Gina Kolata wrote in the NYTimes in the article Study Says Obesity Can Be Contagious in 2007:

Obesity can spread from person to person, much like a virus, researchers are reporting today. When a person gains weight, close friends tend to gain weight, too. [...]

The answer, the researchers report, was that people were most likely to become obese when a friend became obese. [...]

The investigators say their findings can help explain why Americans have become fatter in recent years — each person who became obese was likely to drag some friends with them.

Did that research hold up to the test of time? Does the research suggest as Kolata claims that the effect is causatitive and not only a correlation?

  • 11
    Seems to me that the author is using metaphorical language about how groups of companions often share activities and habits, not actual contagion. Not sure that this question addresses an actual claim. – PoloHoleSet Jan 22 '18 at 15:29
  • 2
    @PoloHoleSet : To the extend that this is an explanation why Americans become fatter the claim has to be that there's more than just a claim about groups of companions often sharing the same traits. – Christian Jan 22 '18 at 15:49
  • 2
    @PoloHoleSet : Social contagion is part of group behavior. – Christian Jan 22 '18 at 16:04
  • 2
    @PoloHoleSet There's nothing in the dictionary definition of the word contagion that implies that it only refers to biological contagion. – Christian Jan 22 '18 at 17:14
  • 4
    @PoloHoleSet I thought so too at first, but looking closer this is a question about human behaviour and the psychology of social influence - which is 100% observable, testable, measurable and on-topic. As you'll see from research quoted below. It's "Does social influence increase obesity" not a quibble about metaphors – user56reinstatemonica8 Jan 22 '18 at 17:27

tl;dr, No.

The effect is real and many lines of inquiry for the underlying causality have been proposed since the initial claim from the question. Since the causes and effects of both obesity and social webs are so complex, no definitive model of causality has been established since.

The central claim holds up very well. As an observation. The language used to describe its way of causality does not so well. That does not mean there are no direct causative effects along the social connections. It means that there is most probably a multitude of effects and the view in that field evolves. The social contagion effect of obesity is an oversimplification in that regard.

A primer on words and definitions.

[…] social scientific research has largely confirmed the thesis that affect, attitudes, beliefs and behaviour can indeed spread through populations as if they were somehow infectious. Simple exposure sometimes appears to be a sufficient condition for social transmission to occur. This is the social contagion thesis; that sociocultural phenomena can spread through, and leap between, populations more like outbreaks of measles or chicken pox than through a process of rational choice.

The term contagion (ken­tâ-jen) itself has its roots in the Latin word contagio, and quite literally means "from touch". Contagion therefore refers to a process of transmission by touch or contact. The Microsoft Dictionary (Microsoft 1997) defines contagion as the

"transmission of a disease by direct contact with an infected person or object; a disease or poison transmitted in this way; the means of transmission; the transmission of an emotional state, e.g. excitement; a harmful influence."

from: Memetics & Social Contagion: Two Sides of the Same Coin?

That means that the point at which strict biology enters the theory is a bit late. Social contagion is not really like a virus, but similar to a virus. (Virus' definition as a life form being contestable ). It is a (n)on living information that spreads like a meme, that is like a meme. And with this kind of concept the network to analyse becomes very complex, cause and effect not easily predictable with common sense or simple experimental protocols:

The Simple Rules of Social Contagion (2014) It is commonly believed that information spreads between individuals like a pathogen, with each exposure by an informed friend potentially resulting in a naive individual becoming infected. However, empirical studies of social media suggest that individual response to repeated exposure to information is far more complex.[…]
We show that there are important and surprising differences between the diffusion of information and a disease stemming from cognitive limitations for processing information. In pathogenic contagion34, people with more incoming contacts are more likely to contract a disease, but in social contagion such people are less likely to become infected. These highly connected users dominate the high-exposure portion of the average exposure response function, giving the false impression that more exposures may be counter-productive. Granted, highly connected users tend to be infected earlier and also to have more followers, increasing their influence once they are infected. Users in a tightly connected core of friends may be repeatedly exposed to information, and the present work demonstrates how the combination of social enhancement and awareness contribute to the observed behavior of users in high k-cores participating in larger cascades.

