Obesity, Mood and Well-Being

Obesity, Mood and Well-Being

In studies of the general population, early studies showed few consistent patterns with
respect to psychosocial distress and obesity, partly due to small samples and varying
assessment tools. The relationship between BMI, smoking status, and depressive
symptoms was studied in a large US national sample, using validated instruments.
The investigators found that the relationship between obesity and depression varied
by sex. Among women, but not men, greater BMI was weakly associated with elevated
reports of depressive symptoms. This relationship remained significant after
controlling for age, years of education, and smoking status, indicating that relative
body weight is weakly related to psychological distress among women but not men. Another US study sought to test the relationships between relative body weight
and clinical depression, suicidal thoughts and suicide attempts in an adult US general
population sample comprising over 40,000 people. Outcome measures were past year
major depression, suicidal thoughts and suicide attempts. Among women, increased
BMI was associated with both major depression and suicide ideation. Among men,
lower BMI was associated with major depression, suicide attempts and suicidal
thoughts. There were no racial differences. Studies of clinical populations have used psychometric instruments for assessment of mental health and psychological functioning in obese individuals and compared them with healthy reference populations. In a much-cited Swedish study ,
severely obese men and women reported distinctly poorer current health and less
positive mood states than the reference subjects, a situation that was worse in women
than in men. Anxiety and/or depression on a level indicating psychiatric morbidity
were more often seen in the obese, again more often in women. The obese subjects
rated their mental well-being worse than chronically ill or injured patients, for example
patients with rheumatoid arthritis, cancer survivors with no recurrence and
spinal-cord injured persons several years after injury. These symptoms improved
with subsequent weight loss from bariatric surgical treatment, providing further support
for the idea that obesity was driving the psychological impairment. In contrast to the widely accepted view that much of the observed psychopathology
associated with obesity is secondary to the obesity itself, one line of research suggests
that psychosocial stress induces central obesity and the metabolic syndrome. Originally suggested by Björntorp and colleagues, subsequent research has been
hampered by largely cross-sectional designs and lack of prospective data. However, a
recent study found that the effect of job strain on subsequent weight change was
dependent on baseline BMI in men but not in women . In the leanest quintile
(BMI 22) at baseline, high job strain and low job control were associated with
weight loss, whereas among those in the highest BMI quintile ( 27), these stress
indicators were associated with subsequent weight gain. No corresponding interaction
between baseline BMI and weight change was seen among women. Furthermore,
the metabolic syndrome, with abdominal obesity as an important determinant, was
recently demonstrated to be closely related to cumulative exposure to work stressors
over 14 years, independent of other relevant risk factors. Employees with chronic
work stress (three or more exposures) were more than twice as likely to have the syndrome
compared to those without work stress. Altered adrenocortical function
induced by stress might influence hepatic lipoprotein metabolism and insulin sensitivity
at target organs, providing a partial explanation for the social inequalities in
obesity and obesity-related disorders. However, given the recent development with
decreasing socioeconomic differences in obesity seen in the US this is obviously a
complex issue.
Other than the conventional view of obesity as a condition carrying both medical
and psychosocial disabilities to the individual, obesity may also been viewed as a sociological
problem deriving from current cultural norms of beauty, normality and socially
acceptable behaviour. In other cultural contexts, where food was less plentiful, obesity
was often considered beautiful. On the other hand, a negative attitude towards obesity,
with stigmatisation of obese individuals, is not entirely a recent phenomenon, with
ascetism and self-denial idealised in many Western societies throughout the centuries.
One of the views driving the stigma of obesity is the notion that it is self-inflicted, with
the cardinal sins of sloth and gluttony emanating from low morals and poor character.
Despite increasing knowledge about the importance of heritability in obesity, and the
societal changes behind the obesity epidemic, these attitudes still prevail.
The growing stigma attached to all degrees of overweight reflects a society with a
contemporary ideal of extreme leanness. There is a belief that this attitude is setting
the stage for an epidemic of dieting and eating disorders.
One of the repeating themes emerging from research on psychosocial aspects of
obesity is the necessity for a gender perspective. Medically, due to the greater likelihood
of central adiposity in men, obesity may be said to confer a greater risk among
males. However, there is much evidence suggesting that the psychological and social
consequences of obesity are far worse for women. Even so, it should be noted that
increased prevalence of body dissatisfaction is occurring in both men and women.
Is there an association between obesity and depression? In Western society, being
overweight has been associated with increased risk for low self-esteem and depression.
It has, however, not been quite clear whether obesity increases the risk of
depression, or if depression increases the risk of obesity, or if there is a reciprocal relation
such that the obese are at increased risk of depression and the depressed are at
increased risk of obesity. Roberts et al. summarised 11 studies studying this association
using cross-sectional or prevalence study designs, with seven of these finding
some evidence of greater risk of depression among the obese. But while seven of these
studies found support for the proposition that the obese are at a greater risk for
depression, evidence was not uniformly robust, and the temporal relation between
obesity and depression was unclear. In their own study of 2,123 adults age 50 and
older, participants reported their height, weight and depressive symptoms during
interviews in 1994 and 1999. Subjects who were obese in 1994 had twice the risk of
becoming depressed in 1999 than subjects who were not obese in 1994. They did not
find any support for depression predicting subsequent obesity, after adjusting for
baseline obesity, or limiting the analyses to the non-obese at baseline. Accordingly, to
date, there is little conclusive evidence that obesity is caused by depression, whereas
obese people do seem more prone to develop future depression.

