The Women’s Health Initiative — a long-term study that has led to discoveries about cancer risks and other health conditions in women — recently came under threat.1 In April, the US Department of Health and Human Services (HHS) announced that it would cut funding for the Women’s Health Initiative, a move that was expected to have a major impact on ongoing research. However, the HHS ultimately reversed this decision, and the initiative can continue — at least for now.
The goals of the Women’s Health Initiative, which was launched in the early 1990s, were to explore major causes of death, disability, and frailty in older women.2 The original study concluded in 2005, but the initiative has continued as extension studies, with annual collections of outcome data for active participants.
“The Women’s Health Initiative … was designed to provide insights about factors that may prevent cardiovascular disease, hip fractures, and cancer in postmenopausal women,” explained Candice A. Price, PhD, program director of the Epidemiology Branch of the Division of Cardiovascular Sciences of the National Heart, Lung and Blood Institute in Bethesda, Maryland. “It remains the largest women’s health study in the United States.”
The original Women’s Health Initiative study (NCT00000611) enrolled 161,808 US women who were 50-79 years at baseline and were followed for up to 20 years.3 A total of 68,132 women were enrolled in 4 randomized clinical trials — 2 on hormone therapy, 1 on calcium and vitamin D supplementation, and 1 on dietary modifications.
“Additionally, thousands of other women have participated in observational arms of the study or its sister studies, which are designed to provide insight about factors that can support healthy aging and longevity in women,” Dr Price explained.
Recent results from Women’s Health Initiative studies have suggested that:
- Hormone therapy is associated with a lower risk of some cancers and a higher risk of others
- Vitamin D and calcium supplementation is associated with a lower risk of colorectal cancer (CRC), breast cancer, and cancer overall
- A dietary intervention is associated with a lower risk of breast cancer death
- Metabolic phenotype and body mass index (BMI) are associated with breast cancer and obesity-related cancers
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with a lower risk of pancreatic cancer.3-8
Hormone Therapy and Cancer
In one Women’s Health Initiative study, researchers found that postmenopausal women who received conjugated equine estrogens (CEE) and medroxyprogesterone acetate (MPA) had an increased risk of breast cancer compared to women who received placebo.3
The study enrolled 16,608 women, and the median follow-up was 5.6 years. The trial was stopped 3.3 years early because the risks of CEE and MPA were found to outweigh the benefits.
Results showed that receiving CEE plus MPA was associated with a 24% increase in breast cancer incidence at 5.6 years compared to placebo (0.43% vs 0.35% annually; hazard ratio [HR], 1.24; 95% CI, 1.01-1.53). At 20 years of follow-up, the breast cancer incidence was still significantly higher with CEE plus MPA than with placebo (0.45% and 0.36%, respectively; HR, 1.28; 95% CI, 1.13-1.45).
“CEE plus MPA also increased mammographic density, frequency of abnormal mammograms, and frequency of breast biopsies,” the researchers wrote. “These results suggested that CEE plus MPA stimulated breast cancer growth and delayed breast cancer diagnosis.”
The researchers also found that, initially, CEE plus MPA was associated with a 39% lower incidence of CRC compared to placebo (0.10% and 0.16%, respectively; HR, 0.61; 95% CI, 0.42-0.87). However, patients who received CEE plus MPA had larger tumors at diagnosis, which suggested delayed detection of CRC in these patients rather than a reduction in the incidence of CRC.
In another Women’s Health Initiative study, researchers compared CEE alone to placebo in 10,739 women who had prior hysterectomy.3 This trial was stopped 1 year early, at a median follow-up of 7.2 years, because the researchers observed an increased risk of stroke with CEE.
During the intervention, there was no significant difference in the rate of breast cancer between patients who received CEE and those who received placebo (0.28% and 0.35%, respectively; HR, 0.79; 95% CI, 0.61-1.02). However, at 10.7 years of follow-up, breast cancer incidence was significantly lower in the CEE group than in the placebo group (0.27% and 0.35%, respectively; HR, 0.77; 95% CI, 0.62-0.95).
