Improving reproductive performance in overweight/obese women with effective weight management
Human Reproduction Update
Improving reproductive performance in overweight/obese women with effective weight management
Robert J.Norman 0
Manny Noakes 1
Ruijin Wu 0
Michael J.Davies 0
Lisa Moran 1
Jim X.Wang 0
0 Reproductive Medicine Unit, University of Adelaide, The Queen Elizabeth Hospital , Woodville Rd, Woodville, SA5011
1 CSIRO Health Sciences and Nutrition , Kintore Ave, Adelaide, SA 5000 , Australia
Obesity and overweight are common conditions in the developed countries and they carry many health consequences, including some reproductive disorders. There is a very high prevalence of obese women in the infertile population and many studies have highlighted the link between obesity and infertility. A large proportion of infertile women have polycystic ovary syndrome (PCOS) which is also linked with increased risk of obesity and other metabolic anomalies. The association between obesity and/or PCOS and hyperinsulinaemia, hyperandrogenism and abnormal secretion of other hormones, such as leptin, underlies many reproductive disorders observed in this population. It has been demonstrated that weight loss can improve the fertility of obese women through the recovery of spontaneous ovulation, whereas others will have improved response to ovarian stimulation in infertility treatment. Therefore, it is proposed that following the initial assessment of infertility and body mass index or other measurement of obesity, various weight management interventions, including diet, exercise or pharmacotherapeutic approaches, should be considered for overweight and obese infertile women.
fertility ?tness/obese/overweight/PCOS/weight loss
There is great concern at the high prevalence of and the increasing
trend to obesity worldwide, especially in Western societies. This is
particularly evident in the USA where >50% of all women are
overweight and 30% obese. In Australia, 67% of men are
overweight or obese and 52% of women are overweight or
obese which constitutes a marked increase over the last 20 years
(Australian Institute of Health and Welfare, 2002)
. The consequent
cost of obesity to national health systems is high
due to the increased morbidity and mortality, including the
risk of several cancers associated with obesity
(Calle et al., 1999,
. The worldwide trend of increasing obesity is attributable to
a combination of reduced exercise, changing dietary composition
and increased energy intake. While increased weight gain among
young children is particularly evident in developed countries,
changing lifestyles in developing countries will see the trend to
obesity extend worldwide. Many ethnic groups who either migrate
to Western societies or adopt a Western lifestyle are prone to
obesity in their changed environment.
reviewed the epidemiology of diabetes in various populations;
the data suggest that genetic tendencies to obesity are unmasked by
geographical differences in food history. The thrifty gene
hypothesis postulates the existence of metabolically thrifty genes that
permit more ef?cient food utilization, fat deposition and rapid
weight gain at occasional times of food abundance, thereby
making the gene bearer better able to survive a subsequent famine.
An alternative theory of the `thrifty phenotype', based on
experimental studies in animals, argues that the capacity for
intergenerational metabolic adaptations to increased energy supply
are easily exceeded among populations exposed to a `lean'
environment for even a single generation
(Hales and Ozanne
Gynaecologists and reproductive scientists have encountered
the reproductive consequences of a society increasing in weight as
a higher frequency of women diagnosed with disorders of
menstruation, infertility, diabetes mellitus in pregnancy and
other signi?cant sequelae
(Sharpe and Franks, 2002)
. In addition,
polycystic ovary syndrome (PCOS), is a condition characterized
by hyperandrogenism and menstrual disturbances, further
complicates the issue
(Norman et al., 2002)
. At the same time, many
advances have been made in recent years on the effect of weight
reduction in improving reproductive function in overweight and
obese infertile women, and there is now a better understanding of
how weight reduction through dieting/exercising leads to
improved reproductive performance. Finally, there have been
interesting reports of how best to achieve and maintain weight
loss through effective weight management.
Obesity, PCOS and reproductive disorders
Obesity, particularly in women with PCOS, can result in many
reproductive disorders. This is due to the complex interaction
between the pituitary gland, pancreas and ovary resulting in a
changed hormonal secretion pattern (Figure 1) The original
descriptions by Stein and Levinthal (1934) emphasized the
association of obesity with PCOS. However, the use of hormone
measurement and ultrasound led to a realization that not all
patients with PCOS suffered from being overweight. Over a third
to 50% of PCOS subjects are overweight or obese
(Balen et al.,
1995; Gambineri et al., 2002)
. Variation in body weight
between PCOS populations in USA and Europe, attributed to
genetic and lifestyle factors, has also been reported recently
(Carmina et al., 2003)
. In PCOS women of Caucasian origin, it is
found that the severity of both metabolic and clinical symptoms is
positively correlated with the body mass index (BMI)
et al., 1995)
. There is also evidence showing that even normal
weight PCOS subjects have increased intra-abdominal fat
(Yildirim et al., 2003).
In subfertile/infertile women with PCOS, overweight or obesity
usually is more prevalent. The relative importance of PCOS status
and overweight/obesity in this group of women is yet to be fully
understood, although increasing evidence suggests that BMI
contributes signi?cantly towards the severity of many problems,
such as the risk of miscarriage
(Wang et al., 2002)
the changed glucose metabolism and consequently modi?ed
androgen secretion in overweight/obese women with PCOS is
the key for assessing the link between obesity and the risk of
various reproductive disorders in this group of women. Leptin is
another key link between obesity and reproductive disorder.
