Diet and lifestyle modifications may be of benefit in the management of polycystic ovary syndrome (PCOS), but there is a paucity of data on these behaviours in women with PCOS. This study aims to address this through a comprehensive investigation of the habitual diet and activity patterns of UK women with PCOS and their alignment with dietary recommendations for health.
A 7-day-estimated food and activity diary and questionnaire was completed by 210 women with PCOS for calculation of activity levels, energy and nutrient intakes and dietary glycaemic index (GI).
Mean (s.d.) body mass index (BMI) was 27.4 (7.3) kg/m2 (n=183), with 53% of women with PCOS having a BMI>25 kg/m2. Of the overweight women, approximately half were not achieving sufficient physical activity to promote weight loss. More frequent eating episodes and a lower BMI were weakly associated (r=−0.158, P=0.034). Mean percentage energy from fat was 38 (7)% (12% energy from saturated fat), with 68% of women with PCOS consuming > 35% energy from fat. Mean dietary GI was higher in obese women with PCOS, compared with healthy weight women with PCOS (55.7 (3.4) and 53.8 (4.0), respectively; P=0.043).
Many women with PCOS are not achieving dietary intakes and levels of physical activity that optimise symptom management and disease prevention. Advice should focus on fat quality and quantity and carbohydrate modification. There is a need for further robust research into the role of dietary GI in the PCOS population.
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, affecting up to 10% of women (Franks, 1995; Lindholm et al., 2008). The presentation of PCOS is heterogeneous in nature, including menstrual irregularity and fertility problems, hirsutism and acne (Diamanti-Kandarakis, 2008). Women with PCOS are also more likely to be overweight and have an increased risk of metabolic syndrome, type 2 diabetes and cardiovascular disease (Ehrmann et al., 1999; Dokras, 2008). The pathogenesis of PCOS is multifactorial; a key component is the association between insulin resistance, compensatory hyperinsulinaemia and hyperandrogenism (Balen, 2004; Carmina, 2006).
Weight loss through dietary restriction and increased physical activity are key management strategies for overweight and obese women with PCOS (Balen et al., 2006). Weight losses of as little as 5% have been shown to reduce insulin levels, improve ovulatory function and reduce serum testosterone (Moran et al., 2003; Stamets et al., 2004; Qublan et al., 2007). Reducing dietary glycaemic index (GI) may be advantageous with demonstrated benefits of low GI diets in non-PCOS insulin resistant populations (McMillian-Price et al., 2006; Barclay et al., 2008). Low GI diets are popular with women with PCOS (Jeanes et al., 2009), yet there is a paucity of data describing the habitual diet and lifestyle of women with PCOS, with just two studies reporting dietary intake of women with PCOS in the United States and one comparison of US and Italian women with PCOS (Carmina et al., 2003; Wright et al., 2004; Douglas et al., 2006). There are no publications describing the habitual diet or snacking habits of UK women with PCOS.
The referral rate to UK dietitians is also surprisingly low, with only 15% of women with PCOS having seen a dietitian (Jeanes et al., 2009; Sharma et al., 2010). Key sources of dietary information for women with PCOS have been reported as the internet and books (Avery and Braunack-Mayer, 2007; Humphreys and Costarelli, 2008; Jeanes et al., 2009). It is of concern that many of these sources are unregulated; there are currently no official UK dietary guidelines available for healthcare professionals advising women with PCOS.
Although increasing physical activity levels have been shown to improve glucose metabolism, insulin sensitivity (Kiddy et al., 1992; Vigorito et al., 2007) and reduce abdominal adiposity independent of weight loss (Ross et al., 2004), evidence from studies reporting the habitual physical activity levels of women with PCOS is relatively scarce.
This study aims to comprehensively investigate the habitual dietary intake and activity levels of women with PCOS in the UK and assess whether dietary and activity recommendations for health are being met. Given the heterogeneity of women with PCOS, this information is essential to accurately characterise their behaviours and hence identify the most relevant targets for lifestyle intervention.
Women with PCOS were recruited through the UK charity Verity via email. The investigators aimed to recruit the maximum number of participants within a 6-month period. Eligibility criteria required participants to be pre-menopausal, aged over 18 years and to provide a self reported diagnosis of PCOS, with date and means of diagnosis. Exclusion criteria included those who were pregnant or breastfeeding (currently or within the last 6 months), those suffering from any medical condition known to independently influence weight, body composition or biochemistry, those receiving treatment or currently suffering from an untreated eating disorder and those taking medication for weight loss (currently or within last 6 months). Ethical approval for the study was granted by Roehampton University Ethics Board, and Verity gave approval to contact their members.
