Diet and nutrition in polycystic ovary syndrome (PCOS): Pointers
for nutritional management
H. FARSHCHI, A. RANE, A. LOVE & R. L. KENNEDY
School of Medicine, James Cook University, Douglas, Australia
PCOS patients are not always markedly overweight but PCOS is strongly associated with abdominal obesity and insulin resis-
tance. Effective approaches to nutrition and exercise improve endocrine features, reproductive function and cardiometabolic
risk proﬁle – even without marked weight loss. Recent studies allow us to make recommendations on macronutrient intake.
Fat should be restricted to 30% of total calories with a low proportion of saturated fat. High intake of low GI carbohydrate
contributes to dyslipidaemia and weight gain and also stimulates hunger and carbohydrate craving. Diet and exercise need to
be tailored to the individual’s needs and preferences. Calorie intake should be distributed between several meals per day with
low intake from snacks and drinks. Use of drugs to either improve insulin sensitivity or to promote weight loss are justiﬁed as
a short-term measure, and are most likely to be beneﬁcial when used early in combination with diet and exercise.
Lifestyle modiﬁcation, nutrition, polycystic ovarian syndrome
The most common endocrine disorder, polycystic ovarian
syndrome (PCOS), is becoming more common due to
increased awareness and the global increase in the pre-
valence of overweight and obesity. It is a heterogeneous
disorder that has been difﬁcult to deﬁne because there is no
single abnormality or diagnostic test that deﬁnes the
syndrome. While precise deﬁnitions are important for
scientiﬁc studies, as a working deﬁnition, the syndrome
may be diagnosed if at least two of the following are present:
. Oligomenorrhea or amenorrhoea associated with de-
creased ovulation. PCOS is the most common cause of
. Hyperandrogenaemia or clinical features of androgen
excess, in the absence of other underlying disease states
. Abnormal ovarian ultrasound with 12 follicles in each
ovary each having a diameter of 2 – 9 mm, or increased
. Increased LH with increased LH/FSH ratio.
The diagnosis is more certain with the presence of an
increasing number of features. Many overweight or obese
women have menstrual irregularity, decreased fertility or
hirsutism without fulﬁlling diagnostic criteria for PCOS.
The pathogenesis and management of these is the same as
for women with PCOS. Speciﬁc treatments for hirsutism
and subfertility have substantially improved management of
PCOS in recent years but do not generally inﬂuence the
underlying condition which is largely due to over-nutrition
and insulin resistance. Even PCOS patients who are not
overweight are often insulin resistant, and modest weight
loss improves outlook in patients of near normal body
weight. The association of PCOS with the abnormalities of
metabolic syndrome (central obesity, dyslipidaemia, hyper-
tension and glucose intolerance) is responsible for the
documented relationship with type 2 diabetes, cardiovas-
cular disease and hormonally-responsive cancers in later life
(Ehrmann 2005; Sartor and Dickey 2005). This paper
reviews our understanding of nutritional aspects of PCOS,
and proposes an approach to diet management and
nutritional therapy in patients with PCOS. The optimal
approach to dietary management of patients with PCOS
remains to be deﬁned (Marsh and Brand-Miller 2005). This
review sets out some general principles around which a
tailored approach to the individual patients can be designed.
Prevalence and association with obesity
The prevalence of PCOS varies between populations, as
does the strength of the association between PCOS and
insulin resistance or obesity. These differences may arise
from genetic factors and from differences in lifestyle.
Furthermore, cultural differences in attitudes to fertility
and racial differences in hirsutism may inﬂuence presenta-
tion. PCOS prevalence among young women in the
reproductive years is generally quoted at 5 – 10%
(Ehrmann 2005). There may also be variation within
populations with ethnic groups who are at high risk of
metabolic syndrome also being at high risk of PCOS. This
may apply, for example, to individuals of Asian descent in
Correspondence: R. L. Kennedy, Department of Medicine, James Cook University, 100 Angus Smith Drive, Douglas, QLD 4814, Australia.
Journal of Obstetrics and Gynaecology, November 2007; 27(8): 762 – 773
ISSN 0144-3615 print/ISSN 1364-6893 online Ó 2007 Informa UK Ltd.
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the UK and to the black population of the USA. A study
from the USA (Azziz et al. 2004) in an unselected
population showed that the prevalence of PCOS for black
and white women were 8.0% and 4.8%, respectively.
Furthermore, the features of PCOS may vary among
different racial groups because of differences in body mass,
diet, and exercise habit (Carmina 2006).
Insulin resistance is present in women with PCOS
independent of body mass. However, obesity in PCOS is
associated with greater insulin resistance, and a higher
incidence of dyslipidaemia and diabetes. The incidence of
diabetes and lipid disorders is higher. At least 50% of
women with PCOS are overweight or obese (Gambineri
2002). Abdominal adiposity or android pattern obesity
(waist – hip ratio 40.85) is also common in PCOS
(Kirchengast and Huber 2001; Yildirim 2003). Android
fat distribution is also present in 70% of lean women with
PCOS, placing them at risk of metabolic disturbances
(Kirchengast and Huber 2001). The risk of glucose
intolerance among women with PCOS is 5- to10-fold
higher than normal and the typical age of onset of impaired
glucose tolerance or diabetes is in the third or fourth
decades, earlier than in the general population (Pelusi et al.
