Self-Reported Polycystic Ovary Syndrome Is Associated With Hypertension: A Northern Finland Birth Cohort 1966 Study


Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting 6% to 18% of reproductive-aged women (1, 2). Even though women with PCOS usually seek medical help for irregular menstruation, hirsutism, or infertility, the syndrome is also characterized by several metabolic risk factors, such as insulin resistance, dyslipidemia, and metabolic syndrome (3). Most women with PCOS are overweight or obese (4), and they also more often present with increased abdominal fat accumulation than weight-matched controls (5). Insulin resistance and hyperandrogenism, together with excess weight, are key features of PCOS.

Although PCOS is strongly associated with many traditional cardiovascular disease (CVD) risk factors (3), it has remained unclear if PCOS is an independent risk factor for hypertension. An Australian study including 26 women with self-reported PCOS and hypertension (mean age, 28 to 33 years) reported that in a normal-weight group, self-reported hypertension was more prevalent in PCOS than in the control group, whereas in the overweight/obese group, the prevalence of hypertension was similar, and in the multivariate regression analysis, PCOS was not significantly associated with hypertension (6). Furthermore, a hospital-based study population of 35 women with PCOS who had underwent wedge resection reported that these women had significantly higher prevalence of hypertension based on hospital discharge register information, even though clinically measured blood pressure (BP) levels were similar between PCOS and control groups (7). In contrast, several studies found comparable 24-hour ambulatory BP levels between PCOS and control groups (8–10). Moreover, the respective roles of body mass index (BMI) and PCOS as risk factors for hypertension are still controversial, as obesity has been reported to be the main determinant of hypertension in women with PCOS in some studies (10), whereas others have claimed that hypertension was more prevalent in PCOS, independently of weight (6, 11). Of note, previous studies have been limited with a small number of study participants (n = 14 to 36) (6–10).

It is well known that increased BP may lead to altered cardiac structure and function and increase the risk of adverse cardiovascular outcome (12). Increased BP leads to a greater workload of the heart, inducing a compensatory cardiac muscle hypertrophy and increased left ventricle pressure, leading to enlargement of the left atrium (12). In a cross-sectional study on 18- to 30-year-old women, women with PCOS displayed higher left atrium size and left ventricular mass index as well as a lower left ventricular ejection fraction and early to late mitral flow velocity ratio, but the role of hypertension was not assessed (13). However, it has been also reported that women with PCOS have similar cardiac structure and function as control women (14, 15). Moreover, even though women with PCOS have an increased prevalence of CVD risk factors and subclinical atherosclerosis, it is still unclear whether women with PCOS have an increased morbidity and mortality due to CVDs (16).

The main goal of this study was to investigate the prevalence of hypertension and antihypertensive medication usage in a population-based setup at ages 31 and 46 years in women with self-reported PCOS (srPCOS) and to determine the respective roles of PCOS and obesity in affecting hypertension and associated echocardiographic examination findings at age 46 years. Second, we aimed to assess whether women with srPCOS have a higher prevalence of cardiovascular morbidity compared with controls by age 46 years.

Materials and Methods

Study population

The study population arises from the Northern Finland Birth Cohort 1966, which is a large prospective general population-based longitudinal birth cohort. All individuals with expected term during 1966 in the two northernmost provinces in Finland (Oulu and Lapland) were included into this birth cohort, and the study population comprised all individuals born alive during that year (12,231 births, 5889 females, 96.3% of all births during 1966 in that area). Enrollment in this database began at the 24th gestational week, and so far, this cohort population has been followed at birth and at ages 1, 14, 31, and 46 years. Postal questionnaires were sent at ages 14, 31, and 46 years, and the current study used these data collection points. At ages of 31 and 46 years, clinical examinations were also performed (, last accessed 9 June 2018).