One paper arriving at the same conclusion of the claim in question is:

The Spread of Obesity in a Large Social Network over 32 Years (2007)
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.

What is problematic here is that the analogy term "virus" used to describe the observed effects of the spread is too deterministic. It is further problematic to describe the effect as "each person who became obese was likely to drag some friends with them." This is far too close to protestant morals of guilt in ethical terms and far too imprecise or downright misleading in practical terms of the presumed mechanisms.

A social contagious model of the obesity epidemic (2016) Obesity has been recognized as a global epidemic by WHO, followed by many empirical evidences to prove its infectiousness. However, the inter-person spreading dynamics of obesity are seldom studied. A distinguishing feature of the obesity epidemic is that it is driven by a social contagion process which cannot be perfectly described by the infectious disease models. In this paper, we propose a novel belief decision model based on the famous Dempster-Shafer theory of evidence to model obesity epidemic as the competing spread of two obesity-related behaviors: physical inactivity and physical activity. The transition of health states is described by an SIS model. Results reveal the existence of obesity epidemic threshold, above which obesity is quickly eradicated. When increasing the fading level of information spread, enlarging the clustering of initial obese seeds, or introducing small-world characteristics into the network topology, the threshold is easily met. Social discrimination against the obese people plays completely different roles in two cases: on one hand, when obesity cannot be eradicated, social discrimination can reduce the number of obese people; on the other hand, when obesity is eradicable, social discrimination may instead cause it breaking out.

There are factors beyond pure social ties at the lowest level of society. Lowest level meaning not social strata but basic blocks and interpersonal connections in a social web – that are implicated in the spread of obesity. That is: really high level propaganda, often disseminated with the best of intentions, sometimes with sinister profit motives and sometimes as purity beliefs:

Pandemic obesity and the contagion of nutritional nonsense. (2003) The United States is the epicenter of an obesity pandemic. As more countries acculturate to a Western lifestyle, rates of obesity and its sequelae are rising steadily in both adults and children. In response, a variety of weight-loss diets emphasizing alternative distributions of macronutrient classes have been promoted with considerable success. Among the most popular is the so-called "Atkins Diet," in which carbohydrate restriction is touted as the key to weight loss. Despite claims, however, evidence that weight loss is enhanced by means other than caloric restriction is lacking. Also lacking is evidence that fad diets produce sustainable weight loss. Most important, fad diets generally ignore or refute what is known about fundamental associations between dietary pattern and human health. Cancer, cholera, and AIDS induce rapid weight loss, highlighting the potential incompatibility of weight loss by any means with health. Available data suggest that long-term weight loss is most consistently achieved by adherence to a fat-restricted diet abundant in grains, vegetables, and fruit, along with regular physical activity, a lifestyle notably conducive to the promotion of overall health. Fad diets, potential harms of which are well characterized, should be presumed "guilty" of incompatibility with human health until or unless proved otherwise; the burden of proof should reside with proponents. In the interim, the clinical and public health communities should work to empower individuals with knowledge needed to reconcile weight control with health promotion; support policies that mitigate obesogenic environmental conditions; and offer unified resistance to the contagion of dietary propaganda.

Different models have been used to at least mathematically model the data and provide a structured approach to interpreting the findings:

Qualitative Stability Analysis of an Obesity Epidemic Model with Social Contagion (2017) We study an epidemiological mathematical model formulated in terms of an ODE system taking into account both social and nonsocial contagion risks of obesity. Analyzing first the case in which the model presents only the effect due to social contagion and using qualitative methods of the stability analysis, we prove that such system has at the most three equilibrium points, one disease-free equilibrium and two endemic equilibria, and also that it has no periodic orbits. Particularly, we found that when considering (the basic reproductive number) as a parameter, the system exhibits a backward bifurcation: the disease-free equilibrium is stable when and unstable when , whereas the two endemic equilibria appear from (a specific positive value reached by and less than unity), one being asymptotically stable and the other unstable, but for values, only the former remains inside the feasible region. On the other hand, considering social and nonsocial contagion and following the same methodology, we found that the dynamic of the model is simpler than that described above: it has a unique endemic equilibrium point that is globally asymptotically stable.