2004). In later life, the risk of developing type 2 diabetes is
potentially increased seven-fold in patients who have had
PCOS (Wild 2002). As in the non-PCOS population,
obesity in PCOS is associated with endothelial dysfunction,
decreased adiponectin and other changes in adipokines that
contribute to metabolic and cardiovascular risk (Carmina
2006). Several mechanisms have been proposed for insulin
resistance in PCOS, including peripheral target tissue
resistance, reduced hepatic clearance or increased pancrea-
tic sensitivity (Ben-Haroush et al. 2004). In obesity, free
fatty acids and tumor necrosis factor-a (TNF-a), released
from adipose tissue may play a key role in pathogenesis of
insulin resistance (Salehi et al. 2004). Other pro-inﬂam-
matory cytokines are also increased, including interleukin-6
(Glintborg et al. 2006) and interleukin-18 (Khang et al.
2006; Escobar-Morreale et al. 2004). As with metabolic
syndrome and type 2 diabetes, plasma adiponectin is
decreased and there is increased leptin and resistin
(Glintborg et al. 2006). The complex pathogenesis of the
condition and its relationship with metabolic syndrome is
demonstrated by a recent study (Corton et al. 2007) where
gene expression proﬁling of visceral fat from patients with
PCOS was carried out. There was increased expression of
pro-inﬂammatory genes, as well as those involved in
regulating immune function, oxidative stress, lipid meta-
bolism, and insulin signaling.
Obesity has signiﬁcant effects on the clinical manifesta-
tions of PCOS: Menstrual/ovulatory disturbances tend to
be more marked in the obese; Androgen levels are higher
contributing to hirsutism and acanthosis nigricans (Mor
et al. 2004). Fertility is decreased and the rate of
spontaneous abortion increased (Wang et al. 2001).
Obesity is clearly a major determinant of many of the
long-term consequences of PCOS including glucose
intolerance and the risk of cardiovascular disease. Both
obesity and insulin resistance are major inﬂuences on
whether patients with PCOS develop features of the
metabolic syndrome (Elting et al. 2001; Goodarzi et al.
2003). The increased risk of endometrial carcinoma in
patients with PCOS may also be more marked in patients
who are obese and insulin resistant (Hardiman et al. 2003).
Patients with PCOS who become pregnant are at increased
risk of developing gestational diabetes (Loctal 2006).
Emotional factors including stress, depression, and dis-
torted body image are important determinants of symp-
toms and presentation, but also of response to treatments,
including lifestyle interventions (Gulseren et al. 2006;
Himelein and Thatcher 2006a,b; Diamanti-Kandarakis
and Economou 2006). The inﬂuence of psychological
factors must always be taken into account when consider-
ing treatment options. Low self esteem and impaired
quality of life are common among women with PCOS
(Coffey et al. 2006), and if the effect of these factors is not
appreciated lifestyle interventions, in particular, are likely
to prove ineffective.
Calorie requirements and restriction
Many studies in overweight and obese subjects have shown
beneﬁcial effects of even modest (5%) weight loss on
well-being, insulin sensitivity, and cardiovascular risk
proﬁle. There is every reason to believe that these beneﬁts
extend to women with PCOS (Marsh and Brand-Miller
2005). Studies in patients with PCOS conﬁrm that modest
weight loss improves glucose tolerance, cardiovascular risk
proﬁle and reproductive function (Crosignani et al. 2003;
Norman et al. 2004; Stamets 2004; Douglas et al. 2006).
Modest weight loss achieved in the short term may also
improve some of the endocrine abnormalities associated
with PCOS: Hyperinsulinaemia contributes both to in-
creased androgen production in response to LH in the
ovary and also to the increased levels of free androgen by
decreasing SHBG. Peripheral aromatisation of androgens
to oestrogen adds to the relatively high oestrogen state
which may increase the long-term risk of certain cancers,
and exacerbate the endocrine abnormalities seen in
patients with PCOS. Short periods of calorie restriction
lead to decreased androgen levels, and this is sufﬁcient in
some patients to restore normal LH pulse frequency and
amplitude with consequent restoration of normal men-
struation. However, LH secretion remains abnormal in
some patients suggesting that they may have intrinsic
abnormalities of pituitary – ovarian axis function (Van Dam
et al. 2002, 2004). Leptin is a hormone that is produced
exclusively by adipocytes and is responsible (in the
physiological state) for decreased feeding, and therefore
energy intake, when the organism is replete. It is also
involved in regulation of reproductive function and
decreased leptin production with weight loss may help to
normalise reproductive function. Ghrelin is a 28-amino-
acid acylated peptide secreted by the stomach in response
to imminent feeding. It is an endogenous ligand for the
growth hormone receptor. Secretion before meals stimu-
lates feeding, decreases energy expenditure and stimulates
gastric motility and acid secretion. Increased ghrelin levels
in patients with PCOS may be part of the abnormal state of
energy balance, and this abnormality is again restored
toward normal with calorie restriction and weight loss
(Norman et al. 2004).
