Seeing Earth's Magnetic Fields: Cryptochromes and Blue Light

Birds Can See Earth's Magnetic Fields -- And We Finally Know How That's Possible

By Michelle Starr

The mystery behind how birds navigate might finally be solved: it's not the iron in their beaks providing a magnetic compass, but a newly discovered protein in their eyes that lets them "see" Earth's magnetic fields.

These findings come courtesy of two new papers -- one studying robins, the other zebra finches.

The eye protein is called "Cry4," and it's part of a class of proteins called "cryptochromes" -- photoreceptors sensitive to blue light, found in both plants and animals. These proteins play a role in regulating circadian rhythms.

There's also been evidence in recent years that, in birds, the cryptochromes in their eyes are responsible for their ability to orient themselves by detecting magnetic fields, a sense called "magneto-reception."

We know that birds can only sense magnetic fields if certain wavelengths of light are available -- specifically, studies have shown that avian magneto-reception seems dependent on blue light.

This seems to confirm that the mechanism is a visual one, based in the cryptochromes, which may be able to detect the fields because of "quantum coherence."

To find more clues on these cryptochromes, two teams of biologists set to work. Researchers from Lund University in Sweden studied zebra finches, and researchers from the Carl von Ossietzky University Oldenburg in Germany studied European robins.

The Lund team measured gene expression of three cryptochromes, Cry1, Cry2, and Cry4, in the brains, muscles and eyes of zebra finches. Their hypothesis was that the cryptochromes associated with magnetoreception should maintain constant reception over the circadian day.

They found that, as expected for circadian clock genes, Cry1 and Cry2 fluctuated daily -- but Cry4 expressed at constant levels, making it the most likely candidate for magnetoreception.

This finding was supported by the robin study, which found the same thing.

"We also found that Cry1a, Cry1b, and Cry2 mRNA display robust circadian oscillation patterns, whereas Cry4 shows only a weak circadian oscillation," the researchers wrote.

But they made a couple of other interesting findings, too. The first is that Cry4 is clustered in a region of the retina that receives a lot of light -- which makes sense for light-dependent magnetoreception.

The other is that European robins have increased Cry4 expression during the migratory season, compared to non-migratory chickens.

Both sets of researchers caution that more research is needed before Cry4 can be declared the protein responsible for magnetoreception.

The evidence is strong, but it's not definitive, and both Cry1 and Cry2 have also been implicated in magnetoreception, the former in garden warblers and the latter in fruit flies.

Observing birds with non-functioning Cry4 could help confirm the role it seems to play, while other studies will be needed to figure Cry1's role.

So what does a bird actually see? Well, we can't ever know what the world looks like through another species' eyes, but we can take a very strong guess.

According to researchers at the Theoretical and Computational Biophysics group at the University of Illinois at Urbana-Champaign, whose researcher Klaus Schulten first predicted magnetoreceptive cryptochromes in 1978, they could provide a magnetic field "filter" over the bird's field of view (like in the picture above).

The zebra finch study was published in the "Journal of the Royal Society Interface," and the robin study was published in "Current Biology."

Devices, Not Drugs: Part I: Sleep Disorders: A Personal Report

by Don Mangus

Here’s a start on my one-man, anecdotal report on all the devices, esoteric research, and alternative treatments I’ve explored over the last year or three.

I feel that technological, dietary, lifestyle, and mind/body treatments for physical and mental health ailments and syndromes are the preferred way to go -- whenever possible. They are underutilized, IMHO.

Why take a drug or risk an operation if you can treat an existing problem treatable with a device? There will likely be fewer harmful or irreversible side-effect/complications, or dangerous drug interactions, with the added benefits of lower cost, and most likely, less pain.

It seems likely that many of our modern health problems are really  the result of our modern lifestyle outstripping the adaptations of our biological evolution.

For instance -- it may be more common and natural for many folks to sleep at several night/day periods during the natural rise and fall of circadian rhythm/hormonal cycles rather than to force the entire sleep experience into a solid, compressed eight-hour block.

This modern-day, Western concept may be simply a cultural result of trying to squeeze more productivity out of post-Industrial Revolution workers. The same goes for the electric light, which artificially extended our wakeful hours. It’s been reported that Thomas Edison deplored sleep as “wasted time.”

Likewise, it seems our sympathetic nervous system has remained at a stage of evolution adapted for quick bursts of “fight or flight” responses to survive the short-term dangers of the Paleolithic Era, rather than the chronic situational stresses common to our modern workplace -- never-ending deadlines, societal pressures, anxiety-producing forcasts of impending crises – as well as just plain old over-stimulation of our senses and minds.