In 1980, at age 14 years, a postal questionnaire including questions about weight and height was sent to 5764 females, and 95% of them (n = 5455) responded with help from their parents. No other clinical data were collected at that age. In 1997, at age 31 years, a postal questionnaire, including questions about health, behavior, work, and social background, was sent to 5608 women, and 4523 (81%) of them responded. In addition, those living in northern Finland or in the Helsinki metropolitan area (n = 4074 women) were invited to a clinical examination. In total, 3127 (77%) women participated in a clinical examination including anthropometric measurements and blood samples for hormonal and metabolic parameters.

In 2012, at age 46 years, comprehensive health research was carried out. A postal questionnaire and invitation to a clinical examination were sent to all individuals alive and with known addresses (n = 5123 women). Of them, 3706 (72%) women responded to the questionnaire and 3280 women (64%) participated in the clinical examination. Postal questionnaires covered all main health-related issues, such as medication use, and all previously made disease diagnoses, lifestyle habits, education, and work. Clinical examination included measurements of height, weight, waist and hip circumference, blood sampling, and cardiovascular health status. A flowchart of the study is presented in Fig. 1.

Definition of PCOS and control populations

At age 31 years, the postal questionnaire included questions on oligo/amenorrhea: “Is your menstrual cycle often (more than twice a year) longer than 35 days?” and excessive body hair: “Do you have bothersome, excessive body hair growth?” Of the women who responded to these questions, 4.1% (n = 125) reported both oligo/amenorrhea and hirsutism (OA+H), after excluding pregnant women, women using hormonal preparations (n = 1459), or not permitting the use of their data for data analysis (n = 41). The validity of this questionnaire to distinguish PCOS cases has already been shown in our previous studies from the same cohort as the women with OA+H present the typical hormonal, metabolic, and psychological characteristics for the syndrome (4, 17–19). At age 46 years, the postal questionnaire included the following question: “Have you ever been diagnosed as having polycystic ovaries and/or polycystic ovary syndrome (PCOS)?” to which 181 responded “yes.” Consequently, women who reported OA+H at age 31 years and/or a diagnosis of polycystic ovaries (PCOs)/PCOS by age 46 years were considered women with srPCOS (n = 279). Women without any PCOS symptoms at age 31 years and without diagnosis of PCO/PCOS by age 46 years were considered controls (n = 1577). More detailed information regarding this issue has been published previously (4).

Definitions of elevated BP and hypertension

The assessment and diagnosis of hypertension were based on the European guidelines (20).

Measured elevated BP

In the clinical examination, brachial systolic and diastolic BP was measured twice at age 31 years and three times at age 46 years with a 1-minute interval after 15 minutes of rest on the right arm of the seated participants using a manual mercury sphygmomanometer at age 31 years and an automated, oscillometric BP device with an appropriately sized cuff (Omron Digital Automatic Blood Pressure Monitor Model M10-IT; Omron, Kyoto, Japan) at age 46 years. Averages of systolic and diastolic BP were calculated, and elevated BP was defined as BP ≥130/85 mm Hg (“measured elevated BP” in the following text) at age 31 or 46 years. Women using antihypertensive medication were excluded from the analysis reporting mean values of systolic and diastolic BP.

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Self-reported use of antihypertensive drugs

Information about antihypertensive medication was gathered from postal questionnaires at age 31 and 46 years, in which study participants reported all their medications, doses, and the reasons for use. The use of antihypertensive drugs was defined as “self-reported use of antihypertensive drugs” at age 31 or 46 years.

Hypertension at age 46 years

In the following text, “hypertension at age 46 years” (or “hypertensive at age 46 years”) is combined information from either self-reported use of antihypertensive medication at age 46 years and/or measured elevated BP at age 46 years.

Self-reported diagnosis of hypertension at age 46 years

Last, we considered separately a group of women with a self-reported diagnosis of hypertension in the questionnaire at age 46 years (“self-reported diagnosis of hypertension at age 46”).


