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Human Reproduction vol.12 no.6 pp.1142–1151, 1997
Menstrual cycle and appetite control: implications for
weight regulation
L.Dye
1
and J.E.Blundell
prior to the onset of menstruation and which are relieved at
or shortly after commencement of menstrual flow. In its most
BioPsychology Group, Department of Psychology, University of
severe form this is also known as premenstrual dysphoric
Leeds, Leeds LS2 9JT, UK
disorder (PMDD) (Gold, 1994)*. Although a large range of
1
To whom correspondence should be addressed
symptoms have been associated with PMS, the more common
symptoms which can be said to characterize the syndrome
Hormonal fluctuations associated with the menstrual cycle
influence appetite control and eating behaviour. Energy include depression, irritability, mood swings, water retention-
intake varies during the reproductive cycle in humans and
based symptoms such as breast tenderness and bloating,
animals, with a periovulatory nadir and a luteal phase
changes in appetite and food cravings. These symptoms can
peak. Patterns of macronutrient selection show less consist-
be measured using subjective rating scales. The distinction
ency but a number of studies report carbohydrate cravings
between PMS and PMDD relates to the severity of the
in the premenstrual phase, particularly in women with
symptoms. PMDD is less prevalent than PMS, affecting ~5%
premenstrual syndrome. The cyclical nature of food crav-
of women. To be clinically significant, it is generally accepted
ings are frequently, but not invariably, associated with
that the symptoms of PMDD that a sufferer experiences must
depression. Fluctuations in appetite, cravings and energy
endure consistently, at a severe level, for at least two cycles
intakeduringthemenstrualcyclemayoccurinparallelwith
(American Psychiatric Association, 1994). For the purposes
cyclical rhythms in serotonin, which can be accompanied
of this review, the term PMS is used to encompass mild and
by affective symptoms. The premenstrual phase can be
severe forms of premenstrual symptoms. Over the years a
considered as a time when women are especially vulnerable
number of assertions have been made about the relationship
to overconsumption, food craving and depression; this is
between the existence of this syndrome and changes in food
often associated with low serotonin activity.
consumption which could influence weight regulation.
Key words: appetite/food craving/menstrual cycle/serotonin
Eating behaviour and appetite control
Particular physiological and psychological characteristics of
Introduction
the menstrual cycle and PMS could influence the expression
In this last decade of the twentieth century, obesity is becoming
of appetite through a variety of mechanisms and processes
an ever increasing public health problem. In turn this has
which influence the control of food intake. The overall regula-
stimulated the current epidemic of dieting (Blundell and Bauer,
tion of eating is complex and can best be envisaged as a
1994). At the same time people are confronted by a vast array
psychobiological system which serves to integrate biological
of food products, and food consumption is heavily promoted.
and environmental influences (e.g. Blundell, 1991). One
Dieting is particularlycommon in young women. It is estimated
important feature of the environment is, of course, the nutri-
that 40–50% of women are on a diet at any one time (Polivy
tional composition of the food supply. Human food intake
and Herman, 1987). Factors which influence the ease of
can be assessed by means of quantitative aspects of food
overconsumption and the difficulty of underconsumption are
consumption such as the energetic value of food and its
likely to be important in the maintenance of a stable body
macronutrient composition (proportion of fat, protein and
weight and in the prevention of the development of obesity.
carbohydrate). Appetite is also represented by qualitative
The regular hormonal fluctuations associated with the men-
aspects such as food choice, food preferences and appreciation
strual cycle may influence appetite control and eating behavi-
of the sensory aspects of food (taste, palatability, mouth-feel
our. In addition, particular conditions associated with the
etc.). In addition, subjective phenomena such as the perception
menstrual cycle, most notably premenstrual syndrome (PMS),
of hunger, fullness and hedonic sensations which accompany
may predispose women to changes in appetite control. It is
therefore important to identify any changes in eating associated eating are also important (Hill et al., 1995). Along with these
with the menstrual cycle in general, and with PMS in particular,
characteristics of consumption are particular food cravings
in order to be able to deal effectively with any implications
and urges to eat food in general or specific food products.
for health and well-being.
Consequently, the phenomenon that scientists and others call
*PMDD replaces late luteal phase dysphoric disorder (LLPDD) in
What is the premenstrual syndrome?
Diagnostic and Statistical Manual of Mental Disorders, 4th edn
The premenstrual syndrome is a collection of behavioural,
(American Psychiatric Association, 1994). LLPDD appeared in a
research appendix to the third edition of this manual.
somatic and physical symptoms which occur in the 7–10 days
1142
© European Society for Human Reproduction and Embryology
Menstrual cycle and appetite control
Figure 1. The fundamental elements influencing the control of food intake. The diagram illustrates how hormonal fluctuations underlying
the menstrual cycle exert direct and indirect effects on the homeostatic system controlling food intake and the pattern of eating.
food intake can be analysed in terms of structured patterns of rhythms, energy balance, and adjustments in various com-
ponents (qualitative and quantitative) of food intake. It followseating (meals, snacks etc.) and nutritional components (selec-
tion of fat, carbohydrate etc.). Subjective sensations (the that hormonal changes could directly alter the biological drive
to modulate eating or could exert an indirect influence byexperience of a drive to eat) accompany these patterns and
may be thought of as causing these adjustments. It follows physiological adjustment so as to make individuals more
susceptible or vulnerable to facilitating or stimulating environ-that any changes induced by the hormonal fluctuations of the
menstrual cycle or by PMS may be detected in various aspects mental forces.
of eating, including changes in hunger, cravings for certain
foods, alteration in meal size or snacking, adjustments in
consumption of fat or carbohydrate and an overall change in
Menstrual cycle changes in food intake
energy intake.
Animal studies
The schematic diagram in Figure 1 indicates how food
intake forms part of a homeostatic system whilst also being Cyclical changes in hunger motivation or food intake have
been observed in many animal species during the oestrusadapted to environmental demands. Two particularly important
features of our current environment are the prevalence of cycle; studies indicate a consistently lower intake around the
time of ovulation. In rodents, feeding is depressed coincidentdieting as a lifestyle for many women, and the abundance of
high-fat, highly palatable foods in the food supply. The with oestrus (Brobeck et al., 1947; Jennings, 1969; Herberg
et al., 1972; Wade, 1972; Leshner and Collier, 1973; Tarttelinhomeostatic system does not operate in symmetrical fashion.
The system appears tobe strongly defended against undereating and Gorski, 1973). However, human and other primate men-
strual cycles are distinctly different to the oestrus cycle of thebut only weakly protected against overconsumption (see Blund-
ell, 1996). Therefore, whereas dieting to lose weight is rodents. Primates have a prolonged luteal phase following
ovulation, which is characterised by elevated levels of circulat-extremely difficult, overconsumption is relatively easy and can
occur passively. In turn, this passive overconsumption is likely ing progesterone (Rosenblatt et al., 1980).
Studies in a number of primate species (see Table I) indicateto lead to weight gain and possibly obesity (Lawton et al.,
1993). This means that any overconsumption (either via that highest food intake occurs consistently in the luteal phase
with the nadir of food intake around the time of ovulationgenerally increased energy intake or involving cravings or
urges for particular foods) which occurs premenstrually is (Krohn and Zuckerman, 1938; Gilbert and Gillman, 1956;
Czaja, 1975; Rosenblatt et al., 1980). An ovulatory decreaselikely to lead to incremental weight gain which, in turn, will
engender accompanying psychological problems. in food intake has also been observed in other mammals
such as pigs (Friend, 1969) goats (Forbes, 1971) and sheepFigure 1 illustrates how hormonal changes underlying the
menstrual cycle can modulate the principles of homeostatic (Tarttelin, 1968).
