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Darrell Wilcox, MD · Medical Director

What's Wrong With Just Aging Naturally?

Quick Answer

Aging without hormone therapy is not a neutral default. It is the path on which a large share of adults meet the leading drivers of death and disability.

Cardiovascular disease remains the number-one U.S. killer, with 915,973 deaths in 2023. Coronary heart disease also becomes common with age (about 18 percent of men and 9 percent of women aged 60 to 79; about one in three men and one in five women aged 80 and older). After fifty, about one in three women and one in five men will have an osteoporotic fracture. A hip fracture is the highest-stakes example: roughly one in five to nearly one in three older adults die within a year, and many survivors never regain independent living. From midlife, lifetime Alzheimer risk is about one in five for women and one in ten for men, and about one in nine Americans aged 65 and older already has clinical Alzheimer dementia. Among adults 60 and older, more than one in four has diabetes, with modeled lifetime risk from young adulthood about one in three. About one in three Americans aged 65 and older reports a disability.

Hormone therapy is not a guarantee against those outcomes. Where randomized trials tested replacement near the menopausal transition, and testosterone in high-risk men for diabetes, several hard endpoints moved: lower all-cause mortality, fewer fractures, fewer early-window cardiovascular events, and less diabetes. Men at high risk for diabetes who were given testosterone in that prevention trial developed diabetes at 12.4 percent against 21.0 percent on placebo, roughly 40 percent fewer cases. Those are trial results with hard endpoints, not projections from mechanism. What follows is the population burden, why hormones sit in the causal chain, what replacement improved, and where the evidence still stops.

On this page

What "aging naturally" actually delivers

"Natural" aging is not an empty backdrop. It is a population trajectory with measurable costs: death, fracture, metabolic disease, cognitive burden, and loss of independence among them.

Cardiovascular disease sits at the top of that list. In 2023 it accounted for 915,973 U.S. deaths. It is still the leading cause of death, about one every 34 seconds. Coronary heart disease alone is already common by the decades when hormones fall: among adults aged 60 to 79, about 18.4 percent of men and 8.5 percent of women have CHD; at age 80 and older the figures rise to 32.5 percent of men and 20.6 percent of women. Those are coronary-disease rates, not the broader American Heart Association tally that folds in hypertension and can make "half of adults have CVD" sound like half already have heart attacks. Declining to intervene on hormones does not erase that backdrop. It accepts the population default against which the early-window cardiovascular trials below are measured.

Bone is next. After age fifty, about one in three women and one in five men will have an osteoporotic fracture over their remaining lifetime. Age-adjusted DXA osteoporosis in U.S. adults 50 and older was 12.6 percent in 2017 to 2018 (19.6 percent of women, 4.4 percent of men), and 27.1 percent among women 65 and older. Between 2000 and 2011, American women aged 55 and older were hospitalized 4.9 million times for osteoporotic fractures, against 2.9 million times for heart attack, 3.0 million for stroke, and 0.7 million for breast cancer. Fractures accounted for more than 40 percent of all hospitalizations across those four conditions, carried the highest age-adjusted admission rate at 1,124 per 100,000 person-years against 668 for heart attack and 687 for stroke, and produced the highest annual hospital cost at 5.1 billion dollars.

A hip fracture is not a setback-and-bounce-back injury for most older adults. Roughly one in five to nearly one in three die within a year after a hip fracture, and among survivors a large share never regain their prior independence. In one registry of 4,912 adults aged 65 and older with an isolated hip fracture, 28 percent had died by twelve months, only 26 percent were living independently, and 46 percent had moderate-to-severe disability. Systematic reviews find that only about 40 to 70 percent of survivors regain prior basic self-care independence, that 10 to 20 percent are newly institutionalized after the fracture, and that among people who were independent beforehand, 20 to 60 percent still need help with various tasks at one to two years. Those figures describe why fracture prevention matters. They do not by themselves prove that hormone therapy prevents death after a hip fracture or restores independence.