So…away we go...

Sleep Devices:

I suffer with Obstructive Sleep Apnea. This sleep disorder is best treated by the “gold standard” of medical devices -- the Continuous Positive Airway Pressure (CPAP) machine. Before I treated this pernicious condition eleven years ago, I was at my wit’s end.

I'd advise my fellow sufferers to avoid painful throat operations or oral jaw-jacking appliances, and to favor the CPAP instead. However, one way or another, the condition should be treated and never ignored.

Not treating chronic OSA can lead to heart damage or even sudden death from arrhythmia-induced cardiac arrest -- so it should be treated. OSA is a very common problem for the general public, and the real money-maker for sleep clinics, and thus easily diagnosed and treated.

Chronic Insomnia is a much, much more difficult condition to treat. I was nearly done-in by a month-long bought of chronic insomnia, and finally had to be hospitalized due to such complications as severe anxiety, depression, , and finally, ceaseless ruminations of suicide. That’s how bad it got. I can fully empathize with the tragic consequences of the sleep-deprived desperation exhibited such celebrities as Michael Jackson, Whitney Houston, and Heath Ledger.

It took two weeks of nightly experiments with various formulations/combinations of heavy-duty “drug cocktails” to stabilize my sleep and mood. Although the intervention worked, these meds are troublesome, and should only be used short-term if possible. I titrated myself off them as much and as soon as possible.

If you have to take them -- you have to -- but there’s a long-term price to pay. From personal experience, I’d strongly recommend avoiding two especially troublesome meds -- Ambien and Zyprexa, if at all possible.

However, if you find yourself suffering from such extreme symptoms as I did, hospitalization is a great idea – it sped up the healing process and the intervention should be considered a necessary Emergency Room situation. Don’t try to “tough it out” or go it alone. Reach out for help.

A Few Things I’ve Learned Along the Way

Natural Supplements: For mild cases of temporary insomnia -- melatonin, valerian root, and l-theanine supplements may help.

Sleep hygiene: it might help in bad-habit or “conditioned” cases. Among the key concepts to try are: a quiet environment (use ear plugs or a “white noise” machine), room and body temperature, and total darkness (use an eye mask).

Also, avoid caffeine, alcohol, exercise, and food too close to bedtime. Avoid over-stimulation from such situations as emotional phone calls, and excessive ruminations about the day’s events or tomorrow’s plans.

Another good trick is to take a warm bath prior to getting into bed. As the body’s temperature cools down, it’s easier to fall asleep.

These CBT techniques work best for very minor, temporary insomnia.

The Effects of Colored Light on Circadian Rhythms, the Light-Dark Cycle, and Melatonin Release:

There’s a theory that “light pollution” profoundly disrupts the natural circadian rhythms/body clock and thus the body’s release of melatonin.

I’m a believer that this theory is very, very valid.

Exposure to bright sunlight for 25 minutes in the morning exposes the body to “blue part” of the light spectrum which inhibits the release of melatonin, and also helps set the natural wake/sleep cycle.

On a side note, on cloudy days -- or for those suffering a bout of Seasonal Affect Disorder (SAD) -- exposure to artificial light from a special blue-light lamp can sometimes bring relief.

I’ve experimented with wearing blue-lensed glasses in the early morning to enhance my wakefulness. These glasses also seem to have an added calming effect on my mood. Although they may make you appear to be a hipster or jazzman, they do seem to be very effective for me.

The biggest factor though, is that later in the evening and night, we subject ourselves to artificial “light pollution” from electric lights, TV screens, computer monitors, light-emitting diodes, etc.

The thing to do here, in the early evening, is to don “blue-blocker” sunglasses (orange or amber colored lenses) which simulate darkness to the body and signal the circadian rhythms to begin a release of melatonin.

I put my “blue-blockers” on when I come home from work, and wear them while using my computer, tablet, reading, and watching TV. They simulate a perpetual sunset.

When I wake in the middle of the night, I also wear them while I read. This very simple device prevents “over-stimulation” from “full-spectrum, white electric light,” and makes it much, much easier to drift back to sleep. I can’t recommend them highly enough for insomniacs.

 What a simple solution – so much better than hypnotic drugs.

An Endorsement of Naps: I love to take an afternoon nap when I can. The best time is naturally, from noon to 3:30 PM. This is the time of a natural lull in alertness in our circadian cycle, but “power napping” is much discouraged by most modern Western work schedules.

I’d nap every day if I could.

More on my other experiments with devices and supplements, later.

Devices, Not Drugs: Orange Glasses

Great Sleep! Reduced Cancer!: A Scientific Approach to Great Sleep and Reduced Cancer Risk by Richard L. Hansler


In 2001 it was discovered that it is only the blue component in ordinary white light that causes melatonin suppression.

