In 1967, Routtenberg and Kuznesof reported a very peculiar phenomenon in rats:
They discovered that when rats were on a restricted feeding schedule (1 hour per day in their experiment) and had free access to a running wheel, their food intake was significantly lower than in control rats, which were on the same feeding schedule but without access to a running wheel. This discrepancy between increased running activity and decreased food intake caused substantial body weight loss, and if rats were not removed from the experimental setup timely, they would eventually die of starvation. This model, later named the activity-based anorexia (ABA) model, is one of the most widely used animal models for the study of anorexia nervosa (AN). (Source)
Of course, rats are not humans. Nonetheless, animal models of anorexia nervosa can inform us of some of the underlying neuropsychological and physiological influences and consequences of … Continue reading →
Cholecystokinin (CCK) is a digestive hormone that stimulates fat and protein digestion, and promotes the feeling of satiety. CCK is released after food consumption to promote digestion (by releasing digestive enzymes from the pancreas and stimulating bile secretion). In rats and monkeys, injection of CCK induces satiety, though it seems (from what I’ve skimmed), the extent to which CCK regulates food intake in humans is not well-established. Previous research on the role of CCK in anorexia nervosa (AN) has found conflicting results, in part because of methodological issues related to measuring levels of CCK. In a recent study, Cuntz and colleagues (2013, freely available online), having developed a better assay for measuring CCK, wanted to clarify its role in AN patients.
The authors had the following goals and hypotheses (I omitted one):
- Objective 1: Compare CCK levels between AN patients and healthy controls before and after a meal
… Continue reading →
In my previous post, I looked at two hormones released during the cephalic phase (gastric secretion that occurs before food is eaten), ghrelin and obestatin, and how they may contribute to runaway eating behavior. Today I’m going to be looking at insulin release during chew and spit (CHSP), a fairly common symptom in eating disorders where the food is tasted, chewed and spit out. Insulin is a small peptide hormone that acts as a key regulator of metabolism; deregulation of insulin signalling plays a role in illnesses such as diabetes and metabolic syndrome. Some people have theorized that CHSP behavior may influence insulin regulation. In fact, there are a number of individuals stating on internet forums that chronic CHSP could lead to insulin resistance, potentially promoting diabetes. As interesting as these theories are, recent data have shown that they are probably not true.
INSULIN RELEASE DURING THE CEPHALIC … Continue reading →
Shelly’s follow-up post on chewing and spitting, an often overlooked symptom in eating disorders. In her first post, Shelly discussed the prevalence of chewing and spitting among eating disorder patients. In this post, Shelly discusses some of the physiological effects of chewing and spitting. Enjoy! – Tetyana
Your body responds to food long before it reaches your stomach. The taste, smell, even the mere sight of food all act to trigger a physiological response, “priming” the gut by stimulating various enzymes required for proper digestion and absorption of nutrients. This is called the “cephalic response”, and it is mediated by a part of the nervous system that’s generally not under conscious control (the autonomic nervous system). Keep in mind, the actual consumption of food is NOT necessary to trigger this reflex.
As you may have already guessed, the act of chewing and spitting … Continue reading →
I used to call them bingeing and purging marathons. If I binged and purged in the morning, chances were, I’d binge and purge throughout the day. The next time I’d eat, I was likely to end up–whether I wanted to or not–bingeing and purging. Not all individuals with bulimia nervosa binge and purge every day (or purge everything they eat, for that matter), but many do, and some binge and purge multiple times a day. In recovery, many people start by trying not to binge and purge before a certain time of the day–because once they binge and purge, it triggers a continuous cycle of bingeing and purging until they become to exhausted or otherwise end up going to bed.
I always wondered why that was, why was it so hard to keep a single episode of bingeing and purging from initiating a repeated cycle of bingeing and purging?
On … Continue reading →
Eating disorders typically begin in adolescence. One common explanation for this is that during adolescence females are increasingly exposed to the media, thin models, and dieting. While this is probably true to some extent, it doesn’t explain why the rates of eating disorders are quite low despite the high levels of exposure to thin models in the media. Out of 100 girls, only a handful develop eating disorders, yet all of them are exposed to the same magazines and TV shows.
This means there must be some other factors that differ between this group of girls. One hypothesis is that hormonal changes during puberty may modulate the genetic risk factors for eating disorders. These changes may “turn on” genes that predispose individuals to eating disorders. Previous research has shown that genetic factors modulate disordered eating (eating disorders have a high heritability), but how? What are the mechanisms of this … Continue reading →