Sleep and Kids

boy-watching-tv-with-remoteIt would be too easy if we put our kids to bed and they fell asleep in the average nine minutes it takes for an adult to drop into the arms of Morpheus. If your child struggles to fall asleep, know that this is not likely to resolve merely by moving from crib to bed. As he ages, there will fewer cries and screams, and more pleas and refusals. Could there be a reason behind this? Maybe television? Video games?

Each child is unique and has his own distinct needs for sleep.  Generally, a preschooler needs 10 to 12 hours a night, maybe with a nap during the day.  The surprise is that the school-age and preteen group benefit from the same, except for the nap.  But, “media use has been shown to negatively affect a child’s sleep,” according to researchers at Seattle’s Children’s Research Institute.  In their randomized controlled study of preschoolers, they found that the children had more than 70 minutes of screen time a day, with a fifth of that after 7 PM.  Almost 20% of the parents interviewed indicated at least one sleep problem with their preschooler.  Daytime TV showing violent behavior exacerbated problems.  (Garrison. 2011)  In a similar study a decade earlier, investigators at Brown University discovered that the sleep domains most affected by television were “bedtime resistance, sleep onset delay, and anxiety around sleep, followed by shortened sleep duration.”  (Owens. 1999)  In both studies—and in several between— it is agreed that a TV in the child’s bedroom compounds the matter and translates into less-than-stellar academic performance.

Recent assaults on Sponge Bob and his kin have raised the hackles of the entertainment industry.  But theirs is not righteous indignation, and transcends the humor of a “Who?  Me?” response.  It has been suspected for decades that the electronic babysitter would require a payback.  If a person believes that life is a series of trade-offs, here’s one of them, usually showing up during the school years, unknowingly invited earlier.

Children who watch fast-paced programs—even for as little as nine minutes — perform poorly in executive function tasks, those that control and regulate other behaviors and abilities, and are necessary for goal-directed activities.  These might include knowing when to start and stop behaviors and when to change them if the situation calls for it.  It also includes being able to plan ahead, to pay attention, and to fine tune memory and motor skills.  Although they are not easy to assess, their absence is noticeable.  (Lillard. 2011)  Teachers have lamented since the 1970’s that too many children start school with five-minute attention spans.

The U.S. is not the only nation facing this problem.  German researchers realized that 25% of their children do not get the ten hours of sleep they need.  They advise that parents and care givers limit TV time in order to prevent the negative consequences of sleep deprivation.  (Heins. 2007)  The Japanese learned that not only TV, but also after-school activities that last past 8 PM can interfere with sleep / wake patterns.  (Oka. 2008)

Other electronic entertainment, not only TV, plays a role in cerebral interference.  Electronics may induce the fight-or-flight state, increase blood pressure and pulse, and disrupt overall brain performance.  The unnatural brightness of the screen can interfere with production of melatonin, the signaling molecule that tells you to fall asleep.  Fast-moving and quick-changing scenes can interrupt the wiring of a young brain, possibly leading to bad dreams and restlessness.  Electromagnetic radiation is a by-product of anything electronic, affecting children more than adults, considering that their brain tissue is more conductive, radio frequency penetration is greater relative to head size, and children will have a longer lifetime exposure than adults.  (Kheifets. 2005)

Problems begin to manifest by age seven, the time when academic load may become a family affair.  When and if you help your child with his homework, you’re sure to notice what all this is about.  A two-hour delay between electronic stimulation and bedtime is not a bad idea.   Prior to that, naturally-paced shows, or even those seemingly in slow motion (Mr. Rogers), can offset, or even prevent, the surreal experiences that occur later. (Christakis. 2011)


Garrison MM, Liekweg K, Christakis DA.
Media use and child sleep: the impact of content, timing, and environment.
Pediatrics. 2011 Jul;128(1):29-35.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

Angeline S. Lillard, PhD,  Jennifer Peterson, BA
The Immediate Impact of Different Types of Television on Young Children’s Executive Function
Pediatrics. Published online September 12, 2011   (doi: 10.1542/peds.2010-1919)

Heins E, Seitz C, Schüz J, Toschke AM, Harth K, Letzel S, Böhler E.
Bedtime, television and computer habits of primary school children in Germany. [Article in German]
Gesundheitswesen. 2007 Mar;69(3):151-7.

Oka Y, Suzuki S, Inoue Y.
Bedtime activities, sleep environment, and sleep/wake patterns of Japanese elementary school children.
Behav Sleep Med. 2008;6(4):220-33.

Leeka Kheifets, PhD, Michael Repacholi, PhD, Rick Saunders, PhD, Emilie van Deventer, PhD
The Sensitivity of Children to Electromagnetic Fields
Pediatrics Vol. 116 No. 2 August 1, 2005 pp. e303 -e313

Dimitri A. Christakis
The effects of Fast-Paced cartoons
Pediatrics. 2011; peds. 2011-2071;  Published Online, 12 Sept., 2011

Gröer M, Howell M.
Autonomic and cardiovascular responses of preschool children to television programs.
J Child Adolesc Psychiatr Ment Health Nurs. 1990 Oct-Dec;3(4):134-8.

Christakis DA, Zimmerman FJ, DiGiuseppe DL, McCarty CA.
Early television exposure and subsequent attentional problems in children.
Pediatrics. 2004 Apr;113(4):708-13.

Al-Khlaiwi T, Meo SA.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population.
Saudi Med J. 2004 Jun;25(6):732-6.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Lack Of Sleep Alters Hormones, Affects Weight

male-sleepySleep disorders are coming under closer scrutiny in a society plagued by their ubiquity, prompted by extraneous and self-induced pressures and obligations.  Discovery of the genetic basis for circadian rhythms has expanded our knowledge of the temporal role of behavior and physiology.  The relationship between sleep deprivation and hormone imbalance is publicized, but disregarded.  That part of the hypothalamus in charge of daily metabolic rhythm is called the suprachiasmatic nucleus, and it controls physical activity and hormone levels, as well as sleep, body temperature, immunity, and digestion.