Melatonin is the hormone that promotes sleep and is a powerful cancer fighter. This book traces the story of how research with animals and humans has demonstrated the health benefits of long periods of darkness that maximize melatonin.

By blocking just the blue light a condition of “virtual darkness” allows enjoyment of normal evening activities while maximizing melatonin flow. The benefits go far beyond better sleep and reducing cancer risk. They include helping to avoid postpartum depression, improving symptoms of ADHD, and helping to stabilize mood in patients with bipolar disorder.

Amazon Customer Reviews

Light and our Lives November 25, 2008
By Rebecca E. Hutchins

As a behavioral optometrist who has long been fascinated by the non-visual portion of the optic nerve, and who recently learned about melanopsin and its implications, this book was meant for me to read. It has an incredible amount of information not readily available on the effects of light at night on our health. The author worked for 40-some years in the lighting industry, and is now concerned enough about the implications of light in insomnia and cancer that he is attempting to find a way to address some of the issues with the use of blue-blocking lenses. I did purchase two pair from the website to compare with those that we use in our office, and found the tint a little hard to handle personally, but I think the topic is a timely and important one, and it is well-handled in this book. I am beginning to believe that Light Pollution and Light at Night may be almost as big an issue to our survival as Global Warming.

Blue light, melatonin, quality of sleep and antioxidant properties April 18, 2012
By J. Duncan

Interesting info on light, the blue spectrum in particular, and how it affects (delays) the start of melatonin production, which affects the onset of sleep. Contains several ideas on how to reduce exposure to blue light, at what times you should consider this, and how even slight exposures late at night (or during the night) can still interfere. UVEX glasses are a cost-effective way to start.

Not sure how - but it works March 24, 2013
By IUS Jan

Dr. Oz promoted this on his television show. I bought the book and the glasses. I am amazed but if you remember to use them (especially if you are on the computer at night) the technologies works. I get drowsy faster and when I go to bed I fall asleep more quickly. I am a believer.

Excerpts From: Clocks, Genes and Sleep

Core components of the circadian transcriptional clock. Brain-and muscle ARNT-like protein (BMAL1) heterodimerizes with CLOCK protein to bind E-box motifs in the promoter regions of downstream target genes, such as Period (Per 1,2) and Cryptochrome (Cry1,2) genes. PERIOD proteins (PERs) heterodimerize with CRYPTOCHROME proteins (CRYs) in order to inhibit CLOCK:BMAL1, thus closing an autoregulatory negative-feedback loop. Blocking activity of CLOCK:BMAL1 in Bmal1 knock-out mice disrupts normal circadian rhythms, and increases reactive-oxygen species (ROS), while concomitantly decreasing memory and lifespan. Circadian clock output regulates a variety of biological and physiological processes, including circadian rhythms, metabolism, learning and memory, ROS/reactive nitrogen species (RNS) homeostasis, aging and longevity, and the cell cycle.

by Malcolm von Schantz, PhD and Simon N Archer, PhD. Journal of the Royal Society of Medicine, Oct. 2003

Genes and Molecules

Information on how circadian rhythms are generated at molecular level comes mainly from studies in mice. The mechanism depends on tightly controlled concerted coexpression of specific clock genes.

Most of these genes are remarkably conserved amongst coelomates — including insects, molluscs and vertebrates — although the precise roles of specific components have drifted during evolution.

At the center of the machinery in mammals are the Period (Per1, Per2 and Per3) and Cryptochrome (Cry1 and Cry2) genes. The protein products of all these oscillate over the 24-hour cycle by inhibiting their own promoters operating in an intricate negative feedback loop.

Sleep Disorders

Sleep has famously been described as being ‘of the brain, by the brain, and for the brain’. Its relation to the circadian clock is less simple to describe. Some disorders of sleep are unrelated to circadian rhythms; others are undoubtedly related to it, particularly the advanced and delayed sleep phase syndromes. In these conditions, sleep occurs either abnormally early or abnormally late. This could theoretically be caused either by an abnormal τ or by abnormal timing of the sleep phase within a circadian cycle of normal periodicity.

Polymorphisms in clock genes can be related to circadian parameters, and the most famous finding so far is a large family where advanced sleep phase syndrome seems to be inherited as a single-gene defect. The condition manifests itself in this family with advanced melatonin, temperature, and sleep/wake rhythms co-segregating with a missense mutation in the Per2 gene. Because of the non-homologous aminoacid substitution, the resulting PER2 protein is phosphorylated less efficiently by casein kinase than the native one—an observation that offers a satisfying mechanistic explanation for the similarity between this phenotype and that of the τ hamster, whose missense mutation in casein kinase I ε results in essentially the same net effect.