PCOS, insulin resistance and hyperandrogenism
Insulin resistance and compensatory hyperinsulinaemia have been
consistently documented in lean and obese women with PCOS in
comparison to weight-matched controls
(Burghen et al., 1980;
Chang et al., 1983; Moller and Flier, 1991; Dunaif, 1997)
severity of insulin resistance is reported to correlate with the
severity of the clinical and metabolic phenotype of PCOS
(Burghen et al., 1980; Robinson et al., 1993)
women displaying hyperandrogenism and ovarian morphology
consistent with PCOS are insulin resistant, whereas ovulatory
women usually are not
(Dunaif et al., 1985, 1987; Robinson et al.,
As insulin resistance is in?uenced strongly by obesity in
(Beard et al., 1987)
, it was initially debated
whether insulin resistance and hyperinsulinaemia are a primary
metabolic disturbance of PCOS or a symptom of the obesity
commonly observed in PCOS
(Ovesen et al., 1993; Holte et al.,
. A synergistic interaction appears to exist with a
degree of insulin resistance and hyperinsulinaemia in lean PCOS
women augmented by the presence of obesity
Gerich, 1990; Dunaif, 1997)
. The extent of this is still debatable, as
not all women with PCOS exhibit hyperinsulinaemia and insulin
(Dale et al., 1992; Ehrmann et al., 1995)
results may in part be explained by the heterogeneity and complex
aetiology of the syndrome, with lean and obese subgroups
displaying varying insulin resistance and metabolic pro?les
(Acien et al., 1999)
. The presence of abdominal obesity is strongly
associated with insulin resistance in subjects without PCOS
(Hollmann et al., 1997). This additionally appears to hold true for
both lean and obese women with PCOS, who may both exhibit
increased abdominal obesity
(Dale et al., 1992; Bringer et al.,
, associated with increased insulin resistance (Pasquali et al.,
An alternative mechanism for insulin resistance in PCOS that
underlies the risk of developing into type II diabetes has been
suggested. De?cient insulin action
(Dunaif et al., 1995)
(Ehrmann et al., 1995)
, increased insulin secretion in
response to dietary stimuli
(Holte et al., 1994a,b)
hepatic clearance of insulin (Ciampelli et al., 1997) are
hypothesized to play an aetiological role in PCOS. Current
research is attempting to elucidate its molecular and genetic
rationale; as yet, no clear consensus has been reached.
Hyperinsulinaemia correlates positively with the presence of
hyperandrogenism in obese and lean women with PCOS. The
hyperandrogenism is postulated to result from both increased
adrenal and ovarian androgen production
(Rosen?eld et al., 1990;
Carmina et al., 1992; Ehrmann et al., 1992, 1995)
. These tissues do
not appear to display insulin resistance whereas ovarian tissues
may have selective resistance to insulin (Wu et al., 2003). This
would agree with the suggested diverging insulin signalling in
(Nestler et al., 1998)
. Androgen overproduction has
been reported both in unstimulated and LH-stimulated ovarian
(Gilling-Smith et al., 1997; Nelson et al., 1999)
response to hyperinsulinaemia
(Poretsky and Kalin, 1987)
Hyperinsulinaemia has additionally been documented as
decreasing serum sex hormone-binding globulin (SHBG) levels
independent of obesity (Haffner, 1996). SHBG is produced in the liver
and helps in the clearance and binding of testosterone. A low
SHBG level will thus result in increased bioavailable testosterone
(Plymate et al., 1988; Nestler et al., 1991)
While there is also abundant evidence associating an increased
BMI with diabetes mellitus, subjects with PCOS in particular have
a substantial added risk of glucose intolerance. In a study from
Adelaide in women with PCOS (aged 20?30 years), 18% of
women with a BMI >30 kg/m2 had impaired glucose metabolism
while 15% of women with normal glucose tolerance showed
conversion to impaired glucose tolerance or frank diabetes when
restudied 5?7 years later
(Norman et al., 2001)
. The deterioration
of glucose metabolism is signi?cantly related to the initial weight
(Wang et al., 2003)
Conway et al. (1993)
also showed that 8% of
lean and 11% of obese women with PCOS had abnormal glucose
PCOS and metabolic syndrome
The endocrine disturbances in PCOS can also result in long-term
consequences. The insulin dysfunction previously discussed may
lead to an increased occurrence of type II diabetes mellitus
and impaired glucose tolerance (IGT) in later adult life
(Dahlgren et al., 1992b; Legro et al., 1999)
. An increased
incidence of hypertension has been reported in PCOS women
compared to non-PCOS subjects
(Dahlgren et al., 1992b; Holte
et al., 1994b; Wild et al., 2000; Elting et al., 2001)
. The above
attributes are found in both pre- and post-menopausal women
(Dahlgren et al., 1992b)
, indicating a possible long-term risk
associated with PCOS.
Together with increased abdominal obesity, this symptom
clustering shows a striking similarity to the metabolic syndrome
. The predominance of these risk factors in women
with PCOS may place them at a higher risk for cardiovascular and
coronary heart disease later in life
(Wild et al., 1990; Birdsall et al.,
. Dahlgren et al. (1992a) showed in a retrospective study an
increased risk pro?le (4?11 fold at ages 40?49 and 50?60 years) of
myocardial infarction (MI) in women with PCOS compared to the
general population. Increased activity of plasminogen activation
inhibitor-I (PAI-I) and C-reactive protein (CRP) associated with
increased risk of MI has been reported in PCOS (Sampson et al.,
1996). There was also an increased fatal MI rate for women with
irregular periods in the Nurses' Health Study
(Rich-Edwards et al.,
. Conversely, long-term follow-up studies have failed to
demonstrate increased circulatory disease mortality with PCOS
(Pierpoint et al., 1998)
. The lack of a uniform de?nition of PCOS
until recently and the heterogeneous nature of this syndrome has
limited our capacity to study the real association between PCOS
and cardiovascular disease. A large, prospective, long-term
follow-up study in a PCOS population with clear and extensive
phenotyping of PCOS abnormalities at baseline is needed, as
recently pointed out by
Obesity and leptin
Leptin plays a potentially important role in human infertility given
the discovery of its regulatory effect on fertility in the mouse
(Castracane and Henson, 2002)
. There is a strong correlation
between serum leptin concentrations and body fat
(Maffei et al.,
1995; Considine et al., 1996; Vicennati et al., 1998)
(Chapman et al., 1997)
in humans. Leptin levels have also been
reported to be increased in women with PCOS
(Brzechffa et al.,
1996; Vicennati et al., 1998)
although this was not supported by
many other studies
(Chapman et al., 1997; Rouru et al., 1997;
Gennarelli et al., 1998)
. There is no clear explanation for this
inconsistency, although the complex interrelation between leptin
and body weight, obesity, body fat distribution and many other
factors means that studies with large sample size and proper
statistical analysis are required for delineating the relationship. On
the other hand, there is a consistent positive association between
leptin levels and obesity
(Brzechffa et al., 1996; Chapman et al.,
1997; Rouru et al., 1997; Gennarelli et al., 1998; Vicennati et al.,
and non-obese women of PCOS were not hyperleptinaemic
(El Orabi et al., 1999). Given the well-established effect of leptin
on ovarian steroidogenesis and ovulation in rodents
(Duggal et al.,
2000; Ryan et al., 2002, 2003)
and in humans
(Agarwal et al.,
1999; Brannian et al., 1999; Lof?er et al., 2001)
, it can be
speculated that the high concentration of leptin might have a role
in the pathogenesis of PCOS and reproductive disorders in?uenced
Obesity and menstrual disorder
Classic studies by Mitchell and Rogers
et al. (1979)
showed that obesity was present at a 4-fold higher rate
in women with menstrual disturbances than in women with normal
cycles. Forty-?ve per cent of amenorrhoeic women were obese
whereas only 9?13% of women with normal periods were
overweight. Furthermore, anovulation was strongly associated
with obesity: grossly obese women had a rate of menstrual
disturbance 3.1-fold more frequent than women in the normal
weight range (BMI 18.5?25.0 kg/m2). Teenage obesity was
positively correlated with menstrual irregularity later in life and
obesity was correlated with abnormal and long cycles, heavy
menstrual ?ow and hirsutism.