The metabolic picture shifts in the same decades. Among U.S. adults aged 60 and older, total diabetes prevalence was 27.3 percent during August 2021 to August 2023 (20.5 percent diagnosed). Modeled lifetime risk of diagnosed diabetes from age 20 sits near 32.8 percent in recent estimates, about one in three. Insulin resistance, visceral fat, and chronic inflammation rise with age and reinforce one another. That midlife change sets the stage for cardiovascular disease, type 2 diabetes, and related disability.

Cognitive burden is part of the same aging arc. At age 45, estimated lifetime risk of Alzheimer dementia is about one in five for women and one in ten for men. About one in nine Americans aged 65 and older already has clinical Alzheimer dementia (roughly 7.4 million people in 2026), with prevalence rising from about 5 percent at ages 65 to 74 to more than one in three at age 85 and older. Nearly one in three older Americans dies with Alzheimer or another dementia. That is population risk, not a hormone-therapy endpoint; prevention of Alzheimer disease by hormone therapy has not been proven.

Functional loss tracks the same decades. In the Administration for Community Living's profile of older Americans (ACS 2022), about 33 percent of adults aged 65 and older report a disability, including 21 percent with serious difficulty walking or climbing stairs and 7 percent with difficulty dressing or bathing. That figure describes how common functional limitation already is after 65. Trials have not shown that hormone therapy prevents frailty or preserves independence; it belongs here as a consequence of aging, not as a claimed therapy endpoint.

Hormone therapy is not a guarantee against any of those outcomes. Where randomized trials tested replacement near the menopausal transition, and testosterone in high-risk men for diabetes prevention, several hard endpoints moved (mortality, fractures, early-window cardiovascular events, and diabetes incidence), which is why "do nothing" is still a decision with a measurable expected cost for people in that window.

Why hormones are part of that story

Several of the changes arriving in midlife are driven by the loss of specific signaling molecules, among them estrogen, progesterone, and testosterone. Those molecules can be replaced, and replacement has been tested in randomized trials with hard endpoints. The case for intervening rests on that observation, not on fear of aging.

Body composition is the clearest everyday illustration. The Study of Women's Health Across the Nation followed body composition by DXA through the menopause transition. Weight climbed steadily through the premenopausal years and did not accelerate at the transition, and the trajectory flattened afterward. What changed was what the weight was made of. At the start of the transition the rate of fat gain doubled and lean mass began to decline, and both continued until roughly two years after the final menstrual period. Because fat rose as lean fell, the sum stayed on the same path. The bathroom scale is the wrong instrument for this question. A woman who reports that her body has changed while her weight has not is describing something real and measurable.

Which hormone drives which half of that shift has been tested directly. Fifty-six healthy men received a GnRH antagonist to clear their own hormone production, then were randomized to combinations of testosterone with or without an aromatase inhibitor, so estrogen and androgen exposure could be varied independently. Changes in fat mass tracked estrogen exposure. Changes in lean mass tracked androgen exposure. The lean-mass effect is dose-dependent: in 61 men given graded weekly testosterone for twenty weeks under GnRH suppression, fat-free mass rose 3.4, 5.2, and 7.9 kg at the 125, 300, and 600 mg doses, with strength and muscle volume rising alongside testosterone concentration. Those were young men rather than older hypogonadal ones, so the magnitudes do not transfer directly, but the relationship is established.

Hormones are not the whole story of aging. They are a controllable piece of it, and the piece that follows has been measured against placebo.

What replacement improved in trials

Survival

A Bayesian meta-analysis pooled nineteen randomized trials covering 16,000 women with a mean age of 55 and 83,000 patient-years of follow-up. Total mortality showed a relative risk of 0.73, with a credible interval of 0.52 to 0.96. Adding eight prospective observational studies produced 0.72, with a tighter interval of 0.62 to 0.82. The authors' Bayesian conclusion was that, on the available evidence, the probability hormone therapy reduces total mortality in younger postmenopausal women is close to certain. That is their probabilistic reading of the pooled data, not a separate clinical claim from this practice.

