levels of follicle-stimulating hormone and estradiol (E2).
RESULTS: Increasing from early to late perimenopause were the number of women who reported five or more symptoms (+14%), hot flushes (+27%), night sweats (+17%) and vaginal dryness (+17%) (all P <.05). Breast soreness-tenderness decreased with the menopausal transition (-21%). Trouble sleeping increased by +6%. The major change in prevalence was from early to late perimenopause, except for insomnia, which showed a gradual increase. Those variables most related to onset of hot flushes were number of symptoms at early perimenopause (P <.05), having an unskilled or no occupation (P <.05), more than 10 pack-years of smoking (P <.01), and decreased E2 (P <.01). The onset of night sweats increased with the change in E2 (P <.05). The onset of vaginal dryness decreased with more years of education (P <.05). Trouble sleeping was predicted by prior lower well-being (P <.01), belief at baseline that women with many interests hardly notice menopause (P <.01), and hot flushes (P <.01).
CONCLUSION: Although middle-aged women are highly symptomatic, the symptoms that appear to be specifically related to hormonal changes of menopausal transition are vasomotor symptoms, vaginal dryness, and breast tenderness. Insomnia reflected bothersome hot flushes and psychosocial factors.
Menopause Makes Your Body Age Faster by Alice Park Time Magazine July 25, 2016 . The hormone loss that accompanies years after menopause may accelerate aging in the body
Menopause, sleepless nights may make women age faster.
Two UCLA studies show menopause, insomnia could increase women’s risk for aging-related diseases by Elaine Schmidt and Mark Wheeler | July 25, 2016
In a pair of studies published today UCLA researchers report that menopause accelerates biological aging and that insomnia, which often accompanies menopause, also has a clear association with age acceleration.
The dual findings suggest both factors could increase women’s risk for aging-related diseases and earlier death. The two studies, published in separate journals, contribute to increasing evidence of the biological clock’s variability.
free full pdf
6) Horiuchi, Shiro. “Postmenopausal acceleration of age-related mortality increase.” The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 52.1 (1997): B78-B92.
It is thus expected that menopause should trigger an acceleration of age-related mortality increase in human females. Life table aging rate patterns for selected industrialized countries generally support this hypothesis. A cause-of-death decomposition analysis indicates that the sex differential in mortality acceleration is mainly due to cardiovascular diseases. Mortality data from seven industrialized countries have shown postmenopausal mortality acceleration clearly,
7) free pdf
Bromberger, Joyce T., et al. “Prospective study of the determinants of age at menopause.” American journal of epidemiology 145.2 (1997): 124-133.
8) Leidy, L. E. “Biological aspects of menopause: across the lifespan.” Annual Review of Anthropology (1994): 231-253.
Longer telomere length in women on HRT
Lee, Duk-Chul, et al. “Effect of long-term hormone therapy on telomere length in postmenopausal women.” Yonsei medical journal 46.4 (2005): 471-479.
Telomeres undergo attrition with each cell division, and telomere length is associated with age-related diseases and mortality in the elderly. Estrogen can influence the attrition of telomeres by diverse mechanisms. This is a retrospective case control study that investigated the influence of long-term hormone therapy (HT) on telomere length in postmenopausal women. We recruited 130 postmenopausal women from 55 to 69 years of age for this study, and divided them into two groups. The first group included 65 women who had been on estrogen and progesterone therapy for more than five years (HT group). The other group was composed of 65 women matched in age to the HT group who had never had HT (non-HT group). The relative ratios of telomere length of study subjects to a reference DNA from a healthy young female were measured using quantitative PCR. Plasma levels of lipid profiles, total antioxidant status (TAS), C-reactive proteins (CRP), fasting glucose levels, and estradiol levels were measured. Age at menopause, vitamin use, and exercise, alcohol, and cigarette smoking histories were also assessed in a questionnaire. Mean duration (± SD) of HT was 8.4 ± 2.3 years. Prevalence of vitamin use and regular exercise were higher in the HT group than in the non-HT group (p<0.01). Relative telomere length ratios in the HT group were significantly greater than those in the non-HT group (p<0.01). HT was significantly correlated with the relative telomere length ratio in multivariate analysis when potential confounding variables were controlled for (p<0.05). In conclusion, telomere lengths were longer in postmenopausal women who had a history of long-term HT than in postmenopausal women without HT. Long-term HT in postmenopausal women may alleviate telomere attrition.