In approaching dietary management, it is important to
take into account the calorie requirements of the indivi-
dual. The recommended daily intake for women is
summarised in Table I. Calorie requirements are higher
for women with higher body mass and, and increase in
relation to activity. It is often useful to focus initially on the
eating pattern and the macronutrient content of the diet
rather than to try to promote both healthy eating and
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weight loss too quickly. Energy deﬁcit can be achieved
either by limiting nutrient intake or by increasing calorie
expenditure. The best approach is a combination of the
two. A daily calorie deﬁcit of as little as 200 kcal/day will
prevent weight gain and promote weight loss in the longer
term. A deﬁcit of 500 kcal/day is needed for the average
person to lose 0.5 kg/week, while a 1,000 kcal deﬁcit is
needed for 1 kg weight loss/week. These deﬁcits are often
hard to achieve in practice, which explains why many
patients ﬁnd it difﬁcult to achieve satisfactory weight loss.
There is a distinct impression, but it is not clear from
published evidence, that women with PCOS ﬁnd it harder
than the average to lose weight. It is important to recognise
that improved abdominal obesity and insulin sensitivity
may occur without an overall change in body weight. In
particular, body composition of patients who exercise
regularly may change with increased lean body mass and
decreased fat mass, but no overall change in weight.
Increased lean body mass (muscle) increases resting energy
expenditure and may help improve hormonal and meta-
bolic parameters in women with PCOS. While the beneﬁts
of modest weight loss have become more widely appre-
ciated in recent years, this should not preclude us from
aiming for as near normal body weight and composition as
possible where this is feasible. To that end, our range of
dietary options is increasing. For example, short-term meal
substitution to achieve calorie deﬁcit is now recognized as
an option for women with PCOS (Moran et al. 2006).
Dietary fat and protein
Fat is the most energy-rich macronutrient component of
the diet containing 9 kcal/g, compared with only 4 kcal/g
for carbohydrate and protein. Furthermore, the body has a
virtually inﬁnite capacity to store fat, particularly in
hyperinsulinaemic individuals. Experiments with fat over-
feeding suggest that fat excess decreases carbohydrate
oxidation with no apparent change in fat oxidation. When
carbohydrate is present in excess, or is inadequately
oxidised, fat deposition is increased through the process
of de novo lipogenesis. Cross-sectional studies indicate that
higher fat intake is associated with impaired insulin
sensitivity, but this relationship is mainly due to obesity
(Riccardi and Rivellese 2000; Vessby 2003). By contrast,
intervention studies showed that a reasonable increase in
total fat intake (from 20% to 40%) had no major impact on
insulin sensitivity (Riccardi ad Rivellese 2000). Hence, a
potential criticism regarding the deleterious effects of high-
protein low-carbohydrate diets on increasing fat intake may
be not applicable, at least in short-term interventions
(McAuley et al. 2005).
Increased consumption of unsaturated fatty acids has
been reported to improve insulin sensitivity in healthy
(Vessby et al. 2001), obese and type 2 diabetic subjects
(Summers et al. 2003). However, the beneﬁcial effects of
the fat quality on insulin sensitivity were observed in
individuals with 537% of total energy intake as fat (Vessby
et al. 2001). A recent investigation (Kasim-Karakas et al.
2004) focused on a diet supplemented in polyunsaturated
fatty acids (PUFA), which have been associated with
positive health beneﬁts in a number of studies. Adminis-
tration of diet supplements with walnuts to increase levels
of linoleic and a-linolenic acids, surprisingly increased
glucose levels, both fasting and during an oral glucose
tolerance test. One explanation might be that total fat
intake in that study was 437% (39 + 1%). There was no
change in levels of insulin or of reproductive hormones.
The longer chain PUFAs, eicosapentaenoic acid and
docosahexaenoic acid which are found in ﬁsh oil have
beneﬁcial effects on metabolic parameters in patients with
diabetes, but speciﬁc evidence relating to PCOS is not
available at this stage. While the Mediterranean diet, rich in
monounsaturated fatty acids (MUFA), has been widely
accepted as a gold standard for healthy diets, its potential
beneﬁts in patients with PCOS have not been documented,
although decreased features of obesity and insulin resis-
tance have been noted in Italian compared with American
patients with PCOS (Carmina 2006). Overall, dietary fat
should account for no more than 30% of the calorie
content of the diet, with a maximum of 10% of calories
coming from saturated fat. The remainder of the fat
content should be as a balanced mixture of unsaturated fat
including cooking oils and spreads. Consumption of trans-
fats – unsaturated fats which, because of internal resonance
in the molecule between double bonds, behave like
unsaturated fats – has been recently linked with increased
risk of anovulatory infertility (Chavarro et al. 2007).
