sleep and fat

EDITORIAL
Sleepless in America

A Pathway to Obesity and the Metabolic Syndrome?

WHETHER ONE IS READING RECENT reports from the Centers for Disease
Control and Prevention, articles in the scientific literature or popular
press, or just glancing around and looking at people in the subway or
the shopping mall, it is apparent that there is a major epidemic in
America: obesity! Obesity is a disease that, in just the past few
decades, has been rising dramatically in developed countries and reached
epidemic levels in the United States. Data from the Behavioral Risk
Factor Surveillance Program (available at: www.cdc.gov/brfss) have
revealed a striking increase, over the past 15 years and across the
United States, in the prevalence of overweight (body mass index [BMI,
calculated as weight in kilograms divided by the square of height in
meters], 25-30) and obesity (BMI 30), and there is recent evidence of an
alarming rise in the proportion of children affected with the disorder.
Besides the social stigma attached to obesity, these trends are cause
for concern because of the risks of secondary complications, including
insulin resistance and type 2 diabetes mellitus, hyperlipidemia,
cardiovascular disease, hypertension, stroke, cancer, and arthritis. The
increase in levels of proinflammatory cytokines and prothrombotic
factors associated with obesity is now recognized as an independent
cause of morbidity and has been targeted by the National Cholesterol
Education Program Adult Treatment Panel as an important independent
contributor to cardiovascular risk. 1 Many fingers are being pointed at
many causes: not enough exercise, high fat foods, poor eating habits,
watching too much television, genetics, family history, fast-food
hysteria, or exposure to advertising luring us to eat unhealthy foods.
Even our early prenatal and postnatal environments may be putting us on
a trajectory for an unhealthy metabolic state later in life.2 A common
denominator may be the excessive intake of carbohydrates encouraged by
the wave of “lowfat” dieting that began in the 1970s. We can even blame
our genes, which evolved in humans engaged in high physical activity
(much of it chasing and looking for food) with eating habits requiring
one to eat as much as possible (and as much meat and fat as possible)
when a meal became available, ie, rarely, as opposed to having the food
lying around us all of the time.

In recent years, a new and unexpected “obesity villain” has emerged,
first from laboratory studies and now, as reported by Vorona et al3 in
this issue of the ARCHIVES, in population-based studies: insufficient
sleep. In a study analyzing 924 patients from 4 primary care practices
in Virginia, a reduced amount of sleep was associated with overweight
and obese status, and patients in the obese group showed a near inverse
linear relationship between weight and reported sleep time. The
relationship between obesity (and associated metabolic and
cardiovascular disorders often referred to as the metabolic syndrome, or
syndrome X 4) and insufficient sleep has only emerged in the past 5
years. In a pioneering study in 1999 by Van Cauter and colleagues, 5 it
was found that sleep restricted to only 4 hours per night for 1 week led
to endocrine and metabolic changes associated with diabetes (insulin
resistance) and weight gain in healthy young men. While the effects were
reversible with normal sleep times, these remarkable, and at the time
surprising findings, led basic and clinical researchers off on the trail
to find the physiological linkages between insufficient sleep and
metabolic function. This work also renewed interest in the role of
insufficient sleep as a cause of many of the metabolic abnormalities
associated with sleep apnea. However, while there is a growing awareness
among some sleep, metabolic, cardiovascular, and diabetes researchers
that insufficient sleep could be leading to a cascade of disorders, few
in the general medical profession or in the lay public have yet made the
connection.

See also pages 25, 35, and 42

For most of us, the news about weight control strikes home as pounds
accumulate with aging or reappear after dieting. Unfortunately, most of
the weight-conscious public, and even the health-care professional
community, still view weight control as a biological black box and
ascribe obesity to indolence and a lack of will. The experience of those
whose body weight is “defended” despite dieting would suggest
otherwise—that weight is controlled much like a thermostat, with
fluctuation around a programmed set point. Yet the obesity magic bullet
has proved elusive because, like other complex diseases (eg,
hypertension, hyperlipidemia, and cancer), multiple genetic and
environmental factors contribute to body weight disregulation and its
secondary complications. An important goal in developing new therapies
for obesity and the metabolic syndrome is to gain a greater
understanding of the elaborate pathways that regulate appetite, food
intake, and energy expenditure and to unravel interactions between
behavior, metabolism, and environment that contribute to long-term
energy constancy. It is of particular interest now to determine the
mechanisms by which acute and/or chronic sleep loss alters this complex
metabolic machinery, as well as the role of the circadian clock in its
regulation of the timing of sleep and metabolic function.6