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Stigmatisation in Obesity

Stigmatisation in Obesity

When considering psychological aspects of obesity, it is widely believed that most
psychological disturbances are more likely to be consequences, rather than causes, of
obesity. One of the most compelling illustrations was reported in the early 1990s,
based on 47 patients who were, on average, 66 kg overweight before surgery for morbid
obesity, who lost 45 kg or more subsequently and who successfully maintained
weight loss for at least 3 years. As a group, they perceived their previous morbid
obesity as having been extremely distressful. Most patients said that they would prefer
to be normal weight with a major handicap (deaf, dyslexic, diabetic, legally blind,
very bad acne, heart disease, one leg amputated) than to be morbidly obese. All
patients said they would rather be normal weight than a morbidly obese multi-millionaire.
Thus obesity, as perceived by obese individuals themselves, is an extremely
serious handicap, although not always perceived as such by others. A recent review
summarised that extreme obesity is associated with significant psychiatric morbidity
and impaired health-related quality of life that in many cases imposes a greater burden
of suffering than the physical complications of obesity.
A second issue is how the obese individuals are treated by others. Negative attitudes
are prevalent, and exacerbated by idealisation of thinness in many Western cultures.
There are numerous examples of obesity-related discrimination, including how
children perceive overweight and obese peers, among employers, students’ ideas
about suitable spouses. In a classic study on childhood stereotypes, young children
associated overweight in children with being lazy, dirty, stupid, cheats and liars. The perception of obesity as a self-inflicted condition creates little sympathy for
the obese. Studies of morbidly obese patients show that in many instances they feel
that they are treated disrespectfully by the medical profession because of their weight,
that people look critically at them and their shopping cart when they go shopping,
and that their spouses and children do not like them to accompany them to social
functions because of their weight. At the workplace, they often feel that they are
placed out of sight of the public and they may be passed over for promotion. When
the 47 patients studied by Rand and Macgregor were asked the same questions
after gastric bypass surgery which they had answered before the surgery, their
responses were dramatically different showing a much more positive view of their
own position. Therefore, these perceptions are reversible, following efficient treatment
of obesity. This demonstrates that the obese suffer not only from negative attitudes
but, in addition, also from frank discriminatory behaviour. Unsuccessful dieting may have negative psychological consequences, due to a sense
of distress, failure and self-blame assumed to accompany the visible consequences of
weight gain. The data supporting this are, however, mixed. In severely obese subjects,
the number of previous dieting attempts was associated with mood disturbance and
anxiety, and was a strong predictor of obesity-related psychosocial problems in women.
In contrast, an evaluation of young women before and after treatment at a weight clinic
did not detect any significant effect of one cycle of weight loss and regain on mood.

