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/

Surfaris "Dune Buggy" 1964

Jim Fuller lead guitar.

https://www.youtube.com/watch?v=CQjNb6ylZoU

Delayed Sleep Phase Disorder

 

 

Sleep Disorders Traced to Genes

by Randy Dotinga

If you like to go to sleep after Conan O'Brien or wake up shortly before lunch, you may have your ancestors to blame.

Researchers at two American universities suspect that night owls inherit their sleep patterns, and they're launching a study that could lead to new gene therapy for everyone from insomniacs to early birds who can't help but hit the sack before prime time.

It may be years, even decades, before gene-based drugs compete with the traditional insomnia remedies of sleeping pills, warm milk or hot toddies.

Researchers only began to seriously explore the genetics of sleep in the mid-1990s, and they're far from determining which genes are in charge of the body clock. Even so, there appears to be a general consensus that many of us don't voluntarily choose to be short sleepers or long sleepers, morning people or night people.

"For some time now, doctors who see people with sleep disorders have been documenting a familial relationship in these things. That's commonly the first way that people start thinking about a particular disease as being genetic, by seeing it cluster in families," said Dr. Walt Klimecki, a geneticist at the University of Arizona who is working with sleep researchers at the University of California at San Diego.
Indeed, researchers have discovered that some people seem to inherit a pesky early-to-sleep/early-to-rise syndrome. A notorious sleep disease -- the rare fatal familial insomnia, which robs people of sleep until they die from lack of it -- also runs in families.

Researchers at UCSD are recruiting Southern California night owls to undergo monitoring and genetic testing to see if their condition is inherited too. The participants have a condition called delayed sleep-phase syndrome and typically prefer to go to bed in the early hours of the morning and wake up after 9 or 10 a.m., when many people are already caffeinated and ready for work.

This sort of behavior won't sound unusual to countless college students or teenagers. But in the most severe cases of the syndrome, simply trying to go to bed earlier doesn't work, according to UCSD sleep researcher Dr. Dan Kripke.

"Some people are quite disabled by delayed sleep phase if their school work or employment requires them to get up early," he said. "They could voluntarily get up in the middle of their sleep period, but after a few days, they become so sleep-deprived, they can't continue to do it for the long run."
Perhaps 1 percent of the population has the disorder, Kripke said.
For reasons that aren't clear, it's much rarer for people to have the opposite condition -- advanced sleep-phase syndrome -- and be unable to postpone sleep past 7 or 8 p.m. Researchers elsewhere have already identified at least one of the genes that appear to cause that problem.

Extremely bright light boxes, which try to reset our internal clocks by making our bodies think it's morning, are a common treatment for sleep-phase disorders. Some patients take melatonin, a signaling hormone that can manipulate the body clock by tricking it into thinking it's dark and time for bed.
The University of Arizona's Klimecki suspects that, as in so many other medical conditions, sleep problems appear when genetics interact with other factors. Just as in illnesses like asthma, genetic predispositions don't necessarily doom someone to an unusual sleep pattern. Years ago, "we used to think of all these diseases as purely genetic," he said. "But now, we're realizing that the environment is really important as well."

Evolution could conceivably play a role too. Natural selection frequently affects both the development of diseases and resistance to them. For instance, an inherited trait that protected people from smallpox in the Middle Ages also appears to keep their descendents from getting AIDS. Klimecki pointed out that some blood disorders may have survived over time because they kept people from getting malaria.

But many more ailments appear to have developed independently from the pressures of evolution, and sleep problems may be among them, Klimecki said.

Once researchers figure out which genes affect sleep, they'll try to understand exactly how they affect the mysterious body clock, which typically resets itself after about 24 hours, and starts our daily cycles -- eating, sleeping and so on -- once again. Hence the term "circadian rhythm" -- "circadian" means "about a day."

Gene research in humans will also provide insight into the daily rhythms of animals.

"Nature uses the same genes and the same code to create the (body) clock in human beings as it does to create the clock in fruit flies," said Dr. Gregory Belenky, director of the Sleep and Performance Research Center at Washington State University at Spokane.