Morning and Eveening Preferences

The gene associated with evening preference that has produced the most interesting results to date in humans is Per3. In a Japanese population, Ebisawa and colleagues reported that a rare single-nucleotide polymorphism causing an aminoacid substitution correlated with delayed sleep phase syndrome.

Our laboratory has studied a more dramatic genetic polymorphism, initially described but not characterized in Ebisawa's paper, encoding an 18-aminoacid tandem repeat sequence, of which humans have either four or five successive copies in each of their Per3 alleles.

By comparing HO-characterized subjects whose scores were around the mean for their gender and age group with those with extreme evening and morning preference, we were able to distinguish an excess p+revalence of the shorter repeat allele in subjects with extreme evening preference. Extending the study to a cohort of patients with delayed sleep phase syndrome, we showed that the association with the shorter allele was even stronger in this population. Thus, although no physiological studies have formally linked the extremes of evening preference and/or long τ with delayed sleep phase syndrome, it would appear from the convergence of their Per3 genotype that such a study is not only worthwhile but long overdue.

Conclusion

In man, the known human clock gene differences appear merely to predict a greater or lesser propensity.

One reason for this difference is that most of the mouse models studied so far have been engineered to abolish the function of a specific gene, rather than carrying a more or less altered form of it. Another is that laboratory rodent strains are highly inbred and thus much more homogeneous with respect to all other clock genes.

The human circadian genotype, being a polygenic trait, is more akin to a hand of cards. Most of us will have a hand containing average cards or a balanced mixture of high and low ones. Only the hands that contain predominantly low or high cards will stand out.

The great majority of us function normally with our allotted circadian phenotype and its interaction with our environment, much as we are able to deal with other aspects of our genetic inheritance.

But the minority who have been dealt a dud hand of the clock genes card game deserve more sympathy and clinical help than they are often accorded.

Our culture trends to associate early waking with virtue and industry, and late sleeping with vice and lassitude. Lack of conformity with this norm is not always a matter of choice: clearly, some people are genetically programmed for an extreme diurnal preference.

Read the whole article at:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC544627/

Excerpts From: Genetic Analysis of Sleep

Genetic Analysis of Sleep

by Amanda Crocker and Amita Sehgal, Howard Hughes Medical Institute, Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia

Almost 20 years ago, the gene underlying fatal familial insomnia was discovered, and first suggested the concept that a single gene can regulate sleep. In the two decades since, there have been many advances in the field of behavioral genetics, but it is only in the past 10 years that the genetic analysis of sleep has emerged as an important discipline.

Major findings include the discovery of a single gene underlying the sleep disorder narcolepsy, and identification of loci that make quantitative contributions to sleep characteristics. The sleep field has also expanded its focus from mammalian model organisms to Drosophila, zebrafish, and worms, which is allowing the application of novel genetic approaches.

Researchers have undertaken large-scale screens to identify new genes that regulate sleep, and are also probing questions of sleep circuitry and sleep function on a molecular level. As genetic tools continue to be refined in each model organism, the genes that support a specific function in sleep will become more apparent. Thus, while our understanding of sleep still remains rudimentary, rapid progress is expected from these recently initiated studies.

The recognition that sleep may be regulated by conserved genetic mechanisms has not yet led to a unified understanding of it. A closely related process—the generation of circadian rhythms—is now explained on the basis of a universal model, largely because of mechanistic studies done in phylogentically very diverse organisms.

If there is a specific neurotransmitter for sleep, it is still hypothetical. Thus, sleep does not appear to be controlled by a singe locus or dedicated genes. It is better understood as a broad system-wide phenomenon.

Hypotheses for sleep include somatic theories (healing of the body and other endocrine functions), cellular metabolic theories (removal of reactive oxidative species and energy replenishment), brain-specific functions such as synaptic plasticity (in adults, this would underlie memory consolidation), or synaptic downscaling.

Genetics provides a new way to address the regulation and function of sleep. While for the past 20 years genetics has been used primarily to verify lesion and pharmacological studies through targeted gene approaches, it can now be used to probe more intricate questions in sleep.

Identification of genes required for sleep homeostasis

The big question remains: Why do we sleep? There is now the growing sense that the function of sleep may fall out of its molecular analysis. Since few sleep-regulating molecules are known, studies are under way to identify novel genes required for sleep. These studies include forward genetic screens as well as genetic manipulation of candidate genes, by focusing on changes in sleep amount as a readout of sleep homeostasis.