The Cochrane review reaches a compatible figure from a different direction. Among women starting within ten years of menopause, all-cause mortality carried a relative risk of 0.70, with a confidence interval of 0.52 to 0.95, graded moderate quality evidence. Among women who started more than ten years out, no mortality benefit appeared at all.

A Finnish registry of 7,258 postmenopausal women experiencing a first acute coronary syndrome found that 42 percent of hormone therapy users died within a year, compared with 52 percent of non-users. That is survival after a cardiac event rather than avoidance of one, and it is observational, but it points the same direction.

Taken together: for women who start near the transition, declining hormone therapy means declining an intervention that lowered death from any cause by roughly a quarter to a third in pooled randomized data.

Bone

Estrogen prevents fractures. In a randomized trial of 16,608 women, total fractures occurred in 8.6 percent of treated women against 11.1 percent on placebo, a hazard ratio of 0.76 with a confidence interval of 0.69 to 0.83. Hip and clinical vertebral fractures fell by 34 percent, total osteoporotic fractures by 24 percent. Bone mineral density at the total hip rose 3.7 percent over three years against 0.14 percent on placebo. The fracture benefit held across every subgroup examined (age, body mass index, smoking status, history of falls, family history of fracture, calcium intake, and baseline bone density), including women in the lowest tertile of fracture risk.

Those women's fracture data come from conjugated equine estrogens with medroxyprogesterone acetate rather than from estradiol with micronized progesterone. The bone effect runs through the estrogen receptor and is not specific to the preparation, and estradiol carries its own FDA-approved indication for prevention of postmenopausal osteoporosis, but the fracture outcomes themselves were measured with the older combination.

For men, testosterone does something similar to the skeleton. In the Testosterone Trials bone substudy, 211 older men with low testosterone were randomized for a year. Trabecular volumetric bone density at the spine rose 7.5 percent against 0.8 percent on placebo, and estimated bone strength at the same site rose 10.8 percent against 2.4 percent. The trial counted six fractures in each arm, which is what a one-year study of 211 men would show whether or not a real fracture benefit exists. Density and strength improved. Fracture prevention in men has not been tested at the scale required to answer it.

Heart

The Danish Osteoporosis Prevention Study randomized 1,006 healthy women aged 45 to 58, recently postmenopausal, to estradiol-based therapy or no treatment. The composite of death, hospitalization for heart failure, or myocardial infarction occurred in 16 treated women against 33 controls, a hazard ratio of 0.48 with a confidence interval of 0.26 to 0.87. The reduction was still present at sixteen years. Over that follow-up there was no excess of cancer overall (hazard ratio 0.92) and no excess of breast cancer specifically (hazard ratio 0.58). That breast-cancer figure is a favorable point estimate from one trial and is underpowered to settle breast-cancer safety for hormone therapy in general; it shows no excess in DOPS, not definitive protection across preparations or populations.

Two imaging trials tested the artery wall directly, both using oral micronized 17-beta-estradiol. In the Estrogen in the Prevention of Atherosclerosis Trial, 222 postmenopausal women without cardiovascular disease were randomized to unopposed estradiol 1 mg daily or placebo for two years. Carotid wall thickness moved slightly backward on estradiol, at minus 0.0017 mm per year against plus 0.0036 mm per year on placebo. Among women not taking lipid-lowering medication, the difference was nearly three times larger. The Early versus Late Intervention Trial with Estradiol asked what happens when the same drug is started at different times. Among 643 women, those within six years of menopause showed carotid wall thickening at 0.0044 mm per year against 0.0078 mm per year on placebo, about half the rate. Among women ten or more years past menopause, there was no difference at all. Same drug, same dose, same endpoint; the only variable that differed was when treatment began.

The Cochrane data agree once read by timing. Women starting within ten years of menopause had coronary heart disease at a relative risk of 0.52, with a confidence interval of 0.29 to 0.96. Women starting later gained nothing and had more strokes. The review's headline conclusion, read without regard to timing, is that hormone therapy offers little cardiovascular benefit, and that is accurate as written. The timing analysis is why it does not settle the question for women near the transition.