Diets that are either low in fat or low in carbohydrate
almost inevitably deliver an increased proportion of calorie
intake as protein. Although it has been controversial, recent
evidence suggests that higher intake of protein improves the
glucose and insulin responses to a glucose load (Gannon
et al. 2003; Farnsworth et al. 2003). Higher protein intake
also increases satiety and may contribute to increasing
postprandial thermogenesis, as well as decreasing abdom-
inal fat. Adequate protein intake is important to protect
lean body mass and to increase muscle in response to
exercise. There have been recent concerns about high
intake of red meat as increased body stores of iron have
been linked to the risk of developing type 2 diabetes.
General advice is that the diet should deliver 20% of its
calories as protein, this may be increased at the expense of
other dietary components for short-term diets designed to
help the patient lose weight or improve glucose tolerance.
Dyslipidaemia in patients with PCOS is an important
determinant of long-term cardiovascular risk. This most
commonly manifests as low HDL-cholesterol but because
triglycerides are often relatively low, a full atherogenic lipid
proﬁle is often not expressed. However, subtle abnormal-
ities including alterations in lipoprotein particle size and
increase LDL II and IV subclasses may contribute to
susceptibility to macrovascular disease (Berneis et al.
2007). Combined oral contraceptives including combina-
tions of the antiandrogenic progestogen cyproterone
Table I. Recommended calorie intake for lean adult females
Sedentary Moderate Active
19 – 30 2,000 2,000 – 2,200 2,400
31 – 50 1,800 2,000 2,200
451 1,600 1,800 2,000 – 2,200
Values are based on BMI of 21.5 kg/m
, women with higher BMI
have greater calorie requirement. Sedentary is equivalent to just
carrying out activities of daily living. Moderately active is
equivalent to walking 1.5 – 3.0 miles per day at 3 – 4 miles per
hour. Active is equivalent to walking more than 3.0 miles per day at
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acetate with ethinyloestradiol are often used to achieve
cycle control, decrease androgenic symptoms, to protect
the endometrium, as well as for their contraceptive action.
Their effect on glucose tolerance and lipid proﬁle is
complex and controversial. It is clear that, in some
individuals, they can increase glucose intolerance and
circulating triglyceride levels (Nader and Diamanti-
Kandarakis 2007). Increased weight during oral contra-
ceptive use may also have an adverse effect on long-term
cardiovascular risk (Vrbikova et al. 2006). The dyslipidae-
mic effect of combined oral contraceptive treatment is
prevented by concurrent use of a statin drug which also
decreases the low-grade inﬂammation (increased C-reac-
tive protein) that often accompanies PCOS (Banaszewska
et al. 2007). A recent report also suggests that statins may
have beneﬁcial effects on the endocrine proﬁle in
PCOS, including decreasing circulating testosterone levels
(Duleba et al. 2006). Low circulating sex hormone binding
globulin (SHBG) has been advocated as a marker for
the dyslipidaemia associated with insulin resistance
(including PCOS) (Chen et al. 2006), although variability
in measured values might preclude its use in routine
practice (Dahan and Goldstein 2006).
The glycaemic load of a diet is deﬁned as the amount of
carbohydrate multiplied by the glycaemic index (GI).
Foods with a high GI deliver carbohydrate rapidly
following ingestion. A high glycaemic load is associated
with an increased risk of diabetes and with poor glycaemic
control in patients with established diabetes. Glycaemic
load can be decreased either by decreasing the amount of
carbohydrate (in an isocaloric diet an increased proportion
of calories are as MUFA or as protein) or by consuming
foods of lower GI. The latter has been shown to improve
insulin sensitivity, decrease post prandial hyperglycaemia,
decease triglycerides and increase HDL-cholesterol (Marsh
and Brand-Miller 2005). Apart from the fact that they have
a low GI, whole grain foods may have a speciﬁc role in
protecting against the development of diabetes. Low-
carbohydrate diets have been controversial and public
interest in these diets has preceded and, to an extent
driven, scientiﬁc interest. We have recently reviewed the
literature relating to the use of these diets in people who
have or are at risk of type 2 diabetes (Kennedy et al. 2005)
Low carbohydrate diets are effective in promoting weight
loss when used for periods up to 6 months. They are only
effective if they deliver fewer calories than are being used
(i.e., they are hypocaloric). They appear to be safe for
short-term use and, indeed, improve cardiovascular risk
proﬁle. The diets used vary in the degree of carbohydrate
restriction. A period of relatively strict carbohydrate
restriction helps at the start of the diet, but the diet does
not have to be severely restricted in carbohydrate to be
effective. Care should be taken to limit the intake of fat,
particularly saturated fat and the diets work best when they
moderately restrict calorie intake and are used alongside a
suitable exercise programme.
Many studies with low-carbohydrate diets have been
carried out over relatively short periods of time. This
limitation has been overcome by more recent studies.
Thus, after 6 months, a greater weight loss with a low-
carbohydrate diet compared with a conventional diet has
been reported (Samaha et al. 2003; Stern et al. 2004), but
the difference between the two diets was not sustained at 12
months (Brehm et al. 2003; Foster et al. 2003). Further
investigations in obese patients demonstrated inconsistency
in terms of weight reduction after 12 months on low-
carbohydrate diets. (McAuley et al. 2005; Dansinger et al.