Breast cancer death rates were also lower in the CEE group than in the placebo group, and this finding persisted through 20 years of follow-up (0.031% and 0.046%, respectively; HR, 0.60; 95% CI, 0.37-0.97).
“For estrogen plus progestin, we do want clinicians to be aware of the fact that, with longer duration, there is this increased risk of breast cancer, whereas, with estrogen alone, we’re not seeing this increased risk of breast cancer, and there may be more latitude in terms of the duration of use with estrogen alone if a woman is doing well on hormone therapy [for menopausal symptoms],” said JoAnn E. Manson, MD, DrPH, a professor of medicine at Harvard Medical School and chief of the Division of Preventive Medicine at Brigham and Women’s Hospital in Boston.
CEE monotherapy “definitely should not be used for the express purpose of trying to prevent cancer . . . because it does have such a complex matrix of benefits and risks,” she added. “But for treatment of moderate to severe or bothersome hot flashes, night sweats, or other menopausal symptoms in early menopause, where a woman will derive quality-of-life benefits, it is very likely that the benefits will outweigh the risks in that scenario.”
At the 2024 ASCO Annual Meeting, researchers reported long-term results on the associations between postmenopausal hormone therapy and ovarian and endometrial cancers.4
Twenty-year follow-up data suggested that CEE plus MPA did not increase the risk of developing ovarian cancer (HR, 1.14; 95% CI, 0.82-1.59; P =.44), dying from ovarian cancer (HR, 1.21; 95% CI, 0.84-1.74; P =.31), or dying after ovarian cancer (HR, 1.37; 95% CI, 0.95-1.98; P =.09) when compared to placebo.
The use of CEE plus MPA was associated with a lower risk of developing endometrial cancer (HR, 0.72; 95% CI, 0.56-0.92; P =.010) and dying after endometrial cancer (HR, 0.68; 95% CI, 0.47-0.97; P =.034) when compared to placebo. However, there was no significant difference in the risk of dying from endometrial cancer between CEE plus MPA recipients and placebo recipients (HR, 0.58; 95% CI, 0.29-1.16; P =.12).
The researchers also found evidence to suggest that CEE monotherapy increased the risk of developing ovarian cancer (HR, 2.04; 95% CI, 1.14-3.65; P =.014), dying from ovarian cancer (HR, 2.79; 95% CI, 1.30-5.99; P =.006), and dying after ovarian cancer (HR, 2.47; 95% CI, 1.26-4.84; P =.006) compared to placebo.
“Hormone therapy has a very complex effect on cancer,” Dr Manson noted.

Calcium Plus Vitamin D and Cancer
In another Women’s Health Initiative trial, researchers tested the health benefits of supplementation with calcium and vitamin D in 36,282 women.5 Participants were randomly assigned to receive calcium plus vitamin D (n=18,176) or placebo (n=18,106).
During cumulative follow-up, supplementation was associated with a 7% lower risk of cancer death when compared to placebo (annualized incidence, 0.50% and 0.54%, respectively; HR, 0.93; 95% CI, 0.87-0.99). However, there were no significant differences in deaths from specific cancers, including CRC, breast cancer, and other cancers.
The researchers also found that, during the intervention phase, women who did not take supplements before randomization but were randomly assigned to receive calcium and vitamin D on study had reductions in the risk of CRC (HR, 0.68; 95% CI, 0.46-0.99), invasive breast cancer (HR, 0.75; 95% CI, 0.60-0.93), and total cancer (HR, 0.85; 95% CI, 0.75-0.96).
These reductions in risk persisted during cumulative follow-up. There were reductions in the risk of CRC (HR, 0.69; 95% CI, 0.54-0.87), invasive breast cancer (HR, 0.81; 95% CI, 0.71-0.94), and total cancer (HR, 0.89; 95% CI, 0.82-0.96) among women who did not take supplements before randomization but were randomly assigned to receive calcium and vitamin D on study. However, there was no reduction in the risk of cancer death for these women (HR, 0.93; CI, 0.82-1.04).