Lake et al. (1997)
studied women at
ages 7, 11, 16, 23 and 33 years and found obesity in childhood and
the early 20s increased the risk of menstrual problems [odds ratio
(OR) 1.75 and 1.59 respectively]. Women who were overweight
(BMI 23.9?28.6 kg/m2) and obese (>28.6 kg/m2) at 23 years of age
were respectively 1.32 and 1.75 times more likely to have
menstrual dif?culties. Girls with menarche at 9, 10 or 11 years
were more likely to have menstrual problems at 16.5 years (OR
1.45 for mild and 1.94 for severe menstrual abnormality), as
Ibanez et al. (1998)
The presence of PCOS may further aggravate the effect of
obesity on menstrual functions. Of 1741 UK subjects with PCOS,
70% had menstrual disturbances and only 22% had normal
menstrual function if their BMI was >30 kg/m2
(Balen et al.,
Kiddy et al. (1992)
found that obese subjects with PCOS
had an 88% chance of menstrual disturbance compared to 72% in
non-obese subjects with PCOS.
In the Nurses' Health Study II (n = 101 073 women), women
with long or highly irregular menstrual cycles (>40 days length)
had a signi?cantly increased relative risk (RR) of developing type
II diabetes mellitus compared to women with a regular menstrual
cycle (26?31 days) (RR = 2.08) after adjustment for BMI. This risk
was more marked in obese women although lean women with
menstrual irregularity also had an increased risk of type II diabetes
mellitus (RR of 1.67, 1.74 and 3.86 for BMI at age 18 of <25, 25?
29 and >30 respectively)
(Solomon et al., 2001)
. This indicates
that reproductive dysfunction is associated with an increase in
metabolic morbidity that is only partially mediated by weight.
Obesity and infertility
Many multiparous women are obese, indeed most obese women
are able to achieve pregnancy readily. In support of this, a large
study of fertile women did not show any relationship between
conception rates and weight or BMI
(Howe et al., 1985)
obese and overweight women are over-represented in
gynaecological and reproductive medicine clinics. Obesity in the teenage
years is more common among married women who never became
pregnant than for married women who did become pregnant
et al., 1979)
. The Nurses' Health Study reported that in 2527
married infertile nurses, the relative risk of ovulatory infertility
was 1.3-fold higher (95% CI 1.2?1.6) in the group with a BMI
range of 24?31 kg/m2 and 2.7-fold higher (2.0?3.7) in women with
a BMI >32 kg/m2
(Rich-Edwards et al., 1994)
. More recent data
from this group show that ovulatory infertility can be largely
attributable to overweight and a sedentary lifestyle
et al., 2002)
. Grodstein et al. (1994a) showed that anovulatory
infertility in 1880 infertile women and 4023 controls was more
common in those with a BMI of >26.9 kg/m2 (RR 3.1, 2.2?4.4)
Even high normal to slightly overweight levels may have an effect
Weight during childhood did not predict adult fecundity, but
weight at 23 years did if the woman was obese (OR 0.69, 0.56?
0.87). Obese women at 23 years were less likely to become
pregnant within 12 months than women of normal weight, while
infertility rate was 33.6% in obese women versus 18.6% in normal
(Lake et al., 1997)
Zaadstra et al. (1993)
found that the upper quartile of BMI
(>33.1 kg/m2) in a group of apparently normal women who were
undergoing donor insemination led to a reduced chance of
pregnancy (OR 0.43). This was a particularly signi?cant study
because few of the women required medication to stimulate
Kusakari et al. (1990)
in Japan found that obesity was
related to anovulation and/or infertility and
Balen et al. (1995)
found that obesity was correlated with higher infertility rates. In
204 North American women
(Green et al., 1988)
, there was a
reduced fertility rate among women who were >20% of ideal body
weight (OR 2.1)?this did not apply to women who had previously
been pregnant. Indeed, obese or overweight subfertile or infertile
women have a lower success rate during infertility treatment
(Koloszar et al., 2002)
. Several reports con?rmed the independent
effect of BMI on fecundity in infertile women treated by assisted
reproductive technology; with very obese women having half the
odds of conception compared to moderate BMI women
et al., 2000; Wittemer et al., 2000; Nichols et al., 2003)
complex interaction between various factors, including infertility
aetiology and body fat distribution, may obscure such a
(Lashen et al., 1999)
. It has been suggested that
intrafollicular hCG concentrations are related to BMI, and this may
explain the concurrent decrease in embryo quality and pregnancy
(Carrell et al., 2001)
Imani et al. (2000)
found that free
androgen index and leptin are the most prominent endocrine
predictors of ovarian response during ovulation induction by
clomiphene citrate. However, more research will be needed for a
better understanding of the association.
Women with central obesity take longer to become pregnant,
indicating that fat distribution plays a role in the chance of
Zaadstra et al. (1993)
have shown that fertile
women with central adiposity take longer to become pregnant than
women of the same BMI with peripheral adiposity. Even lean
women with PCOS have a signi?cantly higher amount of body fat
(Kirchengast and Huber, 2001)
. There is also an
association between central adiposity, anovulatory cycles and
hyperinsulinaemia in adolescent girls born small for gestational
age (SGA) (Ibanez et al., 2002). Ibanez et al. found that ovulation
was restored following metformin treatment and a reduction in
abdominal fat mass. The mechanism of this effect is uncertain but
it is well known that increased central fat distribution is associated
with a higher level of circulating insulin and other features of the
Obesity, miscarriage and other adverse pregnancy outcomes
Weight excess is associated with an increased risk of miscarriage.
In a study of primiparous women seeking a spontaneous pregnancy
(Hamilton-Fairley et al., 1992)
, 11% of women with a BMI 19?
