Studies have shown that a woman’s risk of developing breast cancer is related to her exposure to hormones that are produced by her ovaries (endogenous estrogen and progesterone). Reproductive factors that increase the duration and/or levels of exposure to ovarian hormones, which stimulate cell growth, have been associated with an increase in breast cancer risk. These factors include early onset of menstruation, late onset of menopause, and factors that may allow breast tissue to be exposed to high levels of hormones for longer periods of time, such as later age at first pregnancy and never having given birth.

Conversely, pregnancy and breastfeeding, which both reduce a woman’s lifetime number of menstrual cycles, and thus her cumulative exposure to endogenous hormones (1), are associated with a decrease in breast cancer risk. In addition, pregnancy and breastfeeding have direct effects on breast cells, causing them to differentiate, or mature, so they can produce milk. Some researchers hypothesize that these differentiated cells are more resistant to becoming transformed into cancer cells than cells that have not undergone differentiation (2, 3).

Some pregnancy-related factors have been associated with a reduced risk of developing breast cancer later in life. These factors include:

• Early age at first full-term pregnancy. Women who have their first full-term pregnancy at an early age have a decreased risk of developing breast cancer later in life. For example, in women who have a first full-term pregnancy before age 20, the risk of developing breast cancer is about half that of women whose first full-term pregnancy occurs after the age of 30 (4). This risk reduction is limited to hormone receptor–positive breast cancer; age at first full-term pregnancy does not appear to affect the risk of hormone receptor-negative breast cancer (5, 6).
• Increasing number of births. The risk of breast cancer declines with the number of children borne. Women who have given birth to five or more children have half the breast cancer risk of women who have not given birth (7). Some evidence indicates that the reduced risk associated with a higher number of births may be limited to hormone receptor–positive breast cancer.
• History of preeclampsia. Women who have had preeclampsia may have a decreased risk of developing breast cancer (8–11). Preeclampsia is a complication of pregnancy in which a woman develops high blood pressure and excess amounts of protein in her urine. Scientists are studying whether certain hormones and proteins associated with preeclampsia may affect breast cancer risk (8, 12, 13).
• Longer duration of breastfeeding. Breastfeeding for an extended period (at least a year) is associated with decreased risks of both hormone receptor–positive and hormone receptor–negative breast cancers (6, 14).

Some factors related to pregnancy may increase the risk of breast cancer. These factors include:

• Older age at birth of first child. The older a woman is when she has her first full-term pregnancy, the higher her risk of breast cancer. Women who are older than 30 when they give birth to their first child have a higher risk of breast cancer than women who have never given birth (15).
• Recent childbirth. Women who have recently given birth have a short-term increase in breast cancer risk that declines after about 10 years. The reason for this temporary increase is not known, but some researchers believe that it may be due to the effect of high levels of hormones on the development of cancers or to the rapid growth of breast cells during pregnancy (16).
• Taking diethylstilbestrol (DES) during pregnancy. DES is a synthetic form of estrogen that was used between the early 1940s and 1971 to prevent miscarriages and other pregnancy problems. Women who took DES during pregnancy may have a slightly higher risk of developing breast cancer than women who did not take DES during pregnancy (17). Some studies have shown that daughters of women who took DES during pregnancy may also have a slightly higher risk of developing breast cancer after age 40 than women who were not exposed to DES while in the womb (18), but the evidence is inconsistent (19).

A few retrospective (case-control) studies reported in the mid-1990s suggested that induced abortion (the deliberate ending of a pregnancy) was associated with an increased risk of breast cancer. However, these studies had important design limitations that could have affected the results. A key limitation was their reliance on self-reporting of medical history information by the study participants, which can introduce bias. Prospective studies, which are more rigorous in design and unaffected by such bias, have consistently shown no association between induced abortion and breast cancer risk (20–25). Moreover, in 2009, the Committee on Gynecologic Practice of the American College of Obstetricians and Gynecologists concluded that “more rigorous recent studies demonstrate no causal relationship between induced abortion and a subsequent increase in breast cancer risk” (26). Major findings from these studies include:

• Women who have had an induced abortion have the same risk of breast cancer as other women.
• Women who have had a spontaneous abortion (miscarriage) have the same risk of breast cancer as other women.
• Cancers other than breast cancer also appear to be unrelated to a history of induced or spontaneous abortion.