Sleep deprivation, or even fragmentation, interrupts the machinery that controls energy expenditure and food intake.  A single night of sleep deprivation has been found to increase the risk of obesity by disturbing secretion and function of thyrotropin, cortisol and ghrelin (Benedict. 2011).  Thyrotropin is better known as TSH, the pituitary secretion that regulates the endocrine function of the thyroid gland.   Cortisol is excreted by the adrenal glands to address stress, affecting the metabolism of glucose, protein and fats. Ghrelin regulates appetite by telling you to eat, while its partner, leptin, tells you to stop.  Aberrations of these substances, aggravated by lack of sleep, reduce expenditure of energy during the waking hours.  Because fewer calories are burned, weight gain is almost certain.  Although the mechanisms behind it are not completely understood, “epidemiological evidence indicates that chronic sleep curtailment increases risk of developing obesity.” (Ibid.).

When we run low on energy from lack of sleep, many of us grab a coffee or three and a handful of junk to get a quick fix of comfort food.  That doesn’t last very long, though, does it?  Sleep affects one’s ability to maintain or to lose weight by regulating hormones and metabolism, which includes the way we handle food as part of the range of processes that occur within a living organism.  This entails anabolism (buildup) and catabolism (break down).  Deprivation of sleep is also tied to cardiovascular health and inflammation that is below the radar, called subclinical (Sharma. 2010).

We need about seven and a half hours of sleep each night.  An extra half hour, by the way, won’t help you to lose the last ten pounds.  But moving from five hours to eight might just be able to accomplish that.  It’s all in the hormones.  If you’re sleep-deprived, you have higher levels of ghrelin, telling you to eat.  That means that leptin is in short supply, and you’ll eat more than you need, ending up with more calories in and fewer calories out.  Oops, imbalance.

Apnea, bruxism (teeth grinding), narcolepsy, and insomnia are only a few of the sleep disorders that plague us.  Overcoming these insults can prevent the health conditions that stem from their upswing in modern society.  Besides obesity, impaired glucose tolerance and insulin resistance are real threats.  Losing some sleep for only a single night can upset the apple cart of insulin sensitivity (Donga. 2010).  That may be of significant relevance to a person harboring Type 2 diabetes, and most assuredly will be with Type 1.  What’s interesting is that voluntary sleep deprivation is a characteristic of modern life, where people put more stock into their jobs than into themselves and their families (Bosy-Westphal. 2008).  Here, weight gain from increased energy intake is earned, even without conscious thought.  Once the inborn clock gets out of whack, don’t be surprised by physiological dysregulation of one kind or another (Huang. 2011).

Sleeping as little as possible is not admirable behavior.  High-schoolers and students cramming for college exams are not doing themselves any favors.  Neither is the mom or dad who works into the wee hours, a common activity in industrialized nations.  Since the 90’s, researchers have paralleled sleep deprivation with the rise of obesity, especially in kids (Leproult. 2010) (Knutson. 2008).  Since our hormones vary from day to night, it matters that we keep circadian rhythm aligned with the design of their function.  Shut off the TV and get rid of the computer games at bedtime.  Put the cell phone away while you’re at it.


Benedict C, Hallschmid M, Lassen A, Mahnke C, Schultes B, Schiöth HB, Born J, Lange T.
Acute sleep deprivation reduces energy expenditure in healthy men.
Am J Clin Nutr. 2011 Jun;93(6):1229-36.

Sunil Sharma and Mani Kavuru
Sleep and Metabolism: An Overview
International Journal of Endocrinology. Vol. 2010 (2010), Article ID 270832, 12 pages

Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, Romijn JA.
A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8.

Bosy-Westphal A, Hinrichs S, Jauch-Chara K, Hitze B, Later W, Wilms B, Settler U, Peters A, Kiosz D, Muller MJ.
Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women.
Obes Facts. 2008;1(5):266-73.

Wenyu Huang, Kathryn Moynihan Ramsey, Biliana Marcheva1,and Joseph Bass
Circadian rhythms, sleep, and metabolism
J Clin Invest. 2011;121(6):2133–2141.

Leproult R, Van Cauter E.
Role of sleep and sleep loss in hormonal release and metabolism.
Endocr Dev. 2010;17:11-21.

Knutson KL, Van Cauter E.
Associations between sleep loss and increased risk of obesity and diabetes.
Ann N Y Acad Sci. 2008;1129:287-304.

Spiegel K, Tasali E, Leproult R, Van Cauter E.
Effects of poor and short sleep on glucose metabolism and obesity risk.
Nat Rev Endocrinol. 2009 May;5(5):253-61.

Morris CJ, Aeschbach D, Scheer FA.
Circadian system, sleep and endocrinology.
Mol Cell Endocrinol. 2011 Sep 10. [Epub ahead of print]

Beccuti G, Pannain S.
Sleep and obesity.
Curr Opin Clin Nutr Metab Care. 2011 Jul;14(4):402-12.

Spiegel K, Leproult R, L’hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E
Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin.
J Clin Endocrinol Metab. 2004 Nov;89(11):5762-71.