But body clocks aren't independent timekeepers: They depend on sunlight and darkness. In people who are kept away from the cues of light and dark, such as blind people, body clocks often boost the period of a "day" slightly beyond 24 hours, said Dr. Al Lewy, a sleep researcher at Oregon Health and Science University. In such people, the right time to go to sleep runs later and later each night, causing major disruptions to their lives. For the blind, who are immune to the effects of light boxes, melatonin may be the only treatment.

If researchers do get a handle on the genetics of sleep and the body clock, they may do more than produce gene-based treatments. According to Belenky, doctors could test people like pilots and special armed forces units to determine how they would handle sleep deprivation.

The tests might even give the lie to people who like to think they can easily skip sleep when they're actually not built to miss snooze time.

"People tend to think, 'Oh well, I'd like to get eight (hours), but I can manage with six,'" Belenky said. "But that's not true."


 

From yee Wiki:

Delayed sleep-phase disorder (DSPD), also known as delayed sleep-phase syndrome (DSPS) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder affecting the timing of sleep, peak period of alertness, the core body temperature rhythm, hormonal and other daily rhythms, compared to the general population and relative to societal requirements. People with DSPD generally fall asleep some hours after midnight and have difficulty waking up in the morning.

Affected people often report that while they do not get to sleep until the early morning, they do fall asleep around the same time every day. Unless they have another sleep disorder such as sleep apnea in addition to DSPD, patients can sleep well and have a normal need for sleep. However, they find it very difficult to wake up in time for a typical school or work day. If, however, they are allowed to follow their own schedules, e.g. sleeping from 4 a.m. to noon (04:00 to 12:00), they sleep soundly, awaken spontaneously, and do not experience excessive daytime sleepiness.

The syndrome usually develops in early childhood or adolescence. An adolescent version disappears in adolescence or early adulthood; otherwise DSPD is a lifelong condition. Depending on the severity, the symptoms can be managed to a greater or lesser degree, but there is no all-encompassing cure. Prevalence among adults, equally distributed among women and men, is approximately 0.15%, or 3 in 2,000. It is also genetically linked to ADHD by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm and a high proportion of DSPD among those with ADHD.


DSPD was first formally described in 1981 by Dr. Elliot D. Weitzman and others at Montefiore Medical Center. It is responsible for 7–10% of patient complaints of chronic insomnia. However, as few doctors are aware of it, it often goes untreated or is treated inappropriately; DSPD is often misdiagnosed as primary insomnia or as a psychiatric condition. DSPD can be treated or helped in some cases by careful daily sleep practices, light therapy, and medications such as melatonin and modafinil (Provigil). The former is a natural neurohormone responsible partly and in tiny amounts for the human body clock. At its most severe and inflexible, DSPD is a disability.

For more, go to:
http://en.wikipedia.org/wiki/Delayed_sleep_phase_disorder

A Meditative Moment with Li-Don

Empty your mind of all thoughts.
Let your heart be at peace.
Each separate being in the universe
returns to the common source.
Returning to the source is serenity.
Then you can deal with whatever life brings you.
-- Lao-Tzu

From yee Wiki:

Laozi (Chinese: Lao Tzu; also romanized as Lao Tse, Lao Tu, Lao-Tsu, Laotze, Laosi, Laocius, and other variations, fl. 6th century BCE) was a philosopher of ancient China, best known as the author of the Tao Te Ching (often simply referred to as Laozi). His association with the Tào Té Chīng has led him to be traditionally considered the founder of philosophical Taoism (pronounced as "Daoism"). He is also revered as a deity in most religious forms of Taoist philosophy, which often refers to Laozi as Taishang Laojun, or "One of the Three Pure Ones."

According to Chinese traditions, Laozi lived in the 6th century BCE. Some historians contend that he actually lived in the 5th–4th century BCE, concurrent with the Hundred Schools of Thought and Warring States Period, while some others argue that Laozi is a synthesis of multiple historical figures or that he is a mythical figure.