Initially, elevated food intake in the luteal phase wasregulation. This means that hormonal rhythms will influence
the capability of people to undereat (to maintain dieting), and attributed to increased concentrations of progesterone (Gilbert
and Gillman, 1956). Later, the ovulatory decrease in intakethe ease of overconsumption. It seems appropriate to use this
model to account for the relationship between hormonal was attributed to the appetite-suppressant effects of oestrogen
1143
L.Dye and J.E.Blundell
The time of ovulation represents the nadir of food intake
Table I. Cyclical patterns of food intake in mammals
during the menstrual cycle (Lyons et al., 1989; Gong et al.,
1989; Fong and Kretch, 1993; Johnson et al., 1994). Moreover,
Intake phase
it has been suggested that these changes in eating parallel
Species Highest Lowest Reference
changes in basal metabolic rate across the menstrual cycle
(Solomon et al., 1982; Webb, 1986). Specifically energy
Baboon Luteal Follicular/ Gilbert and Gillman
ovulatory (1956)
expenditure has been shown to increase in the postovulatory
Rhesus monkeys Luteal Ovulatory Rosenblatt et al. (1980)
phase (Webb, 1986). This could be due to separate hormonal
Rhesus monkeys Luteal Ovulatory Czaja (1978)
action on energy intake and expenditure respectively, or to the
Pigtail monkeys Luteal Ovulatory Krohn and Zuckerman
(1938)
driving action of energy intake on some aspect of energy
Pig Pre-ovulatory Friend (1969)
expenditure (such as diet-induced thermogenesis).
Goat Ovulatory Forbes (1971)
One potential explanation for the fluctuations in food intake
Sheep Ovulatory Tarttelin (1968)
Guinea-pig Ovulatory Czaja and Goy (1975)
is alterations to insulin sensitivity during the menstrual cycle.
Rat Oestrus Herberg et al. (1972)
Marsden et al. (1996) assessed carbohydrate metabolism and
insulin sensitivity at receptor and post-receptor level in women
(Czaja, 1975, 1978), the luteal phase increase being thus due
in the follicular or luteal phase of an ovulatory ovarian cycle,
to the inhibitory action of progesterone on oestrogenic activity.
in the physiological target organ adipose tissue. They found a
Given the relatively similar reproductive cycles of primates
reduction in insulin receptor binding in the luteal phase but
and humans, it is to be expected that similar fluctuations in
no change in overall insulin action on adipocyte glucose uptake
food intake should occur during the menstrual cycle, under
and lipolysis. The effect of menstrual cycle phase, i.e. of
natural conditions.
hormone concentrations on insulin binding, is congruent with
impaired insulin sensitivity in conditions where concentrations
Human studies
of oestrogen and progesterone are raised either artificially, as in
In humans, when food intake has been examined in relation
oral contraceptive use, or naturally, as in pregnancy. However,
to the menstrual cycle a distinct pattern of fluctuation has
although receptor binding is altered in the luteal phase,
been observed. Generally, energy intake is higher in the
compensatory change in the post-binding sites allows overall
postovulatory or premenstrual phase of the cycle than in the
insulin action in adipocytes to remain normal.
preovulatory or follicular phase (see Table II for review of
research). Examination of these phases has usually focused on
two 10 day periods either side of ovulation.
Macronutrient intake
In the majority of studies luteal energy intake is significantly
In contrast to cyclic effects on total energy intake, reports
higher than energy intake in the follicular phase. Of 30 studies
about the patterns of macronutrient intake during the menstrual
that compare cycle phases in 37 groups of women, 25 studies
cycle are less consistent (see Table III) and sometimes have
report significantly higher luteal energy intake than follicular
achieved celebrity status.
intake. The remaining 12 comparisons show no significant
There has been some suggestion of significantly increased
effect, though the trend for similar groups in each study is
carbohydrate consumption premenstrually (Dalvit-McPhillips,
invariably in the same direction. The two exceptions are
1983; Hrboticky et al., 1989; Lyons et al., 1989; Brzezinski
Wurtman et al. (1989) and Krakow (1992) who show follicular
et al., 1990), reductions in protein and carbohydrate intake at
energy intake to be non-significantly greater than luteal intake
ovulation (Lyons et al., 1989), and premenstrual increases in
in subjects with no premenstrual symptoms and women not
fat intake (Anantharaman-Barr et al., 1988; Tarasuk and
taking oral contraceptives respectively. Both of these studies,
Beaton, 1991; Johnson et al., 1994) or in fat and protein
however, have some inherent methodological weaknesses. For
intake (Gallant et al., 1987). The increase in carbohydrate
example, in both studies participants were aware of the
consumption has been referred to as carbohydrate craving and
menstrual cycle focus, a factor known to influence reporting
has been regarded as an index of a particular type of eating
(Ruble, 1977), and in Wurtman et al.’s study screening for
disorder (Wurtman, 1993).
PMS was based on retrospective reports which are likely to
There are however, inconsistencies both between and within
amplify any cyclical pattern (Warner et al., 1991).
studies. Results may differ depending on whether actual intake
In contrast, such statistically significant cycle-related trends
(in grams) of a macronutrient or the relative proportion that a
are not observed in women using oral contraceptives
macronutrient contributes to total percentage energy intake is
(Anantharaman-Barr et al., 1988; Krakow, 1992), or women
considered. While absolute intake of a macronutrient may
with anovulatory cycles (Barr et al., 1995). In both of these
increase significantly from the follicular to luteal phase (e.g.