Nedeltcheva AV, Kessler L, Imperial J, Penev PD.
Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance.
J Clin Endocrinol Metab. 2009 Sep;94(9):3242-50. Epub 2009 Jun 30.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Shift Work and Your Health

overworked-workerRotating shifts causes difficulties because it works in opposition to the body’s normal circadian rhythms, the most influential being the sleep/wake cycle.  There is also the matter of social isolation that comes from working when everybody else is asleep, and vice-versa.  One of the complications of changing shifts is the incidence of gastrointestinal upset.  Shift workers have a notoriously high occurrence of ulcers, based partly on disruption of sleep patterns and partly on the activation of H. pylori infection if it is at all present and waiting for the opportunity to strike.  (Pietroiusti, 2006)  (Segawa, 1987)  Chronic fatigue, untimely sleepiness, and even failure to fall asleep are some other physical interruptions caused by shift work.  Among the worst social perturbations is divorce, an element that hits some jobs more than others, law enforcement being a prime example.

Canada’s Institute for Work and Health delved into this topic and found that night work is associated with an increase in breast cancer among women who work rotating shifts for long durations.  (IWH, 2010)  The etiology of breast cancer is mostly uncertain, but about one fourth its incidences can be attributed to genetic factors.  At least a little blame has been put on light at night and its effect on melatonin, the hormone produced by the pineal gland that communicates information about light to different parts of the body in order to regulate biologic rhythms.  When the eye’s pupil detects changes in brightness—night—it sends the sleep message to the brain by way of melatonin.  When this activity gets stymied, melatonin is not able to exert its anti-cancer character, and the risk of breast cancer is elevated after a prolonged time. (Schernhammer, 2001)   (Hansen, 2001)   Melatonin is a popular sleep aid, especially for those experiencing jet lag, but few have associated it with anti-cancer function.  (Knower, 2012)  An interesting realization in this circumstance is the body’s inability to manufacture vitamin D from exposure to natural light, raising the question of the appropriateness of supplementation.  (Shao, 2012)  Among researchers’ quests is the determination of the actual concentrations of vitamin D in women who have survived breast cancer and whether or not insufficiency is prevalent among sufferers, survivors, and healthy controls.  (Trukova, 2012)  (Blask, 2009)

Little is known about sleep taken at night, and even less about sleep taken during the day, when years of natural law dictate otherwise.  Nobody really knows how much sleep is necessary for optimal health.  But there is evidence that long sleepers and very short sleepers have increased mortality.  (Ferrie, 2007)  The first part of sleep lasts about fifteen minutes, and is labeled as Stage 1.  If you are awakened from this stage, you may even deny having been asleep.  Stage 2 occupies about half of sleep time, yet is the least understood part.  Being deprived of this stage results in almost total sleep loss because this is the part from which other stages develop.  This, by the way, is the stage affected by medications and sleep aids.  Stages 3 and 4 are combined into the slow-wave-sleep stage, differing only by the number of delta waves measureable by an EEG.  Contrasted to Stage 2, this is the one common to most persons, and is the one compensated after long periods of sleep deprivation.  This is the one needed for body repair and the activity of growth hormone(s).  Rapid eye movement (REM) sleep is the best known stage and throughout its duration the body is virtually paralyzed and loses its ability to regulate heat.  Dreams, which are deemed necessary to psychological well-being, occur here.  REM, dominating the late stages of sleep episodes, is strongly influenced by circadian rhythm.   Daytime sleep is normally one or two hours shorter than night time sleep.  REM, therefore, is shortened.  This adds to the alertness problems of the night shift.

A modern concern about shift work is increased risk of type 2 diabetes and the metabolic syndrome, compounded by the possible elevation of cardiovascular jeopardy.  This affects women more than men, but the combination of obesity, high triglycerides, and low HDL cholesterol is common to both.  (Karlsson, 2001)  Years of rotating night shift work are associated with weight gain that comes from failed attempts to eat right and from limited time for exercise.  And to think that all this is precipitated by disturbed circadian periodicity.  Eating on the run and mindless snacking are more common among night workers than their daytime counterparts.  Even if day and night workers had the same major CVD factors, the night workers admit to increased job strain and greater at-work physical exertion, both of which contribute to the altered parameters that incite metabolic syndrome.  (Esquirol, 2009)  In Japan, where the work ethic is ubiquitously strong, different work schedules have been associated with a rise in the incidence of diabetes.  (Morikawa, 2005)  (Suwazono, 2006)  Over the long term, changes are evident not only in daily glucose levels, but also in glycosylated hemoglobin (HbA1c), which measures glucose over an extended time.  (Suwazono, 2009)

Workplace cafeterias commonly close at night.  Workers are then left to their own culinary devices, and that often translates to unhealthy eating habits by virtue of convenience and time constraints.  A healthy work force is a boon to productivity and accident prevention, areas in which companies can demonstrate an interest that supersedes complaining about the opposite.  If a company is reactive, it can get you to the First-Aid station or to the HR person for failure to perform.  By being proactive, it can prevent both while saving money on bandages and the expense of training a replacement.

If there is a best-case scenario for shift work, scheduling a rotation that lasts at least six weeks seems to work by affording enough time to adapt one’s circadian dance to the situation.  There are those who prefer steady nights, but that breed is rare.  If we think adapting to factory work schedules is tough, we should look at those who work in the emergency room.  At least some of us have a scapegoat for tight trousers.


Blask DE.
Melatonin, sleep disturbance and cancer risk.
Sleep Med Rev. 2009 Aug;13(4):257-64. Epub 2008 Dec 17.

Costa G.
Shift work and breast cancer. 
G Ital Med Lav Ergon. 2010 Oct-Dec;32(4):454-7.

Esquirol Y, Bongard V, Mabile L, Jonnier B, Soulat JM, Perret B.
Shift work and metabolic syndrome: respective impacts of job strain, physical activity, and dietary rhythms.
Chronobiol Int. 2009 Apr;26(3):544-59.

Ferrie JE, Shipley MJ, Cappuccio FP, Brunner E, Miller MA, Kumari M, Marmot MG.
A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort.
Sleep. 2007 Dec;30(12):1659-66.