“There has been increasing evidence . . . that vitamin D is linked to a reduced risk of advanced cancers,” Dr Manson noted. “This is not a reason to treat with calcium and vitamin D because we did not see a significant reduction in fractures, and there is some increased risk of kidney stones with supplementation. Our recommendation is to focus on diet, on dietary intake of these nutrients.”
However, postmenopausal women who cannot meet the dietary recommendations for calcium and vitamin D through food alone can safely take these supplements, Dr Manson said.
Diet and Cancer
The Women’s Health Initiative trial that was designed to evaluate the effects of a low-fat diet included 48,835 women — 19,541 who were randomly assigned to the dietary intervention and 29,294 who remained on their usual diet.3 The dietary intervention was designed to “reduce total fat consumption to 20% of total energy intake, increase vegetable and fruit intake to at least 5 servings per day, and increase grain intake to at least 6 servings per day,” researchers noted.
At 8.5 years of follow-up, patients in the low-fat diet group did not have a significantly lower risk of breast cancer than those who followed their usual diet (0.42% and 0.46%, respectively; HR, 0.92; 95% CI, 0.84-1.01; P =.09). Similarly, the risk of CRC was no lower in patients who followed the low-fat diet than in patients who followed their usual diet (0.13% and 0.12%, respectively; HR, 1.07; 95% CI, 0.90-1.27; P =.45).
However, during the intervention phase, all-cause mortality after a breast cancer diagnosis was reduced in the low-fat diet group (P =.02). In addition, at a 20-year cumulative follow-up, a reduction in breast cancer death was seen in the low-fat diet group compared to the usual-diet group (0.037% and 0.047% annually, respectively; HR, 0.79; 95% CI, 0.64-0.97; P =.02).
Dr Manson described this as a “key takeaway” from the study. “There are many components of fruits and vegetables that have been implicated in reducing cancer and deaths from cancer,” she noted. “We do think this dietary pattern offers an option for women who are at increased risk of breast cancer seeking to reduce these risks.”
Given the fact that the dietary intervention was associated with a lower risk of breast cancer death, researchers decided to use Women’s Health Initiative data to investigate associations between breast cancer and metabolic syndrome and obesity.6
The researchers analyzed 63,330 patients who had BMI and metabolic syndrome scores determined at study entry. Metabolic syndrome scores were divided into 3 categories (0, 1-2, and 3-4) and included high waist circumference (≥88 cm), high blood pressure (systolic ≥130 mm Hg and/or diastolic ≥85 mm Hg, or hypertension history), history of high cholesterol, and history of diabetes.
For BMI category, patients were divided into underweight or normal weight (BMI, <25 kg/m2), overweight (BMI, 25 to <30 kg/m2), grade 1 obesity (BMI, 30 to <35 kg/m2), and grade 2-3 obesity (BMI, ≥35 kg/m2) groups.
The median follow-up was more than 18.6 years for breast cancer incidence, 23.2 years for breast cancer death, and 20.4 years for death after breast cancer.
In analyses adjusted for BMI, breast cancer incidence was not higher in patients with a higher metabolic syndrome score (3-4 vs 0; P =.42). However, a metabolic syndrome score of 3-4 was associated with a higher risk of death from breast cancer (HR, 1.44; 95% CI, 1.02–2.04; P =.03) and death after breast cancer (HR, 1.53; 95% CI, 1.26-1.85; P <.001) than a score of 0.
In analyses adjusted for metabolic syndrome score, overweight women and obese women had a higher risk of developing breast cancer than women of normal weight (P trend <.001). The highest risk was seen in patients with grade 2-3 obesity (HR, 1.69; 95% CI, 1.52-1.89).
The researchers also found that the risk of death after breast cancer was higher in women who were overweight or obese (P <.001), and the risk of death from breast cancer was higher in women with grade 2-3 obesity (P <.001).
Researchers also used Women’s Health Initiative data to evaluate associations between obesity-related cancers and metabolic phenotype and BMI in an analysis of 20,593 women who were followed for a median of 21 years.7
When compared to patients who were metabolically healthy and of normal weight, the risk of any obesity-related cancer was significantly elevated among patients who were metabolically healthy and overweight or obese (HR, 1.15; 95% CI, 1.00-1.32) and patients who were metabolically unhealthy and overweight or obese (HR, 1.35; 95% CI, 1.18-1.54). There was no significant increase in risk for patients who were metabolically unhealthy and of normal weight (HR, 1.12; 95% CI, 0.90-1.39).