As a part of the clinical examinations at age 46 years, a subpopulation was enrolled to echocardiographic examinations in the Oulu research unit (Fig. 1). As a rule, every second individual attending the clinical examination was randomly enrolled to an echocardiographic examination without any preselection criteria and without the participant’s own wish influencing the enrollment. All participants accepted to take part to the echocardiography. In total, echocardiography was performed in 645 women, including 37 women with srPCOS and 283 control women. Transthoracic two-dimensional echocardiography was performed online by an experienced cardiologist (K.K.), using the General Electric Vivid E9 device with a M5S-D 1.5/4.6-MHz sector transducer for cardiovascular imaging (GE Health Medical, Horten, Norway). All measurements followed the American Society of Echocardiography guidelines (21). In addition, global longitudinal strain was assessed offline using the EchoPac 7 software (automated function imaging) (22). Global strain is a novel indicator of the overall systolic function of the left ventricle and may reveal heart disease at an early stage, when ejection fraction is still normal (23).

Definitions of CVD manifestation and cardiovascular mortality

The International Classification of Diseases, Revisions 8, 9, and 10 (ICD-8, ICD-9, and ICD-10, respectively) diagnostic codes for cardiovascular morbidity and events (I20, I21 to I25, I50, I60 to I63, I63 to I64, I65 to I68, I69, I70, G45, G46) were identified from hospital discharge, hospital outpatient clinic, and basic health care registers, with data covering years 1972 to 2015, 1998 to 2015, and 2011 to 2015, respectively. In Finland, all individuals have a unique personal identification number. The individuals with serious acute illness are treated in public special health care centers, which report the diagnosis to the hospital discharge and hospital outpatient clinic registers. The data from national registers can be linked to an individual. Cardiovascular mortality data were retrieved from the mortality register of Statistics Finland, which covers information about cause of death and time of death.

Statistical methods

Ethical approval

The study followed the principles of the Declaration of Helsinki. The Ethics Committee of the Northern Ostrobothnia Hospital District has approved the research. All participants took part on a voluntary basis and signed an informed consent.


The clinical characteristics of srPCOS and control groups according to the BMI group are shown in Table 1. After BMI adjustment by general linear modeling, the women with srPCOS did not significantly differ from controls regarding waist circumference, serum levels of sex hormone binding globulin, total cholesterol and low-density lipoprotein, and free-androgen index, whereas women with srPCOS had significantly higher serum testosterone and lower high-density lipoprotein concentration than control women (data not shown). The glucose metabolism parameters have already been reported (25).

Prevalence of self-reported diagnosis of hypertension and use of antihypertensive drugs

The prevalence of self-reported diagnosis of hypertension at age 46 years was significantly greater among women with srPCOS compared with controls [Fig. 2(a), P < 0.001] at age 46 years. Furthermore, self-reported use of antihypertensive medication was significantly more common among women with srPCOS compared with control women both at age 31 years [Fig. 2(b), P = 0.022] and 46 years [Fig. 2(c), P < 0.001].

Measured elevated BP at age 31 and 46 years

At age 31 years, normal-weight as well as overweight/obese women with srPCOS had significantly higher systolic and diastolic BP than normal-weight and overweight/obese control women, respectively. At age 46 years, in the normal-weight group, women with srPCOS displayed significantly higher diastolic but not systolic BP compared with controls, whereas there were no significant differences between overweight/obese srPCOS women and overweight/obese controls (Table 1).

At age 46 years, women with srPCOS had significantly more often BP levels ≥140/90 mm Hg than control women [32% (n = 67/207) vs 25% (n = 332/1328), P = 0.027]. Of these 67 women with srPCOS who had BP ≥140/90 mm Hg, 18 (27%) already used antihypertensive medication, whereas 46 (69%) did not. In three srPCOS cases, information about antihypertensive medication was lacking. If a cutoff of 130/80 mm Hg for hypertension was used, as much as 71% (n = 147/207) of women with srPCOS were hypertensive, compared with 59% (n = 777/1328) of control women (P = 0.001).

Echocardiography at age 46 years

The echocardiographic parameters did not significantly differ between srPCOS and control women. However, there was a small, nonsignificant trend toward higher measured values for interventricular septal thickness at diastole, left ventricular mass index, and left atrial systolic volume compared with control women. There were no differences between women with srPCOS and controls in diastolic filling pressure estimated with E/e′ measurement (Table 2). The Cohen d values varied from 0 to 0.33, representing very small or small effect sizes.

