According to the National Sleep Foundation’s 2007 Sleep in America poll, just published by Eileen Chasens and colleagues from the University of Pittsburgh in this month’s issue of Behavior and Sleep Medicine, almost 20% of community-dwelling women aged 40 to 60 years reported sleepiness that consistently interfered with daily life.

Perhaps not surprisingly, the sleepy subsample reported more symptoms of insomnia, restless legs syndrome, obstructive sleep apnea, depression and anxiety, as well as more problems with health-promoting behaviors, drowsy driving, job performance, household duties, and personal relationships.

Further analyses revealed that sleepiness along with depressive symptoms, medical comorbidities, obesity, and lower education were associated with poor self-rated health, whereas menopause status (pre-, peri- or post-) was not.

These results point to the high prevalence of daytime sleepiness in midlife women and suggest that addressing the underlying causes of poor sleep and sleep disruption may be an important measure to improve health in this population.

Obviously, what applies to the midlife women in this study may well also apply to women of other age groups as well as men - and of course our kids.

Perhaps we should all use the long weekend to get more sleep.

AMS
Edmonton, Alberta

p.s. You can now also follow me and post your comments on Facebook

Chasens ER, Twerski SR, Yang K, & Umlauf MG (2010). Sleepiness and health in midlife women: results of the National Sleep Foundation’s 2007 Sleep in America poll. Behavioral sleep medicine, 8 (3), 157-71 PMID: 20582759

Regular readers of these pages will recall previous articles on the discoveryof brown adipose tissue in adult humans.

Brown adipose tissue or BAT is specifically designed to turn calories into heat, thereby significantly affecting metabolic rate.

The current theory is that people who have more BAT, are more obesity resistant and can better handle excess calories. It is estimated that just 50 grams of BAT may help burn several hundred extra calories per day.

This discovery has spawned a huge interest into the functioning and regulation of BAT amongst obesity researchers and many are looking into possible ways of increasing the amount of BAT or of stimulating it to burn more calories.

An article by Tan and colleagues from the University of Texas, San Antonio, TX, released this week in Obesity Reviews, examines the evidence in support of the notion that melatonin, an endogenous peptide intimately linked to the biology of sleep, may play an important role in the regulation of BAT metabolism.

Secreted by the pineal gland at night, melatonin plays a key role in regulating the sleep-wake cycle and many other circadian rhythms in physiological functions like glucose homeostasis or body temperature. Importantly, both natural and artificial light can markedly suppress melatonin production.

In their articles, the authors quote a number of articles showing that in mammals, melatonin not only increases recruitment of brown adipocytes but also elevates their metabolic activity.

Based on these findings, the authors speculate that the hypertrophic effect and functional activation of BAT by melatonin, if also present in humans, may suggest a novel role for melatonin in managing obesity.

Perhaps more importantly, the authors note that the suppression of endogenous melatonin levels due to excessive light exposure after darkness through artificial light sources, may contribute to the obesity epidemic, as exposure to light at night has been shown to dramatically reduce endogenous melatonin production.

Perhaps it may well be this complex physiology linking BAT to melatonin that in part explains the important recent recognition that sleep deprivation may be a key factor in the obesity epidemic in both adults and children.

Perhaps lights out at 9.00 pm may not be such a bad weight management strategy after all?

AMS
Edmonton, Alberta

p.s. You can now also follow me and post your comments on Facebook

Tan DX, Manchester LC, Fuentes-Broto L, Paredes SD, & Reiter RJ (2010). Significance and application of melatonin in the regulation of brown adipose tissue metabolism: relation to human obesity. Obesity reviews : an official journal of the International Association for the Study of Obesity PMID: 20557470

As blogged before, overweight and obese patients frequently present with fibromyalgia, characterized by chronic pain, fatigue and depressed mood.

A paper by Akiko Okifuji from the University of Utah, Salt Lake City, just published in the Journal of Pain, examines the relationship between fibromyalgia and obesity in pain, function, mood, and sleep.

The study examines the impact of obesity on hyperalgesia, symptoms, physical abilities, and sleep in 215 fibromyalgia patients, who also underwent tender point examination, physical performance testing, and 7-day home sleep assessment.

Almost 50% of participants were obese and an additional 30% were overweight.

Obesity was positively related to greater tender point sensitivity, reduced physical strength and lower-body flexibility, shorter sleep duration, and greater restlessness during sleep.

The results confirmed that obesity is a prevalent comorbidity of fibromyalgia and the authors suggest that weight management may need to be incorporated into treatments.

In the paper, Okifuji and colleagues also discuss several potential mechanisms linking obesity to fibromyalgia including alterations in the endogenous opioid system, the endocrine system, and systemic inflammation, whereby adipose-tissue derived cytokines may enhance central sensitization.