conditions, cyclic fluctuations in hormones are absent or
Barr et al., 1995), the percentage of energy intake as, e.g., fat
minimized. In addition, eating trends across the menstrual
or carbohydrate may fail to differ. The well-publicized view
cycle are not seen in women with highly restrained eating
has been that it is carbohydrate intake that increases in the
patterns (Schweiger et al., 1992). This could be due to the
luteal phase (Wurtman et al., 1989). However, there are an
effects of low energy intake on hormonal cycles, or because
equal number of studies which document significant increases
of a tonic inhibition of eating which obscures any underlying
physiological influence. in fat intake at this stage of the cycle. Such results may
1144
Menstrual cycle and appetite control
Table II. Cyclical patterns of energy intake in women
Study Sample size Days measured Energy intake (MJ)
Luteal (L) Menstrual Follicular (F) Ovulatory L versus F
Abraham et al. (1981) 23 35 (whole cycle) nr nr nr nr L . F*
Anantharaman-Barr et al. (1988) 22–8oc 7days pre/7 days post nr nr ns
– 14 noc nr nr L . F*
Barr et al. (1995) 45 – 29 ovulatory 333 days (pre/ovul./post) 3.27 8.01 nr L . F*
– 13 anovulatory 7.91 8.21 nr F . Lns
Brzezinski et al. (1990) 17 PMS – meals 1 day pre/1 day post 7.28 6.04 L . F*
– snacks 3.86 1.80 L . F*
Dalvit (1981) 8 10 days pre/10 days post 8.12 6.02 L . F*
Dalvit-McPhillips (1983) 8 10 days pre/10 days post 7.22 5.22 L . F*
Fong and Kretch (1993) 9 1–28 (whole cycle) 10.46 10.31 9.87 9.39 ns
Gallant et al. (1987) 18 –9 control 233 days (pre/post) 8.09 6.27 L . F*
–9 PMS 6.56 5.71 L . Fns
Giannini et al. (1985) 20 whole cycle nr nr nr nr no cyclical
trend
Gong et al. (1989) 7 1–28 (whole cycle) 8.54 7.89 7.67 7.39 L . F*
Hill and Blundell (1989) 12 – PMS whole cycle nr L . F*
Hrboticky et al. (1985) 8 1 day pre/1 day post 7.72 7.52 L . F
Hrboticky et al. (1989) 10 1 day pre/1 day post nr nr L . F*
Johnson et al. (1994) 26 1–28 (whole cycle) 7.84 7.6 7.15 7.15 L . F*
Krakow (1992) 98 – 47 noc whole cycle 8.23 8.64 8.803 F . Lns
– 47 oc whole cycle 8.86 8.64 8.58 L . Fns
Lariviere et al. (1994) 8 231 days (pre/post) 8.29 7.39 L . F*
Lissner et al. (1988) 23 10 days pre/10 days post 9.77 9.41 L . F*
Lyons et al. (1989) 25 1–28 (whole cycle) 9.13 9.05 8.45 7.87 L . F*
McCoy et al. (1988) 12 7 days pre/7 days post 8.95 8.27 L . F*
Manocha et al. (1986) 11 10 days pre/10 days post 6.74 5.44 L . F*
Martini et al. (1994) 18 3 days pre/3 days post 7.98 7.32 L . F*
Netter et al. (1993) 40 – disturbed eaters 9 days pre/9 days post nr nr L . F*
– non-disturbed nr nr L . F*
Oram (1987) 6 10 days pre/10 days post 11.56 8.74 L . F*
Piers et al. (1995) 13 5 days pre/5 days post 7.12 7.12 ns
Pliner and Fleming (1983) 34 1 days pre/1 days post 8.42 7.49 L . F*
Rogers and Jas (1994) 42 – (snacks) 25 L/17 follicular 3.35 1.46 L . F*
Schweiger et al. (1992) 21 – 13 unrestrained 12 days pre/12 days post 9.42 9.08 L . F*
– 9 restrained 7.21 6.99 L . Fns
Sophos et al. (1987) 9 7 days pre/7 days post 7.79 7.44 L . Fns
Tarasuk and Beaton (1991) 14 10 days pre/10 days post 8.00 7.62 L . F*
Wurtman et al. (1989) 19 – control 1 day pre/1 day post 8.46 8.72 F . Lns
9 – PMS 1 day pre/1 day post 10.02 7.92 L . F*
*Significant difference between luteal and follicular phases (P . 0.05). nr 5 measured but actual intake not reported; oc 5 oral contraceptive; noc 5 no oral
contraceptive; PMS 5 premenstrual syndrome; ns 5 non-significant.
represent general increases in appetite rather than specific or behaviour. This problem is compounded when multiple
phases are compared and degrees of freedom reduced. Further-increases in intake of a particular macronutrient.
more, few studies have taken account of menstrual cycle-
related symptoms, which are most commonly reported in the
Methodological issues
premenstrual phase. These symptoms may influence behaviour
All studies on the menstrual cycle are confronted by formidable
in an indirect way (in contrast to direct hormonal influence).
methodological problems. Studies of food intake and the
Consequently, in our view, research on the pattern of eating
menstrual cycle often contain some serious methodological
and motivation accompanying the menstrual cycle should be
flaws or inconsistencies. These include techniques for recording
critically examined and cautiously interpreted.
food intake, inadequate determination of menstrual cycle
phases, the failure to consider more than two (rather long)
Premenstrual syndrome and food intake
cycle phases and the frequent ‘averaging’ across menstrual
cycles. These methodological problems will reduce the PMS is characterized by the dramatic occurrence of symptoms
in the premenstrual phase, which are relieved following thesensitivity of experiments and may jeopardize the validity of
the conclusions made about the nature of fluctuations in food onset of menstruation. Increases in appetite and/or food crav-
ings are considered characteristic of PMS. A frequent dilemmaintake during the menstrual cycle.
One frequent problem concerns those experiments using which arises in studies of PMS is whether PMS is an extreme
of the normal experience of the menstrual cycle or is asmall numbers of subjects; these studies may not have had
sufficient statistical power to detect small effects in motivation qualitatively different phenomenon.
1145
L.Dye and J.E.Blundell
Table III. Macronutrient intake (% of energy intake) in the follicular (F) and luteal (L) phases
Carbohydrate Fat Protein
Study n FL FL FL
Abraham et al. (1981) 23 nr* nr* nr* nr* nr* nr*
Barr et al. (1995) 29 ovulatory 57.5 56.1 28.9 31.3 12.7 12.4
13 anovulatory 56.3 54.1 30.5 32.9 12.5 13.1
Tarasuk and Beaton (1991) 14 43.8 43.07 36.01 37.56* 14.56 14.12
Dalvit-McPhillips (1983) 8 39.9 55.8* 44.4 32.6* 15.7 11.6
Fong and Kretch (1993) 9 44.2 44.5 41.9 41.7 12.9 13.0
Gallant et al. (1987) 9 43.1 40.9 36.6 37.7* 13.9 15.7*
9 PMS 34.6 40.0 48.8 43.6 15.0 16.0
Johnson et al. (1994) 26 47.5 47.9 35.4 37.4* 15.4 14.7
Lyons et al. (1989) 18 47.0 45.9 35.8 36.8 13.5 13.4
Oram (1987) 6 46.5 42.2 37.1 38.1 14.5 16.4
Schweiger et al. (1992) 9 unrestrained 42.0 43.0 41.0 40.0 13.0 14.0
9 restrained 45.0 39.0 39.0 40.0 13.0 14.0
Sophos (1987) 14 47.3 46.1 36.4 33.7 15.2 15.1
Martini et al. (1994) 18 51.3 50.1 33.1 34.2 15.6 15.6
Hrboticky et al. (1989) 8 54.02 54.09 28.03 28.31 13.35 13.4
Brzezinski et al. (1990) 17 PMS
meals 28.6 32.5* 48.65 48.1* 21.1 17.01
snacks 27.9 32.8* 52.3 50.5* 17.7 15.2
*Significant difference between luteal and follicular phases (P . 0.05). nr 5 measured but actual intake not
reported; PMS 5 premenstrual syndrome.
In relation to food intake, the former view would imply that more calories, protein, fat and vitamin B
6
premenstrually.