Research has shown the following with regard to pregnancy and the risk of other cancers:

• Women who have had a full-term pregnancy have reduced risks of ovarian (27, 28) and endometrial (29) cancers. Furthermore, the risks of these cancers decline with each additional full-term pregnancy.
• Pregnancy also plays a role in an extremely rare type of tumor called a gestational trophoblastic tumor. In this type of tumor, which starts in the uterus, cancer cells grow in the tissues that are formed following conception.
• There is some evidence that pregnancy-related factors may affect the risk of other cancer types, but these relationships have not been as well studied as those for breast and gynecologic cancers. The associations require further study to clarify the exact relationships.

As in the development of breast cancer, exposures to hormones are thought to explain the role of pregnancy in the development of ovarian, endometrial, and other cancers. Changes in the levels of hormones during pregnancy may contribute to the variation in risk of these tumors after pregnancy (30).

Women who have difficulty becoming pregnant or carrying a pregnancy to term may receive fertility treatment. Such treatment can include surgery (to repair diseased, damaged, or blocked fallopian tubes or to remove uterine fibroids, patches of endometriosis, or adhesions); medications to stimulate ovulation; and assisted reproductive technology.

Ovarian stimulation and some assisted reproductive technologies involve treatments that temporarily change the levels of estrogen and progesterone in a woman’s body. For example, women undergoing in vitro fertilization (IVF) receive multiple rounds of hormone treatment to first suppress ovulation until the developing eggs are ready, then stimulate development of multiple eggs, and finally promote maturation of the eggs. The use of hormones in some fertility treatments has raised concerns about possible increased risks of cancer, particularly cancers that are linked to elevated levels of these hormones.

Many studies have examined possible associations between use of fertility drugs or IVF and the risks of breast, ovarian, and endometrial cancers. The results of such studies can be hard to interpret because infertility itself is linked to increased risks of these cancers (that is, compared with fertile women, infertile women are at higher risk of these cancers even if they do not use fertility drugs). Also, these cancers are relatively rare and tend to develop years after treatment for infertility, which can make it difficult to link their occurrence to past use of fertility drugs.

• Breast cancer: The bulk of the evidence is consistent with no increased risk of breast cancer associated with the use of fertility drugs or IVF (31–34). 
• Ovarian cancer: There is some uncertainty about whether treatment for infertility is a risk factor for ovarian cancer. A 2013 systematic review of 25 studies that included more than 180,000 women found, overall, no strong evidence of an increased risk of invasive ovarian cancer for women treated with fertility drugs (35). In one study, women who underwent IVF had an increase in risk of ovarian borderline malignant tumors (36).
• Endometrial cancer: Overall, the use of fertility drugs or IVF does not appear to increase the risk of endometrial cancer (34).

The overall risk of cancer is not elevated in people whose mothers used DES while pregnant compared with the general population (6–8). However, females exposed to DES in utero, commonly called DES daughters, are at increased risk of several specific cancers, including:

• Clear cell adenocarcinoma. DES daughters have about 40 times the risk of developing clear cell adenocarcinoma of the lower genital tract as unexposed women (women who were not exposed to DES prenatally). However, this type of cancer is still rare; approximately 1 in 1,000 DES daughters developed it. The first DES daughters with clear cell adenocarcinoma were very young at the time of their diagnoses (3). Subsequent research has shown that the risk of developing this disease remained elevated as these individuals aged into their 40s and 50s, but it continued to be rare (8, 9).
• Breast cancer. DES daughters may have a slightly increased risk of breast cancer after age 40. A 2006 study from the United States suggested that breast cancer risk is not increased in DES daughters overall but that after age 40, DES daughters have approximately twice the risk of breast cancer as unexposed women of the same age and with similar risk factors (6). A 2011 study also found that a large cohort of DES daughters had nearly twice the risk of developing breast cancer at 40 years or older as unexposed women (10), but a 2019 follow-up study showed that their breast cancer risk has lessened over time (7). It is therefore possible that risk was increased for a limited time at middle age. However, a 2010 study from Europe found no difference in breast cancer risk between DES daughters and women not exposed to DES in utero (8).
• Pancreatic cancer. A 2021 study found that DES daughters had about two times the risk of pancreatic cancer as women in the general population (11). Research is ongoing to determine if the increased risk persists as these individuals get older.
• Cervical precancers. Studies show that DES daughters were about 2 times more likely to have high-grade cell changes in the cervix than females not exposed to DES in utero. Approximately 4% of DES daughters developed these conditions because of their exposure (10). 

Males exposed to DES in utero, referred to as DES sons, have been studied for their risk of testicular and prostate cancers. There is no evidence to date that DES exposure in utero increases the risk of prostate cancer (12, 13).  However, the evidence around testicular cancer is mixed.

People who were exposed to DES in utero may have other health issues or characteristics, including:

Autoimmune conditions.  Concerns have been raised that individuals exposed to DES in utero may have problems with their immune system. However, research thus far suggests that DES daughters do not have an increased risk of autoimmune diseases. Researchers found no difference in the rates of lupus, rheumatoid arthritis, optic neuritis, and idiopathic thrombocytopenia purpura between women who were and were not exposed to DES in utero (16).

Cardiovascular disease.  Individuals exposed to DES have an increased risk of high cholesterol, hypertension, coronary artery disease, and heart attack but not of stroke (17, 18). The associations between prenatal DES exposure and coronary artery disease and heart attack appear to be stronger in DES daughters than DES sons (17).

Pancreatic disorders. One study found a higher risk of pancreatic disorders and pancreatitis (inflammation of the pancreas) in both DES daughters and DES sons compared with unexposed females and males (11). 

Early menopause. DES daughters have more than twice the risk of early menopause (menopause that begins before age 45) as unexposed women. Scientists estimate that 3% of DES-exposed women have experienced early menopause due to their exposure (10).

Depression. One study found a 40% higher risk of depression in DES daughters than in unexposed women (19), but other studies have not found increased risks (20, 21). Prenatal exposure of men to DES was not associated with the risk of depression (21). 

Psychosexual characteristics. Findings from animal studies have raised the possibility that prenatal exposure to DES may influence certain psychological and sexual characteristics of adult men and women. However, a 2003 study found little evidence that such exposure is associated with the likelihood of ever having been married, age at first sexual intercourse, number of sexual partners, or having had a same-sex sexual partner in adulthood (20). 

A study published in 2020 found that DES daughters were about 40% less likely to identify as gay/lesbian or bisexual compared with unexposed women (22). There were indications that DES-exposed men were more likely to be gay or bisexual, but these associations were not statistically significant (22).

Researchers are also studying possible health effects among the children of DES daughters. These groups are called DES granddaughters and DES grandsons, or the third generation. Researchers are studying these groups because studies in animal models suggest that DES may cause DNA changes (i.e., altered patterns of methylation) in mice exposed to the chemical during early development (23). These changes can be heritable and have the potential to affect subsequent generations.

A comparison of the results of DES granddaughters’ pelvic exams with those of their mothers’ first pelvic exams found none of the changes that had been associated with prenatal DES exposure in their mothers (14). However, another analysis showed that DES granddaughters began their menstrual periods later and were more likely to have menstrual irregularities than unexposed women of the same age (that is, women whose mothers were not exposed to DES before birth) (24). The data also suggested that infertility was greater among DES granddaughters than among unexposed women of the same age (25) and that they may have an increased risk of preterm delivery (24). However, this association is based on small numbers of events and was not statistically significant. Researchers will continue to follow these individuals to study the risk of infertility.