Another article in this issue of the ARCHIVES may be related to the
association between sleep loss and obesity found in the article by
Vorona et al.3 Ferreira et al 7 report on data from the Amsterdam Growth
and Health Longitudinal Study and they determine that, starting at 13
years of age, factors such as fatness, fitness, and lifestyle are
important determinants of the metabolic syndrome that affects 10% of the
studied population by the age of 36 years—an indication that the obesity
epidemic in young people is not confined to America. An alarming
statistic defines a major problem among American youth: between 1980 and
2000, the rate of obese young people has risen from 5% to 15%, and
another 15% has moved into that classification in young adulthood. While
this epidemic in our young population has received national attention,
less well-known is the finding that children of all ages in America are
sleeping 1 to 2 hours less per night than they need, according to a
recent poll taken by the National Sleep Foundation.8 While insufficient
sleep has often been associated with the elderly population, the
increasing demands and lifestyles of modern society have imposed
restricted sleep on our youth as well. It is now critical to determine
the importance of a lack of sufficient sleep during the early formative
years in putting our youth on a trajectory toward obesity and the
metabolic syndrome - a trajectory that could be altered if sleep loss
is indeed playing a role in this epidemic.

A new edited book, Obesity in Childhood and Adolescence, 9 will
hopefully raise the clinical community’s awareness of the causes,
consequences, and therapies of obesity in the young. However, it is
noteworthy that none of the 21 chapter titles in this book contain the
word sleep, indicating that the connection between sleep loss and
obesity still is not a major consideration in the war on obesity.
Hopefully, articles such as those in this issue of the ARCHIVES, which,
on the one hand, link sleep loss and obesity, and on the other hand,
define the importance of early habits for obesity and the subsequent
development of the metabolic syndrome, will lead more clinicians to
explore the effects of chronic long-term partial sleep loss on weight
and metabolic function in our children.

It is fascinating to note that genetic and clinical observations both
point to interconnections between sleep and metabolic regulation. The
discovery of the orexins as neuropeptide agonists of orphan signaling
pathways within the energy center of the brain, 10, 11 and the
subsequent identification of the orexin receptor as the causative
genetic defect in the most common form of canine narcolepsy by Mignot
and colleagues, 12 set the stage for investigating neural
interconnections linking sleep and metabolic homeostasis. While these 2
fundamental systems appear to have distinct functions in human
physiology, the discovery of overlapping molecular components suggests a
coregulation that may have coordinated the alternance between periods:
periods of fasting and sleep and periods of wakefulness, food seeking,
and energy storage. A lack of sleep may perturb the homeostatic
coordination of these pathways, activating metabolic pathways that
trigger energy conservation (increased food intake and decreased
expenditure) in excess of the energy cost of increased wakefulness.
Indeed, our recent analysis of leptin-deficient animals suggests that
leptin per se may be necessary for consolidated sleep, since animals
with a genetic absence of leptin display markedly increased sleep
fragmentation and experience increased periods of microsleep during the
active period. 13 In view of observations from experimental models and
human clinical studies on the relationship between the sleep-wake cycle
and fuel homeostasis, it may be opportune to ask whether intervention in
sleep disorders may ameliorate some of the metabolic deficits associated
with overweight and obesity.

