The Doctor Weighs In

The recent American Diabetes Association meetings started off with an interesting presentation on the relationship between sleep disturbances and metabolic abnormalities, such as insulin resistance and Type 2 diabetes. It turns out the relationship between sleep and our overall energy balance is complex, but fascinating and relevant to those of us struggling to keep our weight down and our insulin sensitivity up.

We have known for some time that food shortage or starvation causes reduced sleep in rodents. Conversely, total sleep deprivation is associated with marked overeating or hyperphagia. A study by Spiegel and colleagues, published in the Annals of Internal Medicine (Dec. 7, 2004, 141:11:846-850), looked at the effect of sleep restriction on appetite regulation in humans.

Twelve healthy, young, normal-weight men participated in the study performed at the Clinic Research Center of the University of Chicago. The men were assigned to either 2 days of sleep restriction or 2 days of sleep extension. Individuals in the s leep restriction group were only allowed 4 hours of bed time. The sleep extension group was required to stay in bed for 10 hours. Six weeks after the first study, the groups flip-flopped – the sleep deprived group was sleep extended and vice versa.

Leptin and ghrelin: the “yi and yang” of appetite regulation

All of the men received a glucose infusion as the sole source of their calories so that meal-related fluctuations of hunger and satiety were avoided. Blood was drawn to check whether there were any variations in the levels of two key appetite regulating hormones, leptin and ghrelin. Leptin is a hormone produced by adipocytes, our fat cells. It provides information to the brain about our energy status. High leptin levels are associated with a suppression of appetite. Leptin levels decrease when we experience an acute calorie shortage and increase when there is a surplus of calories. Ghrelin is a hormone that is produced primarily in the stomach. It has the opposite effects of leptin. High ghrelin levels stimulate appetite. The ratio of leptin to ghrelin, then, provides important information to the brain about our current energy balance.

The men were also asked to respond to a standardized set of questions about how hungry they were in general and also how hungry they were for specific food classes, for example sweets; salty foods; starchy foods; fruits and fruit juices; vegetables; and high protein foods, such as meat, poultry and eggs.

And the results show…

Sleep restriction was associated with significant reductions in the appetite suppressing hormone, leptin. The appetite stimulating hormone, ghrelin, on the other hand increased significantly. Sleep restriction relative to sleep extension was associated with an almost 25% increase in hunger ratings. The increase in appetite tended to be greatest for calorie-dense foods with high carbohydrate content (sweets, salty foods, and starch foods), aka “comfort foods.” The increase in appetite for fruits and vegetables was less consistent and of lesser magnitude. Appetite for protein rich foods was not affected by sleep duration. Further analysis revealed that most (70%) of the variance in increased hunger was accounted for by the increase in the ghrelin-to-leptin ratio.

Now all of you who have read my blog on study design will immediately say…hey, wait a minute…this was a very small study, only 12 study subjects. And, they were all young healthy men. Is this really valid? Good point! Spiegel and associates recently reviewed the effects of sleep loss on a number of metabolic parameters, including appetite, and confirm alterations in ghrelin-to-leptin levels in response to sleep disturbances, although they point out that we can't be certain that other factors that regulate appetite, such as adiponectin from fat cells and peptide YY 3-36 from intestinal cells, aren't also playing a role in sleep deprivation-related metabolic disturbances (Journal of Applied Physiology 2005, 99:2008-2019).

This latter review also points out that sleep deprivation exerts marked effects on glucose metabolism and insulin resistance. Recurrent sleep curtailment may be a risk factor for the development of obesity and type 2 diabetes. In fact, another study by Punjabi and Polotsky published in the same journal (Journal of Applied Physiology, 2005,99:1998-2007) showed that individuals with the most disordered sleep, called sleep apnea, seems to develop disturbances in insulin sensitivity and glucose tolerance and may be predisposed to the eventual development of type 2 diabetes. The topic of disordered sleep and diabetes will be the topic of a later blog.

And in closing, I remind you of the words of Ralph Waldo Emerson (doesn't he sounds just like our parents?):

“ Eat well, drink in moderation, and sleep sound, in these three good health abound ”

This blog was originally posted on the PEERtrainer website (www.peertrainer.com) on February 16, 2006.