A central figure in Chinese culture, both nobility and common people claim Laozi in their lineage. He was honored as an ancestor of the Tang imperial family, and was granted the title Táishāng xuānyuán huángdì, meaning "Supreme Mysterious and Primordial Emperor". Throughout history, Laozi's work has been embraced by various anti-authoritarian movements.

Laozi is an honorific title. Lao means "venerable" or "old", such as modern Mandarin laoshi, "teacher". Zi, Wade-Giles transliteration tzu, in this context is typically translated "master". Zi was used in ancient China as an honorific suffix, indicating "Master", or "Sir".

In popular biographies, Laozi's given name was Er, his surname was Li (forming Li Er, 李耳) and his courtesy name was Boiang. Dan is a posthumous name given to Laozi, and he is sometimes referred to as Li Dan.

Excerpts from The PRH (Personal Responsibility for Health) Chronicles by David Katz, M.D.

Like other species, ours lives in the modern world with prehistoric genes and prehistoric tendencies.

Pronghorn antelope that race across the plains of Colorado and Wyoming are beautiful to watch, but to zoologists, they pose something of a mystery. They can run up to 40 miles per hour, and sustain their top speed for more than four miles, even though no existing predator can come close to catching them.

Thousands of years ago, however, such predators -- long-legged wolves and a North American hyena -- did exist. So the pronghorn continue to run for their lives -- from ghosts. They share the genetic makeup of their ancestors, and thus remain what their past required them to be. And so do we.

We, too, have a natural environment. And a world of fast-food drive-through restaurants, fax machines, escalators and email is not it. The nutritional environment we live in is toxic to us. The effects of that toxicity are rampant chronic disease and epidemic obesity. In trying to choose fruits and vegetables over chocolate and cheese, you are fighting your own metabolism, engineered to preserve you through periods of famine.

Epidemic obesity and chronic disease is, like a perfect storm, the product of massive and protean forces. It is an emergency in slow motion, but an emergency just the same. Whereas a hurricane devastates one part of our country over the span of a few days, obesity and attendant chronic disease have been battering at our entire population over a span of decades. The consequences are concisely epitomized by noting that what was "adult-onset" diabetes less than a generation ago is now routinely diagnosed in children under age 10. Other chronic diseases -- heart disease, stroke, and cancer -- are following diabetes down the age curve.

Like any other storm, these threats call for a brisk and well-coordinated crisis response that has yet to materialize fully. Instead, as our bodies expand and our health deteriorates, the body politic has divided into opposing camps claiming personal responsibility, or environmental factors, as the mutually exclusive explanations for our plight. Such polarity translates into partial paralysis, forestalling the cooperative actions needed to curtail this relentless scourge.

That an "obesigenic" environment trumps personal choice, tends to prevail among public health advocates, and with good reason. In 2005 and 2006, the Chicago Tribune highlighted food industry practices, including the use of functional MRI scans of the brain, to determine flavor combinations most conducive to endless eating. An updated overview of food industry efforts underlying the addictiveness of snack foods is the most recent New York Times Magazine cover story. The links between industrial profits and prevailing pandemics is elaborated in a current issue of The Lancet, a prestigious international medical journal.

Realistically, we must invoke both environmental reform and personal responsibility to promote health. After all, if in our enthusiasm for environmental determinism we renounce personal responsibility altogether, we risk both ineffectiveness and irrelevance for failing to consider that you can lead people to carrot juice but you can't make them drink -- any more than you can make them use stairs instead of elevators, rakes instead of leaf blowers, or soccer balls rather than video games.

On the other hand, any fair-minded person must recognize that the playing field of opportunity for weight control is not level. Implying that people struggling with poverty, unsafe neighborhoods, and resource-poor environments are personally "responsible" for their weight can be the literal addition of insult to injury, a blame-the-victim mentality that ignores access, affordability, and social privilege.

What we need, and have thus far mostly failed to pursue, is a diligent attempt to base policies on data rather than reciprocal disparagements. Questionnaires can test what behavioral science calls "self-efficacy," the capacity to take personal control.