2005) The effects of high-protein low-carbohydrate versus
low-protein high-carbohydrate diets on PCOS have been
evaluated only in two experiments (Stamets et al. 2004;
Moran et al. 2003). Both of these studies reported no
signiﬁcant differences in weight loss in terms of the
different protein content of the diets. However, these
studies were very short term (1 and 3 months, respectively).
No signiﬁcant differences were observed between low-
carbohydrate and high-carbohydrate diets on fasting
insulin levels, or insulin sensitivity as assessed by homeo-
static model assessment (HOMA) (Farnsworth et al. 2003;
Layman et al. 2003; Brinkworth et al. 2004). However, a
lower postprandial insulin response was reported in
subjects consuming a low-carbohydrate diet (Farnsworth
et al. 2003; Layman et al. 2003). In one recent study
(Douglas et al. 2006), both fasting and post-challenge
insulin levels were decreased by low-carbohydrate diet.
More marked improvement in triglycerides (Samaha et al.
2003) and HDL-cholesterol (Foster et al. 2003) have been
noted with low-carbohydrate diets compared with conven-
tional diets. Other studies have reported improvements in
LDL-cholesterol particle size (Sharman et al. 2004), LDL
concentration (McAuley et al. 2005; Parker et al. 2002),
and postprandial blood-lipid proﬁle (McAuley et al. 2005).
Low-carbohydrate diets have been associated with deleter-
ious effects on lipid proﬁle when used long term
(Kwiterovich et al. 2003), and thus severe carbohydrate
restriction should be regarded as a short-term measure to
achieve weight loss. Recent trials conﬁrm that restriction of
dietary carbohydrate can lead to improved adipokine levels
towards values that indicate a more normal, insulin-
sensitive state (Cardillo et al. 2006), and along with this
there is an improvement in cardiovascular risk proﬁle
(Nordmann et al. 2006).
Regulation of appetite is complex and ﬂuctuations in
blood glucose may play a part in stimulating appetite and
increasing energy intake. Both insulin and blood glucose
ﬂuctuate more widely in patients with insulin resistance.
This ﬂuctuation commonly gives rise to reactive hypogly-
caemia. For example, Altuntas et al. (2005) studied 64 lean
women with PCOS and showed that reactive hypoglycae-
mia occurred in 50% following a glucose load. The
phenomenon was associated with lower levels of androgen
and prolactin and tended to occur in women with higher
levels of b cell function. Many women with PCOS describe
carbohydrate cravings and cite this as a reason for their
difﬁculty in losing weight. Hypoglycaemia is known to
stimulate feeding behaviour, increasing both total food and
fat intake (Dewan 2004). Glucose sensing neurones are
present in the hypothalamus, basal ganglia, limbic system,
and nucleus tractus solitarius (Levin 2001). Glucose
responsive neurones express the components of the
sulphonylurea receptor (Kir 6.2 and SUR) and glucoki-
nase, and sense increased glucose in a manner akin to the
pancreatic b cell. Another population of glucose sensing
neurones ﬁre in response to decreased glucose. The
components of the glucose sensing mechanism (glucoki-
nase and sulphonylurea receptor) are also present in
neurones that secrete neuropeptide Y (NPY) or pro-
opiomelanocortin (POMC), both of which are involved in
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appetite regulation. Orexins, a group of hormones that
stimulate feeding behaviour, both stimulate glucose-sensi-
tive neurones (Liu et al. 2001), and are secreted by these
neurones (Cai et al. 2005). The neurones also respond to
the potent orexigenic peptide, ghrelin (Chen et al. 2005).
Changes in feeding behaviour during the menstrual cycle
have been well documented with increased fat and total
energy intake during the luteal phase. This may relate to
increased energy requirement and loss of this cyclical
change in energy utilisation may contribute to the increase
in weight that commonly occurs following the menopause
(Reimer et al. 2005). Hyperglycaemia may also play a
direct role by stimulating release of cytokines such as TNF-
a which may be involved in the pathogenesis of insulin
resistance and hyperandrogenaemia (Gonzalez et al. 2006).
Fluctuations in blood glucose may thus arise from the
changes that occur in PCOS but may also contribute to
development of these changes through altered feeding
behaviour, body composition and insulin responses.
The importance of frequency and regularity of eating
patterns is often neglected. There has been, in recent years,
a move away from regular and social eating patterns to
more irregular eating with increased consumption of
convenience and energy-dense snack foods (Harnack
et al. 2000). There has been surprisingly little research on
the inﬂuence of eating pattern on metabolic parameters but
available evidence suggests that it may be an important
determinant of overall nutrient intake and may, to an
extent, govern the metabolic response to food. In a study of
nearly 16,000 adults (Kerver et al. 2006), meal and snack
patterns were good markers for overall nutrient intake.
Those who ate frequently during the day had higher intakes
of carbohydrate, ﬁbre, and a range of micronutrients.