Sleep and metabolism
There have long been theories that sleep is important for metabolism (Benington and Heller 1995). This is supported by the potential role for adenosine, and by reports showing associations between glycogen levels and sleep. In addition, there appears to be anatomic overlap in the regulation of sleep and metabolism.

More recently, genes important for dealing with cellular stress have been implicated in sleep regulation. Through both differential expression profiles and targeted gene approaches, the gene Bip is implicated as a sleep-promoting factor. Bip is important for the unfolded protein response in the endoplasmic reticulum (ER), and is up-regulated following periods of sleep deprivation in mice (Cirelli et al. 2005b). In addition, flies with altered Bip levels show changes in their homeostatic response to sleep deprivation.

Genes important for synaptic modulation

One of the current hypotheses for why we sleep is that it allows for, or even promotes, synaptic downscaling (Tononi and Cirelli 2006). This hypothesis is based on the presumption that, during wakefulness, the interaction of animals with their environment leads to the strengthening of some synapses, while others remain the same. It postulates that synaptic downscaling during sleep promotes efficiency in terms of energy and space, while maintaining the relative ratios of the strength of synapses. This hypothesis has been supported in recent years by differential expression studies of genes whose expression changes with sleep/wake state.

Genes involved in learning and memory

In both mice and flies, many genes important for learning and memory have been targeted for sleep analysis. These include, but are not limited to, CREB, protein kinase A (PKA), cAMP, ERK, cGMP, and some of the ion channels.

Conclusion

Genetics can tell us a lot about what sleep does for organisms, but the potential of this approach has only just started to be recognized in the sleep field. With the generation of conditional and anatomically restricted knockouts (or knock-ins) in mice, we are on the verge of answering many questions.

These include determining the roles of adenosine and BDNF in sleep and memory. In flies, anatomically and/or temporally restricted expression of sleep-regulating transgenes has already been performed.

These approaches have provided great insight into the role of specific signaling pathways in sleep. In the future, this technology will be used to rescue sleep mutants in a region-specific manner, although some of these mutations, such as in ion channels, may turn out to have global effects that cannot be rescued in specific areas.

However, the real power of the fly, worm, and fish models lies in their amenability to unbiased genetic screens. With a process like sleep, about which little is known, we suggest that the best approach is one that is not associated with any preconceived assumptions,

At this point, there is no evidence that a single gene, or subset of genes, acting in a specific subset of neurons is responsible for sleep.

It is more likely that sleep is a network phenomenon. It is also likely that there will be many hypotheses for why we sleep and strong evidence for each, since many of the neurotransmitters and signaling pathways that keep us awake serve other functions.

For instance, orexin is apparently involved in both feeding behavior and maintaining wakefulness. Sleep deprivation results in several impaired processes, some of which may turn out to reflect consequences of increased wakefulness rather than indicating an actual function of sleep.

With the advancement of new genetic tools, it is likely that we will soon see experiments directly testing some of these hypotheses, such as cellular metabolic function and synaptic scaling.

From the data discussed in this review, it is likely that sleep is important for overall homeostatic regulation of the entire organism, possibly down to within-the-cell homeostasis.

It is clear that sleep is a very basic process, and that studying it in model organisms will provide significant insight into why we sleep. In general, advances in genetics in all model organisms will provide a wealth of knowledge for the sleep field in the coming years.

For more detail, read the entire article, as it originally appeared, at:

http://genesdev.cshlp.org/content/24/12/1220.full

Sleep Disturbance Linked to Aging Eye Lens

Bring on the Blues -- Light Therapy! I ordered one of these devices on Amazon to give it a shot!

 

 

Philips goLITE BLU Light Therapy Device

 

 

 

 

By Charles Bankhead, Staff Writer, MedPage Today

Published: September 06, 2011

 

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner

Action Points

• Explain that sleep disturbance correlated significantly with reduced blue light transmission to the retina resulting from aging and yellowing of the lens.
• Point out that the odds of sleep disturbance also increased significantly with the extent of autofluorescence, a measure of lens transmission and yellowing.

Sleep disturbance correlated significantly with reduced blue light transmission to the retina resulting from aging and yellowing of the lens, Danish investigators reported.

Every one% increase in blue light lens transmission reduced the odds of sleep disturbance by five%. The association was similar across age groups and remained significant after controlling for a variety of potential confounders, as reported in the September issue of Sleep.

"To translate the odds ratios into a clinical example, a 50-year-old, nonsmoking, nondiabetic female with a low risk of ischemic heart disease who was in the 97.5% upper normal range of blue light lens transmission ... had a risk of sleep disturbances of 16.4%," Line Kessel, MD, PhD, of Glostrup Hospital and the University of Copenhagen, and co-authors wrote.