Recent studies have found that DES granddaughters and DES grandsons may have a slightly higher risk of cancer (26) and birth defects (27), including hypospadias in DES grandsons (28). However, because each of these associations is based on small numbers of events, researchers will continue to study these groups to clarify the findings.

The women who used DES are now in their 70s and older. These women have already experienced the slight increase in risks of developing (29) and dying from (30) breast cancer documented in follow-up studies in which they participated. No evidence exists to suggest that women who took DES are at higher risk for any other type of cancer (5).

Women who know or believe they were exposed to DES before birth should be aware of the health effects of DES and inform their health care provider about their possible exposure. 

Several major organizations publish guidelines about routine medical examinations and screening for women, but none of them address the needs of DES daughters specifically. These individuals have generally been advised to have an annual medical examination to check for adverse health effects of DES, including abnormal cervical cells and clear cell adenocarcinoma. In the past, that medical examination may have included a pelvic examination (in which the health care provider checks the vulva, vagina, cervix, ovaries, uterus, and rectum for any abnormalities) with a Pap test that collected cells from the cervix and the vagina; colposcopy (examination of the cervix with magnification) has been recommended to follow up on any abnormal findings. 

However, now that the population of DES daughters has become older (the youngest having been born in 1972), the relative benefits and harms of this approach compared with what is recommended for DES-unexposed individuals is unclear. For example, no guidelines address the age at which screening exams can end for these individuals. 

It is generally recommended that DES daughters follow the routine breast cancer screening recommendations for their age group.

Each woman should discuss this question with her health care provider. There is no evidence that hormone replacement therapy is unsafe for DES daughters. However, some clinicians believe that DES daughters should avoid these medications because they contain estrogen (32).

Researchers have conducted both observational studies and randomized controlled trials to look at possible links between someone’s vitamin D level or use of vitamin D supplements and their risk of developing or dying from cancer (11). Randomized trials are considered a stronger design because they control for the possibility that other differences between people, rather than their vitamin D status, explain associations seen in observational studies. However, vitamin supplementation trials are typically limited to testing one daily dosage, as compared with the measurement of a range of blood levels in observational studies. 

Evidence from observational studies

Cancer risk. Observational studies have examined a number of individual cancer sites for possible associations of risk with vitamin D level. Higher vitamin D levels have been consistently associated with reduced risks of colorectal cancer (12) and, to a lesser extent, bladder cancer (13). Studies have consistently shown no association between vitamin D levels and risk of breast, lung, and several other, less common cancers (14–17). By contrast, opposite (i.e., harmful) associations of risk with higher blood vitamin D levels have been suggested for prostate cancer (18) and possibly pancreatic cancer (19, 20).

Cancer mortality. Possible associations between vitamin D status and cancer mortality have generally been studied for all cancers combined. Most meta-analyses (i.e., studies that combine multiple individual studies) of observational studies have found that lower serum vitamin D levels are associated with higher overall cancer mortality (11, 21–24). For example, a meta-analysis of 12 cohort studies found a 14% higher cancer mortality among people with the lowest 25-hydroxyvitamin D levels than among those with the highest levels (22). Similarly, an analysis of approximately 4,000 cancer cases within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial found a 17% lower cancer mortality among men and women in the highest category of vitamin D than in the lowest category (25). 

Evidence from randomized controlled trials

Cancer risk. Most randomized controlled trials have found that vitamin D supplements, with or without calcium, do not reduce the risk of developing cancer overall or of developing specific cancers (11, 26–29). An evidence report prepared for the United States Preventive Serves Task Force (USPSTF) in its assessment of nutrient supplements to prevent cardiovascular disease or cancer found little or no benefit for vitamin D in preventing cancer, cardiovascular disease, and death (30). 