On mechanism, oral estradiol lowers LDL cholesterol and apolipoprotein B by upregulating hepatic LDL receptor expression, the same pathway through which statins and PCSK9 inhibitors produce their benefit, and it raises HDL and lowers lipoprotein(a). How much of the vascular effect runs through the lipid change is unsettled. Estradiol also acts directly on endothelial function and arterial stiffness. The supported imaging claim is slowed or slightly reversed carotid wall thickening rather than reduction of established plaque; coronary calcium and plaque by CT in the early-versus-late trial showed no difference in either group, and neither imaging trial measured heart attacks as a primary endpoint.

Metabolic health and diabetes

In men, the T4DM trial randomized 1,007 men at high risk for type 2 diabetes to testosterone undecanoate or placebo on top of a lifestyle program. At two years, 12.4 percent of treated men had developed diabetes against 21.0 percent on placebo, a relative reduction of roughly 40 percent. The investigators note that HbA1c did not improve despite the improvement in glucose tolerance testing, that suppression of the reproductive axis persisted for up to twelve months after treatment stopped, and that longer evaluation is needed before testosterone is used broadly for diabetes prevention.

In women, the Women's Health Initiative hormone trial followed 15,641 women for 5.6 years and found treated diabetes in 3.5 percent of the hormone group against 4.2 percent on placebo, a hazard ratio of 0.79 with a confidence interval of 0.67 to 0.93. The effect changed little after adjusting for body mass index and waist circumference, which points at insulin sensitivity rather than at weight. Because that trial used conjugated estrogens rather than estradiol, a meta-analysis of fourteen randomized trials of 17-beta-estradiol plus norethisterone acetate matters: it found reductions in HbA1c of 0.65 percentage points, in fasting glucose of 11.05 mg/dL, and in fasting insulin of 1.35 mIU/L. These are estradiol-based data rather than extrapolations from conjugated estrogens.

Cognition: a signal, not proven prevention

The largest body of evidence on hormone therapy and dementia points toward reduced risk. A 2023 meta-analysis assembled 45 observational reports covering 768,866 cases and 5.5 million controls. Hormone therapy use was associated with reduced Alzheimer's disease at a relative risk of 0.78 (0.64 to 0.95) and reduced all-cause dementia at 0.81 (0.70 to 0.94). Estrogen-only therapy specifically came in at 0.86. Stratified by when treatment started, midlife estrogen-only therapy was associated with a 32 percent reduction (relative risk 0.685, interval 0.513 to 0.915). A separate analysis of 379,352 women drawn from a decade of claims data found reduced risk across every neurodegenerative outcome examined, with formulations containing 17-beta-estradiol and progesterone associated with greater reductions than synthetic formulations, and longer duration associated with greater reduction than shorter duration.

There is also randomized evidence on imaging rather than diagnoses. Women who had been on hormone therapy for about a decade were randomized either to continue or to stop, with brain metabolism measured by FDG-PET over two years. Those who continued showed relative preservation of frontal and parietal cortical metabolism. Women continuing unopposed 17-beta-estradiol specifically preserved metabolism in the precuneus and posterior cingulate, the region that declines earliest in Alzheimer's disease. Women who stopped estradiol, and women who continued conjugated equine estrogens instead, declined in that region. Estrogen supports synaptic plasticity, mitochondrial energy metabolism in neurons, and cerebral glucose utilization, and it modulates neuroinflammation. The brain is an estrogen-responsive organ; the loss of that signaling at menopause is a real physiologic event.

What the evidence does not yet support is a claim of prevention. Observational association is not the same as randomized proof, and women who take and continue hormone therapy differ systematically from women who do not. The one randomized trial that followed modern therapy started near menopause (transdermal estradiol with cyclic micronized progesterone) found cognition neither better nor worse than placebo about a decade after randomization. Its authors described the finding as reassurance about long-term neurocognitive safety, alongside no evidence of cognitive improvement or preservation. Estradiol started near menopause has long-term randomized evidence of cognitive safety and a large, consistent, formulation-dependent observational signal pointing toward lower dementia risk. It has not been proven to prevent dementia. Researchers at Weill Cornell and the University of Arizona have called for exactly that trial.