Participants completed a questionnaire and a 7-day estimated food and activity diary (previously used in published studies (Truby et al., 2006)). The questionnaire was designed specifically for this study and included questions relating to diagnosis, self-reported symptoms (What conditions/symptoms do you have as a result of your PCOS?), weight (Is your weight stable?) and any PCOS-related nutritional advice received (Supplementary Data 1; Jeanes et al. 2009). Food diary data were entered into the dietary analysis software package Dietplan 6.3 (Forestfield Software, Horsham, UK) by a registered dietitian. Energy, macro and micronutrient intakes were calculated. National Diet and Nutrition Survey (NDNS) nutrient intakes (Bates et al., 2010) for women aged 19–64 years were used as reference values for comparison. Dietary GI and glycaemic load (GL) were determined, using a previously established method (Frost and Dornhurst, 2000; Barclay et al., 2007; Aston et al., 2008). GI values for foods containing carbohydrate were obtained from published values (Foster-Powell et al., 2002; Aston et al., 2008; Atkinson et al., 2008). Those foods with less than 1% of total energy content from carbohydrate were excluded from GI analysis. Mean dietary GI and GL were classified into high (above 70 and 20, respectively), moderate (56–69 and 10–19.9, respectively) or low (less than 55 and 10, respectively), according to previously established cut-offs (Brand-Miller et al., 1998).
Eating frequency (EF) was defined as the total number of eating and drinking episodes per day (Drummond et al., 1998). The timing of eating episodes was categorised into either morning (0501–1159 h), afternoon (1200–1900 h), evening (1901–0500 h), or all-day, according to previously defined methods (Hampl et al., 2003). Foods were categorised into one of 26 categories and subcategories, based on NDNS data and previous studies (Drummond et al., 1998).
Average daily physical activity levels were calculated from the self-reported diaries, with activities categorised into metabolic equivalents of energy (Ainsworth et al., 2000) and time spent at different levels of activity intensity (low, moderate and vigorous).
Frequencies and descriptive statistics were generated using SPSS version 16.0 (SPSS Inc., Chicago, IL, USA). Data was tested for normality, using the one-way Kolmogorov–Smirnov test. Student’s t-tests were used to compare subcategories of data. A one-sample t-test was used to compare nutrient intakes with the NDNS (2008–2009) data for women aged 19–64 years. Relationships were determined using Pearson correlation. Significance was assumed at P<0.05. All data are presented as mean (s.d.), unless otherwise stated.
Of the 1138 women with PCOS contacted, 210 women completed the study between May and November 2006, a response rate of 18%.
Study population characteristics
The mean (s.d.) self-reported age of the group was 32.6 (6.3) years (n=189), with 97% of participants reporting their ethnicity as British Caucasian (21 did not report their age and two participants did not report their ethnicity). The mean (s.d.) body mass index (BMI) was 27.4 (7.3) kg/m2 (n=183). Forty-four percent were within the healthy range for BMI (18.5–24.9 kg/m2), 53% were overweight or obese (BMI >25 kg/m2) and 3% were considered underweight (BMI<18.5 kg/m2). There were fewer overweight women with PCOS, but a greater proportion of obese women with PCOS, 22% and 31%, respectively. The majority of women with PCOS reported a combination of the classic PCOS symptoms of weight issues (overall weight issues or abdominal adiposity in lean women with PCOS), hirsutism, acne or irregular menses, with 69% of the women with PCOS reporting three or more symptoms. Weight issues were the most common symptom reported by those who were overweight or obese, and hirsutism and irregular menses were the two most commonly reported symptoms in all women (Table 1). Those who reported four or more symptoms had significantly greater BMI (29.1(7.5) kg/m2) than those with less than four symptoms (26.1(6.7) kg/m2) (P=0.006).