For example, the early large randomized Women’s Health Initiative trial found that supplementation with 400 IU vitamin D plus 1000 mg calcium had no effect on the incidence of breast or colorectal cancer among postmenopausal women (31–33). 

More recently, the largest trial of vitamin D supplementation, VITAL, assigned more than 25,000 participants aged 50 and over (men) or 55 and over (women) to receive a daily dose of 2000 IU vitamin D plus fish oil omega-3 fatty acids or of placebo. After 5 years of follow-up, the vitamin D/omega-3 group had the same overall cancer incidence as the placebo group (29). The incidence of breast, prostate, and colorectal cancer was also the same in both groups. Another large trial of vitamin D supplementation, ViDA, conducted among New Zealanders aged 50–84, also found no association between supplementation and the risk of cancer overall (34).  

In addition, findings from several trials cast doubt on the idea that taking vitamin D supplements prevents the development of colorectal adenomas, which can become colorectal cancer. In the VITAL trial, people who took vitamin D supplements did not have a lower risk of colorectal adenomas or serrated polyps at 5 years of follow-up (35). An ancillary study of a randomized trial in US adults with prediabetes and overweight or obesity found that vitamin D supplementation was not associated with incident cancer or colorectal polyps (36). And in the Vitamin D/Calcium Polyp Prevention Study, which studied people who had had at least one adenoma removed during colonoscopy at the start of the study, taking a daily vitamin D supplement did not reduce the risk that adenomas would recur during the following 10 years (37).

Cancer mortality. Several randomized controlled trials have studied whether vitamin D supplements lowers the risk of death from cancer, with varying results (11, 27, 29, 38, 39). For example, in the VITAL trial, vitamin D did not reduce cancer deaths overall, although a mortality reduction was seen in analyses that excluded deaths in the first few years of follow-up (28). In the D-Health trial, which included Australians 60 years and older, a monthly dose of 60,000 IU vitamin D for 5 years also did not reduce cancer mortality (40). 

However, a meta-analysis of 10 randomized controlled trials through 2018 (including the VITAL trial) found that vitamin D supplementation was associated with a slight (13%) reduction in cancer mortality over 3–10 years of follow-up (27). A meta-analysis of 21 randomized trials found no evidence that vitamin D supplementation was associated with reduced mortality from all causes combined or from cardiovascular disease (41). 

Many participants in these trials had blood levels of vitamin D that are considered adequate for overall health. This has led to speculation that any effects of vitamin D supplementation on cancer mortality might be more evident in people with low vitamin D levels (42), and researchers are pursuing this question.

Clinical trials are being conducted to examine the potential benefit of adding vitamin D supplements to other treatments for people with cancer. For example, the phase 3 SOLARIS trial is testing whether adding high-dose vitamin D3 to chemotherapy and bevacizumab would extend the length of time patients with advanced or metastatic colorectal cancer live without their disease getting worse. 

Researchers are also studying vitamin D analogs—chemicals with structures similar to that of vitamin D—which may have the anticancer activity of vitamin D but not the toxic effects of high doses (43). For example, ongoing clinical trials are testing both vitamin D and its analog paricalcitol alone or in combination with other treatments, including immunotherapy and chemotherapy, in patients with pancreatic cancer (44).

Another research question relates to the differing prevalence of vitamin D deficiency among racial/ethnic groups and whether these may contribute to some cancer disparities (45, 46). According to NHANES data for 2011–2014, the prevalence of vitamin D deficiency (defined as a serum 25-hydroxyvitamin D concentration of less than 30 nmol/L) among adults in the United States was 18% among non-Hispanic Black people, 2% among non-Hispanic White people, 8% among non-Hispanic Asian people, and 6% among Hispanic people (4). Black people are also less likely to use vitamin D supplements than White people (47).