Increases in intake for the PMS subjects were smaller than forPMS sufferers experience similar temporal fluctuations in
appetite and intake to ‘normal’ women but at a greater intensity. controls. These data are in contrast to the findings of Dalvit-
McPhillips (1983) which show an increase in carbohydrateThere have, however, been few objective studies of intake in
PMS sufferers. Two studies report luteal intake to be signific- intake premenstrually. The macronutrient data reported by
Dalvit-McPhillips (1983) does not correspond to total energyantly higher than follicular intake (Hill and Blundell, 1989;
Brzezinski et al., 1990), one a non-significant trend in the intakes reported previously from the same women (Dalvit,
1981) and Dalvit’s subjects were not reported to be PMSsame direction (Gallant et al., 1987) and one a non-significant
reversed effect (Wurtman et al., 1989). Both studies which sufferers. Rogers et al. (1992) have suggested that foods which
are preferentially consumed premenstrually tend to be highlyfail to detect effects (Gallant et al., 1987; Wurtman et al.,
1989) are based on far fewer subjects than the studies which palatable and with high hedonic properties. These foods tend
to be high in both carbohydrate and fat. Indeed, the 12%confirm the similar pattern of increased luteal energy intake
in PMS sufferers as non-symptomatic women. Giannini et al. energy increase reported by Hill and Blundell (1989) was
mainly due to a rise in the number of high fat/high carbohydrate(1985) reported a positive relationship between caloric intake
and severity of PMS symptoms. Women who reported more snacks consumed. It is therefore difficult to draw firm conclu-
sions about specific changes in macronutrient consumption.severe symptoms recorded higher caloric intake. However,
while caloric intake was measured by daily intake diaries,
PMS symptoms were assessed by retrospective questionnaire
PMS, mood and food cravings
at the end of the study, a method which tends to exaggerate
symptom reporting. Studies of food craving during the menstrual cycle have
produced a range of findings about both the pattern and natureMore recently, Both-Orthman et al. (1988) found an increase
in subjective ratings of appetite in the premenstrual phase as of food cravings. The predominant trend, however, seems to
be an increase in both the frequency and severity of foodcompared with the postmenstrual phase in both PMS and
control subjects. Levels of reporting in the premenstrual phase craving in the premenstruum. This is clearly depicted in Figure
2, based on data from 5546 women who reported symptomswere significantly higher in the PMS subjects than in the
controls. Concurrent ratings of mood and depression were in a retrospective questionnaire (Dye et al., 1995). Even
allowing for some elevation in reporting given the retrospectivesignificantly correlated with ratings of appetite in the premen-
strual phase for the PMS subjects only, suggesting a relationship nature of the study, a clear increase in food craving in the
premenstrual phase (compared with postmenstrual) is evident.between mood and appetite which distinguishes this group
from the control (non-PMS) group. This coincidence of appetite This pattern is true for severe and moderate food cravings.
Interestingly, for mild food cravings the opposite pattern isincrease and mood change has led to suggestions that these
may be causally linked. observed. This suggests that food cravings are more frequent
and more severe premenstrually, but they can also occur in aConcerning the intake of specific macronutrients Gallant
et al. (1987) found that both control and PMS subjects much weaker form at other points in the menstrual cycle in
the same women.increased carbohydrate intake postmenstrually but consumed
1146
Menstrual cycle and appetite control
Figure 2. Percentage of subjects reporting food cravings (varying
degrees of severity) at three stages of the menstrual cycle. These
Figure 3. Relationship between the incidence of food cravings and
data show a greater frequency and intensity of cravings in the
three phases of the menstrual cycle in three groups of women. The
premenstrual phase. This figure is based on data from a sample of
graph indicates non-depressed women (square symbols), women
5546 women (adapted from Dye et al., 1995).
with chronic depression (diamonds) and women with depression
only during the premenstrual phase (circles). The vertical axis
This tendency for increased food craving in the pre-menstrual
indicates the degree of reported food craving on a scale from 1
(mild) to 4 (severe). (Adapted from Dye et al., 1995.)
phase has been observed in varied samples of women (e.g.
with and without PMS and/or premenstrual depression), sug-
gesting that the experience of PMS sufferers is more severe
but not necessarily qualitatively different from that of normal
women. There does not seem to be a difference in the foods
which are craved (as opposed to frequency or severity) by
PMS or non-PMS subjects. However, it is worth considering
closely whether the craved foods belong to any particular
nutrient category (e.g. carbohydrates).
This is important because of the known effects of food on
mood and the well-documented incidence of mood change
(particularly depression) in the premenstrual phase, especially
in PMS sufferers. Consequently, a relationship between food
craving (possibly for carbohydrate-rich foods) and depression
could occur. The logic of this relationship is that women crave
those particular foods whose consumption would ameliorate
the depression. Some studies have indicated that these two
symptoms may co-exist premenstrually (Cohen et al., 1987;
Figure 4. Relationship between the incidence of food cravings and
Bancroft et al., 1988). A more recent study has clarified the
the severity of depression in three phases of the menstrual cycle.
relationship between food craving and depression.
The vertical axis indicates the severity of reported food craving on
Figure 3 is based on 919 women, selected on the basis of
a scale from 1 (mild) to 4 (severe). Bars indicate concurrent rating
their clear patterns of depression rating during three menstrual
of depression from none to severe during each of three menstrual
cycle phase (horizontal axis). The figure is based on data from a
cycle phases. From the figure, it is evident that depression is
sample of 5546 women (adapted from Dye et al., 1995).
positively related to food craving. In women with ‘chronic’
depression (i.e. depression reported as severe or very severe
in each cycle phase examined) ratings of food craving are food cravings of this PMS group are identical to those of the
‘chronic depressed’ group when their depression ratings areelevated to a ‘moderate’ level at each phase. This contrasts
with the low ratings of food craving observed in women who also the same, but the level of craving falls to that of the non-
depressed group when depression also falls.report no depression at any phase of the cycle (‘non-depressed’
group). This latter group, however, do show a cyclical pattern The relationship between food cravings and depression in
Figure 3 clearly suggests that these menstrual cycle-relatedin their reports of food craving, indicating that a rhythm of
craving can occur in the absence of depression, but at a lower symptoms are not independent. These data, however, are based
on approximately one-fifth of the original data, i.e. thoselevel. The pattern of craving shown by those women who
reported severe or very severe depression only in the premen- women with relatively easily classified temporal patterns of
depression (n 5 919). Figure 4 shows the relationship betweenstrual phase (a feature which characterizes the PMS) confirms
the relationship between food craving and depression. The depression rating and food craving rating during each phase
1147
L.Dye and J.E.Blundell
of the menstrual cycle for a large sample of unselected women 1984) and in response to oestradiol administration (Kato,
1960). In humans, concentration of serotonin (V
max
) is lowest(n 5 5 546). A positive linear relationship between depression
and food craving is evident in each cycle phase. The more premenstrually (Taylor et al., 1984; Tam et al., 1985). There
is evidence that serotonin levels in whole-blood, and plasmasevere the rating of depression, the greater the degree of food
craving. The occurrence of more severe food cravings in and platelet uptake and content are lower premenstrually in
women with PMS (Rapkin et al., 1987; Ashby et al., 1988,the premenstrual phase (in contrast to the menstrual and
postmenstrual phases) is also clear. The interrelationship 1992). Similar fluctuations have been observed in melatonin,
which is synthesized from serotonin (Parry, 1994).between food craving and depression is maintained at all
phases of the menstrual cycle and the size of the sample Neuroendocrine challenge tests have been used to measure
changes in serotonin function. Normally, infusion of thesuggests a robust relationship between these symptoms at all
phases of the menstrual cycle. serotonin precursor
L
-tryptophan (or fenfluramine) produces
an increase in plasma prolactin. In women with PMS, prolactin
responses to a neuroendocrine challenge test are blunted
The role of serotonin in food intake and food craving
premenstrually (Halbreich, 1990; Bancroft et al., 1991). The
neuroendocrine response can be affected by dieting in womenIn recent years, research has identified the neurotransmitter
serotonin [also known as 5-hydroxytryptamine (5-HT)] as a (Goodwin et al., 1987), a factor not controlled for in these
studies.particularly important component of the biological system
influencing eating (Blundell, 1977). Serotonin is implicated in The serotonin agonist, buspirone, has a high affinity for 5-
HT
1A
receptors. Yatham et al. (1989) found that the prolactinthe effects of dietary composition on brain function (e.g.