Clinicians should be aware of the relationship between excess weight and fibromyalgia, which can often pose an important contributor to weight gain and a major barrier to weight management.

AMS
Edmonton, Alberta

Okifuji A, Donaldson GW, Barck L, & Fine PG (2010). Relationship Between Fibromyalgia and Obesity in Pain, Function, Mood, and Sleep. The journal of pain : official journal of the American Pain Society PMID: 20542742

So, as Michelle Obama yesterday announced her childhood obesity initiative, another piece of news on childhood obesity crowded the news wires.

This was a study by Sarah Anderson (Ohio State) and Robert Whitaker (Temple) published as an early release in Pediatrics.

The researchers performed a cross-sectional analysis of a nationally representative sample of 8550 four-year-old US children who were assessed in 2005 in the Early Childhood Longitudinal Study.

The study focussed on the relationship between obesity and three household routines: regularly eating the evening meal as a family (>5 nights per week); obtaining adequate nighttime sleep on weekdays (10.5 hours per night); and having limited screen-viewing (television, video, digital video disk) time on weekdays (2 hours/day).

Analyses were adjusted for the child’s race/ethnicity, maternal obesity, maternal education, household income, and living in a single-parent household.

While the prevalence of obesity was 14.3% among children exposed to all 3 routines (14.5% of the sample), it was 24.5% among those exposed to none of the routines (12.4%).

The odds of obesity associated with exposure to all 3, any 2, or only 1 routine (compared with none) were 0.63, 0.64, and 0.84, respectively.

So if you do have kids ask yourself:

1) Do we regularly sit down for supper as a family?
2) Do my kids regularly get at least 10.5 hrs of sleep?
3) Do my kids have less than 2 hrs of screen time on weekdays?

A “no” to all of the above, probably puts your kids in the high-risk category, a “yes” to all of the above, and your kids are probably doing fine.

Now comes the tough part, i.e. wether or not, if you are not doing all of the above, simply doing these three things will actually change your kids risk for obesity. Or in other words, if you did nothing else, except sit down for dinner, have the kids in bed by 8.30, and limit their screen time, would your kids actually have healthy weights?

I am guessing that it will take far more than that. In fact I would not at all be surprised if the families that do any of the above were probably quite different from the families that don’t. I would indeed expect that these families are different in so many ways that really, these three factors are probably just “markers” rather than the actual explanation for the lower obesity risk.

Indeed, if you did have the time and parenting skills to ensure that your whole family sits down for supper, your kids don’t watch too much TV, and are off to bed at bedtime, then you are probably also doing a lot of other things right.

On the other hand, if your family meals are chaotic, you have no control over your kids’ screen time, and they are still running around at midnight, there are probably other issues that need to be addressed.

So while the findings are interesting (and by no means surprising), I am not exactly sure how they will help us address the childhood epidemic.

Perhaps a well-designed intervention study will show wether or not simply adopting these three “routines” will actually make a difference.

I certainly appreciate any comments or opinions on whether or not any of my readers think this will work.

AMS
Hamburg, Germany

Regular readers of these pages will recall several posts on the importance of adequate restorative sleep for the maintenance of healthy weights. As blogged previously, reduced sleep is not only associated with increased risk for obesity, but sleep deprivation also has profound effects on ingestive behaviour.

A new study by Schmid and colleagues from the University of Luebeck, Germany, published in the Journal of Clinical Endocrinology and Metabolism now shows that sleep deprivation can have profound effects on glucagon levels, a key determinant of glucose control.

Their study examined the effects of a single night of sleep restriction to 4.5 hours vs. a night of 7 hours of sleep in a crossover study in 10 healthy men.

Sleep deprivation not only reduced basal plasma glucagon levels but also glucagon response to a hypoglycemic clamp, but had no effect on circulating concentrations of insulin, C-peptide, epinephrine, norepinephrine, or growth hormone. Basal concentrations of ACTH and cortisol were also reduced after sleep loss during baseline.

This finding provides further evidence for the notion that glucose homeostasis is sensitive to subtle changes in sleep duration.

Importantly, as glucagon is a key hormone that helps maintain normal glucose levels during fasting by inducing the liver to convert stored glycogen into glucose and release it into the bloodstream, lack of glucagon release resulting from sleep deprivation could promote eating in response to hypoglycemia, thereby promoting weight gain. This may be of particular relevance to diabetic patients on hypoglycemic medications, who are particularly prone to hypoglycemic episodes.

This interesting observation clearly supports the notion that ensuring adequate amounts of sleep should be an important cornerstone of weight management.

AMS
Edmonton, Alberta