Observational studies and investigations of biological mechanisms through which vitamin D status and supplementation influence cancer risk are ongoing. Also under study is whether any beneficial effects of vitamin D on cancer outcomes may be restricted to people who have certain genetic variants in genes that metabolize or transport vitamin D (48, 49). For example, a recent analysis of a US population found improved cancer survival primarily among women and men with a specific form of a vitamin D binding protein called GC (25). 

Menopausal hormone therapy (MHT)—also called postmenopausal hormone therapy and hormone replacement therapy—is sometimes used to replace the natural hormones estrogen and progesterone in a woman’s body during and after menopause, when levels of these hormones drop. Providers may recommend MHT to relieve common symptoms of menopause, such as hot flashes and vaginal dryness, and to address long-term biological changes, such as bone loss (osteoporosis), that result from declining levels of estrogen and progesterone.

Like most therapies, MHT has not only potential benefits but also possible harms. People should discuss the likely benefits and harms they might experience with their providers before deciding whether to use MHT and what form to use.  

MHT usually consists of estrogen alone or estrogen plus progestin, a synthetic form of progesterone. The hormones used in MHT are approved by the U.S. Food and Drug Administration (FDA) and come from a variety of plants and animals or are made in a laboratory. The chemical structure of these hormones is similar to those of hormones produced by women’s bodies. MHT can be given in a variety of ways. When the goal is to treat hot flashes and other systemic symptoms or to prevent osteoporosis, it is usually given as a pill, but it can be also be given systemically through the skin (e.g., via a patch, gel, or spray) or via an implant. When the goal is to address genitourinary symptoms such as vaginal dryness, MHT (containing low-dose estrogen only) is applied directly in the vagina (as a cream or suppository).

Which form of MHT is used depends on whether a woman has a uterus. Because estrogen, when used alone (i.e., without progestin) for systemic MHT, is associated with an increased risk of endometrial cancer, estrogen is used alone only in women who have had a hysterectomy. Women who have a uterus—that is, who have not had a hysterectomy—are generally prescribed estrogen plus progestin for systemic MHT. Vaginal estrogen to treat genitourinary symptoms is prescribed regardless of hysterectomy status. 

Non-FDA-approved hormone products, sometimes referred to as “bioidentical hormones,” are custom-mixed (or compounded) drugs that are sometimes sold without a prescription on the internet. Claims that these products are “safer” or more “natural” than FDA-approved hormonal products are not supported by credible scientific evidence. More information about these products can be found on FDA’s Menopause & Hormones: Common Questions fact sheet.

Much of the evidence about the health effects of MHT comes from two randomized clinical trials that were sponsored by the National Institutes of Health as part of the Women’s Health Initiative (WHI):

• The WHI Estrogen-plus-Progestin Study, in which women with a uterus were randomly assigned to receive either a hormone pill containing both estrogen and progestin (Prempro) or a placebo. The median duration of treatment was 5.6 years.
• The WHI Estrogen-Alone Study, in which women without a uterus were randomly assigned to receive either a hormone pill containing estrogen alone (Premarin) or a placebo. The median duration of treatment was 7.2 years.

Both trials were stopped early (in 2002 and 2004, respectively), when it was determined that both types of therapy were associated with specific health risks. 

Findings of follow-up studies of WHI participants and other studies have shown that MHT is associated with both potential benefits and potential harms (1). 