Fernstrom and Wurtman, 1971) and in the control of meal response to a buspirone challenge test was greater during the
luteal phase and suggested that this is due to supersensitivitypatterns and the urge to eat (Blundell, 1992). Since serotonin
is also implicated in physical and psychological symptoms of 5-HT
1A
receptors at this time. These results were confirmed
by Dinan et al. (1990) who excluded the possibility of variableoccurring during the menstrual cycle (and especially in PMS),
a consideration of the role of serotonin may help in the absorption during the menstrual cycle. Buspirone has also been
reported to have beneficial effects on premenstrual symptomsunderstanding of appetite changes related to PMS.
Serotonin has been implicated as the mediating factor in the (David et al., 1987; Rickels et al., 1989), as have other
serotoninergic compounds such as fluoxetine (Rickels et al.,relationship between mood and appetite (Wurtman, 1993).
This hypothesis is based on the evidence that low levels of 1990; Stone et al., 1991; Menkes et al., 1992; Wood et al.,
1992).
D
-Fenfluramine has been shown to be effective inserotonin induce dysphoric mood. It is argued that craving for
particular food products (containing carbohydrates) occurs in suppressing luteal increases in appetite in PMS sufferers (Hill
and Blundell, 1989; Brzezinski et al., 1990). However, theseorder to raise the levels of serotonin in the brain and it has
been suggested that this may be an adaptive mechanism to studies conflict in their findings on mood symptoms.
Thus studies in women with PMS show a consistent trendcompensate for a relative lack of serotonin premenstrually.
Therefore eating CHOs serves as a form of self-medication to toward decreased levels of serotonin premenstrually (Severino,
1994). A recent study (Ulrich et al., 1994) has demonstratedraise mood. The mechanisms through which the carbohydrate
content of the diet influences the uptake of tryptophan into the that central, hypothalamic regulation of follicle stimulating
hormone (FSH) and prolactin release involves serotonin, spe-brain and in turn increases the synthesis of serotonin has been
well described elsewhere (Fernstrom and Wurtman, 1971). cifically 5-HT
3
receptor-mediated processes. There is also well-
documented evidence of serotonin’s role in the regulation ofIt has been demonstrated (Wurtman et al., 1989) that the
deliberate administration of carbohydrate can relieve premen- the oestrous cycle in rodents (Vitale and Chiocchio, 1993).
These data, coupled with evidence of rhythmicity in peripheralstrual depression in PMS sufferers, defined by retrospective
symptom ratings. The consumption of a carbohydrate-rich, serotonin, suggest that while ovarian steroids may modulate the
serotonergic system, serotonin also modulates gonadotrophinprotein-poor evening meal improved mood in PMS sufferers
in the late luteal phase but had no effect on mood in the secretion.
Serotonin is also implicated in the aetiology of depression,follicular phase or in non-symptomatic control subjects. This
is consistent with a carbohydrate-induced increase in serotonin and neuroendocrine findings in women are consistent with a
higher incidence of depression in women than in men (Meltzer,occurring during the premenstruum. However, as noted earlier
there is little evidence for a selective craving for carbohydrate 1990). However, we cannot infer that peripheral serotonin
levels predict central levels in humans, although such afoods premenstrually or for a preferential intake of carbohyd-
rate. Consequently, the idea that individuals attempt to medicate relationship has been demonstrated in non-human primates
(Raleigh and McGuire, 1980). On the basis of the findingthemselves by eating carbohydrate is not yet substantiated.
However, there are other reasons to consider a role for serotonin (McGuire et al., 1983) that the serotonin system of the vervet
monkey may be affected by environmental factors and socialin premenstrual food craving and increased energy intake.
Ovarian steroids may have a modulating role in the sero- interaction, Rapkin (1992) has developed an appealing theory
of physiological deregulation of the serotonin system. Thistonergic system, affecting metabolism, activity and receptors
(Rapkin, 1992; Severino, 1994). Animal studies suggest proposes that physiological down-regulation, i.e. reduction in
serotonin, may produce negative somatic and behaviouralchanges in serotonin levels during the oestrus cycle (Biegon
et al., 1980; McEwen and Parsons, 1982; Fischette et al., symptoms such as those which characterize PMS, whereas
1148
Menstrual cycle and appetite control
women without PMS may be able to minimize deregulation concerned about their weight and shape and are likely to be
dieting. Given the increased susceptibility to risk factors forvia for instance, environmental interaction.
The effects of lowered serotonin are most likely to be overconsumption likely to be present just before menstruation,
dieting will be even more difficult to sustain during this periodobserved in those behaviours most closely regulated by the
neurotransmitter. It can be suggested that the fluctuation in and there are likely to be more frequent occurrences of counter-
regulation (Polivy and Herman, 1985).appetite and energy intake observed in women during the
menstrual cycle reflect cyclical rhythms in serotonin, which To date, however, these hypotheses remain untested because
the prevalence of PMS in dieters, the ease of adherence to amay be accompanied by affective symptoms in women with
PMS but which are present to a lesser degree (or are better diet during the premenstrual phase and the effect of dieting
on premenstrual symptoms have not been studied. This is antolerated) in women without PMS. Serotonin has been shown
to influence both satiation (meal size) and satiety (post-meal area which merits further research.
Since this review concerns the relationship between appetiteinhibition) (Blundell, 1992). During the premenstrual phase,
serotonin activity is relatively low, and therefore there will be control and hormonal conditions linked with reproductive
function, it is worth drawing attention to a possible role forrelatively weaker control over appetite. Indeed it can be
deduced that altered activity at particular serotonin receptors the ob-protein (‘leptin’) (Halaas et al., 1995). It has been
proposed that leptin serves as a signal linking adipose tissue(5-HT
1B
and 5-HT
2C
) modulates the ability to resist risk factors
for overeating and a positive energy balance (Blundell, 1996). to central neural pathways. In animals and humans the plasma
concentrations of leptin correlate well with body mass indexConsequently, during the premenstrual phase individuals will
be more susceptible to many stimuli (internal and environ- (BMI) and percentage body fat. Consequently, this ob-protein
could be the much sought after lipostatic factor. In addition,mental) that facilitate eating and elicit food craving. Thus, the
premenstrual phase of the menstrual cycle can be considered it has been demonstrated that injections of leptin can restore
fertility in mutant mice (ob/ob) which have difficulty reprodu-a time when women are especially vulnerable to overconsump-
tion and craving, and also to depression (due to low sero- cing (Chehab et al., 1996). Injections of leptin also cause an
early onset of reproductive function in normal female micetonin activity).