The majority of women (74.2%, n=147) reported achieving the recommendation for health of at least 30 min of moderate intensity activity per day (Department of Health, 2004). Women within the healthy BMI range reported spending significantly more time in moderate intensity activity (78 (62) min per day) compared with obese women (57(49) min per day) (P=0.041). Forty-eight percent of overweight or obese women reported at least 60 min of moderate intensity activity per day, sufficient activity to promote weight loss (Department of Health, 2004).
Total energy and nutrient intakes reported by women with PCOS were significantly higher when compared with women in the NDNS (Bates et al., 2010) (P<0.01) as shown in Table 2. In women with PCOS, the percentage energy from fat was higher and percentage energy from carbohydrates was slightly lower (not significant), compared with the NDNS. Sixty-eight percent of women with PCOS in this study had a total fat intake greater than 35% contribution to total energy, with saturated fatty acid intake accounting for 12% of total energy, substantially exceeding the reference nutrient intake (<10% energy). Using Goldberg cut-offs, an EI:BMR ratio of less than 1.1 is indicative of under-reporting of dietary intake (Goldberg et al., 1991). Using this cut-off, 17% of participants were considered to be under-reporting, which reduced to 15% when those reporting decreasing weight were excluded.
Total sugar intake accounted for 19% of total energy intake (44% of all carbohydrate consumed). Non-milk extrinsic sugar intake was 10.5% of total energy, exceeding the maximum recommended intakes (<10% of total energy). Non-starch polysaccharide (NSP; 16.5 g) was below the reference nutrient intake of 18 g per day (Department of Health, 1991), yet significantly higher than NDNS values for adult women (13 g, P<0.001).
The mean dietary GI for the women with PCOS was 54.6 (4.2), categorised as low GI (<55), yet only two participants achieved a mean GI of <45 as recommended by Barclay et al. (2008). Over half (54.6%; n=109) of the women with PCOS had a mean dietary GI in the low GI category, 44.9% (n=89) were in the medium GI category and 0.5% (n=1) in the high GI category. Mean dietary GL was 10.9 (2.4), with 38% of the women considered to have a low dietary GL, 62% medium and none found to have high mean dietary GL. Thirteen percent (n=26) of women were both reporting and following a low GI diet, an additional 16% (n=32) reported following a low GI diet, but had mean GI levels >55.
Mean EF including drinks was 8.7 (1.9) episodes per day, and excluding drinks was 5.0 (1.3) episodes per day. Intake of sweet snacks (1.6 (1.0) episodes per day) was significantly higher than savoury snacks (0.75 (0.6) episodes per day; P<0.001). Afternoon eaters consumed more sweet foods (1.9 (1.0)) compared with evening eaters (0.9 (0.5); P<0.001).
Relationships between dietary intake, eating pattern and BMI
A significant difference in dietary GI between healthy weight women with PCOS and obese women with PCOS was found, with the former reporting a lower dietary GI (53.8 (4.0) versus 55.7 (3.4); P=0.043). There was a positive relationship between BMI and dietary GI (r=0.217, P=0.003) for all women with PCOS, although no relationship was observed between dietary GI and energy intake.
There was a significant negative relationship between BMI and EF (r=−0.158, P=0.034) and a trend towards a negative relationship between energy intake and EF for all women with PCOS (r=−0.141, P=0.054).
This study is the first to comprehensively investigate the habitual dietary intake and activity levels of women with PCOS in the UK and assess whether dietary recommendations for health are being met. There are several key findings from the study:
Half of overweight or obese women with PCOS were not achieving sufficient activity to promote weight loss (60 min per day). However, the majority of all women with PCOS (74%) were achieving the recommendations for health of at least 30 min of moderate intensity activity per day.
Percentage energy contribution from fat was significantly higher in women with PCOS, compared with recommended intakes and previously reported intakes of UK women (NDNS values).
Mean dietary GI (54.6) was substantially higher than the recommendation of 45 or less purported to reduce long-term disease risk (Barclay et al., 2008); however, it is in line with an average dietary GI of 56.5 reported for women in the general UK population (van Bakel et al., 2009).
Lean women with PCOS reported a significantly lower mean dietary GI, compared with obese women with PCOS.
More frequent eating episodes was weakly associated with a lower energy intake and lower BMI.