Ha M, Park J.
Shiftwork and metabolic risk factors of cardiovascular disease.
J Occup Health. 2005 Mar;47(2):89-95.

Hansen J.
Light at night, shiftwork, and breast cancer risk.
J Natl Cancer Inst. 2001 Oct 17;93(20):1513-5.

Institute for Work and Health (IWH)
Scientific Symposium, Toronto, 12 April, 2010
Scientific Symposium on the Health Effects of Shift Work

Karlsson B, Knutsson A, Lindahl B.
Is there an association between shift work and having a metabolic syndrome? Results from a population based study of 27,485 people.
Occup Environ Med. 2001 Nov;58(11):747-52.

Knower KC, To SQ, Takagi K, Miki Y, Sasano H, Simpson ER, Clyne CD.
Melatonin suppresses aromatase expression and activity in breast cancer associated fibroblasts.
Breast Cancer Res Treat. 2012 Jan 12.

Kroenke CH, Spiegelman D, Manson J, Schernhammer ES, Colditz GA, Kawachi I.
Work characteristics and incidence of type 2 diabetes in women.
Am J Epidemiol. 2007 Jan 15;165(2):175-83.

Morikawa Y, Nakagawa H, Miura K, Soyama Y, Ishizaki M, Kido T, Naruse Y, Suwazono Y, Nogawa K
Shift work and the risk of diabetes mellitus among Japanese male factory workers.
Scand J Work Environ Health. 2005 Jun;31(3):179-83.

Paul A. Schulte, PhD, Gregory R. Wagner, MD, Aleck Ostry, PhD, et al
Work, Obesity, and Occupational Safety and Health
American Journal of Public Health. Mar 2007; 97:3, 428-436

Pietroiusti A, Forlini A, Magrini A, Galante A, Coppeta L, Gemma G, Romeo E, Bergamaschi A.
Shift work increases the frequency of duodenal ulcer in H pylori infected workers.
Occup Environ Med. 2006 Nov;63(11):773-5.

Prasai MJ, George JT, Scott EM.
Molecular clocks, type 2 diabetes and cardiovascular disease.
Diab Vasc Dis Res. 2008 Jun;5(2):89-95.

Schernhammer ES, Laden F, Speizer FE, Willett WC, Hunter DJ, Kawachi I, Colditz GA.
Rotating night shifts and risk of breast cancer in women participating in the nurses’ health study.
J Natl Cancer Inst. 2001 Oct 17;93(20):1563-8.

Scott AJ.
Shift work and health.
Prim Care. 2000 Dec;27(4):1057-79.

Segawa K, Nakazawa S, Tsukamoto Y, Kurita Y, Goto H, Fukui A, Takano K.
Peptic ulcer is prevalent among shift workers.
Dig Dis Sci. 1987 May;32(5):449-53.

Shao T, Klein P, Grossbard ML.
Vitamin D and Breast Cancer.
Oncologist. 2012 Jan 10.

Suwazono Y, Sakata K, Okubo Y, Harada H, Oishi M, Kobayashi E, Uetani M, Kido T, Nogawa K.
Long-term longitudinal study on the relationship between alternating shift work and the onset of diabetes mellitus in male Japanese workers.
J Occup Environ Med. 2006 May;48(5):455-61.

Suwazono Y, Dochi M, Oishi M, Tanaka K, Kobayashi E, Sakata K.
Shiftwork and impaired glucose metabolism: a 14-year cohort study on 7104 male workers.
Chronobiol Int. 2009 Jul;26(5):926-41.

Trukova KP, Grutsch J, Lammersfeld C, Liepa G.
Prevalence of Vitamin D Insufficiency Among Breast Cancer Survivors.
Nutr Clin Pract. 2012 Jan 6.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Sleep and Weight

sleeping-manAhh, yes, that state of rest for body and soul.  It’s the time when will power and consciousness are suspended, and when body functions are mostly in neutral. Most sleep scientists agree that sleep has considerable value as a recuperative and adaptive function in humans.   Because it takes work for the body to maintain a constant temperature in an environment with temperature ranges, the eight-hour respite affords a chance to reconstitute cells and tissues.  While the body slows down, the brain, on the other hand, revs up its metabolic activity during the REM phase of sleep to get ready for the input of the next day.  Complicated stuff, for sure.

The negative consequences of too little sleep can rattle your chain with fanfare.  Falling asleep at the wheel is scary.  Falling off the pew in church is embarrassing.  Dozing during a business call gets expensive.  And being cranky all day gets you no favors.  But guess what.  Lack of sleep can make you fat, too.  Try to figure that out, since nobody eats when they’re asleep.  Do they?

Just because body functions slow down, it doesn’t mean they stop.  Hormones and other body chemicals are still at work.  Two of those, ghrelin and leptin, are responsible for turning appetite on and off, respectively.  Sleep deprivation seems to crank up the ghrelin and stimulate appetite.  When that happens, you crave more food while losing the sensitivity—or even the common sense—to know when to stop eating.  This problem could well be a circuitous matter:  does fatness cause lack of sleep or is it the other way around, or do they share a common factor?  Hmm.  Michael Breus, sleep researcher extraordinaire, addresses this conundrum in his recently published, “The Sleep Doctor’s Diet Plan:  Lose Weight Through Better Sleep” (Rodale, 2011).  And Dr. Marie-Pierre St-Onge, researcher at the New York Obesity Nutrition Research Center at St. Luke’s-Roosevelt Hospital, adds her expertise by pointing out that sleep-deprived people burn the same number of calories during the day as sound sleepers, but, she adds, eat about three hundred more calories a day.  Since there are 3500 calories in a pound, a person will add that pound to his repertoire in a little less than two weeks (St-Onge, 2011)

The interest in the association of lousy sleep to weight problems is international.  Even in Japan, there’s a St. Luke’s Hospital.  Here, doctors checked out more than 21,000 middle-aged guys’ sleep habits and compared them to individual body mass index, finding that the variability of sleep duration is related to weight gain.  And these participants thought that 6 hours’ sleep was enough (Kobayashi, 2012).  Guess they were wrong.  A year earlier, the same docs at the same hospital compared ~7-hour sleepers to ≤5-hour sleepers, and found weight gain and obesity in the deprived group.  It was interesting to note that there was little difference between the 7-hour and 8-hour subjects (Kobayashi, 2011).  The kicker in the 2011 study is that the investigators also found metabolic syndrome to be related to poor sleep (Kobayashi, Takahashi, et al 2011).