NSAIDs and Pancreatic Cancer
Researchers also used Women’s Health Initiative data to examine whether the use of NSAIDs is associated with the risk of pancreatic cancer.8 Of 117,452 patients included in this analysis, 54,695 were classified as nonusers of NSAIDs, 34,996 as inconsistent users, and 27,761 as consistent users.
At a median follow-up of 17.6 years, consistent use of any NSAID was associated with a lower risk of pancreatic cancer when compared to no use (HR, 0.71; 95% CI, 0.59-0.87). The association was strongest with any dose of aspirin (HR, 0.67; 95% CI, 0.52-0.86) and low-dose aspirin (HR, 0.54; 95% CI, 0.33-0.89) compared to nonuse.
“Consistent uses of non-aspirin NSAIDs (individually or as a class) and acetaminophen were not associated with pancreatic cancer risk,” the researchers wrote.
They also found that NSAID use was associated with a lower risk of pancreatic cancer among patients with diabetes (HR, 0.28; 95% CI, 0.10-0.75) and without diabetes (HR 0.75, 95% CI, 0.61-0.92).
“Additional large prospective studies with careful measurement of prevalent pancreatitis and NSAID type, frequency, and dose are needed to further investigate the possibility of stronger benefit among individuals diagnosed with diabetes,” the researchers concluded.
Disclosures: The Women’s Health Initiative is funded by the National Heart, Lung, and Blood Institute. Study pills for the Women’s Health Initiative trials were donated by Wyeth Ayerst and GlaxoSmithKline Consumer Healthcare. Dr Price and Dr Manson reported having no relevant disclosures. Some study authors disclosed conflicts of interest. Please see the original references for complete disclosure information.
This article originally appeared on Cancer Therapy AdvisorThe Women’s Health Initiative — a long-term study that has led to discoveries about cancer risks and other health conditions in women — recently came under threat.1 In April, the US Department of Health and Human Services (HHS) announced that it would cut funding for the Women’s Health Initiative, a move that was expected to have a major impact on ongoing research. However, the HHS ultimately reversed this decision, and the initiative can continue — at least for now.
The goals of the Women’s Health Initiative, which was launched in the early 1990s, were to explore major causes of death, disability, and frailty in older women.2 The original study concluded in 2005, but the initiative has continued as extension studies, with annual collections of outcome data for active participants.
“The Women’s Health Initiative … was designed to provide insights about factors that may prevent cardiovascular disease, hip fractures, and cancer in postmenopausal women,” explained Candice A. Price, PhD, program director of the Epidemiology Branch of the Division of Cardiovascular Sciences of the National Heart, Lung and Blood Institute in Bethesda, Maryland. “It remains the largest women’s health study in the United States.”
The original Women’s Health Initiative study (NCT00000611) enrolled 161,808 US women who were 50-79 years at baseline and were followed for up to 20 years.3 A total of 68,132 women were enrolled in 4 randomized clinical trials — 2 on hormone therapy, 1 on calcium and vitamin D supplementation, and 1 on dietary modifications.
“Additionally, thousands of other women have participated in observational arms of the study or its sister studies, which are designed to provide insight about factors that can support healthy aging and longevity in women,” Dr Price explained.
Recent results from Women’s Health Initiative studies have suggested that:
- Hormone therapy is associated with a lower risk of some cancers and a higher risk of others
- Vitamin D and calcium supplementation is associated with a lower risk of colorectal cancer (CRC), breast cancer, and cancer overall
- A dietary intervention is associated with a lower risk of breast cancer death
- Metabolic phenotype and body mass index (BMI) are associated with breast cancer and obesity-related cancers
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are associated with a lower risk of pancreatic cancer.3-8
Hormone Therapy and Cancer
In one Women’s Health Initiative study, researchers found that postmenopausal women who received conjugated equine estrogens (CEE) and medroxyprogesterone acetate (MPA) had an increased risk of breast cancer compared to women who received placebo.3
The study enrolled 16,608 women, and the median follow-up was 5.6 years. The trial was stopped 3.3 years early because the risks of CEE and MPA were found to outweigh the benefits.