Recommendation for weight management for overweight women with PCOS
The association between higher BMI and greater number of reported symptoms seen in this study confirms the importance of recommending and supporting overweight women with PCOS to achieve even moderate weight loss in order to confer significant improvements to symptom presentation (Kiddy et al., 1992; Stamets et al., 2004; Qublan et al., 2007). The current study suggests that women with PCOS may be more active than previously reported, with 74% self reporting that they did at least 30 min of moderate intensity activity per day, compared with Humphreys and Costarelli (2008), who reported that only 41% of women with PCOS reported undertaking moderate intensity exercise at least once per week. Additionally the Department of Health (2004) has reported that only 24% of women in the general population are sufficiently active to gain any health benefit, the higher rate of activity reported by the current study cohort may be explained by the reported benefits of physical activity improving some of their PCOS symptoms (Jeanes et al., 2009). However, of concern, 52% of overweight or obese women with PCOS were not achieving sufficient activity of 60 min per day to promote weight loss.
Recommendation for the modification of dietary fat intake
The high total and saturated fat intakes of the current sample are of concern, given that fatty acid intake is shown to influence glucose metabolism through the altering of insulin signalling and cell membrane function, with a diet high in saturated fatty acid associated with a decrease in insulin sensitivity when compared with a high monounsaturated fatty acid (MUFA) diet (Galgani et al., 2008). Furthermore, a review by Risérus (2008) concluded that saturated and trans fatty acids should be replaced with poly unsaturated fatty acids and MUFAs to confer benefits in terms of improving insulin sensitivity and preventing type 2 diabetes mellitus. Riccardi et al. (2004) further demonstrated that a high MUFA diet significantly improved insulin sensitivity, compared with a high saturated fat diet. However, these benefits were not demonstrated when total fat intake exceeded 38% of total energy (Riccardi et al., 2004), as was the case in 50% of the women with PCOS. Therefore, in this population, any benefits from increased MUFA intake may be lost as a result of a high total fat intake. As total dietary fat intake for women with PCOS in the current study was above recommended levels, it is clear that a reduction of total fat intake should focus on lowering saturated fatty acid intake, concurrently with encouragement of the maintenance of MUFA and poly unsaturated fatty acid in women with PCOS.
Support for incorporating low GI foods into the diet
Despite a relatively low percentage of total energy from carbohydrate intake (43%), the high total sugar intake in this population was a cause for concern. This may in part be explained by their more frequent consumption of sweet snacks (1.6 per day), compared with savoury snacks (0.75 per day). Mean dietary GI reported by women with PCOS was similar to the average dietary GI reported by women in the general UK population (54.6 and 56.5, respectively) (van Bakel et al., 2009), higher than Barclay et al.’s (2008) recommendation of 45 or less for the reduction of long-term disease risk. Achieving this recommendation would mean a reduction of approximately 10 units for the average participant in the current study, with only two women already reporting mean GI levels below 45. In addition, the mismatch between women’s perceptions and actual intakes in terms of GI is of note and may indicate a key area for education. Advice provided by dietitians focuses on a reduction in energy intake (78%) and dietary GI (77%), often in combination, although relatively few women with PCOS receive dietary advice from a registered dietitian, which may explain the problems with implementing this type of regime (Jeanes et al., 2009). Despite the lack of studies investigating the effects of low GI diets in women with PCOS specifically, given the potential benefits for glycaemic control, it seems prudent for women to incorporate low GI foods into everyday meals and snacks, whilst also aiming to remain in line with current dietary guidelines for health.
There is some debate regarding the role of low GI diets in weight reduction, yet the majority of evidence suggests that following an ad libitum low GI diet is not an effective means of achieving weight reduction independently (Aston, 2006), although this may help with weight maintenance (Thomas et al., 2007). In the current study, a weak relationship was found between BMI and dietary GI, with significant lower dietary GI reported by healthy weight women compared with obese women, consistent with findings from a recent systematic review (Thomas et al., 2007). Although altered GI diets remain popular for PCOS management, well-controlled studies are needed to confirm the effectiveness of these approaches in both lean and overweight women with PCOS.