In experimentally-induced sleep loss, insulin sensitivity decreases without compensation in beta-cell function, resulting in impaired glucose tolerance and increased risk for diabetes.  Sleep loss down-regulates leptin function, lowers satiety, and up-regulates the appetite enhancing ghrelin.  Increased appetite = increased food intake=weight gain  (Morselli, 2010) (Chamorro, 2011).  Sleep fragmentation—waking every couple hours—causes daytime sleepiness (Mavanji, 2012). We need a study to show that?   In the valiant effort to revitalize, we turn to sugary foods in the hope they’ll provide bursts of energy lasting long enough to get us through the rest of the day.  Empty calories here.  And the energy high is soon followed by an almost audible crash.

With all the studies being performed in this area, you’d think somebody would be working on a remedy.  Maybe we already have one, but don’t know it.  Have you spoken to your doctor about poor sleep?  If you’d rather do it alone, consider a few simple steps.  Go to bed at the same time every night.  The body needs to know when to go to sleep.  Exercise a little bit every day.  That’ll reduce anxiety, one of the biggest reasons for poor sleep.  But don’t do it just before bed.  Do it a few hours beforehand.  If you’re a worrier, keep a journal.  That helps to identify things that aren’t likely to happen, anyway, so you don’t have to worry about them in the first place.  Try not to delay what needs to be done to prepare for the next day.  You’ll only add to the worry list.  Coffee will try to keep you awake for several hours after the last cup in the afternoon, so don’t drink any after, say, 2 or 3 o’clock.  Alcohol will not improve sleep.  It might make you fall asleep faster, but almost certainly will interrupt restorative sleep.  In the AM, drink water before anything else, and get fifteen minutes of sunlight to help reset your circadian clock.

Although the link between sleep loss and weight gain is convincing, the exact science behind the connection is to be determined.  You can always stay up all night and try to catch the leather fairy cutting your belt a little shorter.  Or you can try an alternative sleep aid, such as valerian, melatonin, or a hops sachet under your pillow.  But check with a healthcare professional before you embark.


Chamorro RA, Durán SA, Reyes SC, Ponce R, Algarín CR, Peirano PD.
[Sleep deprivation as a risk factor for obesity].  [Article in Spanish]
Rev Med Chil. 2011 Jul;139(7):932-40.

Knutson KL.
Does inadequate sleep play a role in vulnerability to obesity?
Am J Hum Biol. 2012 Jan 24. doi: 10.1002/ajhb.22219. [Epub ahead of print]

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Relation between metabolic syndrome and sleep duration in Japan: a large scale cross-sectional study.
Intern Med. 2011;50(2):103-7. Epub 2011 Jan 15.

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Association between weight gain, obesity, and sleep duration: a large-scale 3-year cohort study.
Sleep Breath. 2011 Sep 3. [Epub ahead of print]

Kobayashi D, Takahashi O, Deshpande GA, Shimbo T, Fukui T.
Association between weight gain, obesity, and sleep duration: a large-scale 3-year cohort study.
Sleep Breath. 2011 Sep 3. [Epub ahead of print]

Kobayashi D, Takahashi O, Shimbo T, Okubo T, Arioka H, Fukui T.
High sleep duration variability is an independent risk factor for weight gain.
Sleep Breath. 2012 Feb 22. [Epub ahead of print]

Mavanji V, Billington CJ, Kotz CM, Teske JA.
Sleep and obesity: a focus on animal models.
Neurosci Biobehav Rev. 2012 Mar;36(3):1015-29. Epub 2012 Jan 16.

Morselli L, Leproult R, Balbo M, Spiegel K
Role of sleep duration in the regulation of glucose metabolism and appetite.
Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):687-702.

Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.
Insufficient sleep undermines dietary efforts to reduce adiposity.
Ann Intern Med. 2010 Oct 5;153(7):435-41.

Patel SR, Malhotra A, White DP, Gottlieb DJ, Hu FB.
Association between reduced sleep and weight gain in women.
Am J Epidemiol. 2006 Nov 15;164(10):947-54. Epub 2006 Aug 16.

St-Onge MP, Roberts AL, Chen J, Kelleman M, O’Keeffe M, RoyChoudhury A, Jones PJ.
Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals.
Am J Clin Nutr. 2011 Aug;94(2):410-6.

St-Onge MP, McReynolds A, Trivedi ZB, Roberts AL, Sy M, Hirsch J.
Sleep restriction leads to increased activation of brain regions sensitive to food stimuli.
Am J Clin Nutr. 2012 Apr;95(4):818-24.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Sleep Deprivation may Lead to Impaired Insulin Response in Fat Cells

insomniaInsulin response? Huh? It’s just what it says, the way the body responds to insulin and the challenges that excite it in the first place. Insulin, as you recall, is a polypeptide hormone secreted by the islets of Langerhans in the pancreas. (A polypeptide, by the way, is made of two or more amino acids and becomes part of a protein.) Its job is to regulate metabolism of carbohydrates and fats, especially the conversion of glucose to glycogen, which lowers blood glucose levels. Glycogen is the chief carbohydrate storage material in animals, tucked nicely away mostly in the liver and partly in muscle, and can be liberated on demand. With insulin resistance the cells become less sensitive to the effects of insulin. If this happens, the pancreas is provoked to work harder and to release more of the hormone. Thus far, no disease is recognized, only a state wherein the body fails to respond. Sensitivity to insulin is widely different within the general population, so much so that the most insulin-sensitive people might be six times more so than those identified as most resistant. The prevalence of insulin resistance in the United States is about a fourth of the general population.