Women who lose ovarian function early, through premature ovarian insufficiency or removal of the ovaries before the usual age of menopause, carry higher long-term risk across several outcomes including cognition. Estrogen therapy through to the typical age of menopause is supported there, as replacement of something lost early rather than addition of something extra.

Timing

Early near the transition is the favorable window. Late is a different question.

Where hormone therapy was started near the menopausal transition, results were favorable: lower all-cause mortality in pooled randomized trials, a halving of the cardiovascular composite in a ten-year randomized trial, carotid wall thickness holding steady or regressing, a quarter fewer fractures, less diabetes. Where treatment began a decade or more later, results looked different: no mortality benefit, no vascular benefit, and more strokes in the Cochrane late-starter analysis. The dementia signal that raised alarm came from the Women's Health Initiative Memory Study, in women averaging about a decade and a half past menopause, randomized to conjugated equine estrogens plus medroxyprogesterone acetate. That study found roughly double the incidence of probable dementia. That is a late-start, older-preparation finding, not a verdict on modern estradiol with micronized progesterone started near the transition. In pooled randomized data the dementia risk tracked the progestogen rather than the estrogen (estrogen-plus-progestogen relative risk 1.64; estrogen-only 1.19, not statistically significant). Preparation and timing both matter: CEE plus MPA is not the same as estradiol plus micronized progesterone, and early is not the same as late. The useful question is when therapy is started, with which preparation, and in whom.

Honest boundaries

These limits belong in the conversation. They do not erase the benefits above.

  • Venous thromboembolism risk remained elevated even among early starters (relative risk 1.74). Timing does not appear to address it. That risk is tied mainly to the first-pass liver effect of oral estrogen, which is the main reason a transdermal route is often preferred.
  • Hormone therapy has not been proven to prevent Alzheimer's disease or dementia.
  • Trials have not demonstrated that body-composition changes translate into fewer falls, fewer fractures in men, or preserved independence. The Testosterone Trials found only modest effects on walking distance and vitality. The honest claim is about composition and metabolic consequence, not about frailty.
  • Hormone therapy is not a substitute for sleep, physical activity, alcohol moderation, and treatment of sleep apnea. Those factors move bone, brain, heart, and metabolism independently, often by more than any prescription will.
  • Someone already a decade or more past menopause is in a different situation than someone at the transition. The evidence for starting then is weak to unfavorable on several endpoints, and findings from late-start conjugated equine estrogens with medroxyprogesterone acetate do not automatically transfer to estradiol with micronized progesterone started near menopause.

Closing

The people most likely to benefit are those closest to the transition rather than furthest from it, which is the opposite of how hormone therapy is usually approached. Waiting until symptoms become unbearable, or until a decade has passed, forfeits the window in which the evidence looks most favorable.

Aging without hormone therapy is a real choice, and some people should make it. But it should be made knowing what the randomized data show for people who start near the transition: lower mortality, fewer fractures, fewer cardiovascular events, and less diabetes. Declining is not a neutral default. For those early-window endpoints already measured in randomized trials, it is a decision with a measurable expected cost. That is not a claim of dementia prevention or preserved independence, which have not been proven, and the decision deserves to be made deliberately rather than by drift.

Worth bringing to that conversation: bone density, lipids including apolipoprotein B, fasting insulin and HbA1c, a blood pressure measured more than once, a body composition assessment rather than a weight, and an honest account of how long it has been since the last menstrual period.

If you are weighing this decision and want the actual numbers applied to your own history rather than a general reassurance, that is a conversation worth having with a physician. If you are already a patient at one of my clinics, bring it up at your next visit.