Previous studies in the general population have demonstrated that increased EF may contribute to increased energy intake in women (Drummond et al., 1998; Hampl et al., 2003), indicating women who eat more frequently may be at greater risk of weight gain. However, other researchers have concluded that regular eating episodes can actually help with weight management and improve insulin sensitivity in obese women (Farshchi et al., 2005) and propose that the same would also be true for women with PCOS. Drummond et al. (1998), using a similar methodology to the current study, reported that women in the general population had a mean of 4.4 eating episodes per day (excluding drinks), lower than the eating frequencies for women with PCOS reported here (five eating episodes per day (excluding drinks)). Women with PCOS frequently report food cravings and difficulty losing weight, which may be linked to eating pattern and eating behaviour (Hirschberg et al., 2004; Herriot et al., 2008), perhaps evidenced by the significant negative relationship between BMI and EF, and the weak negative trend between energy intake and EF. The findings from this study highlight a need for future studies designed specifically to investigate the relationship between eating behaviour and BMI in women with PCOS.
Study participants were recruited through the charity Verity, which may have lead to a non-representative sample of women with PCOS, as these were women more likely to be better informed. The use of a 7-day-food and activity diary has enabled comprehensive dietary analysis; however, the limitations of self-reported intake and activity are well established (Gibson, 2006). The mean age of the women was also relatively young, and therefore, more likely to be physically active (Department of Health, 2004), and any complications of PCOS may not have presented yet. The majority (96%) of women who took part in the study were Caucasian, an overrepresentation of this ethnic group, when compared with the general population (92% Caucasian, Office for National Statistics, 2010). This is particularly important, as previous literature has indicated a high prevalence of PCOS in South Asian and Black populations (Wijeyaratne et al., 2002; Azziz et al., 2006), indicating the need to target these ethnic groups in future research.
This research has shown that, even in a self-selected and therefore potentially-motivated sample of women with PCOS, many of whom were not overweight, dietary intakes and eating patterns may not be optimal for management of their symptoms and reduction of future disease risks. The importance of focusing lifestyle interventions to promote weight management through physical activity and dietary advice on quality and quantity of fat, as well as carbohydrate modification, has been highlighted alongside the need for further robust research into the role of dietary GI and GL, and eating patterns in the PCOS population, specifically in order to inform the development effective lifestyle guidelines.
Ainsworth BE, Haskell WL, Whitt MC, Irwin ML, Swartz AM, Strath SJ et al. (2000). Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc 32, 498–516.
Aston L (2006). Glycaemic index and metabolic disease. Proc Nutr Soc 65, 125–134.
Aston L, Gambell JM, Lee DM, Bryant SP, Jebb SA (2008). Determination of the glycaemic index of various staple carbohydrate-rich foods in the UK diet. Eur J Clin Nutr 62, 279–285.
Atkinson F, Foster-Powell K, Brand-Miller JC (2008). International tables of glycemic index and glycemic load values: 2008. Diabetes Care 31, 2281–2283.
Avery J, Braunack-Mayer A (2007). The information needs of women diagnosed with Polycystic Ovarian Syndrome - implications for treatment and health outcomes. BMC Women′s Health 7, 9.
Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W et al. (2006). Position statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab 91, 4237–4245.
Balen A (2004). The pathophysiology of poylcytic ovary syndrome: trying to understand PCOS and its endocrinology. Best Pract Res Clin Obstet Gynaecol 18, 685–706.
Balen A, Dresner M, Scott E, Drife J (2006). Should obese women with polycystic ovary syndrome receive treatment for infertility? BMJ 332, 434–435.
Barclay A, Flood VM, Rochtchina E, Mitchell P, Brand-Miller JC (2007). Glycemic index, dietary fiber, and risk of type 2 diabetes in a cohort of older Australians. Diabetes Care 30, 2811–2813.
Barclay A, Petocz P, McMillan-Price J, Flood V, Prvan T, Mitchell P et al. (2008). Glycemic index, glycemic load, and chronic disease risk—a meta-analysis of observational studies. Am J Clin Nutr 87, 627–637.
Bates B, Lennox A, Swan G (2010). National Diet and Nutrition Survey: headline results from Year 1 of the Rolling Programme (2008/2009). Available at: http://www.food.gov.uk/science/dietarysurveys/ndnsdocuments/ndns0809year1, accessed 28th September 2010.
Brand-Miller JC, Allwan C, Mehalski K, Brooks D (1998). The glycaemic index of further Australian foods. Proc Nutr Soc 22, 110.
Carmina E (2006). Metabolic syndrome in polycystic ovary syndrome. Minerva Ginecol 58, 109–114.
Carmina E, Legro R, Stamets K, Lowell J, Lobo R (2003). Difference in body weight between American and Italian women with polycystic ovary syndrome: influence of the diet. Hum Reprod 18, 2289–2293.
