People Getting Substantially Fatter Thanks to Our Unhealthy Environment, Says Study

People have gotten fatter in the past 50 years, and scientists believe our environments could be to largely to blame. What is known as an obesogenic environment could heighten our chances of having an unhealthy body mass index from the time we are in the womb until we die, warned the authors of the study published in the journal The BMJ.

Study co-author Maria Brandkvist of the Department of Public Health and Nursing at the Norwegian University of Science and Technology, Trondheim told Newsweek: "Our genetic propensities for obesity may make it easier for some and more difficult for others to make healthy lifestyle choices. For those with genetic predisposition to obesity, today's environment may make these healthy lifestyle choices even more difficult. We cannot change our genes, however, we can influence the environment in which we live."

The term describes an environment which makes it easier for a person to gain, rather than lose, weight. This include variables like how close grocery stores are, and how easy it is for an individual to access safe sidewalks and parks. Toxins and microbes could also play a part, the researchers said. Experts believe changing the environments we inhabit could be an important tool for tackling the obesity epidemic which the World Health Organization says affected more than 650 million in 2016.

To find out why levels of obesity worldwide have almost tripled since 1975, scientists in Norway studied data collected periodically on 118,959 people in Nord-Trøndelag County between 1963 to 2008. The people were aged between 13 to 80-years-old in Nord-Trøndelag County, and the cohort was representative of the Norwegian population, according to the authors.

The participants took part in a tuberculosis screening program running between 1963 to 1975, which the researchers linked to information from the Nord Trøndelag Health Study (Hunt) on the same individuals. The Hunt study gathered information including body mass index (BMI), as well as the participants' health, lifestyle, their living situation, and measures like their blood pressure. The team also looked at the genes of 71,860 of the Hunt participants. The data was sorted into five categories according to whether the individuals were genetically predisposed for obesity.

The authors found the average BMI in Norway "increased substantially" between the 1960s and the 2000s, and started rising between the mid-1980s and mid-1990s. Those born after 1970 had a "substantially" higher BMI as young adults when compared with those born before.

Those genetically predisposed to obesity saw the biggest increases in BMI. In the 1960s, men who were at most genetic risk had a BMI 1.2kg/m2 higher on average than those with the smallest risk. By the 2000s, this had risen to 2.09kg/m2. In women, the figures were 1.77 kg/m2 in the 1960s and 2.58 kg/m2 in the 2000s, respectively. The findings held even when factors associated with weight like smoking were taken into account.

The size and scope of the study stands in contrast to past works which had smaller cohorts, a short follow-up time, and relied on participants to report their own weight, the researchers argued.

As the study was observational, the scientists couldn't find a cause for this increase in obesity. But they think the higher BMIs could be explained by the obesogenic environment interacting with an individual's genetics.

While eating too much and not moving enough are contributors to the obesity epidemic, "the underlying cause is likely a complex combination of globalisation, industrialisation, and other societal, economic, cultural, and political factors," the authors wrote.

Study co-author Maria Brandkvist of the Department of Public Health and Nursing at the Norwegian University of Science and Technology, Trondheim told Newsweek: "One explanation could be that those with a genetic predisposition for obesity will gain more weight by eating more unhealthy foods when these are made readily available."

She explained: "We might find clues [for the origins of the obesity epidemic] if we look back to how we lived our lives in the 1960s; when it was not as easy or even possible to make certain unhealthy lifestyle choices. What and how much did we eat, how much did we sleep and how much did we move?"

"The obese are often stigmatized for having unhealthy lifestyle choices. Acknowledging the importance of the obesogenic environment and its amplification of our genetic differences, can help destigmatize obesity."

Dr. Jo Lewis, of the University of Cambridge Metabolic Network, who did not work on the study, told Newsweek that population-based studies can be limited because research participants are generally healthier than the general population, and also noted the cohort of The BMJ paper was relatively homogenous.

"The rising prevalence of obesity is driven by changes in the environment including the consumption of high calorie foods and reduced levels of physical activity," she said.

"However, within a given environment, there is considerable variation in body weight; some people are particularly susceptible to severe obesity, whilst others remain thin. Family, twin and adoption studies have consistently demonstrated that 40 to 70 percent of the variation in body weight can be attributed to heritable factors."

Clare Llewellyn, associate professor of obesity at University College London who wasn't involved in the work, pointed out to Newsweek: "They [the study authors] didn't actually measure the environment, so this study doesn't shed any light on which aspects of the 'obesogenic' environment are causing those who are genetically susceptible to obesity to gain weight at a faster pace than those who are genetically at lower risk."

Professor John Wilding, who leads clinical research into Obesity, Diabetes and Endocrinology at the University of Liverpool and didn't work on the study, told Newsweek the study questions the widely held belief that obesity is a problem of failed willpower.

"It emphasizes the point that much of the rapid change in obesity that has occurred in the last few years is a result of genetic predisposition combined with an unfavorable environment; those with high genetic risk are most vulnerable to the current obesogenic environment," he said. "We can't change people's genes, but substantial changes to the food and physical activity environment may make it easier to tackle the obesity epidemic at a public health level. For individuals, some will need medical treatment."

Llewellyn echoed Wilding's sentiment, and told Newsweek: "I hope that this study will help to move the narrative away from obesity as a matter of individual responsibility and personal blame, to more helpful discussions about how we can change the environment to make healthier choices easier for everyone—especially those living in poverty. Obesity is not a lifestyle choice."

This study is the latest in a swathe attempting to understand why people are the weight they are. In January, a separate team of scientists concluded a person's genes can affect whether they are fat or thin, with the odds stacked against obese people.

Researchers wanted to understand why the body weight of people who who live in similar environments can vary greatly, and why some people appear to easily keep a healthy body size while others struggle. The findings were published in the journal PLOS Genetics.

This article has been updated with comment from John Wilding and Clare Llewellyn.

Uncommon Knowledge

Newsweek is committed to challenging conventional wisdom and finding connections in the search for common ground.

Newsweek is committed to challenging conventional wisdom and finding connections in the search for common ground.

About the writer


Kashmira Gander is Deputy Science Editor at Newsweek. Her interests include health, gender, LGBTQIA+ issues, human rights, subcultures, music, and lifestyle. Her work has also been published in the The Independent, The Independent on Sunday, The i Newspaper, the London Evening Standard and International Business Times UK.

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