(Chehab et al., 1997). These effects may occur because leptin
signals the amount of body fat and because reproductive
Dieting and the menstrual cycle
function is normally switched off when levels of body fat fall
too low. In humans it is known that leptin levels are very lowMost of this discussion has been concerned with the effects
of hormonal changes on food intake. It should be borne in in patients with anorexia nervosa (Grinspoon et al., 1996) and
that female athletes with amenorrhea fail to display a diurnalmind, however, that food intake also affects hormones, and
therefore food intake will affect the rhythm of the menstrual rhythm of leptin (Laughlin and Yen, 1997). Although the role
of leptin in appetite control in humans remains to be verified,cycle. One major dimension here is the concept of dieting,
which may involve ~40% or more of the female population. some interaction between leptin, serotonin and reproductive
hormones could shed further light on appetite fluctuationsDieting can be defined as self-induced attempts to restrict food
consumption and to control the pattern of eating. Therefore within the menstrual cycle. However, at the moment this idea
should be considered speculative.dieting is likely to influence measured food consumption, food
choice and other aspects of eating. Pirke (1987) and Pirke
et al. (1989) have shown that dieting causes menstrual irregular-
Conclusions
ities. The ovarian cycle was disrupted by either disturbed
follicular development, i.e. the lack of development of a It is clear that PMS is a clinical phenomenon with implications
for health and well-being. However, considerable methodologi-dominant follicle and low levels of oestrogen, or by luteal
phase defects, i.e. impaired progesterone secretion by the cal problems face researchers who investigate PMS and other
phenomena associated with the menstrual cycle. A wide varietycorpus luteum. The former effect results in absolute infertility,
the latter in significantly compromised fertility. In addition, of characteristics and events have been attributed to the rhythm
of the menstrual cycle and to the premenstrual phase inepisodic luteinizing hormone secretion during the follicular
phase was altered by dieting. Three major factors which particular. Definitive statements cannot yet be made about
certain issues. However, we feel that the following generalinfluence this relationship have been identified: (i) age: younger
women are more susceptible to diet-induced menstrual irregu- conclusions can be drawn from the published body of research;
(i) Orderly fluctuations in eating and other measures of foodlarities; (ii) amount of weight loss: the greater the weight loss
the higher the likelihood of menstrual irregularities; (iii) the consumption do occur during the menstrual cycle. Generally
there is an increase in energy intake and appetite during thenature of the diet: vegetarian diets affect the cycle more than
a non-vegetarian diet, even when both cause the same amount pre-menstrual phase (when compared to the ovulatory or
postmenstrual phases); (ii) This increase in energy intake andof weight loss.
It follows that any studies on the relationship between appetite during the premenstrual phase also occurs in women
who suffer from PMS. In these women the appetite changeshormonal state, food cravings and eating should take into
account the prevalence of dieting among women in the study may be experienced with greater intensity and given increased
psychological emphasis; (iii) During the premenstrual phasesample. This is particularly important in studies on PMS since
it is known that a large proportion of PMS sufferers are food cravings are increased in frequency and intensity. Food
1149
L.Dye and J.E.Blundell
Cohen, I.T., Sherwin, B.B. and Fleming, A.S. (1987) Food cravings, mood
craving appears to be more severe in women with PMS; (iv)
and the menstrual cycle. Horm. Behav., 21, 457–470.
Food craving is positively related to depression during the
Czaja, J.A. (1975) Food rejection by female rhesus monkeys during the
menstrual cycle. Food craving is more intense when depression
menstrual cycle and early pregnancy. Physiol. Behav., 14, 579–587.
Czaja, J.A. (1978) Ovarian influences on primate food intake: Assessment of
is severe, and depression is greater during the premenstrual
progesterone actions. Physiol. Behav., 21, 923–928.
phase. Food craving is linked to depression in women with
Czaja, J.A. and Goy, R.W. (1975) Ovarian hormones and food intake in
PMS; (v) These changes in appetite and cravings indicate the
female guinea pigs and rhesus monkeys. Horm. Behav. 6, 329–349.
probability of active or passive overconsumption of food
Dalvit, S.P. (1981) The effect of the menstrual cycle on patterns of food
intake. Am. J. Clin. Nutr., 34, 1811–1815.
during the premenstrual phase and in women with PMS. In
Dalvit-McPhillips, S.P. (1983) The effect of the human menstrual cycle on
turn, this suggests a potential for weight gain; (vi) Changes in
nutrient intake. Physiol. Behav., 31, 209–212.
serotonin metabolism are implicated in the vulnerability to
David, D., Freeman, A. and Harrington, T.M. (1987) Buspirone for anxious
risk factors, increased food consumption, food craving and
women in a primary care environment: a multicenter open evaluation. Adv.
Therapy, 4, 251–264.
depression during the premenstrual phase. These phenomena
Dinan, T.G., Barry, S., Yatham, L.N. et al. (1990). The reproducibility of the
could be treated by behavioural, nutritional or pharmaceutical
prolactin response to buspirone: relationship to the menstrual cycle. Int.
strategies designed to influence the synthesis and/or synaptic
Clin. Psychopharm., 5, 119–123.
activity of serotonin.
Dye, L., Warner, P. and Bancroft, J. (1995) Food craving during the menstrual
cycle and its relationship to stress, happiness of relationship and depression.
J. Affect. Dis., 34, 157–164.
Fernstrom, J.D. and Wurtman, R.J. (1971) Brain serotonin content: Increase
References
following ingestion of carbohydrate diet. Science, 174, 1023–1025.
Fischette, C.T., Biegon, A. and McEwan, B.S. (1984) Sex steroid modulation
Abraham, S.F., Beaumont, P.J., Argall, W.J. and Haywood, P. (1981) Nutrient
of the serotonin behavioural syndrome. Life Sci., 35, 1197–1206.
intake and the menstrual cycle. Aust. NZ. J. Med., 11, 210–211.
Fong, A.K.H. and Kretch, M.J. (1993) Changes in dietary intake, urinary
American Psychiatric Association (1994) Diagnostic and Statistical Manual
nitrogen and urinary volume across the menstrual cycle. Am. J. Clin. Nutr.,
of Mental Disorders, 4th edn. American Psychiatric Association,
57, 43–46.
Washington, DC.
Forbes, J.M. (1971) Physiological changes affecting voluntary food intake in
Anantharaman-Barr, H.G., Clavien, H., Gmunder, B. and Pollett, P.E. (1988)
ruminants. Proc. Nutr. Soc., 30, 135–142.
Nutrient intake and the menstrual cycle. Int. J. Obesity, 143.
Friend, D.W. (1969) Self-selection of feeds and water by swine during
Ashby, C.R. Jr., Carr, L.A., Cook, C.L. et al. (1988) Alteration of platelet
pregnancy and lactation. J. Anim. Sci., 32, 658–666.
serotonergic mechanism and monoamine oxidase activity in premenstrual
sundrome. Biol. Psychiat., 24, 225–233.
Gallant, M.P., Bowering, J., Short, S.H. et al. (1987) Pyridoxine and magnesium
status of women with premenstrual syndrome. Nutr. Res., 7, 243–252.
Ashby, C.R. Jr, Carr, L.A, Cook, C.L. et al. (1992) Inhibition of serotonin
uptake in rat brain synaptosomes by plasma from patients with premenstrual
Giannini, A.J., Price, W.A., Loiselle, R.H. and Giannini, M.C. (1985)
syndrome. Biol. Psychiat., 31, 1169–1171.
Hyperphagia in premenstrual tension syndrome. J. Clin. Psychiat., 46,
436–437.
Bancroft, J., Cook, A. and Williamson, L. (1988) Food craving, mood and
the menstrual cycle. Psychol. Med., 18, 855–860.
Gilbert, C. and Gillman, J. (1956) Changing pattern of food intake and appetite
duringthemenstrualcycleofthe baboon(Papio ursinus) with a consideration
Bancroft, J., Cook, A., Davidson, D. et al. (1991) Blunting of neuroendocrine
of some of the controlling endocrine factors. S. Afr. J. Med. Sci., 21, 75–88.
responses to infusion of
L
-tryptophan in women with perimenstrual mood
change. Psychol. Med., 21, 305–312.
Gold, J. H. (1994) Historical perspective of Premenstrual Syndrome. In
Gold, J.H. and Severino, S.K. (eds), Premenstrual Dysphorias; Myths and
Barr, S.I., Janelle, K.C. and Prior, J.C. (1995) Energy intakes are higher
Realities. American Psychiatric Association, New York.
during the luteal phase of ovulatory menstrual cycles. Am. J. Clin. Nutr.