 The most common condition related to insulin resistance is obesity, now a public health concern in its own right and a risk factor for type 2 diabetes, hypertension, and coronary artery disease.  Losing weight increases the body’s sensitivity to insulin. Just a ten percent drop in weight can make a big difference. Of course, exercise enters the picture because it encourages the muscles to use glucose and gets rid of the spare tire. A high-fiber diet reduces levels of blood insulin and lowers risk of developing high blood pressure. Then there are drugs, decidedly the last resort. But there is now another factor that enters the scene, one to which we pay too little attention and take for granted—sleep, that marvelous cyclical event that restores body, mind and spirit.

A very recent study announced that fat cells need sleep as much as the cells in the brain.  Lack of sleep and limited sleep have a direct and harmful effect on fat, a state that could lead to major health issues, including obesity and type 2 diabetes by increasing risk for insulin resistance. Under conditions controlled for calorie intake and physical activity, subjects in a cross-over study (where they change places after an allotted time) were allowed 4.5 or 8.5 hours of sleep. Insulin response in the fat cells was measured afterward. It was found that response to insulin after sleep restriction was 30% lower, dropping fat cell function to that of an obese or diabetic person, despite being physically fit (Broussard, 2012). Because many of us are sleep deprived, this is a significant finding, portending obesity, diabetes and other metabolic concerns.

Fat, or adipose tissue, serves an important function as an energy depot, and also prevents body heat loss and provides an elastic padding between organs. Having a density of about 0.9 kilogram per liter compared to muscle’s 1.06 kg/L, fat will float quite easily. Weight loss does not automatically make fat cells disappear; they merely shrink, waiting to balloon again under the right conditions. Fat may even become an active organ that sends chemical signals to other parts of the body, possibly triggering sickness and disease (ACS, 2010). Two of those signalers are leptin, which controls appetite, and adiponectin, a protein hormone that regulates glucose and fatty acid catabolism.

A single night of sleep deprivation may evoke hepatic insulin resistance and decrease glucose disposal rate, thereby affecting peripheral insulin sensitivity and disturbing more than one metabolic pathway (Donga, 2010). This upset of energy balance likewise presages disease manifestations that include thyroid dysregulation and weight gain (Bosy-Westphal, 2008). Where does weight gain fit in here? It seems that sleep deprivation stimulates the activity of ghrelin, a hormone produced by stomach cells that turns hunger on. Leptin is its counterpart. A French analysis of sleep-deprived men noted their consumption of as much as twenty-two percent more calories on the day after sleep restriction than they did with ample sleep (Brondel, 2010). These reports demonstrate a link between sleep loss and risk for chronic disorders (Chamorro, 2011).

The feverish pitch of world citizenship compromises our sleeping hours.  Instead of the eight we need, many of us are lucky to see five or six. What used to be a complaint of college students has become a contagion that affects an increasing number of us.  Medications and defined sleep disorders aside, the time for sleep needs to be assigned and followed, lest we open the door to the unwelcomed guests that accompany deprivation. One of the simplest steps to restore the time for sleep is to learn to say “no” so you can eliminate the other gremlins of sleep loss that include acne, insomnia and a sensitive stomach.  If work worries keep you awake at night, look for ways to stop taking a fortune out of your bank of well-being, since renegade glucose metabolism is not a sweet deal.


ACS News Service Weekly PressPac: October 13, 2010
New evidence that fat cells are not just dormant storage depots for calories

Bosy-Westphal A, Hinrichs S, Jauch-Chara K, Hitze B, Later W, Wilms B, Settler U, Peters A, Kiosz D, Muller MJ.
Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women.
Obes Facts. 2008;1(5):266-73.

Brondel L, Romer MA, Nougues PM, Touyarou P, Davenne D.
Acute partial sleep deprivation increases food intake in healthy men.
Am J Clin Nutr. 2010 Jun;91(6):1550-9.

Broussard JL, Ehrmann DA, Van Cauter E, Tasali E, Brady MJ.
Impaired insulin signaling in human adipocytes after experimental sleep restriction: a randomized, crossover study.
Ann Intern Med. 2012 Oct 16;157(8):549-57.

Orfeu M. Buxton, Milena Pavlova, Emily W. Reid, Wei Wang, Donald C. Simonson, Gail K. Adler
Sleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men
Diabetes. Sep 23 2010;59(9):2126-2133.

Chamorro RA, Durán SA, Reyes SC, Ponce R, Algarín CR, Peirano PD.
Sleep deprivation as a risk factor for obesity
Rev Med Chil. 2011 Jul;139(7):932-40.

Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, Romijn JA.
A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8. Epub 2010 Apr 6.

Knutson KL, Van Cauter E.
Associations between sleep loss and increased risk of obesity and diabetes.
Ann N Y Acad Sci. 2008;1129:287-304.

Reynolds AC, Dorrian J, Liu PY, Van Dongen HP, Wittert GA, Harmer LJ, Banks S.
Impact of five nights of sleep restriction on glucose metabolism, leptin and testosterone in young adult men.
PLoS One. 2012;7(7):e41218. Epub 2012 Jul 23.