Hypertensive women with PCOS had significantly higher values for measured interventricular septal thickness at diastole, left ventricular mass index, and left atrial systolic volume compared with normotensive controls. Estimated left ventricular filling pressure (E/e′) was also increased in hypertensive women with PCOS compared with normotensive controls, suggesting modest alterations in diastolic function in this PCOS subgroup. Left ventricular systolic function was mildly decreased in hypertensive women with PCOS (assessed by global strain), even though the difference in left ventricular ejection fraction was not statistically significant compared with other groups. The Cohen d values varied from 0.33 to 0.82. Similarly, hypertensive control women exhibited significant unfavorable changes in the echocardiography parameters compared with their normotensive counterparts, and the Cohen d values varied from 0.46 to 0.62 (Table 3).

Binary logistic regression analysis

In the crude univariate binary logistic regression analysis, srPCOS was significantly associated with hypertension (crude OR = 1.99; 95% CI, 1.40 to 2.52) at age 46 years, and this association remained significant (AOR = 1.78; 95% CI, 1.32 to 2.40) in the adjusted regression analysis (adjustment for consumption of alcohol, smoking, education, and use of combined contraceptive pills). In addition, in the regression analysis including also overweight/obesity at age 46 years as a covariate, srPCOS was associated with an increased risk of hypertension at age 46 years by 1.5-fold (AOR = 1.56; 95% CI, 1.14 to 2.13), independently of overweight/obesity (AOR for overweight/obesity at age 46 years = 3.62; 95% CI, 2.92 to 4.49).

Prevalence of CVD manifestations by age 46 years

The prevalence of any CVD was twice as high in women with srPCOS than in controls (6.8% vs 3.4%, P = 0.011), and the prevalence of myocardial infarction was already significantly higher in women with srPCOS (1.8% vs 0.5%, respectively, P = 0.034) at this early premenopausal age (Table 4). By age 46 years, two women with srPCOS, but no woman in the control group, had died as a result of ischemic heart disease.


To our knowledge, this is the largest general population-based prospective study with repeated cross-sectional assessments of Caucasian women with PCOS, providing well-documented information about hypertension based on the use of antihypertensive medication, diagnosis of hypertension set by a physician, and clinically measured BP level. Our main findings were that women with PCOS were significantly more often hypertensive and diagnosed with hypertension and more often used antihypertensive medication compared with controls. Moreover, elevated BP was associated with unfavorable changes in echocardiographic parameters in hypertensive women with srPCOS compared with normotensive women. Last, premenopausal women with srPCOS exhibited significantly increased cardiovascular morbidity, even though these results need to be interpreted with caution because of the small number of cases.

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In the current study, women with srPCOS more often had hypertension at age 46 years and had significantly greater diastolic and systolic BP at age 31 years than control women, regardless of BMI. In addition, at age 46 years, normal-weight women with srPCOS had significantly higher diastolic but not systolic BP compared with normal-weight controls, whereas the difference between srPCOS and control women vanished in the overweight/obese groups. In line with the present findings, previous cross-sectional studies including adolescent (11) and young reproductive-aged women (6) have reported significantly higher BP levels in normal-weight women with PCOS compared with normal-weight controls, whereas overweight and obese PCOS and control groups had a similar prevalence of hypertension (6, 11). These findings, in keeping with ours, suggest that PCOS has an independent effect on BP levels, even in young, normal-weight women. Of note, however, in the regression analysis, overweight/obesity was associated with hypertension by a greater odds ratio that for srPCOS, outlining the important role of excess weight as a determinant of hypertension in women with PCOS. In addition, after including also the known potential effect modifiers/risk factors for elevated blood pressure (alcohol consumption, education, smoking, physical activity, diabetes, obstructive sleep apnea, and dyslipidemia) in the regression analysis, the results did not change (data not shown). In contrast, some studies found comparable 24-hour ambulatory BP levels between PCOS and control groups, but that finding might be due to small study populations (8–10). Of note, our study population included only women of Caucasian ethnicity and may therefore differ from other populations regarding the prevalence of hypertension and other cardiovascular risk factors, as race/ethnicity has also been reported to affect these risks in women with PCOS (26). Our results are therefore best generalized to Caucasian populations.