Those who ate less frequently had higher intakes of fat,
cholesterol, protein and sodium. Lower micronutrient
intake was associated with skipping breakfast. Our recent
experiments on lean (Farshchi et al. 2004a,b) and obese
(Farshchi et al. 2005a) women showed that a regular meal
frequency leads to higher postprandial energy expenditure,
lower energy intake and improved impaired insulin
sensitivity compared with irregular eating in 2-week
interventions. In a further study (Farshchi et al. 2005b),
breakfast consumption was associated with a lower energy
intake and improved insulin sensitivity compared with
breakfast omission. If such effects seen after only 2 weeks of
irregular eating or omitting breakfast are sustained in the
long term, they could lead to weight gain and thus
contribute to the development of obesity. Chapelot et al.
(2006) have conﬁrmed that less frequent major eating
episodes may lead to increased fat mass and increased
levels of leptin. The optimal frequency of food intake has
yet to be determined, but a regular pattern with low intake
from snacks seems to be desirable. Ghrelin levels increase
in response to anticipation of food (Drazen et al. 2006),
and this response is learned. Since this and other orexigenic
hormones increase energy intake and decrease energy
expenditure, there is a strong argument for regular but
not too frequent eating episodes in individuals who wish to
control or lose weight. The importance of breakfast may
not just relate to the distribution of energy intake and
thermic response to food. Individuals who missed breakfast
in the Go¨ teburg Adolescence Study (Sjoberg et al. 2003)
were more likely to smoke, drink alcohol, eat more
carbohydrate and have decreased micronutrient intake.
Although further long-term studies in obese and PCOS are
required, it appears that regular eating including breakfast
can help in weight management and also improve insulin
Exercise and PCOS
There is a surprisingly scant literature on the role of
exercise in managing patients with PCOS. What we know,
and what we recommend, must therefore come largely
from studies involving non-PCOS subjects. We currently
recommend 30 min of exercise on at least 5 days of the
week to maintain weight, and for healthy lifestyle. Recent
studies showed that 60 – 75 min of moderate-to-high
intensity of physical activity promotes a greater long-term
(12 – 18 months) weight loss compared with the conven-
tional recommendation for optimum health (Jeffery et al.
2003; Jakicic et al., 2003). Accumulation of exercise in
frequent short periods of physical activity appears to have
similar inﬂuence in long-term weight loss programmes.
Activity related to daily living and leisure time activity is an
important determinant of body weight but not of the
response to weight management programmes. A realistic
approach to exercise depends on the assessment of the
patient’s current exercise habits, preferences regarding type
of exercise, and inclination to undertake exercise. The
following options for exercise should be discussed with the
. Aerobic exercise. This is important for cardiovascular
ﬁtness and to increase energy expenditure as part of a
weight loss programme. It is important to recognise
that the overweight and unﬁt patient may have limited
capacity for aerobic exercise
. Exercises to increase suppleness and ﬂexibility.
Although they may not greatly increase calorie ex-
penditure, such exercises may increase engagement
with an exercise programme, decrease risk of injury
with exercise, and promote a sense of well-being
. Endurance exercise. For patients who cannot manage
high-intensity exercise, prolonged lower level activity is
an appropriate way to gain ﬁtness and to increase
energy expenditure. Walking with a pedometer can be a
very useful approach to begin to increase energy
. Resistance training. Increasing muscle strength and
mass with weight training has been neglected as a
means of improving function and body composition
until recently. The high metabolic rate of muscle means
that muscle mass is an important determinant of resting
energy expenditure and resistance training is now
regarded as a highly acceptable way to inﬂuence weight,
body composition, and insulin sensitivity (Poehlman
et al. 2000; Borg et al. 2002).
Pharmacological treatment should obviously only be
considered as an adjunct to lifestyle management, and
only when the latter has been shown not to have controlled
symptoms and signs on its own. However, the beneﬁts
For personal use only.