24.9 kg/m2, 14% with BMI 25?27.9 kg/m2 and 15% of those
>28 kg/m2 miscarried (OR 1, 1.26 and 1.37 respectively). Women
>82 kg are more likely to miscarry than thinner women (OR 2.7 for
82?95 kg and 3.4 for >95 kg)
(Bohrer and Kemmann, 1987)
even a mild increase in BMI (25?28 kg/m2) leads to a signi?cantly
higher risk of pregnancy loss (OR 1.37, 1.18?1.60) following
gonadotrophin ovulation induction in some series
(HamiltonFairley et al., 1992; Pettigrew and Hamilton-Fairley, 1997)
pregnancies achieved by assisted reproduction treatment, we also
showed a marked increase in the risk of miscarriage in overweight
and obese women independent of PCOS
(Wang et al., 2002)
Another recent study in women receiving donated oocytes also
observed obesity as an independent risk factor for miscarriage
. Obesity is also a risk factor for early pregnancy
loss after assisted reproduction treatment
(Fedorcsak et al., 2000)
although it was found unrelated to preclinical pregnancy loss
(Winter et al., 2002)
The adverse effect of overweight and obesity on pregnancy and
obstetric outcome is well known. Some of the American studies on
massively obese women indicate high health risks and resultant
increased costs to the health system
(Galtier-Dereure et al., 2000)
for example cost in increased requirement for infertility treatment
(Rich-Edwards et al., 2002)
. High pre-pregnancy weight is
associated with an increased risk of pregnancy-induced
hypertension, toxaemia, gestational diabetes, urinary infection,
macrosomia, Caesarean section, and increased hospitalization
et al., 1999; Michlin et al., 2000)
. PCOS per se seemed to have
little effect on pregnancy outcomes other than increased risk of
(Mikola et al., 2001)
, although studies with
large sample size are needed to distinguish the effect of PCOS and
the confounding effect of overweight and obesity.
Obesity and response to infertility treatment
Most studies show conclusive evidence that increasing BMI is
associated with an increased requirement for clomiphene citrate.
In several of these, large doses of clomiphene (up to 200 mg per
day) were required to ensure ovulation in the heaviest women
(Shepard et al., 1979; Lobo et al., 1982; Friedman and Kim 1985;
Dickey et al., 1997)
. Doses of gonadotrophins required to induce
ovulation are also increased in anovulatory women and those
requiring ovarian stimulation for any reason
(McClure et al.,
. Increased weight and BMI in PCOS lead to impaired
response to standard doses of clomiphene citrate, although most
obese women with this condition will respond to larger doses
(Crosignani et al., 1994)
Fedorcsak et al. (2001)
obesity, independent from hyperinsulinaemia, was related to lower
oocyte recovery on IVF and increased total FSH requirements for
stimulation. A similar observation has been made with
gonadotrophin ovulation induction in non-PCOS women
(Loh et al.,
Improvement of reproductive function through weight management and dietary intervention
Weight loss may impact on reproductive functioning for several
reasons, which broadly encompass the effect of a reduction in fat
and/or lean tissue mass, related changes in some endocrinological
parameters and metabolism and even improvement in self-esteem.
The effect of weight loss on reproductive functioning depends on
initial body weight and probably the amount of weight lost.
Modest weight losses of ~10% in obese women have been
demonstrated to be effective in improving hormonal pro?les,
menstrual regularity, ovulation, and pregnancy rates
(Falsetti et al.,
1992; Kumar et al., 1993; Clark et al., 1995; Galletly et al., 1996;
Hollmann et al., 1996; Norman and Clark, 1998)
over as little as 4 weeks with weight losses of 5?10% of initial
body weight can reduce hyperandrogenism and circulating insulin
(Hamilton-Fairley et al., 1993; Clark et al., 1995; Clark et al.,
1998; Huber-Buchholz et al., 1999; Wahrenberg et al., 1999)
addition, the intergenerational tracking of maternal adiposity
through perinatal mechanisms indicates a potential to reduce the
risk of obesity in the offspring by controlling obesity in the mother
(Foreyt and Poston, 1998)
Weight loss improves insulin resistance and hormone pro?le
Attenuating insulin resistance has become a target in normalizing
hyperandrogenism and anovulation in PCOS. Weight loss
improves insulin sensitivity and short-term reproductive ?tness
in overweight women and PCOS subjects and is additionally
crucial for improving short- and long-term metabolic health. This
can be accomplished through dietary control and exercise with the
overall aim of energy expenditure exceeding energy intake over a
short or medium period. Caloric restriction improves insulin
sensitivity measured through euglycaemic hyperinsulinaemia
(Andersen et al., 1995; Holte et al., 1995)
glucose:insulin ratios (Pasquali et al., 1986), homeostasis model
(Moran et al., 2003)
, oral glucose tolerance test
(Pasquali et al., 1989;
HamiltonFairley et al., 1993; Jakubowicz and Nestler, 1997)
(Kiddy et al., 1989; Botwood et al., 1995; Wahrenberg
et al., 1999; Pasquali et al., 2000; Van Dam et al., 2002)
Weight loss in PCOS women also decreases hyperlipidaemia
(Andersen et al., 1995; Moran et al., 2003)
cytochrome P450c17a activity
(Jakubowicz and Nestler, 1997)
and improves adipocyte lipolysis
(Wahrenberg et al., 1999)
Following weight loss, metabolic and endocrine variables were
improved to a level similar to that of BMI-matched non-PCOS
(Holte et al., 1995)
, indicating a positive role of dietary
treatment in restoring reproductive and metabolic function to
overweight women with PCOS.
Location of adipose tissue reduction is also important in
restoring metabolic and reproductive function
(Holte et al., 1995;
Huber-Buchholz et al., 1999)
Holte et al. (1995)
demonstrated that weight loss in women resulted in reduction of
truncal? abdominal fat and that endocrine and metabolic
improvements between intervention and control groups were removed after
adjusting for truncal?abdominal fat. Weight loss also decreases
hyperandrogenism (measured as decreases in free androgen index,
free or total testosterone and increases in SHBG) and improves
menstrual function, ovulation and fertility
(Kiddy et al., 1989;
Pasquali et al., 1989; Kiddy et al., 1992; Hamilton-Fairley et al.,
1993; Botwood et al., 1995; Holte et al., 1995; Jakubowicz and
Nestler, 1997; Van Dam et al., 2002; Moran et al., 2003)
consistently documented are changes in LH with reductions
(Pasquali et al., 1989), increases
(Van Dam et al., 2002)
(Kiddy et al., 1992; Holte et al., 1995;
Jakubowicz and Nestler, 1997)
Although it is anecdotally reported that women with PCOS have
dif?culty in achieving and maintaining weight loss, this has not
been speci?cally examined. No differences in weight loss have
been observed between subjects with and without PCOS following
isocaloric 5000?6000 kJ/day (1190?1428 kcal/day) diets for 2?7
(Jakubowicz and Nestler, 1997; Pasquali et al., 2000)
in our unpublished study in subjects with (n = 20) and without
PCOS (n = 12) over 4 months of energy restriction. This has not
been investigated under less restrictive or self-managed dieting
regimes. It is suggested that women with PCOS may exhibit
possible abnormalities in energy expenditure. While resting
energy expenditure (REE) does not differ between women with
PCOS and weight-matched controls
(Segal and Dunaif, 1990;
Robinson et al., 1992)
, postprandial thermogenesis (PPT) has been
found either not to differ
(Segal and Dunaif, 1990)
or to be
(Robinson et al., 1992)
in women with PCOS.
