One factor accounting for this may well be the lack of timely access to sleep testing.
Now, a study by Hirsch Allen and colleagues from the University of British Columbia Hospital Sleep Clinic, published in the Annals of the American Thoracic Society, examined the relationship between severity of sleep apnea and travel times to the clinic in 1275 patients referred for suspected sleep apnea.
After controlling for a number of confounders including gender, age, obesity and education, travel time was a significant predictor of OSA severity with each 10 minute increase in travel time associated with an apnea-hypopnea-index increase of 1.4 events per hour.
The most likely explanation for these findings is probably related to the fact that the more severe the symptoms, the more likely patients are to travel longer distances to undergo a sleep study.
Thus, travel distance may well be a significant barrier for many patients accounting for a large proportion of undiagnosed sleep apnea – at least for milder forms.
Given the often vast distances in Canada one can only wonder about just how much sleep apnea goes under diagnosed because of this issue.
Now a study by Robert Eckel and colleagues, published in Current Biology, illustrates how sleep deprivation and timing of meals can markedly alter insulin sensitivity.
Studies were conducted in 16 healthy young adults (8w) with normal BMI. Following a week of 9-hr-per-night sleep schedules, subjects were studied in a crossover counterbalanced design with 9-hr-per-night adequate sleep (9-hr) and 5-hr-per-night short sleep duration (5-hr) conditions lasting 5 days each, to simulate a 5-day work week. Sleep was restricted by delaying bedtime and advancing wake time by 2 hr each.
Energy balanced diets continued during baseline, whereas food intake was ad libitum during scheduled wakefulness of 5- and 9-hr conditions.
Overall, the simulated 5-day work week of 5-hr-per-night sleep together with an ad libitum diet resulted in a 20% decrease in oral and intravenous insulin sensitivity, which was compensated for by increased insulin secretion..
These changes persisted for up to 5 days after restoring 9-hr sleep opportunities.
The authors also showed that shifting circadian rhythm resulted in morning wakefulness and eating during the biological night, a factor that may promote weight gain over time.
Now, Christophe Varin and colleagues from the Centre National de la Recherche Scientifique, Paris, France, in a paper published in the Journal of Neuroscience describe how glucose regulates key neurones in the brain to induce sleepiness.
Their studies in mice focussed on sleep-active neurons located in the ventrolateral preoptic nucleus (VLPO), critical in the induction and maintenance of slow-wave sleep (SWS).
Using both in vivo and ex vivo patch clamp studies, the researchers show that a rise in extracellular glucose concentration in the VLPO can promote sleep by increasing the activity of sleep-promoting VLPO neurons.
As the researchers note,
“The extracellular glucose concentration monitors the gating of KATP channels of sleep-promoting neurons, highlighting that these neurons can adapt their excitability according to the extracellular energy status… Glucose-induced excitation of sleep-promoting VLPO neurons should therefore be involved in the drowsiness that one feels after a high-sugar meal. This novel mechanism regulating the activity of VLPO neurons reinforces the fundamental and intimate link between sleep and metabolism.”
Apart from helping unravel the biology of a phenomenon that every parent of a young child is well aware of, this research raises a number of interesting clinical questions.
Does overconsumption of high-sugar foods necessitate counteracting these effects with caffeine? Is this why sugar-sweetened pop generally contains caffeine (to not put you to sleep)?
Does this also explain the practice of eating a bedtime snack to fight insomnia?
And what does this mean for people with poorly controlled diabetes: do they need to drink more coffee than people without diabetes to get through their day? (not something I’ve heard of).
For all my Canadian readers (and any international readers planning to attend), here just a quick reminder that the deadline for early bird discount registration for the upcoming 4th Canadian Obesity Summit in Toronto, April 28 – May 2, ends March 3rd.
To anyone who has been at a previous Canadian Summit, attending is certainly a “no-brainer” – for anyone, who hasn’t been, check out these workshops that are only part of the 5-day scientific program – there are also countless plenary sessions and poster presentations – check out the full program here.
To register – click here.
The title of this post may sound like a “no-brainer”, but the research literature on the long-term health benefits of weight loss from longitudinal intervention studies in people with severe obesity is much thinner than most people would expect.
Thus, a new study from our group, that looks at the relationship between changes in body weight and changes in health status over two years in patients with severe obesity enrolled in the Alberta Population-based Prospective Evaluation of the Quality of Life Outcomes and Economic Impact of Bariatric Surgery (APPLES) study, published in OBESITY, may well be of considerable interest.
As described previously, APPLES is a 500-patient cohort study in which consecutive, consenting adults with BMI levels > 35 kg/m2 were recruited from the Edmonton Adult Bariatric Specialty Clinic. The 500 patients enrolled were between 18 and 60 years old and were either wait-listed (n=150), beginning intensive medical treatment (n=200) or had just been approved for bariatric surgery (n=150). Complete follow-up data at 24 months was available for over 80% of participants.
At study enrollment, the proportion of patients who reported >2 and >3 chronic conditions was 95.4% and 85.8%, respectively. The most common single chronic conditions at baseline were joint pain (72.2%), anxiety or depression (65.4%), hypertension (63.4%), dyslipidemia (60.4%), diabetes mellitus (44.6%), gastrointestinal reflux disease (35.4%), and sleep apnea (33.5%).
After 2 years, just over 50% of participants had maintained a weight loss > 5%, with a mean weight change for the entire cohort of about 13 kg.
Losing > 5% weight was associated with an almost 2-fold increased likelihood of reporting a reduction in multimorbidity at 2-year follow-up, whereby outcomes varied between treatment groups: in the surgery group, the top three chronic conditions that decreased in prevalence over follow-up were sleep apnea (43% at baseline vs. 25% at 2 years,), dyslipidemia (60% vs. 47%), and anxiety or depression (59% vs. 47%); in the medically treated group anxiety or depression (69% vs. 57%) and joint pain (77% vs. 67%); and none in the wait-listed group.
As expected, any reduction in multimorbidity was associated with a clinically important improvement in overall health status.
In summary, this paper not only documents the considerable multimorbidity associated with severe obesity, it also documents the clinically important improvement in health status associated even with a rather modest 5% weight loss over 2 years in these individuals.