Joseph Bass, MD, PhD Fred W. Turek, MD
Financial Disclosu None. Correspondence: DrBass, Northwestern
University Feinberg School of Medicine and ENHRI Pancoe-Evanston
Northwestern Healthcare Life Sciences Pavilion, 2200 Campus Dr, Room
4405, Evanston, IL 60208-3500(j-bass @northwestern.edu)

REFERENCES
1. Ford ES. Prevalence of the metabolic syndrome in US populations.
Endocrinol Metab Clin North Am. 2004;33:333-350.
2. Gluckman PD, Hanson MA. The developmental origins of the metabolic
syndrome. Trends Endocrinol Metab. 2004;15:183-187.
3. Vorona R, Winn MP, Babineau TW, Eng BP, Feldman HR, Ware JC.
Overweight and obese patients in a primary care population report less
sleep than patients with a normal body mass index. Arch Intern Med.
2005;165:25-30.
4. Reaven G. Syndrome X. In: DeGroot LJ, Jameson JL, eds.
Endocrinology.4th ed. Philadelphia, Pa: WB Saunders Co; 2001:954-958.
5. Spiegel K, Leproult R, Van Cauter E. Impact of sleep debt on
metabolic and endocrine function. Lancet. 1999;354:1435-1439.
6. Van Cauter E, Copinschi G, Turek FW. Endocrine and other biologic
rhythms. In: DeGroot L J, Jameson JL, eds. Endocrinology.4th ed.
Philadelphia, Pa: WB Saunders Co; 2001:235-256.
7. Ferreira I, Twisk JWR, van Mechelen W, Kemper HCG, Stehouwer CDA.
Development of fatness, fitness, and lifestyle from adolescence to the
age of 36 years: determinants of the metabolic syndrome in young
adults:theAmsterdam Growth and Health Longitudinal Study. Arch Intern
Med. 2005;165:42-48.
8. National Sleep Foundation. The 2004 NSF National Sleep in America
Poll. Available at: www.sleepfoundation.org. Accessed October 7, 2004.
9. Kiess W, Marcus C, Wabitsch M, eds. Obesity in Childhood and
Adolescence. Leipzig, Germany: Karger; 2004. Pediatric and Adolescent
Medicine; vol 9.
10. Sakurai T, Amemiya A, Ishii M, et al. Orexins and orexin receptors:
a family of hypothalamic neuropeptides and Gprotein-coupled receptors
that regulate feeding behavior. Cell. 1998;92:573-585.
11. de Lecea L, Kilduff TS, Peyron C, et al. The hypocretions:
hypothalamus-specific peptides with neuroexcitatiry activity. Proc Natl
Acad Sci U S A. 1998;95:322 327.
12. Lin L, Faraco J, Li R, et al. The sleep disorder canine narcolepsy
is caused by a mutation in Hypocretin (Orexin) receptor 2 gene. Cell.
1999;98:365-376.
13. Shelton JK, Kosaka N, Perrino C et al. Role of leptin in sleep
consolidation and circadian rhythmicity. Sleep. 2004;27(suppl):A31.
(REPRINTED) ARCHINTERNMED/VOL 165, JAN 10,2005 WWW.ARCHINTERNMED.COM

"Bob (this one)" wrote in message
...
EDITORIAL
Sleepless in America

A Pathway to Obesity and the Metabolic Syndrome?

In a study analyzing 924 patients from 4 primary care practices
in Virginia, a reduced amount of sleep was associated with overweight
and obese status, and patients in the obese group showed a near inverse
linear relationship between weight and reported sleep time.

The relationship of less sleep causing increasing obesity may not be a
direct cause, but rather a result of less activity causing you to need less
sleep for body repair. I find this is true for myself. The more physically
active I am, the more sleep I need.
Also, I believe that if an overweight person's appetite is more or less
insatiable, then staying up longer gives them another hour or 2 to eat more.

On Mon, 29 Aug 2005 14:06:40 GMT, "Tom G" wrote:

The relationship of less sleep causing increasing obesity may not be a
direct cause, but rather a result of less activity causing you to need less
sleep for body repair. I find this is true for myself. The more physically
active I am, the more sleep I need.
Also, I believe that if an overweight person's appetite is more or less
insatiable, then staying up longer gives them another hour or 2 to eat more.

My doc told me (last year when I was being tested for Sleep Apnoea)
that there was a reasonably strong correlation between lack of good
(restful) sleep and insulin resistance. Certainly, when I began
treating my apnoea and got the first good sleep I had managed in years
I began to lose weight WITHOUT making any changes to my diet and
exercise regime.