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Darrell Wilcox, MD · @wellnessdoc_4everyoung on Instagram

References

  1. Salpeter SR, Cheng J, Thabane L, Buckley NS, Salpeter EE. Bayesian meta-analysis of hormone therapy and mortality in younger postmenopausal women. Am J Med. 2009;122(11):1016-1022. PMID 19854329.
  2. Boardman HMP, Hartley L, Eisinga A, et al. Hormone therapy for preventing cardiovascular disease in post-menopausal women. Cochrane Database Syst Rev. 2015;(3):CD002229. PMID 25754617.
  3. Tuomikoski P, Salomaa V, Havulinna A, et al. Decreased mortality risk due to first acute coronary syndrome in women with postmenopausal hormone therapy use. Maturitas. 2016;94:106-109. PMID 27823727.
  4. Cauley JA, Robbins J, Chen Z, et al. Effects of estrogen plus progestin on risk of fracture and bone mineral density: the Women's Health Initiative randomized trial. JAMA. 2003;290(13):1729-1738. PMID 14519707.
  5. Singer A, Exuzides A, Spangler L, et al. Burden of illness for osteoporotic fractures compared with other serious diseases among postmenopausal women in the United States. Mayo Clin Proc. 2015;90(1):53-62. PMID 25481833.
  6. Snyder PJ, Kopperdahl DL, Stephens-Shields AJ, et al. Effect of testosterone treatment on volumetric bone density and strength in older men with low testosterone. JAMA Intern Med. 2017;177(4):471-479. PMID 28241231.
  7. Schierbeck LL, Rejnmark L, Tofteng CL, et al. Effect of hormone replacement therapy on cardiovascular events in recently postmenopausal women: randomised trial. BMJ. 2012;345:e6409. PMID 23048011.
  8. Hodis HN, Mack WJ, Lobo RA, et al. Estrogen in the prevention of atherosclerosis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2001;135(11):939-953. PMID 11730394.
  9. Hodis HN, Mack WJ, Henderson VW, et al. Vascular effects of early versus late postmenopausal treatment with estradiol. N Engl J Med. 2016;374(13):1221-1231. PMID 27028912.
  10. Wittert G, Bracken K, Robledo KP, et al. Testosterone treatment to prevent or revert type 2 diabetes in men enrolled in a lifestyle programme (T4DM): a randomised, double-blind, placebo-controlled, 2-year, phase 3b trial. Lancet Diabetes Endocrinol. 2021;9(1):32-45. PMID 33338415.
  11. Margolis KL, Bonds DE, Rodabough RJ, et al. Effect of oestrogen plus progestin on the incidence of diabetes in postmenopausal women: results from the Women's Health Initiative Hormone Trial. Diabetologia. 2004;47(7):1175-1187. PMID 15252707.
  12. Cui W, Zhao L. The influence of 17-beta-estradiol plus norethisterone acetate treatment on markers of glucose and insulin metabolism in women: a systematic review and meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2023;14:1137406. PMID 37265701.
  13. Greendale GA, Sternfeld B, Huang M, et al. Changes in body composition and weight during the menopause transition. JCI Insight. 2019;4(5):e124865. PMID 30843880.
  14. Chao J, Rubinow KB, Kratz M, et al. Short-term estrogen withdrawal increases adiposity in healthy men. J Clin Endocrinol Metab. 2016;101(10):3724-3731. PMID 27482750.
  15. Bhasin S, Woodhouse L, Casaburi R, et al. Testosterone dose-response relationships in healthy young men. Am J Physiol Endocrinol Metab. 2001;281(6):E1172-E1181. PMID 11701431.
  16. Snyder PJ, Bhasin S, Cunningham GR, et al. Effects of testosterone treatment in older men. N Engl J Med. 2016;374(7):611-624. PMID 26886521.
  17. Nerattini M, Jett S, Andy C, et al. Systematic review and meta-analysis of the effects of menopause hormone therapy on risk of Alzheimer's disease and dementia. Front Aging Neurosci. 2023;15:1260427. PMID 37937120.
  18. Kim YJ, Soto M, Branigan GL, Rodgers K, Brinton RD. Association between menopausal hormone therapy and risk of neurodegenerative diseases: implications for precision hormone therapy. Alzheimers Dement (N Y). 2021;7(1):e12174. PMID 34027024.