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Socioeconomic Status and Obesity

Socioeconomic Status and Obesity

Is it relevant, when discussing individual determinants of obesity, to consider the
common assumption that specific psychological and/or risk factor profiles are
causally related to obesity? The reverse question must also be asked: what is the evidence
that psychological and socioeconomic characteristics are not the consequences,
but rather the causes, of the obese state?
There has been a strong interest in studying the relation between socioeconomic status (SES) and obesity. Previous studies have shown that the association between
SES and obesity may vary by population, sex and age . H owever, a p erson’s body
weight status may also affect his/her education and occupational opportunities,
which subsequently affect his/her SES. A good understanding of the association
between obesity and SES has many important public health and policy implications,
particularly for the prevention and management of obesity. It is well known that obesity
is more prevalent in the lower socioeconomic classes and that this pattern is more
common among women than men. Even so, there is a varying relation of SES with
obesity between countries at different stages of development .
A landmark review of studies published prior to 1989 on SES and obesity proposed
that obesity in the developing world would be essentially a disease of the socioeconomic
elite . However, in a recent review from developing countries, the authors concluded from the studies they had
reviewed that obesity in the developing world is no longer a disease of groups with
higher SES. Additionally, the burden of obesity in each developing country tends to
shift towards the groups with lower SES as the country’s gross national product
increases. They also concluded that the shift of obesity in women with low SES apparently
occurs at an earlier stage of economic development than it does for men.
Socioeconomic gradients with respect to obesity, even in the Western world, are both
heterogeneous and in transition. For example, it has long been accepted that in the US
population, groups with low SES are at greater risk to be obese than people of high SES.
This perception, however, was challenged in a recent study . Based on nationally
representative data collected in the National Health and Nutrition Examination Surveys
from American adults since the 1970s, the findings indicated an overall trend of a weakening
association between SES and obesity, with differing patterns across ethnic groups.
In a study of children and young people grouped by race, sex, and age, different results
were observed in the association between overweight and SES. Between 1988–1994 and
1999–2002, the ratio in the prevalence of overweight in adolescent boys with a low or
high SES decreased from 2.5 to 1.1 and from 3.1 to 1.6 in girls (fig. 1) . Consistently
across almost all SES groups, the prevalence of overweight was much higher in blacks
than in whites, indicating highly complex patterns in the association of SES and overweight
. The authors speculated that television viewing might have been the primary
type of inactivity in poor adolescents during the early part of the period they were
studying, whereas computers and computer games became more widely accessible and
264 Rosengren · Lissner
affordable during the more recent part of the observation period, especially in high SES
groups. Accordingly, the energy intake and expenditure patterns of all adolescents
regardless of SES, particularly for white adolescent boys, became more similar, resulting
in smaller economic disparities of the proportion of overweight subjects. Similarly, data
from the US show that in the 70s there was as much as a 50% relative difference in obesity
prevalence among those with less than high school education, compared to people
with college education, but by 1999–2000, the difference had decreased to 14% .
Similar observations of a decreasing socioeconomic gradient in obesity were reported
in one Swedish study of young adults . These findings underline that individual
characteristics are probably not the main cause of the current obesity epidemic. In addition,
changing patterns of consumption and of physical activity directly affect socioeconomic
differences in a way that is not always predictable.
The other side of the obesity-SES association is whether obesity can be shown to be a
risk factor for subsequent changes in SES. Among the first studies indicating that obesity
might affect social mobility was based on a Swedish population-based sample of
women examined in the late 1960s showing that the shift toward higher socioeconomic
level since childhood was more common in normal-weight than in overweight women
. However, this study did not establish which subjects were already overweight
as children. One US study, which classified adolescents and young adults as being
overweight or normal at baseline, found that the overweight group, 7 years later, were
less often married, had lower income and had completed fewer years of education.
These prospective findings were independent of initial SES, suggesting that obesity created
a situation of downward social mobility, and, in addition, more often occurring in
women than in men. Thus, in addition to the physical health consequences of obesity,
obese people, particularly obese women, suffer from social stigmatization, prejudice,
and discrimination . In a Swedish longitudinal study, no social difference in overweight
was observed at age 16 years but at 30 years educational level was associated with
overweight, reflecting the cumulative influence of multiple adverse circumstances experienced
from adolescence to young adulthood .
Potential mechanisms for an effect of obesity on subsequent social status have
been proposed, the most obvious being related to the stigmatisation experienced by
the obese. Leanness is often equated with beauty, success, fitness and self-control.
Obesity, on the other hand, is considered as undesirable as leanness is desirable, for
reasons that are more often related to cosmetic concerns than to actual or potential
medical complications. Specific examples for discrimination may be seen in the areas
of marital, employment and educational opportunities. If obesity has both social
causes and effects, a self-perpetuating cycle may be created that reinforces the relationship
between low SES and obesity.

