There is a wealth of CVD literature on the determinants of obesity. Using a broad
frame of reference, I have grouped risk factors into six categories (age, period and birth
cohort; energy balance; sex and gender; smoking; genetics; and psychosocial,
socioeconomic and –cultural factors) to highlight the interconnections between several sets of factors. Intentionally I have focused on the obesity risk factors that are most
individual characteristics and environments, further indicating how adult obesity is a
multifactorial public health concern that requires methodologies that can study multiple
contributors (risk factors) simultaneously.
1. Age, Period and Birth Cohort Effects
Excessive weight gain beyond what is required for normal development and
maturation at any time point in the life course is concerning and can have metabolic
implications. Weight gain early in life is a public health concern as overweight or obese
children and adolescents are at extremely heightened increased risk for overweight or
obese in adulthood and therefore may remain at higher risk for CVD throughout their
lives [64-67].
Similarly, weight gain in adulthood may lead to the development of
overweight/obesity for the first time in adulthood or the intensification of obesity-related
CVD risk. For example, longitudinal studies of weight gain have shown that it predicts a
number of CVD risk factors throughout adulthood in a number of populations including
Mexican Americans [68, 69]. With respect to outcomes, weight gain since 18 years old
(based on self-report) has been shown to a risk factor for all-cause mortality later in life
(specifically CVD-related deaths and non-smoking-related cancers) in the Nurses’ Health Study [70]. This association was independent of one’s early adulthood body mass (self- reported BMI at 18 years of age). Importantly, weight gain in adulthood is more likely to
lead to the deposition of extra weight in the abdomen, where fat is most metabolically
detrimental [71].
Adults have been at the forefront of the obesity epidemic as compared to their
children/adolescents [58]. Yet in addition to age-related disparities, there have been
marked period effects in the obesity epidemic since the 1980s. The interaction of these
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individuals born in the US in the midst of the obesity epidemic (after 1980) carry a larger
burden of obesity than seen in other cohorts [72]. Although the exact genetic and
environmental etiologic mechanisms are unclear, weight gain during adulthood may
exacerbate the public health burden experience by birth cohorts from the obesity
epidemic [71].
2. Energy Balance
Presumably the current obesity epidemics seen in developed nations like the US
are due to a continued imbalance between energy intake and expenditure [58]. In
developing countries transition from a tradition to a Westernized diet, the adaptation of
an urbanized lifestyle or other cultural practices (‘reverse acculturation’) has been associated with a nutrition transition leading to population-level increases in obesity.
However, on an individual level poor diet or physical activity have been challenging to
quantify and change in epidemiology and public health.
3. Sex and Gender
Women tend to have higher percentages of body fat than men, which they store
preferentially in subcutaneous rather than visceral depots. As such at a given BMI (e.g.
30 kg/m2) women on average have higher percentages body fat and less fat free or bone mass than men [58]. Among parous women, both gestational weight gain and post-
partum weight retention are considered risk factors for obesity [73]. Moreover,
independent of aging effects menopause has been documented to associate with
increased weight gain and shifts in body composition towards more central adiposity [74,
75].
In addition to evidence of a biological basis of differences in obesity prevalence
between men and women, women’s weight appears to vary more across SES
weight and obesity may also be engendered through complex social processes or
cultural roles.
4. Smoking
Generally current smoking and tobacco use has been associated with lower
average body weight and therefore less overweight and obesity [58]. Yet this
generalization does not hold for all current smokers. While it has been demonstrated that
weight is generally lower among adult smokers (ages 25-44), and higher among former
adult smokers, this trend has not been found in younger smokers (ages 16-24) [76]. In
addition, suggested weight control effects of smoking may dissipate over time, as long-
term smokers (20 years and older) have been shown to be heavier than never or former
smokers, and heavy smokers are more likely to be obese, and have greater abdominal
obesity, than both other smokers and non-smokers [77, 78]. Additionally, an individual’s weight may increase after smoking cessation [58]. Evidence supports the role of nicotine
in metabolic pathways, although the biologic mechanisms are still unclear.
5. Psychosocial, Socio-Economic and -Cultural Factors
Psychosocial stress [79] and depression [80] are risk factors for adult obesity.
More specifically a variety of sources of perceived psychosocial stressors, such as work
and caregiving stress, childhood adversity, and financial insecurity have been associated
with modest increases in obesity over time [81]. Previous reports also describe
increasing obesity prevalence with lower SES; yet the mechanism is likely complex and
may be bidirectional in nature (i.e. obesity may influence one’s ability for SES advances through the life course) [82]. When studies have jointly assessed the influence of socio-
economic and -cultural factors on BMI and obesity, variability in SES-gradients is evident
by racial/ethnic group. Furthermore, the differences in BMI across racial/ethnic groups
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distinct role that sociocultural factors may play in determining one’s body image and access to health care, which could impact the accuracy of self-reported measures (e.g.
Aim 1 of body weight), and in determining an individual’s burden of obesity (e.g. gene- environment interactions).
Acculturation is a multi-dimensional process of cultural adaptation that begins
when individuals from more than one culture come into continuous contact with each
other, which results in the maintenance and development of cultural practices with one
or both cultures [9, 83, 84]. Work by Berry has outlined four potential strategies during
the process of acculturation: integration, assimilation, separation and marginalization [9,
84].
Yet the role of acculturation in public health disparity research and its
operationalization has been widely debated [85-89]. The concept of acculturation has
been criticized in the field of public health for not involving the structural factors that
might also account for health disparities [90]. Additionally, uni-directional and uni-
dimensional measures of acculturation are based on the assumption that the host
culture is static and that any observed change in the individual is due to their
assimilation in the host culture. Such measures therefore have been criticized for their
ability to differentiate between the varied components of acculturation (e.g. individuals
that have successfully integrated the cultural influences of both cultures to their benefit,
and those who have become equally marginalized from both cultures) [84].
6. Genetics
Above I have already described some of the environmental risk factors for
obesity. Yet obesity is a multifactorial disease due to a combination of environmental
and genetic influences [91, 92]. Estimates of the heritability of obesity range between 40-
cases of obesity. Monogenic forms of extreme obesity can be grouped into three main
etiologic categories [91]. First, several occur in the genes involved in the hypothalamic
leptin-melanocortin system that regulates energy balance. Second, the genes involved in
the neurodevelopment of the hypothalamus can also be distributed to produce extreme
obesity. Lastly, extreme obesity has been associated with a handful of pleiotropic
syndromes due to the dysfunction of the primary cilium. Given that monogenic forms of
extreme obesity explain a small portion of the heritability of obesity, most of the
heritability may be explained by less impactful but more common genetic variations.
Below I will describe the current state of evidence on the population-level genetic
influences on obesity, which are the exposures of interest in this dissertation.