  19. Rasgon NL, Geist CL, Kenna HA, Wroolie TE, Williams KE, Silverman DHS. Prospective randomized trial to assess effects of continuing hormone therapy on cerebral function in postmenopausal women at risk for dementia. PLoS One. 2014;9(3):e89095. PMID 24622517.
  20. Maki PM. Minireview: effects of different HT formulations on cognition. Endocrinology. 2012;153(8):3564-3570. PMID 22673228.
  21. Gleason CE, Dowling NM, Kara F, et al. Long-term cognitive effects of menopausal hormone therapy: findings from the KEEPS Continuation Study. PLoS Med. 2024;21(11):e1004435. PMID 39570992.
  22. Mosconi L, Nerattini M, Williams S, Fink M. New horizons in menopause, menopausal hormone therapy, and Alzheimer's disease. J Clin Endocrinol Metab. 2025;110(4):911-921. PMID 39815764.
  23. Centers for Disease Control and Prevention / National Center for Health Statistics. Deaths: Leading Causes for 2023. NCHS Data Brief No. 521. December 2024.
  24. Chêne G, Beiser A, Au R, et al. Gender and incidence of dementia in the Framingham Heart Study from mid-adult life. Alzheimers Dement. 2015;11(3):310-320. PMC4092061. PMID 24418058.
  25. International Osteoporosis Foundation. Epidemiology of osteoporosis and fracture (synthesis citing Kanis JA; Melton LJ III remaining-lifetime osteoporotic fracture risk after age 50: approximately 1 in 3 women and 1 in 5 men).
  26. Palaniappan LP, et al. 2026 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association. Circulation. 2026. DOI 10.1161/CIR.0000000000001412. PMID 41562125.
  27. Alzheimer's Association. 2026 Alzheimer's Disease Facts and Figures. Alzheimers Dement. 2026. DOI 10.1002/alz.71345.
  28. Sarafrazi N, Wambogo EA, Shepherd JA. Osteoporosis or low bone mass in older adults: United States, 2017–2018. NCHS Data Brief No. 405. 2021.
  29. Koyama AK, Cheng YJ, Brinks R, et al. Trends in lifetime risk and years of potential life lost from diabetes in the United States, 1997-2018. PLoS One. 2022;17(5):e0268805. PMID 35609056.
  30. Administration for Community Living. 2023 Profile of Older Americans (American Community Survey 2022 disability estimates).
  31. Giummarra MJ, Ekegren CL, Gong J, et al. Twelve month mortality rates and independent living in people aged 65 years or older after isolated hip fracture: a prospective registry-based study. Injury. 2020;51(2):420-428. PMID 31810636.
  32. Dyer SM, Crotty M, Fairhall N, et al. A critical review of the long-term disability outcomes following hip fracture. BMC Geriatr. 2016;16:158. PMC5010762. PMID 27590604.
  33. Gwira JA, Fryar CD, Gu Q. Prevalence of Total, Diagnosed, and Undiagnosed Diabetes in Adults: United States, August 2021–August 2023. NCHS Data Brief No. 516. November 2024.

Related

This content is for educational purposes only and does not constitute medical advice or a diagnosis. Whether hormone therapy is appropriate for any individual depends on personal and family history, timing relative to menopause, route of administration, and an individualized assessment of risks and benefits. Hormone therapy is not FDA-approved for the prevention of cardiovascular disease, dementia, or diabetes, and is not approved as an anti-aging therapy. Several of the findings described above come from observational studies, which can show association but not causation. Trials cited used varying preparations, and findings from conjugated equine estrogens with medroxyprogesterone acetate do not necessarily apply to bioidentical estradiol and micronized progesterone. Individual results vary, and no outcome is guaranteed. Always consult your own physician before starting, stopping, or changing any hormone regimen. Dr. Wilcox's current state licensure is listed on the About page.