Results showed that receiving CEE plus MPA was associated with a 24% increase in breast cancer incidence at 5.6 years compared to placebo (0.43% vs 0.35% annually; hazard ratio [HR], 1.24; 95% CI, 1.01-1.53). At 20 years of follow-up, the breast cancer incidence was still significantly higher with CEE plus MPA than with placebo (0.45% and 0.36%, respectively; HR, 1.28; 95% CI, 1.13-1.45).
“CEE plus MPA also increased mammographic density, frequency of abnormal mammograms, and frequency of breast biopsies,” the researchers wrote. “These results suggested that CEE plus MPA stimulated breast cancer growth and delayed breast cancer diagnosis.”
The researchers also found that, initially, CEE plus MPA was associated with a 39% lower incidence of CRC compared to placebo (0.10% and 0.16%, respectively; HR, 0.61; 95% CI, 0.42-0.87). However, patients who received CEE plus MPA had larger tumors at diagnosis, which suggested delayed detection of CRC in these patients rather than a reduction in the incidence of CRC.
In another Women’s Health Initiative study, researchers compared CEE alone to placebo in 10,739 women who had prior hysterectomy.3 This trial was stopped 1 year early, at a median follow-up of 7.2 years, because the researchers observed an increased risk of stroke with CEE.
During the intervention, there was no significant difference in the rate of breast cancer between patients who received CEE and those who received placebo (0.28% and 0.35%, respectively; HR, 0.79; 95% CI, 0.61-1.02). However, at 10.7 years of follow-up, breast cancer incidence was significantly lower in the CEE group than in the placebo group (0.27% and 0.35%, respectively; HR, 0.77; 95% CI, 0.62-0.95).
Breast cancer death rates were also lower in the CEE group than in the placebo group, and this finding persisted through 20 years of follow-up (0.031% and 0.046%, respectively; HR, 0.60; 95% CI, 0.37-0.97).
“For estrogen plus progestin, we do want clinicians to be aware of the fact that, with longer duration, there is this increased risk of breast cancer, whereas, with estrogen alone, we’re not seeing this increased risk of breast cancer, and there may be more latitude in terms of the duration of use with estrogen alone if a woman is doing well on hormone therapy [for menopausal symptoms],” said JoAnn E. Manson, MD, DrPH, a professor of medicine at Harvard Medical School and chief of the Division of Preventive Medicine at Brigham and Women’s Hospital in Boston.
CEE monotherapy “definitely should not be used for the express purpose of trying to prevent cancer . . . because it does have such a complex matrix of benefits and risks,” she added. “But for treatment of moderate to severe or bothersome hot flashes, night sweats, or other menopausal symptoms in early menopause, where a woman will derive quality-of-life benefits, it is very likely that the benefits will outweigh the risks in that scenario.”
At the 2024 ASCO Annual Meeting, researchers reported long-term results on the associations between postmenopausal hormone therapy and ovarian and endometrial cancers.4
Twenty-year follow-up data suggested that CEE plus MPA did not increase the risk of developing ovarian cancer (HR, 1.14; 95% CI, 0.82-1.59; P =.44), dying from ovarian cancer (HR, 1.21; 95% CI, 0.84-1.74; P =.31), or dying after ovarian cancer (HR, 1.37; 95% CI, 0.95-1.98; P =.09) when compared to placebo.
The use of CEE plus MPA was associated with a lower risk of developing endometrial cancer (HR, 0.72; 95% CI, 0.56-0.92; P =.010) and dying after endometrial cancer (HR, 0.68; 95% CI, 0.47-0.97; P =.034) when compared to placebo. However, there was no significant difference in the risk of dying from endometrial cancer between CEE plus MPA recipients and placebo recipients (HR, 0.58; 95% CI, 0.29-1.16; P =.12).