Women with srPCOS showed no statistically significant changes in echocardiographic features, although some unfavorable trends were observed (increase in left atrial size, intraventricular septum thickness, and left ventricular mass). These changes are recognized as an adaptation of the heart to elevated levels of BP and are thought to predispose later to heart failure with preserved ejection fraction (27). Hypertensive women with srPCOS had significantly higher values for left atrial size, intraventricular septum thickness, and left ventricular mass compared with normotensive controls, whereas normotensive srPCOS and control groups had comparable cardiac structure and function, suggesting that elevated BP is an important determinant of the cardiac structure and function in women with PCOS. The relatively small number and young age of the women studied most likely explain why there were only few statistically significant differences in the echocardiographic parameters. The results of previous studies investigating cardiac structure and function in PCOS have been inconsistent. Two previous studies, investigating PCOS women in their 20s and 30s, reported significantly greater left atrial diameter and left ventricular mass in women with PCOS, independently of BMI, suggesting the early beginning of heart failure with preserved ejection fraction or abnormalities in the filling phase of the left ventricle (13, 28). In contrast, other studies have not reported any significant difference in the echocardiographic parameters between women with PCOS and controls (14, 15). The controversial findings of these previous studies might be explained by the differences in the age and ethnicity of the study groups as well as the criteria used for the diagnosis of PCOS.

In the current study, women with srPCOS had a significantly higher prevalence of acute myocardial infarction by age 46 years than control women, and the prevalence of any CVD diagnosis was twice as high in the PCOS group, even though these were premenopausal women. However, these results need to be interpreted with caution, as the number of affected women with overt CVD was very small. Likewise, no firm conclusions can be drawn with regard to the risk of CVD mortality in the current study because the numbers were so small (two vs none). Previous studies have reported inconsistent findings with regard to the risk of cardiovascular morbidity in women with PCOS, possibly because of variable study designs and ages of the participants. Recently, a Danish study reported that the event rate for CVD was significantly higher in premenopausal PCOS population compared with controls (29). Also, a nationwide, register-based study of PCOS women aged 30 years reported that PCOS was associated with a twofold higher risk of stroke and thrombosis, whereas the risk of other CVD was not significantly increased (30). A 20-year, retrospective cohort study reported a significantly increased odds ratio for myocardial infarction and a significant correlation with age, history of hypertension, and smoking with cardiovascular outcome in patients with PCOS (31). On the contrary, a 21-year follow-up study of 35 postmenopausal women with PCOS who had a history of wedge resection showed a similar prevalence of myocardial infarction and stroke between PCOS and control groups (7), and a retrospective observational study did not find any increased risk for large-vessel disease in women with PCOS (mean age 30 years) (32). In addition, a recent study reported that women with high postmenopausal androgen levels and retrospectively diagnosed with PCOS did not display an elevated risk for CVD (33). It has been postulated that later age at menopause and, consequently, more prolonged estrogen exposure could alleviate the CVD burden in PCOS despite the high CVD risk profiles commonly present in these women. However, whether this is due to lack of reliable data for the diagnosis and/or the fact that the women in most studies have been too young for detecting CVD events remains to be resolved in future, longitudinal studies.

The modest difference in BP levels observed in women with srPCOS is significant, as an increase of BP of 1.5 to 2 mm Hg has been shown to have a marked impact on CVD risk at a population level (34). In that study, the reduction of even mildly and/or moderately elevated BP to normal levels was associated with a reduced risk of CVDs (34). Of note, at age 46 years, one-third of the women with srPCOS displayed measured BP levels over the generally accepted cutoff value for starting antihypertensive medication (BP ≥140/90 mm Hg). Furthermore, of the women with srPCOS who had BP ≥140/90 mm Hg, 27% were hypertensive despite the use of antihypertensive medication, and even worse, over two-thirds of them (69%) were probably not aware of their elevated BP levels. The follow-up evaluation of these women in the future will reveal whether the cardiovascular risk actually increases further in women with PCOS and clarify the respective roles of the risk factors linked to PCOS with regard to cardiovascular morbidity.