et al. (1992)
calculated that this difference in PPT between PCOS
and controls would account for a weight gain of 1.9 kg per year if
maintained in the long-term.
Weight loss improves reproductive functions
When fertility is a problem, the primary goal of treatment is to
normalize serum androgens and restore reproductive function,
simply achieved by reducing insulin resistance through a decrease
in weight and abdominal fat. Studies of weight loss through
lifestyle modi?cation have indicated that improvements in fertility
occur with modest weight loss (~5% of initial body weight) and
study-end BMI of >30 kg/m2
(Kiddy et al., 1992; Hollmann et al.,
Crosignani et al. (2003)
recently showed that there is a
parallel improvement in anthropometric indices, ovarian
physiology and fertility rate induced by diet.
Foreyt and Poston (1998)
also suggested that modest weight losses of ~10% of initial weight
are effective in improving hormonal pro?les, menstrual regularity,
ovulation, and pregnancy rates.
In 11/25 women who responded to weight loss with
improvements in menstrual cyclicity (ovulation and menstrual cycle
length), a signi?cant reduction in fasting insulin and homeostasis
model assessment insulin resistance index (HOMA) was observed
compared to subjects who showed no improvement in menstrual
cyclicity with weight loss
(Moran et al., 2003)
. Where PCOS is
present, this is consistent with the proposed aetiology of insulin
resistance. It would be of great clinical use to be able to identify
these subjects prior to commencement of a treatment strategy in
order to target successful interventions.
Short- and long-term management of weight loss
Weight management for women has been vigorously
recommended by many authors
(Hoeger 2001; Norman et al., 2002)
Short-term weight loss has been achieved in overweight PCOS
subjects with very low calorie diets (VLCD) (330?421 kcal/day)
(Kiddy et al., 1989; Hamilton-Fairley et al., 1993; Andersen et al.,
1995; Wahrenberg et al., 1999; Van Dam et al., 2002)
moderate caloric restriction (1000?1500 kcal/day for 3?6 months)
(Pasquali et al., 1986, 1989, 2000; Kiddy et al., 1992; Andersen
et al., 1995; Holte et al., 1995; Jakubowicz and Nestler, 1997;
Moran et al., 2003)
. There is evidence that energy restriction
alone, independent of weight loss, improves reproductive
(Moran et al., 2003)
, which has implications for the
management of infertility compared to the longer-term prevention
Despite the short-term bene?ts of severe caloric restriction,
sustained long-term weight loss is more dif?cult to achieve
, and if weight is regained the manifestations of
PCOS may return. In a review of 17 studies of long-term outcome
for dietary treatment of obesity in general populations,
concluded that ~15% of subjects maintain weight
loss (all or 9?11 kg) with success rates of up to 14 years of
observation. Although physical activity, behaviour modi?cation
and continued support are associated with attenuating weight
(Ayyad and Andersen, 2000)
, it is unclear which dietary
strategies are optimal in a free-living situation. Some evidence
indicates that weight is maintained more effectively and
compliance is increased when an ad libitum low fat, high carbohydrate
dietary pattern (~30% of daily energy as fat and 55% as
carbohydrate) is followed over longer periods of time, compared
to ?xed energy diets.
Toubro and Astrup (1998)
compared 1 year
weight maintenance with an ad libitum low fat, high carbohydrate
diet after 13.5 kg initial weight loss in 43 obese adults; 65% of the
ad libitum group and 40% of the ?xed energy group maintained a
weight loss of >5 kg after 2 years. In a cross-sectional study,
et al. (1998)
assessed the dietary patterns of 438 subjects from the
National Weight Control Registry who maintained a weight loss of
30 kg for 5.1 years. Subjects who successfully maintained weight
reported continued consumption of a low energy and low fat diet.
A systematic evaluation of six randomized controlled trials using
partial meal replacement plans for weight management suggests
that these types of interventions can safely and effectively produce
signi?cant sustainable weight loss and improve weight-related risk
factors of disease
(Heyms?eld et al., 2003)
. The ef?cacy of this
approach in PCOS has not been assessed.
Finally, pharmacotherapeutic approaches may also be an option
for long-term weight loss maintenance. Sibutramine and orlistat
are two weight loss drugs currently approved for obesity treatment,
which have been associated with signi?cantly greater weight loss
than that seen with dieting alone
(Thearle and Aronne, 2003)
there is little work reported using these drugs in the context of
improving fertility or infertility treatment, such as assisted
reproductive techniques or ovulation induction, so it will not be
further discussed here.
Using insulin-sensitizing agents
Therapeutic use of insulin-sensitizing agents such as metformin,
diazoxide, troglitazone and D-chiro-insotol (a mediator of the
action of insulin at the receptor level) in the treatment of PCOS
have resulted in amelioration of hyperinsulinaemia and
(Nestler et al., 1989; Velazquez et al., 1994; Dunaif
et al., 1996; Nestler et al., 1999; Pasquali et al., 2000; Ibanez et al.,
. This provides both support for the link between
hyperinsulinaemia and hyperandrogenism and an additional
potential pharmaceutical target for improvement of both
conditions. It has thus been postulated that hyperinsulinaemia is a key
metabolic abnormality in PCOS. Metformin, however, is not
effective for grossly obese women
(Ehrmann et al., 1997)
studies found that metformin induced weight loss
although this remains to be con?rmed
The use of metformin for infertile women with PCOS receiving
infertility treatment has become popular in the last few years. A
recent systematic review found that metformin is effective, alone
or together with ovulation induction agent, for the ovulation
induction of PCOS women
(Lord et al., 2003)
Appetite, ghrelin and weight management
Discrepancies in appetite regulation may exist. Some investigators
have claimed that bulimia is a common ?nding in PCOS, but
others have not con?rmed this. There has been much interest in the
appetite regulation function by hormone ghrelin (Figure 2).
