A sedentary lifestyle plays a significant role in obesity. Worldwide there has been a large shift towards less physically demanding work, and currently at least 30% of the world’s population gets insufficient exercise. This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home. In children, there appear to be declines in levels of physical activity due to less walking and physical education. World trends in active leisure time physical activity are less clear.
The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland found an increase and a study from the United States found leisure-time physical activity has not changed significantly. A 2011 review of physical activity in children found that it may not be a significant contributor.In both children and adults, there is an association between television viewing time and the risk of obesity.
A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.
Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient food energy is present. As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present. People with two copies of the FTO gene (fat mass and obesity associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele.
The differences in BMI between people that are due to genetics varies depending on the population examined from 6% to 85%.
Obesity is a major feature in several syndromes, such as Prader–Willi syndrome, Bardet–Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term “non-syndromic obesity” is sometimes used to exclude these conditions.) In people with early-onset severe obesity (defined by an onset before 10 years of age and body mass index over three standard deviations above normal), 7% harbor a single point DNA mutation.
Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight. Different people exposed to the same environment have different risks of obesity due to their underlying genetics.
The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely to survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies. This theory has received various criticisms, and other evolutionarily-based theories such as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.
Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing’s syndrome, growth hormone deficiency, and some eating disorders such as binge eating disorder and night eating syndrome.
However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness. The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.
Certain medications may cause weight gain or changes in body composition; these include insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, certain anticonvulsants (phenytoin and valproate), pizotifen, and some forms of hormonal contraception.
Obesity in developed countries is correlated with economic inequality, While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.
Though it is accepted that energy consumption in excess of energy expenditure leads to obesity on an individual basis, the cause of the shifts in these two factors on the societal scale is much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.
The correlation between social class and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant differences were seen among men of different social classes.
In the developing world, women, men, and children from high social classes had greater rates of obesity. An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.
Among developed countries, levels of adult obesity, and percentage of teenage children who are overweight, are correlated with income inequality. A similar relationship is seen among US states: more adults, even in higher social classes, are obese in more unequal states.
Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness.
In undeveloped countries the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns. Attitudes toward body weight held by people in one’s life may also play a role in obesity. A correlation in BMI changes over time has been found among friends, siblings, and spouses. Stress and perceived low social status appear to increase risk of obesity.
Smoking has a significant effect on an individual’s weight. Those who quit smoking gain an average of 4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years. However, changing rates of smoking have had little effect on the overall rates of obesity.
In the United States the number of children a person has is related to their risk of obesity. A woman’s risk increases by 7% per child, while a man’s risk increases by 4% per child. This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.
In the developing world urbanization is playing a role in increasing rate of obesity. In China overall rates of obesity are below 5%; however, in some cities rates of obesity are greater than 20%.
Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world. Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.
Consistent with cognitive epidemiological data, numerous studies confirm that obesity is associated with cognitive deficits.Whether obesity causes cognitive deficits, or vice versa is unclear at present.
The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown to differ between lean and obese people. There is an indication that gut flora can affect the metabolic potential. This apparent alteration is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.
The use of antibiotics among children has also been associated with obesity later in life.An association between viruses and obesity has been found in humans and several different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.
A number of reviews have found an association between short duration of sleep and obesity. Whether one causes the other is unclear. Even if shorts sleep does increase weight gain it is unclear if this is to a meaningful degree or increasing sleep would be of benefit.
Certain aspects of personality are associated with being obese. Neuroticism, impulsivity, and sensitivity to reward are more common in people who are obese while conscientiousness and self-control are less common in people who are obese.
Loneliness is also a risk factor.