Big, Bigger, Obese

With Christmas around the corner we tend to overindulge. Oh, all these cookies and the huge family dinners! But why is it that some people really struggle with gaining too much weight, whereas others seem to stay slim, even though they apparently eat the same amount? Let's talk about the neuroscience of overeating:

How We Can and Cannot Influence Our Body Weight

Image by Nancy White via Flickr

More and more people in our society are labeled obese. No longer just a problem in Western society, obesity is rising in developing countries as well. In 2008, half a billion adults worldwide suffered from obesity according to the definition of the World Health Organization (WHO). In 2012, the WHO stated that more than 40 million kids worldwide are overweight or obese. Childhood obesity is also associated with a higher risk of obesity in adulthood [1].
But what is the reason behind the obesity epidemic? Can we blame everything on fast food chains and lack of exercise? Or are there some intrinsic factors involved as well?

It’s Not Us ...
The existence of a common ‘fat gene’ causing the obesity epidemic is a myth. However, many genes increase the risk of being obese. By 2006, only 176 cases were reported where obesity is directly caused by a single-gene mutation. The Human Obesity Gene Map shows a total of 127 obesity candidate genes [2]. Identified genetic abnormalities include leptin deficiency, proopiomelanocortin mutations, and melanocortin 3 receptor abnormalities. These mutations all come with multiple detrimental effects [3].

MANY GENES ARE IDENTIFIED 

RISK FACTORS FOR OBESITY

Control of food intake is intrinsically organized by our endocrine system. The pancreatic enzyme amylin suppresses appetite via brainstem mechanisms. Cholecystokinin (CCK) is produced in the intestine and slows down gastric emptying. This helps you get the satisfying feeling of being full after eating. On the other hand, the stomach hormone ghrelin stimulates appetite when the stomach is empty.
Other hormones play an important role in long-term control of body weight. The pancreatic hormone insulin reduces energy intake. Leptin has the same effect, but is produced by adipose tissue. Neuropeptide Y and orexin are produced in the hypothalamus and stimulate appetite. All of these hormones are suggested as neuroendocrine targets for obesity therapy on the molecular level [4,5].
Classic twin studies in the 1980s and 1990s, which relied on pairs of identical and fraternal twins, suggest that 40-70% of variation in body size is due to genetic factors [6]. However, this does not explain the currently expanding obesity epidemic.

... But This Is
Changes in nutrition and activity patterns of children and families over the past decades have most likely had the biggest impact on the current childhood obesity epidemic. Family factors are crucial in the prevention of obesity. Parents that put unreasonable restrictions on their children's diet, pressure their children to eat certain foods, and excessively monitor the child’s behavior may do more harm than good. Such behavior is consistently linked to pediatric weight gain. On the other hand, leading by example, such as parental intake of fruit and vegetables, encourages healthy nutrition in children.
Portion sizes and the caloric value of foods have increased over the past few decades. Nearly 20% of the difference in energy intake is due to increased portion size [7]. The increased added sugar content of foods and beverages coincides with the obesity epidemic. Several epidemiological studies focusing on this issue conclude that intake of sugar-sweetened beverages is strongly correlated with body mass index (BMI).

OVERWEIGHT PARENTS INCREASE 

CHILD OBESITY RISK 13X

 

Reduced activity is also a major factor in the obesity epidemic. Sitting on a couch and watching television increases the risk of obesity [3]. Lack of sleep leads to increased food intake and may reduce physical activity as well (see also "Eat Well and Sleep Sound" 2014 - Volume 7 - Issue 3 ). Meta-analyses calculated an increased risk for obesity of 56-89% for children who sleep less. This is a vicious circle, because increased BMI in children is associated with reduced sleep duration due to an increase in adipose tissue deposits [8].

A Little Bit of Both
Epigenetics also play a role. Some genetic factors might only come into play when the right environmental stimuli are present. Lack of food during pregnancy increases the risk of adulthood obesity, as was shown in Dutch children born in the 1944-1945 famine [9]. Late introduction of solid foods reduces the odds of obesity at the age of 10 years [10]. Adiposity rebound is the point at which body fat levels are lowest and from then on will only increase (usually at 5-6 years of age). Having two overweight parents at this time increases the risk of obesity thirteen times [11]!
Though certain inherited predispositions do exist, our environment is the biggest factor when it comes to obesity risk. Recently, increased luxury, comfort, and meals with higher calories may have created this epidemic, but it is up to us to change this!

[1] WHO on overweight and obesity, http://bit.ly/18pCdAN
[2] Rankinen et al, Obesity, 2006
[3] Skelton et al, Pediatr Clin North Am, 2011
[4] De Kloet and Woods, Curr Opin Endocrinol Diabetes Obs, 2010
[5] Crocker and Yankovski, Endocrinol Metab Clin North Am, 2009
[6] Farooqi and O’Rahilly, Arch Dis Child, 2000
[7] McConhay et al, J Am Diet Assoc, 2004
[8] Bayer et al, Sleep, 2009
[9] Willyard, Nature, 2014
[10] Seach et al, Int J Obes, 2010
[11] Whitaker et al, Pediatrics, 1998

by Judith Houtman, PhD student AG Heppner
This article originally appeared September 2014 in Volume 07, Issue 03 "Nature vs Nurture".