Sebastian M Schmid, Manfred Hallschmid, Kamila Jauch-Chara, Britta Wilms, Hendrik Lehnert, Jan Born, Bernd Schultes
Disturbed glucoregulatory response to food intake after moderate sleep restriction.
Sleep (impact factor: 5.05). 01/2011; 34(3):371-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Sweet Sweep of Sleep

sleepy-womanAhh, the sweet balm that soothes the nerves and restores the soul at the end of the day. Sadly, for some of us it is elusive, and its intangible rewards sporadic. Sleep. It can get interrupted, disrupted and corrupted. Even in its worst state, sleep can be the most desired gift for the time.

There have been thousands of sleep studies over the years, but science still isn’t completely sure why we need it. “Completely” is the key word. One goofy answer is that we sleep to cure sleepiness. It’s agreed that sleep gives the body a chance to rejuvenate. That we know about rapid eye movement sleep (REM) shows that sleep is not a totally static process for the brain. Asleep, it still needs calories. The amount of sleep a person needs is purely singular, and depends on his or her circadian rhythm, which is that twenty-four-hour cycle of biological activities that occur regularly and dependably regardless of illumination. What sleep experts look for are maximum melatonin levels and minimum core body temperature, reporting that one should be asleep at least six hours before lowest temp is achieved. When these occur just after the middle of the sleep cycle, the timing is deemed to be just right (Wyatt, 1999) (Dijk, 2002) (Taillard, 2011).

Too much sleep can be as unhealthy as too little. Where lack of sleep can increase the chance of accidents and CVD issues, a plethora might increase risk of other-cause mortality (Ferrie, 2007). Because animals with brains sleep, we might infer that it’s a needed pastime. Regardless of who and how much, the fact is that we heal better when we sleep, the immune system gets a chance to recoup, memory and cognitive function improve, and a general restoration takes place. And now there’s another reason to cut Z’s…the prevention of Alzheimer’s disease and related cognitive disorders.

Whether it’s more hypothetical than proven, a new study released by the University of Rochester hints that a good night’s sleep can ward off Alzheimer’s disease (Xie, 2013). Lead author, Maiken Nedergaard, notes that sleep serves a vital function, a collective term that includes washing debris out of the brain. The brain produces toxic waste as it works every day. This new study says that while we sleep the brain shrinks in size, allowing the spaces between brain cells to enlarge so that junk can be washed out by the cerebral spinal fluid that is pumped around it (Underwood, 2013).

Researchers in Nedergaard’s lab noticed that mice whose brains were probed while conscious would sometimes fall asleep. When that happened, cerebrospinal fluid would rush into the brain’s interstitial space and wash away cellular debris. Delving into the phenomenon, they observed that the brain’s glial cells, a web of connective tissue that supports neurons, expand during wakefulness to reduce the space between cells and shut off the movement of fluid. During sleep, the interstitial volume changes again.

Interstitial fluid is a solution that bathes the area around cells with a concoction that contains sugars, salts, fatty acids, amino acids, coenzymes, hormones, and neurotransmitters. Different areas of the body have different concentrations of these substances. Little attention was paid to the area between cells before Nedergaard’s investigation because that was considered just space (Herculano-Houzel, 2013).  The brain’s drainage system was termed the glymphatic system, a functional waste management setup that removes extracellular proteins and metabolic waste products from the pathway, but reliant upon the glia instead of a dedicated, albeit absent, lymphatic network.

To double-check their findings, scientists injected the mouse brains with proteins that parallel those implicated in Alzheimer’s disease (AD)—the amyloids. These were washed away faster from the brains of sleeping mice than their awake peers. It is the accumulation of these soluble proteins at the synapses that is believed by some to initiate the disease (Tomiyama, 2010) (Esparza, 2013).

Fragmented sleep is that which does not include much slow-wave sleep and is not refreshing. Total time asleep is less than normal, affecting about a third of all adults. Unfragmented-consolidated sleep is divided into two periods with a gap between. This “bi-phasic” sleep is common and is something people can adjust to. Fragmented sleep is characteristic of Alzheimer’s and Parkinson’s patients, though it is common to the aging process. However, there is debate about whether increased fragmentation is a normal part of aging or indicative of an underlying pathology. Regardless, it is associated with cognitive performance (Lim, 2013). In any case, it’s unpleasant to experience the next day’s sleepiness. There are pharmaceutical sleep aids, but the natural ones, such as valerian and melatonin, are safer.

Melatonin is produced in the brain, but decreases with age and in those with Alzheimer’s disease. There are data from clinical trials demonstrating that melatonin can slow the progression of cognitive impairment in AD patients by protecting neural cells from amyloid-mediated toxicity and by arresting the formation of plaques in the first place (Lin, 2013). As a noted anti-oxidant, melatonin is able to scavenge the free radicals that are likewise implicated in AD etiology (He, 2010), and to improve mitochondrial energy metabolism (Cheng, 2006) (Liu, 2013). Produced in the pineal gland from tryptophan, melatonin, as a sleep aid, lowers body temperature and blood pressure, a condition required for sound sleep.

If sleep can clear the abnormal accumulation of neurotoxins (Rothman, 2012), and if melatonin can help resolve dysfunctional sleep patterns, then this bag of ideas might just hold more than water.


Orfeu M. Buxton, Sean W. Cain, Shawn P. O’Connor, James H. Porter, Jeanne F. Duffy,
Wei Wang, Charles A. Czeisler and Steven A. Shea
Adverse Metabolic Consequences in Humans of Prolonged Sleep Restriction Combined with Circadian Disruption
Sci Transl Med. 11 April 2012; Vol. 4 Issue 129: p. 129ra43

Cheng Y, Feng Z, Zhang QZ, Zhang JT.
Beneficial effects of melatonin in experimental models of Alzheimer disease.
Acta Pharmacol Sin. 2006 Feb;27(2):129-39.