"[In contrast] a similar ... 50-year-old female who was in the 2.5% lower normal range of blue light lens transmission ... had a risk of having sleep disturbances of 37.9%."

The odds of sleep disturbance also increased significantly with the extent of autofluorescence, a measure of lens transmission and yellowing.

Regulation of sleep patterns and circadian rhythms occurs through the retinohypothalamic tract in response to stimulation of retinal ganglions, primarily by blue light.

With aging, the lens acquires a yellowish discoloration from accumulation of chromophores that preferentially absorb in the short wavelength region of the light spectrum. The authors hypothesized that lens yellowing might act as a filter for blue light in older people, who are more prone to sleep disturbance.

"Theoretically, the aging process of the lens of the eye may be an important causative factor in sleep disorders," the authors wrote.

To examine the relationship between lens aging and sleep disturbance, investigators recruited participants from an ongoing epidemiologic study (Inter99 Eye Study) of associations between ophthalmic parameters and health.

The study of lens aging and sleep disturbance involved 970 people, ages 30 to 60. The study population consisted of 142 participants with a high risk of ischemic heart disease, 107 with newly diagnosed type 2 diabetes, 11 participants with a history of diabetes, 147 participants with impaired glucose tolerance, and a miscellaneous group of 61 participants. The control group had 502 participants.

Investigators assessed sleep disturbance by means of questionnaires and prescriptions for sleeping medications. Lens aging was determined by autofluorometry. Sleep disturbance was defined as answering "yes" to "having trouble sleeping and/or purchasing a sleep medication in the past year."

Overall, the prevalence of sleep disturbance was 24.4%. and more than 80% of participants with sleep disturbances said the problem occurred frequently and required treatment with sleep medication. The prevalence ranged from a high of 32.5% of participants, ages 55 to 60, to a low of 15.7% in participants ages 30 to 35 (P=0.0002).

Sleep disturbance affected women more often than men (32.2% versus 18.4%, P<0.0001). It also was more common in participants with diabetes (30.7% versus 22.5% for normoglycemic individuals, P=0.016) and smokers (28.6% versus 21.0% of nonsmokers, P=0.007).

The inverse association between sleep disturbance and blue light lens transmission was represented by an odds ratio (OR) of 0.95 per 1% increase in lens transmission (95% CI 0.93 to 0.97, P<0.0001).

Adjustment for age, sex, diabetes, smoking, and risk of ischemic heart disease resulted in an OR of 0.97 (95% CI 0.95 to 0.99, P=0.016).

The findings are consistent with the hypothesis that decreased blue light transmission reduces stimulation of retinal ganglions containing melanopsin, which has a key role in photoentrainment of circadian rhythms.

"Melanopsin is stimulated by predominantly blue light with a maximum absorption around 480 nm in humans, the very part of the visible spectrum that is mostly affected by the aging process of the human lens," the authors wrote.

"The results of the present study indicate that the spectral characteristics of the light reaching the retina, and specifically the total amount of blue light that penetrates the refractive media of the eye, may have a profound impact on sleep quality, most likely mediated via reduced ocular photic regulation of melatonin secretion," they added.

"Our results support that choosing the right indoor lighting conditions may have a beneficial effect on sleep and that blue light therapy might be used to modulate circadian sleep disorders," they concluded.

The study had some limitations including the risk that some patients were misclassified because sleeping medication may be used for other conditions, such as benzodiazepines for anxiety.

The study received no industry support, and the authors had no relevant disclosures.

Primary source: Sleep
Source reference:
Kessel L, et al "Sleep disturbances are related to decreased transmission of blue light to the retina caused by lens yellowing" Sleep 2011; 34: 1215-1219.

Paul Spector M.D.: Being in the Dark Is a Good Thing: Darkness and Disease

You don't hear much about light pollution. And when you do, it's usually a story about wildlife or greenhouse gases or stargazing. That's about to change.

Recent research has drawn a connection between dim light exposure at night and depression. T
he investigators found that light, comparable to the levels of light pollution surrounding cities, not only triggered depression in animal models but also increased specific inflammatory molecules in the hippocampus, a part of the brain involved in mood disorders. When the inflammatory molecules were blocked, the depression lifted.

We have known for some time that inflammation is associated with many diseases. In fact, it seems as if it is an essential condition for most of them. A Who's Who of inflammatory illnesses would number over 100 and include Alzheimer's, atherosclerosis, arthritis, Parkinson's, cancer and mood disorders. The connection with mood disorders was first appreciated when depression was found to be more prevalent in those with inflammatory disorders than in the general population.