The strengths of this study are the general population-based cohort study design, high participation and response rates, and low dropout rates. We have also previously reported that there were no significant differences between dropout and follow-up groups of women with OA+H at age 31 years (4). Importantly, BP was clinically measured at both ages 31 and 46 years. We were not able to adjust the results for some potential confounding factors (high sodium or low potassium intake, family history, stress and use of nonsteroidal anti-inflammatory drugs), but adjustment for alcohol consumption, education, smoking, physical activity, diabetes, obstructive sleep apnea, and dyslipidemia did not change the results. The cardiovascular event diagnoses were based on hospital discharge and outpatient registers, which have been shown to have a very high coverage and accuracy (88% to 98%) for vascular diseases in Finland (35). The main limitation of this study is that the definition of PCOS is based on self-reported symptoms and diagnosis of PCOS, as that may be prone to misdiagnosis. However, we have previously shown that the presence of both self-reported oligoamenorrhea and hirsutism can accurately identify women with the typical endocrine, metabolic, and psychological profiles of PCOS (17–19), with oligoamenorrhea always being self-reported data. Moreover, the presence of both oligoamenorrhea and hirsutism fulfills both Rotterdam and National Institutes of Health criteria for PCOS. Despite this, our results suggest that even women with srPCOS, who probably have milder hormonal and metabolic alteration than women with PCOS attending clinics, have increased risk for hypertension and CVDs. Another limitation of the diagnosis is that the questionnaire at age 46 years did not distinguish between those women with PCOs and those with established PCOS. However, women with PCO were reported to show a similar metabolic status as control women (36), and thus we would expect that the differences between the PCOS and control groups would have been even greater if we would have been able to exclude women with PCOs only. Other limitations of this study include the relatively small number of women in the echocardiographic analysis and of those who had a diagnosis of CVD.

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In conclusion, hypertension and use of antihypertensive medication were significantly more common among women with srPCOS compared with controls, and srPCOS was significantly associated with hypertension, independently of overweight/obesity. Moreover, normal-weight women with srPCOS displayed significantly higher BP levels than normal-weight controls already in their 30s. The hypertensive srPCOS women showed a consistent trend toward unfavorable changes in the cardiac structure and function, exposing them later to increased risk of heart failure with preserved ejection fraction. In addition, an increased prevalence of cardiovascular morbidity was already apparent in premenopausal women with srPCOS. Our results support strongly the recommendation of the Androgen Excess and PCOS (AE-PCOS) Society about the ideal BP for women with PCOS to be 120 mm Hg systolic and 80 mm Hg diastolic or lower (37). They are also in line with the results of the randomized, multicenter trial (Systolic Blood Pressure Intervention Trial) (38), recommending a goal of systolic BP level <120 mm Hg for people at high cardiovascular risk. Last, the present findings strengthen further the need for early systematic screening and efficient treatment of hypertension in women with PCOS, as recommended by the AE-PCOS Society (37) and the international evidence-based guideline for PCOS (39), as well as the importance of an active prevention and treatment of obesity in this particular group of women. Future prospective longitudinal studies are needed to establish the cause-effect relationship of PCOS and hypertension.




We thank the late Professor Paula Rantakallio for launching the Northern Finland Birth Cohort, the participants in the 31- and 46-year studies, and the Northern Finland Birth Cohort project center.