Bone Density after Menopause
Felson, David T., et al. “The effect of postmenopausal estrogen therapy on bone density in elderly women.” New England Journal of Medicine 329.16 (1993): 1141-1146.
Estrogen therapy prevents bone loss in postmenopausal women who take it early in the postmenopausal period. The risk of fracture is highest much later in life, however. We studied whether bone mass in elderly women was affected by earlier estrogen use and how long women needed to take estrogen for it to have a beneficial effect on bone density later in life.
METHODS: In 1988 and 1989, we measured bone mineral density at the femur, spine, shaft of the radius, and ultradistal radius in 670 white women in the Framingham Study cohort (mean age, 76 years; range, 68 to 96). These women had been followed prospectively through menopause and had been asked repeatedly about estrogen therapy. After excluding women who began taking estrogen after a fracture, we investigated whether postmenopausal estrogen therapy affected bone density; in these analyses we adjusted for age, weight, height, cigarette smoking, physical activity, and age at menopause.
RESULTS: A total of 212 women (31.6 percent) had received estrogen therapy (mean estimated duration of treatment, 5 years). Only women who had taken estrogen for 7 to 9 years or for 10 or more years had significantly higher bone mineral density than women who had not taken estrogen (7 to 9 years of treatment, P < 0.05 at sites in the femur and the spine; > or = 10 years, P < 0.05 at all sites except the spine). In the women less than 75 years of age who had taken estrogen for seven or more years, the bone density was, averaging all sites, 11.2 percent greater than in women who had never received estrogen. Among women 75 years of age and older in whom the duration of therapy was comparable, bone density was only 3.2 percent higher than in women who had never taken estrogen.
CONCLUSIONS: For long-term preservation of bone mineral density, women should take estrogen for at least seven years after menopause. Even this duration of therapy may have little residual effect on bone density among women 75 years of age and older, who have the highest risk of fracture.
HRT prevents Heart Disease After Menopause
J Womens Health (Larchmt). 2006 Jan-Feb;15(1):35-44.
Hormone therapy and coronary heart disease: the role of time since menopause and age at hormone initiation.
Grodstein F1, Manson JE, Stampfer MJ.
Apparently discrepant findings have been reported by the Women’s Health Initiative (WHI) trial compared with observational studies of postmenopausal hormone therapy (HT) and coronary heart disease (CHD).
METHODS: We prospectively examined the relation of HT to CHD, according to timing of hormone initiation relative to age and time since menopause. Participants were postmenopausal women in the Nurses’ Health Study, with follow-up from 1976 to 2000. Information on hormone use was ascertained in biennial, mailed questionnaires. We used proportional hazards models to calculate multivariable adjusted relative risks (RR) and 95% confidence intervals (CI). We also conducted sensitivity analyses to determine the possible influence of incomplete capture of coronary events occurring shortly after initiation of HT.
RESULTS: Women beginning HT near menopause had a significantly reduced risk of CHD (RR = 0.66, 95% CI 0.54-0.80 for estrogen alone; RR = 0.72, 95% CI 0.56-0.92 for estrogen with progestin). In the subgroup of women demographically similar to those in the WHI, we found no significant relation between HT and CHD among women who initiated therapy at least 10 years after menopause (RR = 0.87, 95% CI 0.69-1.10 for estrogen alone; RR = 0.90, 95% CI 0.62-1.29 for estrogen with progestin). Among women who began taking hormones at older ages, we also found no relation between current use of estrogen alone and CHD (for women aged 60+ years, RR = 1.07, 95% CI 0.65-1.78), although there was a suggestion of possible reduced risk for combined HT (RR = 0.65, 95% CI 0.31-1.38). In sensitivity analyses, we found that the incomplete capture of coronary events occurring shortly after initiation of HT could not explain our observation of a reduced risk of coronary disease for current users of HT.
CONCLUSIONS: These data support the possibility that timing of HT initiation in relation to menopause onset or to age might influence coronary risk.
Arthritis After Menopause
CECIL, RUSSELL L., and Benjamin H. Archer. “Arthritis of the menopause: a study of fifty cases.” Journal of the American Medical Association 84.2 (1925): 75-79.
Estrogen Alone and Joint Symptoms in the Women’s Health Initiative Randomized Trial
Chlebowski, Rowan T., et al. “Estrogen alone and joint symptoms in the Women’s Health Initiative randomized trial.” Menopause (New York, NY) 20.6 (2013).