61, 39–43.
Gong, E. J., Garrel, D. and Calloway, D. H. (1989) Menstrual cycle and
voluntary food intake. Am. J. Clin. Nutr. 49, 252–258.
Biegon, A., Bercovitz, H. and Samuel, D. (1980) Serotonin receptor
concentration during the estrus cycle of the rat. Brain Res., 187, 221–225. Goodwin, G.M., Fairburn, C.G. and Cowen, P.J. (1987) Dieting changes
serotonergic function in women, not men: implications for the etiology of
Blundell, J. E. (1977) Is there a role for serotonin (5-hydroxytryptamine) in
anorexia nervosa? Psychol. Med., 17, 839–842.
feeding? Int. J. Obesity, 1, 15–42.
Grinspoon, S., Gulick, T., Askari, H. et al. (1996) Serum leptin levels in
Blundell, J. E. (1991) The biology of appetite. Clin. Appl. Nutr., 1, 21–31.
women with anorexia-nervosa. J. Clin. Endocrinol. Metab., 81, 3861–3863.
Blundell, J. E. (1992) Serotonin and the biology of feeding. Am. J. Clin. Nutr.,
Halaas, J.L., Gajiwala, K.S., Maffei, M. et al. (1995) Weight-reducing effects
55, 1555–1595.
of the plasma protein encoded by the obese gene. Science, 269, 543–546.
Blundell, J. E. (1996) Food intake and body weight regulation. In Bouchard, C.
Halbreich, U. (1990) Gonadol hormones and antihormones, serotonin and
and Bray, G. (eds), Regulation of Body Weight: Biological and Behavioural
mood. Psychopharm. Bull., 26, 291–295.
Mechanisms. Wiley, Chichester, pp. 111–133.
Herberg, L.J., Pye, J.G and Blundell, J.E. (1972) Sex differences in the
Blundell, J.E. and Bauer, B. (1994) Eating disorders in relation to obesity:
hypothalamic regulation of food hoarding: hormones versus calories. Anim.
semantics or facts? In Ditschuneit, H., Gries, F.A. Hauner, H. et al. (eds.),
Behav., 20, 186–191.
Obesity in Europe, 1993. Libbey, London, pp. 9–14.
Hill, A.J. and Blundell, J.E. (1989) Food selection, body weight and the
Both-Orthman, B., Rubinow, D.R., Hoban, M.C. et al. (1988) Menstrual cycle
premenstrual syndrome (PMS): effect of the
D-
fenfluramine. Appetite,
phase-related changes in appetite in patients with premenstrual syndrome
12, 215.
and in control subjects. Am. J. Psychiat., 145, 628–631.
Hill, A.J., Rogers, P.J. and Blundell, J.E. (1995) Techniques for the
Brobeck, J.R., Wheatland, M. and Strominger, J.L. (1947) Variations in
experimental measurement of human eating behavior and food intake: a
the regulation of energy exchange associated with estrus, diestrus and
practical guide. Int. J. Obesity, 19, 361–375.
pseudopregnancy in rats. Endocrinology, 15, 73–101.
Hrboticky, N. L., Leiter, L.A. and Anderson, G.H. (1985) Effects of menstrual
Brzezinski, A.A., Wurtman, J.J., Wurtman, R.J. et al. (1990) d-Fenfluramine
cycle and
L
-tryptophan on food intake in lean women. Int. J. Obesity, 9, A45.
suppresses the increased calorie and carbohydrate intakes and improves the
Hrboticky, N., Leiter, L.A. and Anderson, G.H. (1989) Menstrual cycle effects
mood of women with premenstrual depression. Obstet. Gynecol., 76,
on the metabolism of tryptophan loads. Am. J. Clin. Nutr., 50, 46.
296–301.
Jennings, W.A. (1969) Voluntary running and the estrous variation in food
Chehab, F.F., Lim, M.E. and Lu, R. (1996) Correlation of the sterility defect
intake in the rat. Psychol. Rep., 25, 199–203.
in homozygousobese female mice by treatment with the human recombinant
leptin. Nature Genet., 12, 318–320.
Johnson, W.G., Corrigan, S.A., Lemmon, C.R. et al. (1994) Energy regulation
over the menstrual cycle. Physiol. Behav., 56, 523–527.
Chehab, F.F., Mounzih, K., Lu, R. and Lim, M.E. (1997) Early onset of
reproductive function in normal female mice treated with leptin. Science, Kato, R. (1960) Serotonin content of rat brain in relation to sex and age.
J. Neurol. Chem., 5, 202.275, 88–90.
1150
Menstrual cycle and appetite control
Krakow, K. (1992) Gibt es ein Zyklusabha
¨
ngiges Erna
¨
hrungsverhalten? Rapkin, A. (1992) The role of serotonin in premenstrual syndrome. Clin.
Obstet. Gynecol., 35, 629–636.Unpublished dissertation, Fachhochschule Mu
¨
nster.
Rickels, K., Freeman, E. and Sondheimer, S. (1989) Buspirone in treatment
Krohn, P.L. and Zuckerman, S. (1938) Water metabolism in relation to the
of premenstrual syndrome. Lancet, 1, 777.
menstrual cycle. J. Physiol., 88, 369–378.
Rickels, K., Freeman, E.W., Sondheimer, S. and Albert, J. (1990) Fluoxetine
Lariviere, F., Moussallu, R. and Garrel, D.R. (1994) Increased leucine flux
in the treatment of premenstrual syndrome. Curr. Ther. Res., 48, 161–166.
oxidation during the luteal phase of the menstrual cycle in women. Am.
J. Physiol., 267, E422–E428.
Rogers, P.J. and Jas, P. (1994) Menstrual cycle effects on mood, eating and
food choice. Appetite, 23, 289.
Laughlin, G.A. and Yen, S.C.C. (1997) Hypoleptinemia in women athletes:
Rogers, P.J., Edwards, S., Green, M.W. and Jas, P. (1992) Nutritional influences
Absence of a diurnal rhythm with amenorrhea. J. Clin. Endocrinol. Metab.,
on mood and cognitive performance: the menstrual cycle, carreine and
82, 318–321.
dieting. Proc. Nutr. Soc., 51, 343–351.
Lawton, C.L., Burley, V.J., Wales, J.K. and Blundell, J.E. (1993) Dietary fat
Rosenblatt, H., Dyrenfurth, I., Ferin, M. and Vande-Wiele, R.L. (1980) Food
and appetite control in obese subjects — weak effects on satiation and
intake and the menstrual cycle in rhesus monkeys. Physiol. Behav., 24,
satiety. Int. J. Obesity, 17, 409–416.
447–449.
Leshner, A.I. and Collier, G. (1973) The effects of gonadectomy on the sex
Ruble, D.N. (1977) Premenstrual symptoms: a reinterpretation. Science, 197,
differences in dietary self-selection patterns and carcass compositions of
291–292.
rats. Physiol. Behav., 11, 671–676.
Schweiger, U., Tuschl, R.J. Platte, P. et al. (1992) Everyday eating behaviour
Lissner, L., Stevens, J., Levitsky, D.A. et al. (1988) Variations in energy
and menstrual function in young women. Fertil. Steril., 57, 771–775.
intake during the menstrual cycle: implications for food intake research.