which accrue when insulin sensitivity is improved with drug
therapy can be useful to demonstrate what could be
achieved with sustained lifestyle interventions. Also, there
is increasing evidence that drug treatments to improve
insulin sensitivity are a useful adjunct to lifestyle interven-
tions. Speciﬁc aspects of PCOS such as menstrual
irregularity, anovulatory infertility and hirsutism may
require speciﬁc treatment. For many patients, the greatest
symptomatic relief, as well as improved long-term prog-
nosis, could be gained by dealing with the underlying
causes of the condition – insulin resistance and overweight/
obesity. These two aspects can be treated separately with
modern drugs, and both the patient and the clinician
should be informed about the likely beneﬁts and limitations
Management of insulin resistance is with metformin, a
biguanide drug, or with the thiazolidinediones (rosiglita-
zone or pioglitazone) which are agonists at the peroxisome
proliferator activator receptor-g (PPARg) receptor. Use of
these drugs should be considered at an earlier stage in
patients who have impaired fasting glucose or impaired
glucose tolerance to prevent or delay progression to type 2
diabetes, and in patients who have developed diabetes to
improve diabetic control. Metformin is extensively used in
patients with PCOS, not only because of its effects on
glucose homeostasis, but also because by decreasing insulin
resistance it leads to favourable changes in androgens and
gonadotrophins (Checa et al. 2005). The latter has proved
to be useful in restoring ovulatory function and thus fertility,
either used alone or in combination with clomiphene
citrate. This effect of metformin is not necessarily conﬁned
to women who are either overweight or who have overt
insulin resistance (Goldenberg et al. 2005). Metformin does
not promote weight loss. Metformin added to a hypocaloric
diet may decrease some of the features of abdominal obesity
– speciﬁcally decreased leptin levels consistent with the loss
of visceral fat which may contribute to improvement in a
number of features of PCOS (Pasquali et al. 2000; Tang
et al. 2006). The drug is usually well tolerated, although up
to 30% of patients may experience gastrointestinal side-
effects. Lactic acidosis is a very rare side effect but
sufﬁciently serious to warrant the drug not being used in
patients with cardiac, renal or hepatic failure. One of the
difﬁculties in using metformin or other insulin sensitising
drugs for PCOS is the lack of a readily available marker to
document successful treatment or to guide dosage. Recent
evidence suggests that the combination of metformin and
lifestyle intervention has sustained beneﬁcial effects on
weight maintenance and cardiovascular risk proﬁle that
might last for up to four years (Glueck et al. 2006;
Gambineri et al. 2006). In addition to affording some
protection from macrovascular damage, use of metformin
with suitable lifestyle advice has been shown to improve
microvascular function (Topcu et al. 2006; Alexandraki
et al. 2006). The drug has been shown to decrease systemic
levels of advanced glycation end products (AGEs) which
contribute to vascular and renal complications of insulin
resistant states (Diamanti-Kandarakis et al. 2007). As
conﬁdence with use of metformin in PCOS grows, and as
scientiﬁc evidence supporting its use accumulates, the drug
is increasingly being used in younger patients, including
adolescents, with PCOS (De Leo et al. 2006; Mastorakos
et al. 2006; Glueck et al. 2006).
There is increasing evidence for the use of thiazolidine-
diones in patients with PCOS. Side-effects include weight
gain, peripheral oedema, anaemia and changes in liver
tests. Rosiglitazone has been shown to improve glucose
tolerance and insulin sensitivity in patients with PCOS,
although it does not necessarily produce marked improve-
ment in other endocrine parameters (Belli et al. 2004). In a
head-to-head study with metformin, rosiglitazone was
reported to be more useful where the features were
predominantly those of insulin resistance, while metformin
additionally ameliorates features of a high androgen state
(Mitkov et al. 2006). It may, however, usefully be
combined with oestrogen and/or antiandrogen treatment
to produce beneﬁts in features related to insulin resistance
and hyperandrogenaemia (Lemay et al. 2006). Pioglitazone
tends to have more marked beneﬁcial effect on cardiovas-
cular risk factors, and may be beneﬁcial in insulin-resistant
patients who fail to respond to metformin (Glueck et al.
2003; Glintborg et al. 2006). The drug may be used singly
or in combination with metformin. Increased weight with
the glitazone drugs relates to increased subcutaneous fat
which is due to the drugs increasing fat cell differentiation
and growth in fat depots that do not contribute, or have a
beneﬁcial effect on, cardiovascular risk. The resultant
decrease in circulating triglycerides and non-esteriﬁed fatty
acids contributes to improved insulin sensitivity but has no
inﬂuence on the overall body composition and energy
expenditure (Smith et al. 2005). Decreased adiponectin
and increased resistin are features of PCOS and insulin
resistance (Gulcelik et al. 2006; Escobar-Morreale et al.
2006), and these features are partly normalised during
treatment with thiazolidinediones (Majuri et al. 2007).
Additionally, these drugs can decrease some of the changes
found in association with non-alcoholic steatohepatitis
(NASH) and low-grade inﬂammation (Rautio et al. 2007).
Modern drugs to assist with weight loss and maintenance
are certainly effective in some patients, and appear to be
safe if used within guidelines. Orlistat is a gastrointestinal
lipase inhibitor that decreases absorption of ingested fat by
up to 30%. Although its use leads to gastrointestinal side-
effects in up to one-third of cases, it appears to be a very
safe drug and is now widely used in treatment of PCOS.
The beneﬁcial effect on insulin resistance and in decreasing
androgen levels is equivalent to that achieved by metformin
(Jayagopal et al. 2005). Advanced glycation end-products
are reactive molecules produced by glycation of proteins
and lipids, and are involved in pathogenesis of diabetic
complications. Orlistat may decrease assimilation of these
products for the diet (Diamanti-Kandarakis et al. 2006).