Department of Health (1991). Dietary Reference Values for Food Energy and Nutrients for the United Kingdom. Report on Health and Social Subjects 41. The Stationary Office. HSMO: London.
Department of Health (2004). At Least Five a Week: Evidence on the Impact of Physical Activity and its Relationship to Health. A Report from the Chief Medical Officer. Department of Health Publications: London.
Diamanti-Kandarakis E (2008). Polycystic ovarian syndrome: pathophysiology, molecular aspects and clinical implications. Expert Rev Mol Med 10, e3.
Dokras A (2008). Cardiovascular disease risk factors in polycystic ovary syndrome. Semin Reprod Endocrinol 26, 39–44.
Douglas C, Norris L, Oster R, Darnell B, Azziz R, Gower B (2006). Difference in dietary intake between women with polycystic ovary syndrome and healthy controls. Fertil Steril 86, 411–417.
Drummond S, Crombie NE, Cursiter MC, Kirk TR (1998). Evidence that eating frequency is inversely related to body weight status in male, but not female, non-obese adults reporting valid dietary intakes. Int J Obes Relat Metab Disord 22, 105–112.
Ehrmann DA, Barnes RB, Rosenfield RL, Cavaghan MK, Imperial J (1999). Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovary syndrome. Diabetes Care 22, 141–146.
Farshchi H, Taylor MA, Macdonald IA (2005). Beneficial metabolic effects of regular meal frequency on dietary thermogenesis, insulin sensitivity, and fasting lipid profiles in healthy obese women. Am J Clin Nutr 81, 16–24.
Foster-Powell K., Holt S, Brand-Miller J (2002). International table of glycemic index and glycemic load values. Am J Clin Nutr 76, 55–56.
Franks S (1995). Polycystic ovary syndrome. N Engl J Med 333, 853–861.
Frost G, Dornhurst A (2000). The relevance of the glycaemic index to our understanding of dietary carbohydrates. Diabet Med 17, 336–345.
Galgani J, Uuauy R, Aguirre CA, Díaz EO (2008). Effect of the dietary fat quality on insulin sensitivity. Br J Nutr 100, 471–479.
Gibson RS (2006). Measuring food consumption of individuals. In: Gibson RS (ed.). Principles of Nutritional Assessment, 2nd edn. Oxford University Press: New York.
Goldberg G, Black AE, Jebb SA, Cole TJ, Murgatroyd PR, Coward WA et al. (1991). Critical evaluation of energy intake using fundamental principles of energy physiology: Derivation of cut-off limits to identify under-recording. Eur J Clin Nutr 45, 569–581.
Hampl JS, Heaton CL, Taylor CA (2003). Snacking patterns influence energy and nutrient intakes but not body mass index. J Hum Nutr Diet 16, 3–11.
Herriot A, Whitcroft S, Jeanes Y (2008). An retrospective audit of patients with polycystic ovary syndrome: the effects of a reduced glycaemic load diet. J Hum Nutr Diet 21, 337–345.
Hirschberg A, Naessén S, Stridsberg M, Byström B, Holtet J (2004). Impaired cholecystokinin secretion and disturbed appetite regulation in women with PCOS. Gynecol Endocrinol 19, 79–87.
Humphreys L, Costarelli V (2008). Implementation of dietary and general lifestyle advice among women with polycystic ovarian syndrome. J R Soc Promot Health 128, 190–195.
Jeanes Y, Barr S, Smith K, Hart KH (2009). Dietary management of women with polycystic ovary syndrome in the United Kingdom: the role of dietitians. J Hum Nutr Diet 22, 551–558.
Kiddy D, Hamilton-Fairley D, Bush A, Short F, Anyaoku V, Reed MJ et al. (1992). Improvement in endocrine and ovarian function during dietary treatment of obese women with polycystic ovary syndrome. Clin Endocrinol 36, 105–111.
Lindholm A, Andersson L, Eliasson M, Bixo M, Sundstrom-Poromaa I (2008). Prevalence of symptoms associated with polycystic ovary syndrome. Int J Gynaecol Obstet 102, 39–43.