The researchers also found evidence to suggest that CEE monotherapy increased the risk of developing ovarian cancer (HR, 2.04; 95% CI, 1.14-3.65; P =.014), dying from ovarian cancer (HR, 2.79; 95% CI, 1.30-5.99; P =.006), and dying after ovarian cancer (HR, 2.47; 95% CI, 1.26-4.84; P =.006) compared to placebo.
“Hormone therapy has a very complex effect on cancer,” Dr Manson noted.

Calcium Plus Vitamin D and Cancer
In another Women’s Health Initiative trial, researchers tested the health benefits of supplementation with calcium and vitamin D in 36,282 women.5 Participants were randomly assigned to receive calcium plus vitamin D (n=18,176) or placebo (n=18,106).
During cumulative follow-up, supplementation was associated with a 7% lower risk of cancer death when compared to placebo (annualized incidence, 0.50% and 0.54%, respectively; HR, 0.93; 95% CI, 0.87-0.99). However, there were no significant differences in deaths from specific cancers, including CRC, breast cancer, and other cancers.
The researchers also found that, during the intervention phase, women who did not take supplements before randomization but were randomly assigned to receive calcium and vitamin D on study had reductions in the risk of CRC (HR, 0.68; 95% CI, 0.46-0.99), invasive breast cancer (HR, 0.75; 95% CI, 0.60-0.93), and total cancer (HR, 0.85; 95% CI, 0.75-0.96).
These reductions in risk persisted during cumulative follow-up. There were reductions in the risk of CRC (HR, 0.69; 95% CI, 0.54-0.87), invasive breast cancer (HR, 0.81; 95% CI, 0.71-0.94), and total cancer (HR, 0.89; 95% CI, 0.82-0.96) among women who did not take supplements before randomization but were randomly assigned to receive calcium and vitamin D on study. However, there was no reduction in the risk of cancer death for these women (HR, 0.93; CI, 0.82-1.04).
“There has been increasing evidence . . . that vitamin D is linked to a reduced risk of advanced cancers,” Dr Manson noted. “This is not a reason to treat with calcium and vitamin D because we did not see a significant reduction in fractures, and there is some increased risk of kidney stones with supplementation. Our recommendation is to focus on diet, on dietary intake of these nutrients.”
However, postmenopausal women who cannot meet the dietary recommendations for calcium and vitamin D through food alone can safely take these supplements, Dr Manson said.
Diet and Cancer
The Women’s Health Initiative trial that was designed to evaluate the effects of a low-fat diet included 48,835 women — 19,541 who were randomly assigned to the dietary intervention and 29,294 who remained on their usual diet.3 The dietary intervention was designed to “reduce total fat consumption to 20% of total energy intake, increase vegetable and fruit intake to at least 5 servings per day, and increase grain intake to at least 6 servings per day,” researchers noted.
At 8.5 years of follow-up, patients in the low-fat diet group did not have a significantly lower risk of breast cancer than those who followed their usual diet (0.42% and 0.46%, respectively; HR, 0.92; 95% CI, 0.84-1.01; P =.09). Similarly, the risk of CRC was no lower in patients who followed the low-fat diet than in patients who followed their usual diet (0.13% and 0.12%, respectively; HR, 1.07; 95% CI, 0.90-1.27; P =.45).
However, during the intervention phase, all-cause mortality after a breast cancer diagnosis was reduced in the low-fat diet group (P =.02). In addition, at a 20-year cumulative follow-up, a reduction in breast cancer death was seen in the low-fat diet group compared to the usual-diet group (0.037% and 0.047% annually, respectively; HR, 0.79; 95% CI, 0.64-0.97; P =.02).
Dr Manson described this as a “key takeaway” from the study. “There are many components of fruits and vegetables that have been implicated in reducing cancer and deaths from cancer,” she noted. “We do think this dietary pattern offers an option for women who are at increased risk of breast cancer seeking to reduce these risks.”