Daniel A. Cohen, Wei Wang, James K. Wyatt, Richard E. Kronauer, Derk-Jan Dijk, Charles A. Czeisler and Elizabeth B. Klerman
Uncovering Residual Effects of Chronic Sleep Loss on Human Performance
Sci Transl Med. 13 January 2010; Vol. 2 Issue 14: p. 14ra3

Dijk DJ, Lockley SW.
Integration of human sleep-wake regulation and circadian rhythmicity.
J Appl Physiol. 2002 Feb;92(2):852-62.

Dragicevic N, Copes N, O’Neal-Moffitt G, Jin J, Buzzeo R, Mamcarz M, Tan J, Cao C, Olcese JM, Arendash GW, Bradshaw PC.
Melatonin treatment restores mitochondrial function in Alzheimer’s mice: a mitochondrial protective role of melatonin membrane receptor signaling.
J Pineal Res. 2011 Aug;51(1):75-86.

Dragicevic N, Smith A, Lin X, Yuan F, Copes N, Delic V, Tan J, Cao C, Shytle RD, Bradshaw PC.
Green tea epigallocatechin-3-gallate (EGCG) and other flavonoids reduce Alzheimer’s amyloid-induced mitochondrial dysfunction.
J Alzheimers Dis. 2011;26(3):507-21.

Dragicevic N, Delic V, Cao C, Copes N, Lin X, Mamcarz M, Wang L, Arendash GW, Bradshaw PC.
Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer’s mice and cells.
Neuropharmacology. 2012 Dec;63(8):1368-79.

Esparza TJ, Zhao H, Cirrito JR, Cairns NJ, Bateman RJ, Holtzman DM, Brody DL.
Amyloid-β oligomerization in Alzheimer dementia versus high-pathology controls.
Ann Neurol. 2013 Jan;73(1):104-19.

Ferrie JE, Shipley MJ, Cappuccio FP, Brunner E, Miller MA, Kumari M, Marmot MG.
A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort.
Sleep. 2007 Dec;30(12):1659-66.

He H, Dong W, Huang F.
Anti-amyloidogenic and anti-apoptotic role of melatonin in Alzheimer disease.
Curr Neuropharmacol. 2010 Sep;8(3):211-7.

Suzana Herculano-Houzel
Sleep It Out
Science. 18 October 2013; Vol. 342 no. 6156: pp. 316-317

Huang Y, Potter R, Sigurdson W, Santacruz A, Shih S, Ju YE, Kasten T, Morris JC,
Effects of age and amyloid deposition on Aβ dynamics in the human central nervous system.
Arch Neurol. 2012 Jan;69(1):51-8.

Jáuregui-Barrutia A, Tijero-Merino B, Gómez-Esteban JC, Zarranz JJ.
Sleep disorders in Parkinson’s disease: REM sleep behaviour disorder and restless legs syndrome.
Rev Neurol. 2010 Feb 8;50 Suppl 2:S15-9.

Ju YE, McLeland JS, Toedebusch CD, Xiong C, Fagan AM, Duntley SP, Morris JC, Holtzman DM
Sleep quality and preclinical Alzheimer disease.
JAMA Neurol. 2013 May;70(5):587-93.

Lee JW, Lee YK, Ban JO, Ha TY, Yun YP, Han SB, Oh KW, Hong JT.
Green tea (-)-epigallocatechin-3-gallate inhibits beta-amyloid-induced cognitive dysfunction through modification of secretase activity via inhibition of ERK and NF-kappaB pathways in mice.
J Nutr. 2009 Oct;139(10):1987-93.

Lim AS, Kowgier M, Yu L, Buchman AS, Bennett DA.
Sleep Fragmentation and the Risk of Incident Alzheimer’s Disease and Cognitive Decline in Older Persons.
Sleep. 2013 Jul 1;36(7):1027-1032.

Lin L, Huang QX, Yang SS, Chu J, Wang JZ, Tian Q.
Melatonin in Alzheimer’s disease.
Int J Mol Sci. 2013 Jul 12;14(7):14575-93.

Liu XJ, Yuan L, Yang D, Han WN, Li QS, Yang W, Liu QS, Qi JS.
Melatonin protects against amyloid-β-induced impairments of hippocampal LTP and spatial learning in rats.
Synapse. 2013 Sep;67(9):626-36.

Ni C, Tan G, Luo A, Qian M, Tang Y, Zhou Y, Wang J, Li M, Zhang Y, Jia D, Wu C, Guo X.
Melatonin premedication attenuates isoflurane anesthesia-induced β-amyloid generation and cholinergic dysfunction in the hippocampus of aged rats.
Int J Neurosci. 2013 Apr;123(4):213-20.

Rothman SM, Mattson MP.
Sleep disturbances in Alzheimer’s and Parkinson’s diseases.
Neuromolecular Med. 2012 Sep;14(3):194-204.

Taillard J, Philip P, Claustrat B, Capelli A, Coste O, Chaumet G, Sagaspe P.
Time course of neurobehavioral alertness during extended wakefulness in morning- and evening-type healthy sleepers.
Chronobiol Int. 2011 Jul;28(6):520-7.

Tomiyama T.
Involvement of beta-amyloid in the etiology of Alzheimer’s disease
Brain Nerve. 2010 Jul;62(7):691-9.

Emily Underwood
Sleep: The Brain’s Housekeeper?
Science. 18 October 2013; Vol. 342 no. 6156: p. 301

Wyatt JK, Ritz-De Cecco A, Czeisler CA, Dijk DJ.
Circadian temperature and melatonin rhythms, sleep, and neurobehavioral function in humans living on a 20-h day.
Am J Physiol. 1999 Oct;277(4 Pt 2):R1152-63.

Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T, Deane R, Nedergaard M.
Sleep drives metabolite clearance from the adult brain.
Science. 2013 Oct 18;342(6156):373-7.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.