So the medical community has targeted anything that causes chronic inflammation as something to nip in the bud. The big players here have been stress, Western diet (high in fat and processed foods), and sedentary lifestyle. Now we may have to add light at night (LAN).

This shouldn't come as a complete surprise. We evolved in an environment that alternated between light and dark. Over tens of thousands of years, this was an environmental constant. In this setting, our cells developed a kind of clock that is organized on a daily (circadian) pattern. Disrupt that rhythm and the trouble begins.

In the 100 years that widespread use of electric bulbs has become the norm, our genome has not adapted. Genetic change does not occur that rapidly. We are still wired for darkness at night, and artificial light disrupts our circadian rhythms. A growing body of research suggests that artificial light at night increases the risk for a variety of diseases including obesity and certain cancers.

If you think about some of the most common symptoms of depression, this story makes more sense. Circadian cycles, sleep, hunger-satiety, and memory are typically altered in depression. People with depression describe difficulty sleeping or excessive sleep. They often relate that their "clock is off." They complain of a loss of appetite or an inability to stop eating.

Depression's capacity to impair memory is so profound that depressives have been misdiagnosed as suffering from dementia, a memory disorder.

The brain centers that control these functions (hunger-satiety, circadian cycles-sleep, memory) are located in the hypothalamus.[Bingo! That's the part of the brain adversely affected by light at night, according to the recent research.

Over the past century there has been a dramatic increase in the incidence of depression, sleep disorders and obesity. This new data suggest that at least part of this increase could be due to the ever-growing exposure to light at night.

Imagine if we were to discover that light plays a major role in the obesity epidemic. I can see the headline now: "My Nightlight Made Me Fat."

So how might you respond to these findings?

Does your bedroom look like a NASA control room when you turn off the lights? Does your phone, TV, cable, computer, fax, printer, smoke alarm, etc. emit light? Do your curtains eliminate all light from outside?

For once, we may want to be in the dark.

For more by Paul Spector, M.D., click here.

David K. Randall: Rethinking Sleep

Vincent van Gogh , The Siesta (after Millet), December 1889-January 1890, oil on canvas, H. 73; W. 91 cm, Musée d'Orsay.

Sometime in the dark stretch of the night it happens. Perhaps it’s the chime of an incoming text message. Or your iPhone screen lights up to alert you to a new e-mail. Or you find yourself staring at the ceiling, replaying the day in your head. Next thing you know, you’re out of bed and engaged with the world, once again ignoring the often quoted fact that eight straight hours of sleep is essential.

Sound familiar? You’re not alone. Thanks in part to technology and its constant pinging and chiming, roughly 41 million people in the United States — nearly a third of all working adults — get six hours or fewer of sleep a night, according to a recent report from the Centers for Disease Control and Prevention. And sleep deprivation is an affliction that crosses economic lines. About 42 percent of workers in the mining industry are sleep-deprived, while about 27 percent of financial or insurance industry workers share the same complaint.

Typically, mention of our ever increasing sleeplessness is followed by calls for earlier bedtimes and a longer night’s sleep. But this directive may be part of the problem. Rather than helping us to get more rest, the tyranny of the eight-hour block reinforces a narrow conception of sleep and how we should approach it. Some of the time we spend tossing and turning may even result from misconceptions about sleep and our bodily needs: in fact neither our bodies nor our brains are built for the roughly one-third of our lives that we spend in bed.

The idea that we should sleep in eight-hour chunks is relatively recent. The world’s population sleeps in various and surprising ways. Millions of Chinese workers continue to put their heads on their desks for a nap of an hour or so after lunch, for example, and daytime napping is common from India to Spain.

One of the first signs that the emphasis on a straight eight-hour sleep had outlived its usefulness arose in the early 1990s, thanks to a history professor at Virginia Tech named A. Roger Ekirch, who spent hours investigating the history of the night and began to notice strange references to sleep. A character in the “Canterbury Tales,” for instance, decides to go back to bed after her “firste sleep.” A doctor in England wrote that the time between the “first sleep” and the “second sleep” was the best time for study and reflection. And one 16th-century French physician concluded that laborers were able to conceive more children because they waited until after their “first sleep” to make love. Professor Ekirch soon learned that he wasn’t the only one who was on to the historical existence of alternate sleep cycles. In a fluke of history, Thomas A. Wehr, a psychiatrist then working at the National Institute of Mental Health in Bethesda, Md., was conducting an experiment in which subjects were deprived of artificial light. Without the illumination and distraction from light bulbs, televisions or computers, the subjects slept through the night, at least at first. But, after a while, Dr. Wehr noticed that subjects began to wake up a little after midnight, lie awake for a couple of hours, and then drift back to sleep again, in the same pattern of segmented sleep that Professor Ekirch saw referenced in historical records and early works of literature.