Given the fact that the dietary intervention was associated with a lower risk of breast cancer death, researchers decided to use Women’s Health Initiative data to investigate associations between breast cancer and metabolic syndrome and obesity.6
The researchers analyzed 63,330 patients who had BMI and metabolic syndrome scores determined at study entry. Metabolic syndrome scores were divided into 3 categories (0, 1-2, and 3-4) and included high waist circumference (≥88 cm), high blood pressure (systolic ≥130 mm Hg and/or diastolic ≥85 mm Hg, or hypertension history), history of high cholesterol, and history of diabetes.
For BMI category, patients were divided into underweight or normal weight (BMI, <25 kg/m2), overweight (BMI, 25 to <30 kg/m2), grade 1 obesity (BMI, 30 to <35 kg/m2), and grade 2-3 obesity (BMI, ≥35 kg/m2) groups.
The median follow-up was more than 18.6 years for breast cancer incidence, 23.2 years for breast cancer death, and 20.4 years for death after breast cancer.
In analyses adjusted for BMI, breast cancer incidence was not higher in patients with a higher metabolic syndrome score (3-4 vs 0; P =.42). However, a metabolic syndrome score of 3-4 was associated with a higher risk of death from breast cancer (HR, 1.44; 95% CI, 1.02–2.04; P =.03) and death after breast cancer (HR, 1.53; 95% CI, 1.26-1.85; P <.001) than a score of 0.
In analyses adjusted for metabolic syndrome score, overweight women and obese women had a higher risk of developing breast cancer than women of normal weight (P trend <.001). The highest risk was seen in patients with grade 2-3 obesity (HR, 1.69; 95% CI, 1.52-1.89).
The researchers also found that the risk of death after breast cancer was higher in women who were overweight or obese (P <.001), and the risk of death from breast cancer was higher in women with grade 2-3 obesity (P <.001).
Researchers also used Women’s Health Initiative data to evaluate associations between obesity-related cancers and metabolic phenotype and BMI in an analysis of 20,593 women who were followed for a median of 21 years.7
When compared to patients who were metabolically healthy and of normal weight, the risk of any obesity-related cancer was significantly elevated among patients who were metabolically healthy and overweight or obese (HR, 1.15; 95% CI, 1.00-1.32) and patients who were metabolically unhealthy and overweight or obese (HR, 1.35; 95% CI, 1.18-1.54). There was no significant increase in risk for patients who were metabolically unhealthy and of normal weight (HR, 1.12; 95% CI, 0.90-1.39).
NSAIDs and Pancreatic Cancer
Researchers also used Women’s Health Initiative data to examine whether the use of NSAIDs is associated with the risk of pancreatic cancer.8 Of 117,452 patients included in this analysis, 54,695 were classified as nonusers of NSAIDs, 34,996 as inconsistent users, and 27,761 as consistent users.
At a median follow-up of 17.6 years, consistent use of any NSAID was associated with a lower risk of pancreatic cancer when compared to no use (HR, 0.71; 95% CI, 0.59-0.87). The association was strongest with any dose of aspirin (HR, 0.67; 95% CI, 0.52-0.86) and low-dose aspirin (HR, 0.54; 95% CI, 0.33-0.89) compared to nonuse.
“Consistent uses of non-aspirin NSAIDs (individually or as a class) and acetaminophen were not associated with pancreatic cancer risk,” the researchers wrote.
They also found that NSAID use was associated with a lower risk of pancreatic cancer among patients with diabetes (HR, 0.28; 95% CI, 0.10-0.75) and without diabetes (HR 0.75, 95% CI, 0.61-0.92).
“Additional large prospective studies with careful measurement of prevalent pancreatitis and NSAID type, frequency, and dose are needed to further investigate the possibility of stronger benefit among individuals diagnosed with diabetes,” the researchers concluded.
Disclosures: The Women’s Health Initiative is funded by the National Heart, Lung, and Blood Institute. Study pills for the Women’s Health Initiative trials were donated by Wyeth Ayerst and GlaxoSmithKline Consumer Healthcare. Dr Price and Dr Manson reported having no relevant disclosures. Some study authors disclosed conflicts of interest. Please see the original references for complete disclosure information.
This article originally appeared on Cancer Therapy Advisor