Conversely, when I stopped sleeping well (due to stressors from
circumstances outside my control) the loss stopped again. Doesn't
seem to matter that eating and exercise patterns are no different from
those I had when I was losing, if I'm not sleeping well (and I'm not)
then I won't lose.

Aramanth

"Aramanth Dawe" wrote in message
news
On Mon, 29 Aug 2005 14:06:40 GMT, "Tom G" wrote:

The relationship of less sleep causing increasing obesity may not be a
direct cause, but rather a result of less activity causing you to need
less
sleep for body repair. I find this is true for myself. The more
physically
active I am, the more sleep I need.
Also, I believe that if an overweight person's appetite is more or
less
insatiable, then staying up longer gives them another hour or 2 to eat
more.

My doc told me (last year when I was being tested for Sleep Apnoea)
that there was a reasonably strong correlation between lack of good
(restful) sleep and insulin resistance.

Insulin resistance is mainly due to life style factors of eating too much
and inactivity, which would then set a person up for sleep problems. Lack of
sleep may then aggravate the insulin resistance.
Just as it is hard to lose weight because of being insulin resistant, a
person shouldn't blame the symptom before the life style factors that caused
the weight gain in the first place.

Certainly, when I began
treating my apnoea and got the first good sleep I had managed in years
I began to lose weight WITHOUT making any changes to my diet and
exercise regime.

Do you think that in your case that lack of good sleep causes insulin
resistance and metabolic syndrome? I think that relieving the symptom of
lack of sleep affected the other factors in good favor.


Conversely, when I stopped sleeping well (due to stressors from
circumstances outside my control) the loss stopped again.

Yes. Stress is not good for sleep.

Doesn't
seem to matter that eating and exercise patterns are no different from
those I had when I was losing, if I'm not sleeping well (and I'm not)
then I won't lose.

In your case, a lack of sleep may be more of a cause than a symptom, but
I believe that for the majority of people, lack of sleep is another self
feeding symptom of metabolic disease.

Aramanth

Aramanth Dawe wrote:
On Mon, 29 Aug 2005 14:06:40 GMT, "Tom G" wrote:

The relationship of less sleep causing increasing obesity may not be a
direct cause, but rather a result of less activity causing you to need less
sleep for body repair. I find this is true for myself. The more physically
active I am, the more sleep I need.
Also, I believe that if an overweight person's appetite is more or less
insatiable, then staying up longer gives them another hour or 2 to eat more.

My doc told me (last year when I was being tested for Sleep Apnoea)
that there was a reasonably strong correlation between lack of good
(restful) sleep and insulin resistance. Certainly, when I began
treating my apnoea and got the first good sleep I had managed in years
I began to lose weight WITHOUT making any changes to my diet and
exercise regime.

Conversely, when I stopped sleeping well (due to stressors from
circumstances outside my control) the loss stopped again. Doesn't
seem to matter that eating and exercise patterns are no different from
those I had when I was losing, if I'm not sleeping well (and I'm not)
then I won't lose.

Aramanth

I also have to wonder (without extensively reviewing these studies
myself) how well the covariate of sleep apnea or other obstructive
airway disorders were controlled for in these studies. It's well-known
that being fat can increase one's risk for airway obstruction, which
can decrease restful sleep. So, it would make sense that the fatter you
are, the less restful sleep you get...

wrote:

I also have to wonder (without extensively reviewing these studies
myself) how well the covariate of sleep apnea or other obstructive
airway disorders were controlled for in these studies. It's well-known
that being fat can increase one's risk for airway obstruction, which
can decrease restful sleep. So, it would make sense that the fatter you
are, the less restful sleep you get...

I concur. Before I started, I had bad airway obstruction when I slept.
My wife was very concerned. With 20 lbs off, my wife notes that I still
breathe badly while asleep, but nowhere near as bad as before.
Additionally, I am sleeping a lot better, though there are too many
variables to really explain it (new apartment, new pillow, getting
accustomed to my wife's cat, weight loss, vitamins, etc). I am looking
forward to sleeping better as I get closer to goal. One more bit of
motivation.

Hollywood, 264/244.5/218