Ghrelin is a 28 amino acid acylated peptide produced primarily
by the endocrine cells in the stomach and is secreted into the
(Kojima et al., 1999)
. It stimulates growth hormone
(GH) secretion through its action as an endogenous ligand for the
hypothalamic?pituitary growth hormone secretagogue receptor
(GHS-R) The GHS-R is widespread throughout the body,
indicating multiple roles for ghrelin in addition to its GH-secreting
actions. In particular, ghrelin has been implicated as an important
regulatory peptide in a number of physiological processes in the
brain and the periphery including food intake, body weight
regulation and endocrine pancreatic function and glucose
metabolism (Muccioli et al., 2002).
Ghrelin increases sharply immediately prior to onset of feeding.
Once feeding has commenced, plasma ghrelin drops to reach a
trough 1?2 h post-meal before returning to baseline values
(Cummings et al., 2001, 2002; English et al., 2002)
. In obesity,
fasting ghrelin is decreased
(Tschop et al., 2001)
postprandial decrease may be impaired
(English et al., 2002)
potentially compromising meal termination. Following weight
loss, fasting ghrelin increases and the impaired post-meal response
(Cummings et al., 2002)
. These data support a
potential role of ghrelin in the pathogenesis of human obesity.
There is a paucity of data on ghrelin homeostasis in PCOS.
Fasting ghrelin is decreased in subjects with PCOS compared to
controls in some
(Pagotto et al., 2002; Scho? et al., 2002)
(Orio et al., 2003)
Pagotto et al. (2002)
observed no change in fasting plasma ghrelin following 7 months
of a hypocaloric diet (1200?1400 kcal/day) for either PCOS (n =
10) or non-PCOS (n = 10) age- and weight-matched subjects
(Pagotto et al., 2002)
. However, in a pilot study, our group
observed higher fasting plasma ghrelin in non-PCOS compared to
PCOS overweight subjects and a greater increase in fasting ghrelin
for non-PCOS subjects following 16 weeks of weight loss (Moran
et al., 2003). There was a greater improvement in postprandial
ghrelin response following weight loss for non-PCOS compared to
the PCOS subjects (unpublished data). There is thus a suggestion
that both fasting and postprandial ghrelin homeostasis is impaired
in PCOS and that weight loss may partially restore normal ghrelin
homeostasis. This indicates that ghrelin is down-regulated in
obesity with the consequence of decreasing satiety signals with
feeding, potentially leading to a predisposition to
overconsumption for subjects with PCOS.
The bene?t of weight management through lifestyle change
In some studies, a reduced emphasis was put on caloric restriction
while more emphasis was placed on lifestyle changes. These
included educating subjects on the adoption of general healthy
eating practices in conjunction with moderate amounts of
(Clark et al., 1995, 1998; Huber-Buchholz et al.,
. These principles may be easier to sustain than a lifestyle
change and thus are likely to improve lifelong maintenance of a
healthy weight. The effect of exercise on improving insulin
sensitivity independent of weight loss has also been documented
(Goodyear and Kahn, 1998)
. Lifestyle changes can also aid in
normalizing hyperlipidaemia and hypertension in reducing the risk
for cardiovascular disease and diabetes mellitis, including the 25%
reduction of fasting insulin and triglycerides and 10% reduction in
weight and blood pressure
(Noakes et al., 1999)
Longer-term lifestyle studies indicate that improvements in
fertility occur with modest weight loss (~5% of initial body
weight) and study-end BMI of >30 kg/m2.
Clark et al. (1995)
conducted a prospective study including a weight loss component
to determine whether it could help infertile, overweight,
anovulatory women. A weekly programme of behavioural change
in relation to exercise and diet for 6 months resulted in an average
weight loss of 6.3 kg, a restoration of ovulation in 12 of the 13
subjects and pregnancy in 11 women. Fasting insulin and
testosterone concentrations dropped signi?cantly. A further
(Clark et al., 1998)
of the same protocol involved 67
anovulatory women in an exercise and dietary intervention for 6
months. Women in the study lost an average of 10.2 kg or 3.7 kg/
m2 (10% reduction of BMI) with 60 of the 67 anovulatory subjects
resuming spontaneous ovulation. Of these women, 52 achieved a
pregnancy, 45 of which resulted in a live birth. A low fat (~30% of
energy and saturated fat ~10% of energy), moderate protein and
moderate carbohydrate intake and increased consumption of ?bre,
wholegrain breads and cereals and fruit and vegetables in
conjunction with moderate regular exercise (30?60 minutes/day)
is proposed to aid in weight loss and maintenance both in the
general population and in obese infertile women with PCOS
Furthermore, lifestyle modi?cation through diet and exercise
programmes in obese subjects with PCOS improves psychological
parameters (self-esteem, anxiety, mean depression scores and
scores on general health questionnaire)
(Galletly et al., 1996)
addition to reproductive outcomes
(Clark et al., 1995, 1998;
Huber-Buchholz et al., 1999)
. While the effect of long-term
weight loss on reduction in diabetic risk has not been studied
speci?cally in PCOS, lifestyle change with altered diet and
increased physical activity is associated with signi?cant reduction
in the risks of developing diabetes mellitus in the general
(Knowler et al., 2002)
. Furthermore, these
interventions are superior to those of medication such as metformin
(Doggrell, 2002; Diabetes Prevention Program Research Group,
Addressing a number of lifestyle factors can improve long-term
reproductive and metabolic health. Exercise aids in management
of infertility through reducing insulin resistance
, limiting lean muscle mass loss in weight loss
(Garrow and Summerbell, 1995) and aiding in maintenance of a
(Skender et al., 1996)
. Furthermore, combining
exercise and dietary intervention together will increase the success
of the regime
(Skender et al., 1996; Frost et al., 2002)
reviews indicate that improved weight maintenance is aided
enormously by exercise (Fogelholm et al., 2000). Smoking is a
major risk factor for female sub-fertility, expressed as time to
pregnancy and early pregnancy loss, for pre-term birth and low
birthweight in babies
(Satcher, 2001; Winter et al., 2002)
levels of alcohol intake have been associated with reduced fertility
and increased risk of spontaneous abortion
(Grodstein et al.,
. Cognitive behaviour therapy and reduction of
psychosocial stressors can aid both in weight loss and maintenance of the
(Wing, 1992; Skender et al., 1996)
weight loss in a group environment additionally provides
psychological support (Galletly et al., 1996). Modifying additional factors
such as alcohol consumption, smoking, cognitive behaviour
therapy and use of a group environment can increase the
longterm success and maintenance of weight loss and reproductive and
metabolic improvements and has been previously successfully
(Clark et al., 1995, 1998; Huber-Buchholz et al., 1999)
Dietary interventions: what diet?