While joint symptoms are commonly reported after menopause, observational studies examining exogenous estrogen influence on joint symptoms provide mixed results. Against this background, estrogen alone effects on joint symptoms were examined in post hoc analyses in the Women’s Health Initiative randomized, placebo-controlled clinical trial.
Methods 10,739 postmenopausal women with prior hysterectomy were randomized to receive daily oral conjugated equine estrogen (0.625 mg/d) or matching placebo. The frequency and severity of joint pain and joint swelling were assessed by questionnaire at entry and year 1 from all participants and in a random 9.9% subsample (n=1062) following years 3 and 6. Logistic regression models were used to compare frequency and severity of symptoms by randomization group. Sensitivity analyses evaluated adherence influence on symptoms.
Results At baseline, joint pain and swelling were closely comparable in the randomization groups (about 77% with joint pain and 40% with joint swelling). After one year, joint pain frequency was significantly lower in the estrogen alone compared to the placebo group (76.3% vs 79.2%, P=0.001) as was joint pain severity and the difference in pain between randomization groups persisted through year 3. However, joint swelling frequency was higher in the estrogen alone group (42.1% vs 39.7%, P=0.02). Adherence adjusted analyses strengthen the estrogen association with reduced joint pain but attenuated the estrogen association with increased joint swelling.
Conclusions The current findings suggest that estrogen alone use in postmenopausal women results in a modest but sustained reduction in the frequency of joint pain
skin aging estrogen
14) Thornton, M. Julie. “Estrogens and aging skin.” Dermato-endocrinology 5.2 (2013): 264-270.
The menopause causes hypoestrogenism, accelerating age-related deterioration of the skin. Estrogen administration has positive effects on human skin by delaying or preventing skin aging manifestations,
15) Stevenson, Susan, and Julie Thornton. “Effect of estrogens on skin aging and the potential role of SERMs.” Clinical interventions in aging 2.3 (2007): 283.
Hormone replacement therapy (HRT) has been shown to increase epidermal hydration, skin elasticity, skin thickness (Sator et al 2001), and also reduces skin wrinkles
Post-menopausal skin has been shown to have increased dryness (Sator et al 2004), decreased elasticity (Henry et al 1997; Sumino et al 2004), and increased wrinkling (Dunn et al 1997).
16) Wend, Korinna, Peter Wend, and Susan A. Krum. “Tissue-specific effects of loss of estrogen during menopause and aging.” Frontiers in endocrinology 3 (2012): 19.
a number of studies have established an essential function of E2 in skin biology. Therefore, E2 may offer an appropriate treatment option to prevent or delay age-associated alterations of the skin by affecting dermal fibroblasts, epidermal keratinocytes, or hair follicles.
17) Emmerson, Elaine, and Matthew J. Hardman. “The role of estrogen deficiency in skin ageing and wound healing.” Biogerontology 13.1 (2012): 3-20.
18) Verdier‐Sévrain, Sylvie, Frederic Bonte, and Barbara Gilchrest. “Biology of estrogens in skin: implications for skin aging.” Experimental dermatology 15.2 (2006): 83-94.
Estrogen and Neuroprotection
19) Engler-Chiurazzi, E. B., M. Singh, and J. W. Simpkins. “From the 90׳ s to now: A brief historical perspective on more than two decades of estrogen neuroprotection.” Brain research 1633 (2016): 96.
neuroprotective actions of estrogen, and specifically 17β-estradiol, identified by early investigations, remain well-documented.
Preliminary investigations suggested that estrogen-containing therapies typically given for the management of disruptive menopausal symptoms could reduce AD risk, attenuate disease-associated cognitive deficits, and modulate brain substrates known to be dysregulated by the condition, such as the cholingeric system.
20) Engler-Chiurazzi, E. B., et al. “Estrogens as neuroprotectants: Estrogenic actions in the context of cognitive aging and brain injury.” Progress in neurobiology (2016).
Here we provide a summary of the biological actions of estrogen and estrogen-containing formulations in the context of aging, cognition, stroke, and traumatic brain injury.
21) Chakrabarti, Mrinmay, et al. “Estrogen receptor agonists for attenuation of neuroinflammation and neurodegeneration.” Brain research bulletin 109 (2014): 22-31.
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Jeffrey Dach MD
7450 Griffin Road Suite 190
Davie, Fl 33314
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