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The Sociology of Obesity

The Sociology of Obesity

The current obesity epidemic is largely driven by environmental factors, including nutritional transition
towards refined and fatty foods with the growing production of energy-dense food at relatively low cost,
increased access to motor vehicles, mechanisation of work and sedentary lifestyles. These influences in
modern society are modified by individual characteristics. Ultimately, energy intake in excess of caloric
expenditure causes obesity, but why this occurs in some but not all individuals is not known. Obesity is
more prevalent in the lower socioeconomic classes but even so, there is a varying relation of socioeconomic
status with obesity between countries at different stages of development and, even in the
Western world, socioeconomic gradients with respect to obesity are both heterogeneous and in transition.
Potential mechanisms for an effect of obesity on subsequent social status have been proposed, the
most obvious being related to the stigmatisation experienced by the obese. Obesity seems to be
causally related to mood disturbances, whereas there is no conclusive evidence that the reverse is true.
When considering psychological aspects of obesity, depressive symptoms are more likely to be consequences,
rather than causes of obesity.

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adiponectin obesity

adiponectin obesity

Adiponectin was discovered independently by several laboratories, hence its various
names: Acrp30 (adipocyte complement-related protein of 30kDa), apM1 (adipose
most abundant gene transcript 1), adipoQ and GBP28 (gelatin-binding protein of
28kDa) . Adiponectin is composed of an N terminal sequence, hypervariable
domain, 15 collagenous repeats and a C terminal domain. A trimeric form of
adiponectin is secreted by adipocytes and gives rise to higher order complexes, i.e.
dimers of trimers (hexamers, low molecular weight, LMW) and six trimers (18-mers,
high molecular weight, HMW) through noncovalent bonding. HMW adiponectin is thought to be the bioactive form in plasma. In contrast, trimeric and hexameric
adiponectin is predominant in the cerebrospinal fluid. Adiponectin also undergoes
posttranslational modifications including glycosylation . Although there is
structural similarity between the globular (head) of adiponectin and TNF- , these
adipokines do not appear to be functionally related.
In contrast to other polypeptide hormones, adiponectin circulates at very high
concentrations ( g/ml), raising the possibility that a smaller cleaved product mediates
its action on various tissues. Total and HMW adiponectin are more abundant
in females, partly due to suppression of adiponectin by androgens in males.
Adiponectin is inversely related to adiposity, in contrast to leptin and most
adipokines. Thus, adiponectin is markedly reduced in obesity and rises with prolonged
fasting and severe weight reduction. Adiponectin, particularly HMW, is
increased by thiazolidinediones (TZDs) and mediates the insulin sensitizing effect of
this class of antidiabetic drugs. A role for adiponectin in glucose homeostasis
is further exemplified by hepatic insulin resistance in rodents and humans lacking
adiponectin. In contrast, adiponectin treatment enhances insulin sensitivity,
primarily by suppressing glucose production. Adiponectin produced in
bacteria has been shown to decrease glucose, stimulate fatty acid oxidation and
reduce body weight and fat; however, these are likely to be pharmacological effects
since bacterially derived adiponectin is incapable of forming high order complexes. Administration of full length or globular adiponectin via systemic or intracerebroventricular
injection induces thermogenesis, fatty acid oxidation and weight
loss in mice. These actions are abrogated in agouti mice (Ay/a), indicating a crucial
role for melanocortin signaling in the central action of adiponectin.
Hypoadiponectinemia is related to insulin resistance, inflammation, dyslipidemia
and cardiovascular risk among various populations. Lack of adiponectin promotes
atherosclerosis in rodents. Adiponectin reverses this by inhibiting monocyte
190 Ahima · Osei adhesion, macrophage transformation, proliferation and migration of smooth muscle
cells in blood vessels. Studies have implicated activation of AMPK and inhibition of
nuclear factor B (NF- B) and vascular adhesion molecules as putative mechanisms
underlying the effects of adiponectin on the vascular system. Adiponectin also
exerts a protective action in myocardial remodeling in response to acute ischemiareperfusion. Adiponectin-deficient mice had increased myocardial apoptosis
and infarct size than wild-type. Importantly, adiponectin treatment diminished
infarct size, apoptosis and TNF- production in both knockout and wild-type mice.
These actions appear to be mediated through activation of AMPK, induction of
cyclooxygenase-2-dependent synthesis of prostaglandin E2.
Adiponectin receptors (AdipoR1 and AdipoR2) contain seven transmembrane
domains, but are structurally and functionally distinct from G-protein-coupled receptors. AdipoR1 is abundant in muscle and binds with high affinity to globular
adiponectin and low affinity to the full-length protein, whereas AdipoR2 is enriched in
liver and has intermediate affinity for globular and full-length adiponectin. Both
receptors mediate the phosphorylation and activation of AMPK. Although studies
have failed to demonstrate a blood-brain transport of adiponectin, both AdipoR1
and AdipoR2 are distributed widely in the brain. Injection of adiponectin into
the 4th ventricle depolarized AdipoR1 and AdipoR2-positive neurons in the area
postrema, suggesting a potential mechanism for its central adiponectin action.
In a recent study, adenovirus-mediated expression of AdipoR1 and AdipoR2 activated
AMPK and peroxisome proliferator-activated receptor (PPAR)- in the liver of
lepr null mice, reduced gluconeogenesis and increased fatty acid oxidation.
Targeted disruption of AdipoR1 prevented adiponectin-induced AMPK activation,
whereas disruption of AdipoR2 decreased PPAR- activity. Disruption of both
AdipoR1 and AdipoR2 abolished adiponectin binding and induced steatosis, inflammation,
oxidative stress, insulin resistance and glucose intolerance. Together, these
results support a role of AdipoR1 and AdipoR2 as major mediators of adiponectin
action on glucose and lipid metabolism.