Potential benefits of MHT include: 

• relief of hot flashes, night sweats, vaginal dryness, and painful intercourse with systemic and local estrogen or systemic estrogen plus progestin for as long as MHT is taken
• lower risk of hip and vertebral fractures with systemic estrogen or estrogen plus progestin for as long as MHT is taken (2–5)
• lower risk of breast cancer with systemic estrogen (3, 5, 6)
• lower risk of death from breast cancer with systemic estrogen (6, 7)

Potential harms of systemic MHT include:

• increased risk of vaginal bleeding with estrogen plus progestin (8) that may require assessment by endometrial biopsy (because bleeding is a risk factor for uterine cancer)
• increased risk of urinary incontinence with both estrogen alone and estrogen plus progestin (2, 9)
• increased risk of dementia with both estrogen alone and estrogen plus progestin when taken by those 65 years or older (10–14)
• increased risk of stroke, blood clots, and heart attack with estrogen alone and estrogen plus progestin for as long as MHT is taken (2–5)
• increased risk of endometrial cancer in people with an intact uterus with estrogen alone
• increased risk of breast cancer with prior use of estrogen plus progestin for at least a decade after use is discontinued (6, 15, 16)
• increased breast density with estrogen plus progestin, making mammography less effective and also increasing breast cancer risk (17–20)
• increased risk of death from lung cancer with estrogen plus progestin (21)

Importantly, MHT is not associated with an increased risk of death from all causes (7).

Women who have had breast cancer in the past are often advised to avoid MHT because some studies suggest that it may increase the risk of breast cancer recurrence (22, 23). However, other studies have not shown an increased risk. For example, a Danish cohort study of postmenopausal women treated for early-stage breast cancer showed no increased risk of recurrence or mortality associated with the use of vaginal or systemic MHT (24).

Many studies have also been done to investigate whether MHT is safe for women who have experienced premature or severe menopausal symptoms as a result of cancer treatments that reduce hormone levels. A 2020 clinical practice statement from the Society of Gynecologic Oncology concluded that the benefits of MHT are likely to outweigh the risks for most people with epithelial ovarian, early-stage endometrial, and cervical cancer as well as for people with BRCA1 or BRCA2 gene mutations or Lynch syndrome and no history of breast cancer (25). However, the statement recommended against the use of MHT in women with advanced endometrial cancer, uterine sarcoma, or endometrioid or low-grade serous ovarian cancer.   

Women who are seeking relief from hot flashes and vaginal dryness should talk with their health care provider about whether to take MHT, the possible risks of using MHT, what formulation might be most appropriate for them, and possible alternative ways to address their symptoms. FDA advises women to use MHT for the shortest time and at the lowest dose possible to control menopausal symptoms.

Women who are concerned about the changes that occur naturally with the decline in hormone production that occurs during menopause can make changes in their lifestyle and diet to reduce the risk of certain health effects. For example, eating foods that are rich in calcium and vitamin D or taking dietary supplements containing these nutrients may help to prevent osteoporosis. 

Medications may be an option to reduce certain changes that come with menopause. For instance, three non-hormonal treatments are approved by the FDA to treat symptoms of menopause: fezolinetant (Veozah) and paroxetine (Brisdelle), to treat moderate to severe hot flashes associated with menopause, and ospemifene (Osphena), to treat moderate to severe pain with sexual activity due to menopause-associated vaginal changes. Other non-hormonal therapies suggested by the North America Menopause Society for relief of menopausal hot flashes include selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, oxybutynin, gabapentin, and cognitive behavioral therapy (26).  

Bone loss can be prevented with several FDA-approved drugs, such as alendronate (Fosamax), raloxifene (Evista), and risedronate (Actonel).

Some women seek relief from menopausal symptoms with complementary and alternative therapies. Some of these remedies contain phytoestrogens, which are estrogen-like compounds derived from plant-based sources such as soy products, whole-grain cereals, oilseeds (primarily flaxseed), legumes, or black cohosh. However, the North America Menopause Society does not recommend supplements, herbal remedies, or acupuncture for relief of hot flashes (26).

A 2016 systematic review and meta-analysis of randomized clinical trials of phytoestrogen-containing therapies found that some of these were associated with modest reductions in the frequency of hot flashes and vaginal dryness (27). According to the National Center for Complementary and Integrative Health, there is little information on the long-term safety of the use of natural products for menopausal symptoms, and some can have harmful side effects or interact with other drugs a woman may be taking.