It seemed that, given a chance to be free of modern life, the body would naturally settle into a split sleep schedule. Subjects grew to like experiencing nighttime in a new way. Once they broke their conception of what form sleep should come in, they looked forward to the time in the middle of the night as a chance for deep thinking of all kinds, whether in the form of self-reflection, getting a jump on the next day or amorous activity. Most of us, however, do not treat middle-of-the-night awakenings as a sign of a normal, functioning brain.

Doctors who peddle sleep aid products and call for more sleep may unintentionally reinforce the idea that there is something wrong or off-kilter about interrupted sleep cycles. Sleep anxiety is a common result: we know we should be getting a good night’s rest but imagine we are doing something wrong if we awaken in the middle of the night. Related worries turn many of us into insomniacs and incite many to reach for sleeping pills or sleep aids, which reinforces a cycle that the Harvard psychologist Daniel M. Wegner has called “the ironic processes of mental control.”

As we lie in our beds thinking about the sleep we’re not getting, we diminish the chances of enjoying a peaceful night’s rest.

This, despite the fact that a number of recent studies suggest that any deep sleep — whether in an eight-hour block or a 30-minute nap — primes our brains to function at a higher level, letting us come up with better ideas, find solutions to puzzles more quickly, identify patterns faster and recall information more accurately. In a NASA-financed study, for example, a team of researchers led by David F. Dinges, a professor at the University of Pennsylvania, found that letting subjects nap for as little as 24 minutes improved their cognitive performance.

In another study conducted by Simon Durrant, a professor at the University of Lincoln, in England, the amount of time a subject spent in deep sleep during a nap predicted his or her later performance at recalling a short burst of melodic tones. And researchers at the City University of New York found that short naps helped subjects identify more literal and figurative connections between objects than those who simply stayed awake.

Robert Stickgold, a professor of psychiatry at Harvard Medical School, proposes that sleep — including short naps that include deep sleep — offers our brains the chance to decide what new information to keep and what to toss. That could be one reason our dreams are laden with strange plots and characters, a result of the brain’s trying to find connections between what it’s recently learned and what is stored in our long-term memory. Rapid eye movement sleep — so named because researchers who discovered this sleep stage were astonished to see the fluttering eyelids of sleeping subjects — is the only phase of sleep during which the brain is as active as it is when we are fully conscious, and seems to offer our brains the best chance to come up with new ideas and hone recently acquired skills. When we awaken, our minds are often better able to make connections that were hidden in the jumble of information.
Gradual acceptance of the notion that sequential sleep hours are not essential for high-level job performance has led to increased workplace tolerance for napping and other alternate daily schedules.

Employees at Google, for instance, are offered the chance to nap at work because the company believes it may increase productivity. Thomas Balkin, the head of the department of behavioral biology at the Walter Reed Army Institute of Research, imagines a near future in which military commanders can know how much total sleep an individual soldier has had over a 24-hour time frame thanks to wristwatch-size sleep monitors. After consulting computer models that predict how decision-making abilities decline with fatigue, a soldier could then be ordered to take a nap to prepare for an approaching mission. The cognitive benefit of a nap could last anywhere from one to three hours, depending on what stage of sleep a person reaches before awakening.

Most of us are not fortunate enough to work in office environments that permit, much less smile upon, on-the-job napping. But there are increasing suggestions that greater tolerance for altered sleep schedules might be in our collective interest. Researchers have observed, for example, that long-haul pilots who sleep during flights perform better when maneuvering aircraft through the critical stages of descent and landing.

Several Major League Baseball teams have adapted to the demands of a long season by changing their sleep patterns. Fernando Montes, the former strength and conditioning coach for the Texas Rangers, counseled his players to fall asleep with the curtains in their hotel rooms open so that they would naturally wake up at sunrise no matter what time zone they were in — even if it meant cutting into an eight-hour sleeping block. Once they arrived at the ballpark, Montes would set up a quiet area where they could sleep before the game. Players said that, thanks to this schedule, they felt great both physically and mentally over the long haul.

Strategic napping in the Rangers style could benefit us all. No one argues that sleep is not essential. But freeing ourselves from needlessly rigid and quite possibly outdated ideas about what constitutes a good night’s sleep might help put many of us to rest, in a healthy and productive, if not eight-hour long, block.

David K. Randall is a senior reporter at Reuters and the author of “Dreamland: Adventures in the Strange Science of Sleep.”