The most important determinant of dietary intervention for weight
loss is energy balance, though for many other reasons various
types of diet have been proposed and tested. Most studies have
looked at carbohydrate-deplete, fat-depleted diets with caloric
restriction as the model for long-term sustained weight loss.
However, some consumer support groups promote high protein,
low carbohydrate or low glycaemic index (GI) diets as being more
effective for therapeutic outcomes in this condition. There is no
de?nite evidence to support or refute this approach. Long-term
weight loss may be more effective with low fat, high carbohydrate
diets comprising unre?ned foods such as whole-grain, pasta,
brown rice, etc., but the evidence for this is inconsistent and
(Saltzman et al., 2001; Poppitt et al., 2002)
None of these studies have been conducted in women with PCOS.
The traditional food pyramid emphasizes a low fat, high
carbohydrate diet with secondary emphasis on unre?ned
carbohydrate. Recent research recommends actively restricting foods
high in glycaemic load such as potatoes and re?ned grain products
such as white bread; limiting dairy products to one or two servings
a day; replacing unhealthy saturated fat with healthier unsaturated
vegetable oils; and emphasizing whole grains, fruits and
(Willett and Stampfer, 2003)
. The greater emphasis on a diet
lower in glycaemic load through minimizing re?ned carbohydrate
and using unsaturated fats more liberally is the key feature of this
pyramid, although whether this approach is successful as a strategy
to achieve energy restriction has not been directly tested other than
in one very short-term (6 day) small trial
(Dumesnil et al., 2001)
There are many diets on offer to consumers and few have any
scienti?c credibility. However, recent publications have shown
that mortality is reduced by adherence to a Mediterranean diet
2003; Trichopoulou et al., 2003)
and the use of high protein, low
carbohydrate diets has been shown to be associated with better and
more sustained weight loss (Foster et al., 2003).
Alternative strategies suggest that increasing dietary protein or
reducing dietary glycaemic/load may aid in weight loss. Increasing
dietary protein at the expense of carbohydrate is proposed to aid
weight loss through an increased satiating and thermogenic effect
of protein, but evidence for the latter is limited
may also increase insulin sensitivity through preserving lean body
mass in weight loss. Decreasing dietary glycaemic load is
proposed to improve cardiovascular risk pro?le and is additionally
proposed to aid weight loss through an increased satiating effect of
low GI foods.
Dietary protein: the effect of increasing dietary protein in weight
Baba et al. (1999)
reported a decreased fall in resting energy
expenditure (REE) with weight loss in a high protein (HP)
compared to a low protein (LP) diet (?555.7 kJ compared to ?
1614.1 kJ). However,
Luscombe et al. (2003)
showed a similar
reduction in REE for both HP and LP diets. This may be explained
by the difference in protein intake between the two studies (45%
compared to 28% respectively for the HP diets) and we propose to
repeat these measurements with an increased protein intake (35?
40% of daily intake). In short-term studies, e.g. 24 h, HP diets
increase postprandial thermogenesis (PPT) and REE compared to
high carbohydrate or fat diets with equal calories
(Robinson et al.,
1990; Mikkelsen et al., 2000; Luscombe et al., 2002)
et al. (2003) reported a 28% increased thermic effect of feeding for
a HP compared to a LP meal, corresponding to a difference of 1.3
kg in weight over 6 months. With the potential for reduced PPT in
(Robinson et al., 1992)
, this may lead to signi?cant
differences in weight loss or maintenance. We propose that a
further increase in dietary protein (35?40% of daily intake) may
aid in weight loss and maintenance of a reduced weight by
minimizing the normal fall in energy expenditure seen in weight
While greater decreases in weight and fat composition were
observed with HP compared to LP ad libitum diets
(Skov et al.,
, no signi?cant differences have been observed in isocaloric
diets for weight and body fat
(Lean et al., 1997; Luscombe et al.,
2002; Moran et al., 2003)
. In a prior weight loss study in women
with type II diabetes, we observed a greater decrease in total (5.3
versus 2.8 kg) and abdominal (1.3 versus 0.7 kg) fat for a HP
compared to a LP diet
(Parker et al., 2002)
. These studies modestly
increased protein (30% of daily intake); a more substantial
increase (35?40%) has not yet been explored for >4 weeks. Protein
is more satiating than carbohydrate or fat (Poppitt et al., 1998), as
shown by a 2000 kJ energy intake difference between ad libitum
HP and LP diets
(Skov et al., 1999)
. This increased satiating effect
may aid dietary compliance or weight maintenance, particularly in
a free-living situation. Qualitatively Layman et al. (2003) reported
a greater level of satiety and satisfaction following 10 weeks of an
isocaloric HP (30% protein) compared to a LP (16% protein) diet.
Oral and intravenous protein or amino acids stimulate insulin
release, both singly and synergistically with glucose
(Gannon et al.,
Baba et al. (1999)
reported no difference in
fasting insulin levels between HP and LP diets. However, a 17%
decrease in insulin sensitivity was reported for a HP compared to a
(Piatti et al., 1994)
. In weight loss, reduction of lean body
mass (LBM) has important implications for maintaining metabolic
rate and improving insulin sensitivity through increasing skeletal
muscle insulin-mediated glucose uptake. While no positive effect
of increasing dietary protein on sparing LBM was found
et al., 1999)
, Piatti et al. (1994) found a decreased reduction in
LBM with increasing dietary protein through an effect of
proteolysis and maintenance of whole-body nitrogen levels.