"Real science" wants of course a clear cut causality, with experimental data to support the hypothesis and make forecasting and prognosis more robust:

Experimental evidence of massive-scale emotional contagion through social networks (2014)
Significance: We show, via a massive (N = 689,003) experiment on Facebook, that emotional states can be transferred to others via emotional contagion, leading people to experience the same emotions without their awareness. We provide experimental evidence that emotional contagion occurs without direct interaction between people (exposure to a friend expressing an emotion is sufficient), and in the complete absence of nonverbal cues.

Abstract: Emotional states can be transferred to others via emotional contagion, leading people to experience the same emotions without their awareness. Emotional contagion is well established in laboratory experiments, with people transferring positive and negative emotions to others. Data from a large real-world social network, collected over a 20-y period suggests that longer-lasting moods (e.g., depression, happiness) can be transferred through networks [Fowler JH, Christakis NA (2008) BMJ 337:a2338], although the results are controversial. In an experiment with people who use Facebook, we test whether emotional contagion occurs outside of in-person interaction between individuals by reducing the amount of emotional content in the News Feed. When positive expressions were reduced, people produced fewer positive posts and more negative posts; when negative expressions were reduced, the opposite pattern occurred. These results indicate that emotions expressed by others on Facebook influence our own emotions, constituting experimental evidence for massive-scale contagion via social networks. This work also suggests that, in contrast to prevailing assumptions, in-person interaction and nonverbal cues are not strictly necessary for emotional contagion, and that the observation of others’ positive experiences constitutes a positive experience for people.

Among the multitude of effects in this complex phenomenon:

The role of social networks in the development of overweight and obesity among adults: a scoping review (2015) Although it is increasingly acknowledged that social networks are important to our understanding ofoverweight and obesity, there is limited understanding about the processes by which such networks shapetheir progression. This paper reports the findings of a scoping review of the literature that sought to identify the key processes through which social networks are understood to influence the development of overweight and obesity.
Included papers addressed a wide range of research questions framed around six types of networks: a paired network (one’s spouse or intimate partner); friends and family (including work colleagues and people within social clubs); ephemeral networks in shared public spaces (such as fellow shoppers in a supermarket or diners in a restaurant); people living within the same geographical region; peers (including co-workers, fellow students, fellow participants in a weight loss programme); and cultural groups (often related to ethnicity).
As individuals are embedded in many of these different types of social networks at any one time, the pathways of influence from social networks to the development of patterns of overweight and obesity are likely to be complex and interrelated.
Included papers addressed a diverse set of issues: body weight trends over time; body size norms or preferences; weight loss and management; physical activity patterns; and dietary patterns.

| improve this answer | |
  • So basically it's a coincidence? – LateralTerminal Jan 24 '18 at 15:50
  • 1
    @LateralTerminal Coincidence might be a bit of an understatement. "Correlated" seems more accurate, so far as I understand it. The environmental circumstances that lead to one individual to becoming obese are shared by peers in the same environment. They have correlated outcomes, for that reason. – Alexander - Reinstate Monica Feb 5 '18 at 21:47
  • @Alexander edited answer says "tl;dr, No." So it seems like a coincidence to me. – LateralTerminal Feb 5 '18 at 21:51
  • 2
    As in no, there is no causal link that person A becoming obese will directly cause person B to have an increased chance of becoming obese. That doesn't mean there isn't an external factor that make both person A and B to become obese, in a correlated way. – Alexander - Reinstate Monica Feb 5 '18 at 21:57

You must log in to answer this question.

Not the answer you're looking for? Browse other questions tagged .