Sibutramine is a centrally-acting inhibitor of serotonin
and noradrenaline uptake. It is marginally more effective
than orlistat as a weight-controlling drug but its use is
limited to 1 – 2 years since it consistently increases pulse
rate and blood pressure. It should not be used in patients
with uncontrolled hypertension. Used in patients with
PCOS, sibutramine improves glucose tolerance and
decreases androgen levels (Sabuncu et al. 2003; Filippatos
et al. 2005). It also decreases levels of leptin and resistin
and increases adiponectin, all of which are associated with
improved insulin sensitivity and decreased risk of type 2
diabetes (Karabacak et al. 2004). Other drugs to assist
with weight control are in development. The most
immediately promising of these is rimonabant, an
inhibitor of the cannabinoid-1 receptor (CB-1). This
drug has been shown in extensive trials, both in Europe
and North America, to promote weight loss and
improvement in cardiovascular risk proﬁles in overweight
For personal use only.
patients (Van Gaal et al. 2005; Despres et al. 2005; Pi-
Sunyer et al. 2006). Although there is no speciﬁc evidence
relating to PCOS at present, there is every reason to
believe that Rimonabant will prove useful in this condi-
tion. There is a distinct possibility that weight manage-
ment drugs will not only prove useful overall, but that
speciﬁc agents might be selected to match the underlying
problem with calorie intake and that these drugs may be
useful singly or in combination with other drugs to treat
the features or natural history of PCOS. There are no
speciﬁc data at present relating to the role of bariatric
surgery in managing patients with PCOS. While surgi-
cally-induced weight loss clearly may restore fertility and
improve cardiovascular risk proﬁle, potential risks have to
be considered carefully (Merhi 2007).
PCOS is a complex disorder due, in part but not
exclusively to, insulin resistance and overweight. In
practice, its management is often not entirely satisfactory
from the patient’s point of view. Treatment of PCOS
may be divided as follows: (1) Attention to lifestyle
factors including diet and exercise. (2) Management of
speciﬁc aspects such as menstrual irregularity, anovula-
tory infertility, and hirsutism. (3) Dietary and exercise
interventions to promote weight loss and improve glucose
tolerance. (4) Pharmacological interventions to improve
insulin sensitivity or to assist with weight loss. A scheme
for management of the overweight or insulin resistant
patient with PCOS is proposed in Figure 1. Although
Figure 1. Approach to the patient with PCOS.
For personal use only.
there has been a general increased interest in the role of
lifestyle modiﬁcation to favourably alter the clinical
features of PCOS, much of what has been learned is
by inference from the non-PCOS population. There is
relatively little speciﬁc information on nutritional recom-
mendations for patients with PCOS (Stein 2006; Hoeger
2006). The focus, to date, has been on the macronu-
trient components of the diet. Evidence is beginning to
emerge that micronutrients are also important. Thus,
there may be beneﬁts to supplementation with omega-3
fatty acids and antioxidants (Stein 2006), and low
vitamin D levels in some patients may contribute to
the metabolic features of the syndrome (Hahn et al.
2006). Some early evidence supports non-pharmacologi-
cal treatment including herb and nutritional supplements
(Dennehy 2006; Westphal et al. 2006).
As PCOS is principally a disease of over-nutrition, the
primary management in most cases should centre on a
nutritional approach. Based on published information
summarised in this review, certain recommendations can
be made about diet and exercise in patients with PCOS.
These are summarised in Table II. An approach which
deals with the fundamental problem in PCOS will help to
improve the multiple facts of the disease and to protect the
patient from the long-term consequences including, type 2
diabetes and cardiovascular disease. A rational approach to
lifestyle management in PCOS will help the practitioner
engage with the patient, and allow both practitioner and
patient to approach this complex disorder in a rational
manner. PCOS is largely a disease of lifestyle. As it
becoming more commonly diagnosed, it is mandatory for
health professionals dealing with PCOS patients to have
some knowledge of how lifestyle factors inﬂuence the
disorder and how they may be changed to alter prognosis
without an undue reliance on the short-term use of
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Table II. Diet and exercise in PCOS
1. Daily energy requirement of 2,000 – 2,400 kcal for patient of average build who is not too active. Avoid restricting this too much to
2. Exercise regularly: 30 min of moderate exercise daily will help to maintain body weight. More prolonged or vigorous exercise may
be needed to produce weight loss.
3. Eat no more than 30% of daily calories as fat, restricting saturated fat to 510% total calories. Use low fat spreads and dairy
4. Carbohydrate should count for 45 – 55% of the diet initially. Keep intake of reﬁned carbohydrate down. Concentrate on low
glycaemic index (GI) foods, those high in ﬁbre and wholegrain foods.
5. Diet of higher protein content may improve satiety and insulin sensitivity. Start with 20% of daily energy as protein, but this may be
increased by substituting for carbohydrate in those who have difﬁculty controlling eating or maintaining weight.
6. Avoid too much red meat. Eat oily ﬁsh at least once per week to supply long-chain essential fatty acids (omega-3, polyunsaturated
7. Eat at least ﬁve portions of fruit or vegetable per day. This promotes satiety, supplies ﬁbre and maintains the micronutrient content
of the diet.
8. Eat regularly and focus food intake on three (maximum four) meals per day. Breakfast is an important meal.
9. Avoid calorie-dense snacks as they promote hyperinsulinaemia and drive hunger. Make sure that drinks are counted in daily
calorie intake estimated – fruit juices and alcoholic drinks are often forgotten but are rich in calories and carbohydrates.
10. Even modest weight loss has health beneﬁts. Achieving this requires energy restriction – modest 200 kcal deﬁcit (decreased
intake or increased utilisation will lead to 5% weight loss in 6 months for many. A 500 kcal per day energy deﬁcit usually equates
to weight loss of up to 0.5 kg/week.
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