Financial Support: This work was supported by grants from the Finnish Medical Foundation, the North Ostrobothnia Regional Fund, Academy of Finland (project grants 315921, 104781, 120315, 129269, 1114194, 24300796, 295760), Center of Excellence in Complex Disease Genetics and SALVE, the Sigrid Juselius Foundation, University Hospital Oulu and University of Oulu (75617), Medical Research Center Oulu, National Institute for Health Research (UK), Genesis Research Trust (UK), NHLBI grant 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01), NIH/NIMH (5R01MH63706:02), ENGAGE project and grant agreement HEALTH-F4-2007-201413, EU FP7 EurHEALTHAgeing-277849 from the European Commission and the Medical Research Council (UK) (G0500539, G0600705, G1002319, G0802782, PrevMetSyn/SALVE), and the MRC, Centenary Early Career Award.

Disclosure Summary: The authors have nothing to disclose.


— Update: 17-02-2023 — found an additional article PCOS & High Blood Pressure: Know The Connection & Safeguard Your Health from the website for the keyword can pcos cause hypertension.

High blood pressure is among the many health risks for women with PCOS. High blood pressure is known as a “silent killer” because it strikes without any warning signs. By the time you realize that you have high blood pressure, most of the damage is already done. If you have PCOS, you need to be extra careful to prevent high blood pressure. Let’s find out more about PCOS and high blood pressure.

PCOS And High Blood Pressure: What’s The Connection?

Here are some reasons that explain the connection between PCOS and high blood pressure.


Obesity is the biggest reason behind high blood pressure in PCOS patients. More than 80% of women with PCOS in the US are overweight or obese. Fats stored in the body release a hormone called leptin. This hormone is directly involved in increasing blood pressure. So the more deposits of fat a person has, more is the activity of leptin in increasing blood pressure.

Insulin Resistance

Another reason for high blood pressure in women with PCOS is insulin resistance. In fact, high blood pressure and insulin resistance have a cause-effect relationship. It means that either can be the cause of the other. High levels of insulin increase the levels of sodium and calcium in the blood, making it thicker and sluggish. Thick and viscous blood exerts more pressure on the arterial walls, increasing blood pressure.

Excess Male Hormones

Excess male hormone levels are associated with an increase in the thickness of the walls of the carotid artery. The carotid artery is a major blood vessel arising from the heart. This artery supplies oxygen-rich blood to the head and neck regions of the body. If the walls of the carotid artery become thick, it ultimately leads to an increase in blood pressure.

Activity in the Nervous System

PCOS patients have a greater activity in the sympathetic nervous system, which is directly linked with high blood pressure. High levels of male hormones, obesity, and insulin resistance also stimulate the autonomic nervous system, which is also key in regulating blood pressure.

Tips To Reduce The Risk Of High Blood Pressure

As we have seen, there’s a strong link between PCOS and high blood pressure. Addressing individual symptoms of PCOS, such as hypertension and excess male hormones, is the most effective way of reducing the risk of high blood pressure.

Diet and lifestyle changes, such as exercise, are always considered as the first line of therapy for PCOS. They can reduce obesity, improve insulin sensitivity and reduce excess male hormones. Here are some dietary considerations to follow to minimize the risk of PCOS and high blood pressure:

  • Monitor your salt intake: According to the American Heart Association, an average adult eats way more sodium than what is recommended. Prepared meals, frozen and canned foods contain a lot of sodium. Always check nutrition labels for salt content before buying any processed foods.
  • Eat more fruits, vegetables, nuts, seeds, and legumes: These foods are rich in magnesium, potassium, and calcium; all of these minerals counter the effects of high sodium and bring down your blood pressure. The DASH (Dietary Approaches to Stop Hypertension) diet proves that including fresh fruits and vegetables in your diet can help in reducing blood pressure. The DASH diet recommends 4 to 5 servings per day of fruits and vegetables and 4 to 5 servings per week of nuts, seeds, and legumes.
  • Eat good fats: Fatty fish, avocados, nuts and olive oil have high amounts of Omega-3 fatty acids, which have a blood-pressure lowering effect.

PCOS And High Blood Pressure: Parting Words

Uncontrolled high blood pressure can damage blood vessels. It can also affect the key organs of the body, such as the heart, the eyes, the limbs, the kidneys, etc. If you have PCOS, monitor your blood pressure regularly and make the necessary changes to your diet and your lifestyle to keep it under check.

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About the Author: Tung Chi