The prevalence of obesity has increased substantially over the past 30 years. We performed a quantitative analysis of the nature and extent of the person-to-person spread of obesity as a possible factor contributing to the obesity epidemic.
We evaluated a densely interconnected social network of 12,067 people assessed repeatedly from 1971 to 2003 as part of the Framingham Heart Study. The body-mass index was available for all subjects. We used longitudinal statistical models to examine whether weight gain in one person was associated with weight gain in his or her friends, siblings, spouse, and neighbors.
Discernible clusters of obese persons (body-mass index [the weight in kilograms divided by the square of the height in meters], ≥30) were present in the network at all time points, and the clusters extended to three degrees of separation. These clusters did not appear to be solely attributable to the selective formation of social ties among obese persons. A person's chances of becoming obese increased by 57% (95% confidence interval [CI], 6 to 123) if he or she had a friend who became obese in a given interval. Among pairs of adult siblings, if one sibling became obese, the chance that the other would become obese increased by 40% (95% CI, 21 to 60). If one spouse became obese, the likelihood that the other spouse would become obese increased by 37% (95% CI, 7 to 73). These effects were not seen among neighbors in the immediate geographic location. Persons of the same sex had relatively greater influence on each other than those of the opposite sex. The spread of smoking cessation did not account for the spread of obesity in the network.
Network phenomena appear to be relevant to the biologic and behavioral trait of obesity, and obesity appears to spread through social ties. These findings have implications for clinical and public health interventions.
The prevalence of obesity has increased from 23% to 31% over the recent past in the United States, and 66% of adults are overweight.1,2 Proposed explanations for the obesity epidemic include societal changes that promote both inactivity and food consumption.3 The fact that the increase in obesity during this period cannot be explained by genetics4,5 and has occurred among all socioeconomic groups1 provides support for a broad set of social and environmental explanations. Since diverse phenomena can spread within social networks,6-10 we conducted a study to determine whether obesity might also spread from person to person, possibly contributing to the epidemic, and if so, how the spread might occur.
Whereas obesity has been stigmatized in the past, attitudes may be changing.11,12 To the extent that obesity is a product of voluntary choices or behaviors, the fact that people are embedded in social networks and are influenced by the evident appearance and behaviors of those around them suggests that weight gain in one person might influence weight gain in others. Having obese social contacts might change a person's tolerance for being obese or might influence his or her adoption of specific behaviors (e.g., smoking, eating, and exercising). In addition to such strictly social mechanisms, it is plausible that physiological imitation might occur; areas of the brain that correspond to actions such as eating food may be stimulated if these actions are observed in others.13 Even infectious causes of obesity are conceivable.14,15
We evaluated a network of 12,067 people who underwent repeated measurements over a period of 32 years. We examined several aspects of the spread of obesity, including the existence of clusters of obese persons within the network, the association between one person's weight gain and weight gain among his or her social contacts, the dependence of this association on the nature of the social ties (e.g., ties between friends of different kinds, siblings, spouses, and neighbors), and the influence of sex, smoking behavior, and geographic distance between the domiciles of persons in the social network.
The Framingham Heart Study was initiated in 1948, when 5209 people were enrolled in the original cohort.16 The Framingham Offspring Study began in 1971, when most of the children of members of the original cohort and their spouses were enrolled in the offspring cohort.17 There has been almost no loss to follow-up other than death in this cohort of 5124 people; only 10 people left the study. In 2002, the third-generation cohort, consisting of 4095 children of the offspring cohort, was initiated. All participants undergo physical examinations (including measurements of height and weight) and complete written questionnaires at regular intervals.
For our study, we used the offspring cohort as the source of 5124 key subjects, or “egos,” as they are called in social-network analysis. Any persons to whom the egos are linked — in any of the Framingham Heart Study cohorts — can, however, serve as “alters.” Overall, 12,067 living egos and alters were connected at some point during the study period (1971 to 2003).