University College London research suggest long-term stress can result in higher levels of obesity

People who suffer long-term stress may also be more prone to obesity, according to research by scientists at UCL which involved examining hair samples for levels of cortisol, a hormone which regulates the body’s response to stress.

The paper, published in the journal Obesity, showed that exposure to higher levels of cortisol over several months is associated with people being more heavily, and more persistently, overweight.

The prevalence of overweight and obesity has markedly increased during the past few decades. Stress has been suggested as one environmental factor that may contribute to the development of obesity. In this review, we discuss the role that exposure to chronic stress may play in the development of obesity, with particular attention to the effects of chronic psychosocial stress. Of particular importance is the effect that social stress has on dietary preference, food consumption, and regional distribution of adipose tissue.

Chronic stress has long been hypothesised to be implicated in obesity – people tend to report overeating and ‘comfort eating’ foods high in fat, sugar and calories in times of stress, and the stress hormone cortisol plays an important role in metabolism and determining where fat is stored.

Previous studies looking at the link between cortisol and obesity relied mainly on measurements of the hormone in blood, saliva or urine which may vary according to the time of day and other situational factors. These studies failed to capture long-term cortisol levels.

Obesity and its associated health risks have risen dramatically in the past few decades. Sedentary lifestyle and easy accessibility to highly palatable nutrient-dense foods creates an environment that promotes overweight and obesity. Chronic social stress, often arising from poor interpersonal relationships, job or unemployment stress, poor self-esteem, and low socioeconomic status has been associated with obesity and its associated illnesses. Chronic activation of the SNS and HPA axis contribute to a anabolic state that promotes fat storage within visceral depots, which increases the risk of dyslipidemia, type 2 diabetes, cardiovascular disease, and other facets of the metabolic syndrome. Stress can also enhance weight gain and fat deposition through changes in feeding behavior. Chronic stress is known to alter the pattern of food intake, dietary preference, and the rewarding properties of foods.

Animal models, such as colony housing of rodents and nonhuman primates have provided invaluable insight into the mechanisms by which obesity may arise from social stress exposure. Although the ideal model to study effects of stress on humans is, of course, humans, ethical and logistical issues often preclude such studies. Human responses to social stress also vary widely among individuals, and it is impossible to completely control for aspects of individual personal experience. For these reasons, ethologically relevant animal models of social stress can fill an important void in understanding how social stress may contribute to obesity.

Of course, there are some aspects that cannot be modeled in animals. Some emotions experienced in response to social stress such as shame, guilt, and self-consciousness are considered by most to be unique to humans. Therefore, it is important to consider animal studies as a complement to studies in humans that may provide insight into the neural mechanisms and genetic factors that underlie stress-associated illness. This in turn may facilitate the development of interventions that may prevent and/or treat stress-related metabolic dysfunction.

Separately research conducted by Dr Sarah Jackson (UCL Epidemiology and Public Health) involved 2,527 men and women aged 54 and older taking part in the English Longitudinal Study of Ageing, taking data over a four-year period.

In the research, the scientists took a lock of hair 2cm long from each participant which was cut as close possible to a person’s scalp – this represented approximately two months’ hair growth with associated accumulated levels of cortisol.  They also examined the participants’ weight, body mass index and waist circumference and how hair cortisol related to the persistence of obesity over time.

They found that people who had higher levels of cortisol present in their hair tended to have larger waist circumference measurements, were heavier, and had a higher body mass index (BMI).  Individuals classified as obese on the basis of their BMI (≥30) or waist circumference (≥102cm in men, ≥88cm in women) had particularly high levels of hair cortisol.

“These results provide consistent evidence that chronic stress is associated with higher levels of obesity,” said Dr Sarah Jackson (UCL Epidemiology and Public Health) who led the research. “People who had higher hair cortisol levels also tended to have larger waist measurements, which is important because carrying excess fat around the abdomen is a risk factor for heart disease, diabetes, and premature death.”

“Hair cortisol is a relatively new measure which offers a suitable and easily obtainable method for assessing chronically high levels of cortisol concentrations in weight research and may therefore aid in further advancing understanding in this area.”

There were limitations to the study, which included the fact the data was from an older population in which levels of cortisol may differ relative to younger adults and the sample was almost exclusively white. It is not currently known whether chronically elevated cortisol levels are a cause or a consequence of obesity.

Credit : University College London & National Library of Medicine


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