Sunday, April 8, 2012

Some Other Causes of Obesity

Food Reward
 
The food reward hypothesis of obesity suggests that ‘rewarding’ foods (reward being "a process that reinforces behavior") leads to overconsumption of calories and an upregulation of the body fat setpoint.
 
Stephan Guyenet has often discussed food reward.  See Food Reward: a Dominant Factor in Obesity: Part 1, 2, 3, 4, 5, 6, 7 and 8; The Case for the Food Reward Hypothesis of Obesity: Part 1 and 2; Why Do We Eat? A Neurobiological Perspective: Part 5 and 6; and Seduced by Food: Obesity and the Human Brain
 
J Stanton has discussed food reward and related concepts in Why Are We Hungry: Part 1, 2, 3, 4, 5, 6, 7 and 8.  Paul Jaminet has discussed food reward here
 
Some of the difficulties of food reward is that palatability and reward aren’t necessarily inherent properties of food (they can vary from person to person), and the Cafeteria diet is one of the arguments in favour of food reward, but (in my opinion) 28/31 of the foods in the Cafeteria diet are junk food [1], so it’s difficult to tease apart food reward related effects of the Cafeteria diet from other (metabolic/gut/etc) effects of junk food.  That being said, perhaps the main reason people eat junk food is because it’s rewarding/palatable, so food reward can definitely influence people’s choices, which is certainly a relevant issue in the modern food environment.
 
* Food reward is not addiction.  This is discussed in some of the posts I linked
 
Sleep Loss
 
Shorter sleep duration is associated with a higher BMI.  Sleep loss studies tend to find decreases in leptin, increases in ghrelin (a hormone that stimulates appetite) and increased calorie intake [2].  Sleep restriction also increases activity of brain reward centres in response to unhealthy food [3] and increases pro-inflammatory cytokines [4]
 
Sleep can affect how weight is lost during calorie restriction.  In a cross-over study 10 overweight adults did moderate calorie restriction for two blocks of 14 days.  One group was told to sleep for 8.5 hours, the other for 5.5 hours.  Both groups lost the same amount of weight (2.9 vs. 3.0 kg), but with 8.5 hours of sleep they lost approximately 50% lean mass and 50% fat, but with 5.5 hours of sleep they lost 80% lean mass and 20% fat* [5]
 
 
8.5 Hours of Sleep
5.5 Hours of Sleep
Weight Lost as Fat (kg)
1.4
0.6
Weight Lost as Fat-Free Mass (kg)
1.5
2.4
Total Weight Loss (kg)
2.9
3.0
 
Circadian rhythm is also important.  In rats on DIO, dim light during the sleep cycle exaggerates the inflammation and weight gain [6], while timed feeding to promote circadian rhythms almost completely protects against DIO [7]
 
* From this graph you can see 12h sleep group released more leptin than the 8h group and yet most people wouldn’t consider an 8h night to be result in sleep debt [2]. 

 
** A related quote from Stephan Guyenet on the study:
 
“That illustrates one of the reasons why I'm skeptical of simple calorie restriction as a means of fat loss. When the body "wants" to be fat, it will sacrifice lean mass to preserve fat tissue. For example, the genetically obese Zucker rat cannot be starved thin. If you try to put it on a severe calorie-restricted diet, it will literally die fat because it will cannibalize its own lean mass (muscle, heart, brain, etc.) to spare the fat. That's an extreme example, but it illustrates the point.”
 
Impaired Leptin Transport
 
Most the research on leptin resistance discusses SOCS3 and/or PTP1B, but there are a few papers that discuss impaired leptin transport across the blood brain barrier.  A review paper [8] mentions the following things decrease leptin transport
 
·         Ovariectomising mice
·         Aging
·         Overfeeding and underfeeding
·         Triglycerides
·         C-reactive protein (CRP)
 
Besides overfeeding and underfeeding, the two that are most modifiable are triglycerides and CRP, which doesn’t change much because inflammation and MD/ER stress are largely responsible for elevated C-reactive protein and triglycerides, and the major mechanisms of leptin resistance (SOCS3 and PTP1B).  Elevated triglycerides are a result of insulin resistance and
 
* Adrenaline, insulin and glucose increase leptin transport

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