Piatti et al. increased dietary protein more severely (45% protein)
than Skov et al. (25% protein). Furthermore, an increased ratio of
fat/LBM loss was reported with weight loss with an isocaloric HP
(30% protein) compared to a LP diet (16% protein) (6.36
compared to 3.92 kg)
(Layman et al., 2003)
. A prior study also
indicated that total LBM was preserved to a greater extent in
weight loss in hyperinsulinaemic females on a HP (30% protein)
compared to a LP diet (15% protein) (?0.1 kg compared to?1.5 kg)
(Farnsworth et al., 2003)
Signi?cant improvements in total cholesterol, triglycerides and
low-density lipoprotein cholesterol (LDL-C) are observed in
studies with no weight loss
(Wolfe and Piche, 1999)
compared to LP diets. In overweight women with PCOS, we
observed a 10% decrease in high-density lipoprotein (HDL-C) for
a LP diet with no change for a HP diet after weight loss (Moran
et al., 2003). In weight loss, improvements in total cholesterol/
(Moran et al., 2003)
(Layman et al., 2003)
and total cholesterol and LDL-C
(Parker et al., 2002)
reported for isocaloric HP compared to LP diets. For ad libitum LP
and HP diets, Skov et al. (1999) demonstrated a reduction in
plasma triglycerides for the HP diet with no change for the LP diet.
However, these changes in lipids are not consistently reported.
Farnsworth et al. (2003)
also noted a greater lowering of plasma
triglycerides on the HP diet in hyperinsulinaemic women.
Glycaemic load: the effect of altering glycaemic load in weight
Glycaemic index (GI) is a classi?cation index of carbohydrate
foods based on their effects on blood glucose response over 2 h,
and glycaemic load (GL) is the product of the GI and the amount of
Moderate GI 55?70
Mini Wheats?, Kelloggs Nutrigrain?,
Kelloggs Sustain?, Uncle Toby's
Basmati rice, white bread
Pontiac variety potato, new potato,
Banana, pineapple, raisins, rockmelon
High GI >70
Sanitarium Puffed Wheat?,
Kelloggs Rice Bubbles?,
Sanitarium Weet Bix?
Calrose?, white rice, brown rice,
Baked potato, instant potato
Cordial, soft drinks, orange juice
Popcorn, boiled-type lollies
Sucrose (table sugar), honey
Glucose, maltose (in malt)
(Jenkins et al., 1984)
. Table I lists GI
grouping of some common types of food. Dietary GI and GL are
positively associated with risk of coronary artery disease and type
(Salmeron et al., 1997; Liu et al., 2000)
intervention studies have shown that weight maintenance low GI
diets may lower daylong glucose levels, glycated haemoglobin
(HBA1c), triglyceride and total cholesterol concentrations
compared to high GI diets (Brand et al., 1991). The effect of low GI
diets on improving insulin sensitivity is more controversial.
et al. (1999)
documented 27% lower fasting insulin after 24 days
following a low GI diet compared to a high GI diet. However, no
differences in insulin sensitivity were found between the two diets.
Reduced GI foods have been shown to result in increased
satiety, decreased hunger and lower voluntary food intake in 15/16
single day studies
(Brand-Miller et al., 2002)
. This has not been
investigated in longer-term weight loss settings, but a reduced ad
libitum energy intake may also occur
(Brand-Miller et al., 2002)
In this scenario, increasing dietary protein will also decrease the
GL through decreasing the total amount of carbohydrate. An
additive effect may additionally exist between the two factors. A
signi?cant recent study
(Dumesnil et al., 2001)
examined low GI?
low fat?HP ad libitum diet compared to the conventional
American Heart Association (AHA) moderate protein high
carbohydrate diets for the treatment of the atherogenic metabolic
risk pro?le over 6 days. This is the ?rst study to examine the
combined effects of increasing dietary protein and decreasing
dietary GI. The AHA diet was associated with signi?cant increases
in hunger and decreases in satiety whereas the low GI?low fat?HP
ad libitum diet reduced energy intake by 25%. The low GI?low
fat?HP diet was associated with an improved metabolic risk pro?le
whereas the AHA diet increased triglycerides by 28% and
decreased HDL-C by 10%
(Dumesnil et al., 2001)
. It is possible
that a HP?low GI diet may optimally improve glycaemic control,
lipid pro?les and insulin sensitivity compared to other dietary
interventions. A HP?low GI diet may also aid in long-term weight
loss and maintenance of a reduced weight due to the increased
satiating effects of low GI foods compared to other dietary
interventions but this has yet to be con?rmed.
Summary and recommendation for weight management of
There is well-established evidence for the detrimental effect
of overweight and obesity on women's reproductive function;
this is further complicated by the presence of PCOS in many
infertile women. In addition, the distribution of body fat is
also related to the reduction or even loss of fertility. So far,
most research has indicated that overweight and obese conditions
lower the concentration of SHBG and increase androgen, insulin
and leptin secretion and insulin resistance, leading to
hyperinsulinaemia and hyperandrogaenmia. However, there is limited
understanding of the details of how these changes affect human
reproductive function. On the other hand, weight loss has
been shown to improve metabolic function, hormonal pro?le
and lead to marked recovery or improvement of reproductive
Therefore the recommendation for overweight/obese patients
with infertility is closely related to the rami?cation of this
problem. They should have their height, weight and waist
circumference recorded at their ?rst consultation and at regular
intervals thereafter. Once the patient has been classi?ed as
overweight or obese, then weight management should be offered
as a ?rst line treatment option.
Dietary intervention and increased physical activity remain the
optimal treatment strategy for overweight/obese women with
PCOS. A relatively small weight loss (~5 kg) can improve insulin
resistance and hyperandrogenism, menstrual function and fertility,
and large changes in weight may not be needed to restore
reproductive function. Weight loss can also improve long-term
metabolic health and realistic and achievable target weight loss
goals can be set for women. Obesity and overweight can be treated
by a variety of strategies including dietary management, physical
activity, behaviour modi?cation, pharmacotherapeutic treatment
and surgery. Dietary management with lifestyle modi?cation as an
objective should be adopted initially with pharmacological and
other interventions reserved for use when weight-loss regimes
have proved unsuccessful.
Since the overall emphasis is to achieve and maintain a reduced
weight, attempts should be made to establish sensible eating
patterns and a healthy lifestyle. A number of alternative dietary
approaches to the conventional low fat?high carbohydrate regime
such as partly modi?ed diets or moderately HP?lower
carbohydrate diets which are consistent with a healthy eating plan may
assist in maintaining an energy restricted diet. The other lifestyle
factors, such as alcohol intake, smoking and psychosocial
stressors, should also be addressed. A group environment can
provide support for weight loss and maintenance of weight loss. At
the same time, it is necessary to tailor intervention to an
individual's weight and current dietary and exercise patterns.
The use of a dietician is warranted to aid in the evaluation of
dietary intake and eating patterns and in individualizing an
appropriate dietary approach.
Supported by the University of Adelaide, NHMRC (Australia),
CSIRO Human Nutrition and The Reproductive Medicine Unit,
University of Adelaide.
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