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Leptin

Leptin

The discovery of leptin more than a decade ago was a major turning point in our understanding
of adipokines. Mice and humans homozygous for the leptin gene mutation
develop hyperphagia, severe early-onset obesity, insulin resistance preceding obesity,
excess lipid accumulation outside adipose tissue (steatosis), and neuroendocrine abnormalities,
notably, hypothalamic hypogonadism and tertiary hypothyroidism.
Moreover, there is evidence for immunosuppression in congenital leptin deficiency. Leptin is expressed and secreted mainly by adipocytes, but low levels are present in the gastric fundus, mammary gland, placenta, pituitary and skeletal muscle. Leptin has a relative molecular mass of 16kDa and circulates in free or bound forms. The latter represents leptin bound mainly to its soluble receptor and is thought
to be inactive. The concentration of leptin is higher in obese than lean individuals.
Leptin falls rapidly during fasting and increases gradually during feeding. Studies in
rodents and human indicate a link between these changes in leptin and insulin.
Higher leptin level in women is explained partly by increased production in subcutaneous
adipose tissue and stimulation by estrogens. On the other hand, leptin is suppressed
by androgens in males. Chronic glucocorticoid exposure, TNF- and IL-6
increase leptin, while adrenergic stimulation decreases leptin. Leptin exhibits a
diurnal rhythm, peaking at night in humans and in the morning in rodents.
A pulsatile leptin rhythm has also been recognized in humans, although the underlying
mechanisms and functional significance are unknown.
Five leptin receptor isoforms, LRa–LRe, are derived from alternate splicing of lepr
mRNA. LRa is the predominant ‘short leptin receptor’ which lacks the key
cytoplasmic domain required for signaling through the JAK/STAT (signal transduction
and activators of transcription) pathway. LRa is abundantly present in brain capillary
endothelium and peripheral tissues, and is thought to mediate leptin transport.

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Adipokines in Obesity

Adipokines in Obesity

Adipose tissue is the source of soluble mediators (adipokines), secreted mainly by adipocytes. Leptin acts
on the brain and peripheral organs to regulate energy homeostasis and the neuroendocrine axis.
Adiponectin regulates glucose and lipid metabolism by targeting the liver and skeletal muscle. Adiposederived
proinflammatory cytokines, vasoactive peptides, coagulation and complement factors, visfatin,
vaspin and retinol-binding protein signal through paracrine and hormonal mechanisms. Understanding
the biology of adipose tissue and the rapidly growing list of adipokines provides new insights into normal
physiological regulation, as well as the pathogenesis and treatment of obesity, diabetes and disorders
of lipid metabolism and cardiovascular system.

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