McMillian-Price J, Petocz P, Atkinson F, O’Neill K, Samman S, Steinbeck K et al. (2006). Comparison of 4 diets of varying glycemic load on weight loss and cardiovascular risk reduction in overweight and obese young adults. Arch Intern Med 166, 1466–1475.
Moran LJ, Noakes M, Clifton PM, Tomlinson L, Norman RJ (2003). Dietary composition in restoring reproductive and metabolic physiology in overweight women with polycystic ovary syndrome. J Clin Endocrinol Metab 88, 812–818.
Office for National Statistics (2010). United Kingdom population by ethnic group. United Kingdom Census. Available at: www.statistics.gov.uk, accessed 8 April 2010.
Qublan H, Yannakoula E, Al-Qudah MA, El-Uri FI (2007). Dietary intervention versus metformin to improve the reproductive outcome in women with polycystic ovary syndrome. A prospective comparative study. Saudi Med J 28, 1694–1699.
Riccardi G, Giacco R, Rivellese AA (2004). Dietary fat, insulin sensitivity and the metabolic syndrome. Clin Nutr 23, 447–456.
Risérus U (2008). Fatty acids and insulin sensitivity. Curr Opin Clin Nutr Metab Care 11, 100–105.
Ross R, Janssen I, Dawson J, Kungl AM, Kuk JL, Wong SL et al. (2004). Exercise-induced reduction in obesity and insulin resistance in women: a randomized controlled trial. Obes Res 12, 789–798.
Sharma A, Walker DM, Atiomo W (2010). National survey on management of weight reduction in PCOS women in the United Kingdom. Eur J Obstet Gynecol Reprod Biol 152, 181–185.
Stamets K., Taylor D, Kunselman A, Demers L, Pelkman C, Legro R (2004). A randomized trial of the effects of two types of short-term hypocaloric diets on weight loss in women with polycystic ovary syndrome. Fertil Steril 81, 630–637.
Thomas DE, Elliott EJ, Baur L (2007). Low glycaemic index or low glycaemic load diets for overweight and obesity. Cochrane Database Syst Rev 18, CD005105.
Truby H, Baic S, deLooy A, Fox KR, Livingstone MB, Logan CM et al. (2006). Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from the BBC ‘diet trials’. BMJ 332, 1309–1314.
van Bakel M, Kaaks R, Feskens EJ, Rohrmann S, Welch AA, Pala V et al. (2009). Dietary glycaemic index and glycaemic load in the European Prospective Investigation into Cancer and Nutrition. Eur J Clin Nutr 63, S188–S205.
Vigorito C, Giallauria F, Palmonba S, Cascella T, Manguso F, Lucci R et al. (2007). Beneficial effects of a three-month structured exercise training program on cardiopulmonary functional capacity in young women with polycystic ovary syndrome. J Clin Endocrinol Metab 92, 1379–1384.
Wijeyaratne CN, Balen AH, Barth JH, Belchetz PE (2002). Clinical manifestations and insulin resistance (IR) in polycystic ovary syndrome (PCOS) among South Asians and Caucasians: is there a difference? Clin Endocrinol 57, 343–350.
Wright CE, Zborowski JV, Talbott EO, McHugh-Pemu K, Youk A (2004). Dietary intake, physical activity, and obesity in women with polycystic ovary syndrome. Int J Obes Relat Metab Disord 28, 1026–1032.
Funding from Roehampton University.
The authors declare no conflict of interest.
Supplementary Information accompanies the paper on European Journal of Clinical Nutrition website
About this article
Cite this article
Barr, S., Hart, K., Reeves, S. et al. Habitual dietary intake, eating pattern and physical activity of women with polycystic ovary syndrome. Eur J Clin Nutr 65, 1126–1132 (2011). https://doi.org/10.1038/ejcn.2011.81
- polycystic ovary syndrome
- feeding behaviour
- motor activity
Indian Journal of Obstetrics and Gynecology Research (2021)
Associations of diet, physical activity and polycystic ovary syndrome in the Coronary Artery Risk Development in Young Adults Women’s Study
BMC Public Health (2021)
Journal of Functional Morphology and Kinesiology (2020)
Physical activity and sedentary behaviour in women with and without polycystic ovary syndrome: An Australian population‐based cross‐sectional study
Clinical Endocrinology (2020)
Nutritional and dietary aspects in polycystic ovary syndrome: insights into the biology of nutritional interventions
Gynecological Endocrinology (2020)