Severino, S.K. (1994) A focus on 5-hydroxytryptamine (serotonin) and
Am. J. Clin. Nutr., 48, 956–962.
psychopathology. In Gold, J.H. and Severino, S.K. (eds), Premenstrual
Lyons, P.M., Truswell, A.S., Mira, M. et al. (1989) Reduction of food intake
Dysphorias; Myths and Realities. American Psychiatric Association, New
in the ovulatory phase of the menstrual cycle. Am. J. Clin. Nutr., 49,
York.
1164–1168.
Solomon, S.J., Kurzer, M.S. and Calloway, D.H. (1982) Menstrual cycle and
Marsden, P.J., Murdoch, A. and Taylor, R. (1996) Adipocyte insulin action
basal metabolic rate in women. Am. J. Clin. Nutr., 36, 611–616.
during the normal menstrual cycle. Hum. Reprod., 11, 968–974.
Sophos, C.M., Worthington-Roberts, B. and Childs, M. (1987) Diet and body
McCoy, C., Donne, B. and Andrews, J.F. (1988) Energy intake during the
weight during the human menstrual cycle. Nutr. Rep. Int., 36, 201–211.
menstrual cycle; little change at ovulation. Proc. Nutr. Soc., 48, 25a.
Stone, A.B., Pearlstein, T.B. and Brown, W.A. (1991) Fluoxetine in the
McEwen, B.S. and Parsons, B. (1982) Gonadal steroid action on the brain:
treatment of late luteal phase dysphoric disorder. J. Clin. Psychiat., 52,
neurochemistry and neuropharmacology. Annu. Rev. Pharmacol. Toxicol.,
290–293.
22, 555–598.
Tarasuk, V. and Beaton, G.H. (1991) Menstrual cycle patterns in energy and
McGuire, M.T., Raleigh, M.J. and Johnson, C. (1983) Social dominance in
macronutrient intake. Am. J. Clin. Nutr., 53, 442–447.
adult male vervet monkeys: Behaviour–biochemical relationships. Soc. Sci.
Tam, W.Y.K., Chan, M-Y., Lee, P.H.K. (1985) The menstrual cycle and platelet
Inform., 22, 311–318.
5-HT uptake. Psychosom. Med., 47, 352–362.
Manocha, S., Choudhuri, G. and Taylor, B. (1986) A study of dietary intake
Tarttelin, M. F. (1968) Cyclical variations in food and water intake in ewes.
in pre- and postmenstrual period. Hum. Nutr.: App. Nutr., 40A, 213–216.
J. Physiol., 195, 29–30.
Martini, M.C., Lampe, J.W., Slavin, J.L. and Kurzer, M.S. (1994) Effect of
Tarttelin, M.F. and Gorski, R.A. (1973) The effects of ovarian steroids on
the menstrual cycle on energy and nutrient intake. Am. J. Clin. Nutr., 60,
food and water intake and body weight in the female rat. Acta Endocrinol.,
895–9.
73, 551–568.
Meltzer, H.Y. (1990) Role of serotonin in depression. Ann. NY Acad. Sci.,
Taylor, D.L., Matthew, R.J., Beng, T.H. and Weimann, M.L. (1984) Serotonin
600, 486–499.
levels and platelet uptake during premenstrual tension. Neuropsychobiology,
Menkes, D.B., Taghavi, E., Mason, P.A. et al. (1992) Fluoxetine treatment of
12, 16–18.
severe premenstrual syndrome. Br. Med. J., 305, 346–347.
Ulrich, U., Nowara, I. and Rossmanith, W.G. (1994) Serotoninergic control
Netter, P., Daume, E., Laschefsui, U. et al. (1993) Consumption of food,
of gonadotrophin and prolactin secretion in women. Clin. Endocrinol., 41,
emotional states and reproductive hormones during the menstrual cycle in
779–785.
disturbed and non-disturbed eaters. In Lehnert, H., Hurison, R., Weiner, H.
Vitale, M.L. and Chiocchio, S.R. (1993) Serotonin, a neurotransmitter involved
et al. (eds), Endocrine and Nutritional Controlof Basic Biological Functions.
in the regulation of luteinizing hormone release. Endocrine Rev. 14, 480–493.
Hogrefe and Huber, Wien.
Wade, G.N. (1972) Gonadal hormones and behavioural regulation of body
Oram, E. L. (1987) The effect of menstrual cycle on patterns of nutrient
weight. Physiol. Behav. 8, 523–534.
intake. Proc. Nutr. Soc., 46, 128a.
Warner, P., Bancroft, J., Dixson, A. and Hampson, M. (1991) The relationship
Parry, B.L. (1994) Biological correlates of premenstrual complaints. In
between perimenstrual depressive mood and depressive illness. J. Affect.
Gold, J.H. and Severino, S.K. (eds), Premenstrual Dysphorias; Myths and
Dis., 23, 9–23.
Realities. American Psychiatric Association, New York.
Webb, P. (1986) 24-hour energy expenditure and the menstrual cycle. Am. J.
Piers, L.S., Diggavi, S.N., Rijskamp, J. et al. (1995) Resting metabolic rate
Clin. Nutr., 44, 614–619.
and thermic effect of a meal in the follicular and luteal phases of the
Wood, S.H., Mortola, J.F., Chan, Y-F. et al. (1992) Treatment of premenstrual
menstrual cycle in well-nourished indian women. Am. J. Clin. Nutr., 61,
syndrome with fluoxetine: a double-blind, placebo-controlled, crossover
296–302.
study. Obstet. Gynecol., 80, 339–344.
Pliner, P. and Fleming, A.S. (1983) Food intake, body weight and sweetness
Wurtman, J.J. (1993) Nutritional Intervention in Premenstrual Syndrome.In
preferences over the menstrual cycle in humans. Physiol. Behav., 30,
Smith, S. and Schiff, I. (eds), Modern Management of Premenstrual
663–666.
Syndrome. W.W.Norton & Co., New York.
Pirke, K.M. (1987) Dia
¨
t und Sto
¨
rungen des Menstruationszyklus. Mu
¨
nch.
Wurtman, J.J., Brzezinski, A., Wurtman, R.J. and Laferrere, B. (1989) Effect
Med. Wsch., 129, 913–914.
of nutrient intake on premenstrual depression. Am. J. Obstet. Gynecol., 161,
Pirke, K.M., Laessle, R.G., Schweiger, U. et al. (1989) Dieting causes
1228–1234.
menstrual irregularities in normal weight young women through impairment
Yatham, L.N., Barry, S. and Dinan, T.G. (1989) Serotonin receptors, buspirone,
of episodic luteinizing hormone secretion. Fertil. Steril., 51, 263–268.
and prementrual syndrome. Lancet, 2, 1447–1448.
Polivy, J. and Herman, C.P. (1976) Clinical depression and weight change: a
complex relation. J. Abn. Psych. 85, 338–340.
Received on September 9, 1996; accepted on March 19, 1997
Polivy, J. and Herman, C.P. (1985) Dieting and bingeing: a causal analysis.
Am. J. Psychol., 40, 193–201.
Polivy, J. and Herman, C.P. (1987) Diagnosis and treatment of normal eating.
J. Consult. Clin. Psychol., 55, 635–644.
Raleigh, M.J. and McGuire, M.T. (1980) Biosocial pharmacology. McLean
Hosp. J., 2, 73–86.
Rapkin, A.J., Edelmuth, E., Chang, L.C. et al. (1987) Whole-blood serotonin
in premenstrual syndrome. Obstet. Gynecol., 70, 533–537.
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