Who does, and who does not, have the knowledge, skills, and resources to compensate for the obesigenic modern environment? We can, and should, find out, and devise means of providing personal control and empowerment where they're lacking, making environmental changes -- such as the elimination of junk foods from schools, or the addition of sidewalks to a suburban neighborhood -- where necessary.

At some point, the interaction of environment and behavior does come down to choice, and we can ask individuals to make good ones -- just as we can ask them to make personal preparations for a dangerous storm. But the levees will remain our collective responsibility.

To read the entire series, go to:

http://www.huffingtonpost.com/david-katz-md/personal-responsibility-for-health_b_2746292.html?utm_hp_ref=healthy-living

The Magnificent Marvin, Again

I took this low-res iPad photo of the very small MDM painting in my Dallas apartment. The scene shows a tent campsite with a landed helicopter at the far right.

Coming to Alaska in 1947 not as a painter but as a geologist, Marvin Mangus spent many field seasons working for the U. S. Geological Survey in Northern Alaska and Canada. While mapping, exploring, and surveying for oil, he made the most of his access to remote, dramatic scenery by studying and painting the landscape. A solid figure on the Alaskan art scene for almost fifty years, Mangus received formal training in the early 1950s from such prominent artists as Eliot O'Hara, Roger Rittase, and William Walter. His record includes more than 50 solo exhibitions and several group exhibitions in Washington D. C., at the Corcoran Gallery of Art, the Smithsonian institution, and the Arts Club. He was one of the first artists to be awarded a solo exhibition at the Anchorage Museum of History and Art after it opened in 1969.

Most of Marvin Mangus' work balances lively brushwork and interest in painterly surface with the artist's profound respect for representational appearance.

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

In the News: One Week of Sleep Deprivation Disrupts DNA Expression

A Third of Americans at Risk

A new study shows how lack of sleep wreaks havoc on the gene mechanisms that control metabolism, stress, and immunity. Over one-third of Americans are sleep-deprived.

by Ashik Siddique

Are you getting enough rest? You probably know that poor sleep is bad for you, but a new study shows exactly how your body suffers from a lack of sleep.

A new study shows how just one week of insufficient sleep alters the normal functions of over 700 genes, causing a wide range of serious negative effects on your health.

Previous studies have linked a long-term sleep deprivation with obesity, heart disease, cognitive impairment, and other negative health outcomes, but the molecular mechanisms that lead to such declines were not fully clear until now. 

In one of the first studies of the effects of sleep deprivation on the human "transcriptome," or the set of messenger molecules for the human genome, British researchers have showed that over time, insufficient sleep directly alters gene expression responsible for processes like immune responses, stress, and metabolism, which have a wide range of negative downstream effects.

The study, conducted by scientists at Surrey University in England, was published online in the journal Proceedings of the National Academy of Sciences on Feb. 25, 2013.

The researchers examined gene expression in 26 healthy volunteers who were deprived of sleep.

The participants in the sleep restriction condition were allowed only about 6 hours of sleep a night for seven consecutive nights, while the control group was allowed 10 hours of sleep.

At the end of the week, both groups were kept awake for a 40-hour period during which blood RNA samples were collected, then allowed 12 hours of constant sleep to recover.

Both groups were observed in a sleep center, with their sleep quality recorded throughout with standard polysomnography measures. A battery of tests was used during their waking hours to assess their cognitive performance and how they felt about their sleep quality each day.

In addition, researchers assayed levels of the hormone melatonin, which regulates biological rhythm and sleep cycles.

RNA analysis of the blood samples revealed that 711 genes were up- or down-regulated by insufficient sleep, meaning that their normal activity either decreased or intensified.

Every gene, or unit of DNA, is responsible for the creation of a protein involved in some bodily process. RNA is the "messenger chemical" that leads from DNA (the unchanging genetic code) to protein creation. If gene expression is turned up or down from its normal levels, it can cause a domino effect that leads to dramatic changes in the human body.

The genes altered by sleep deprivation in this study were involved in regulating sleep homeostasis, stress response, and metabolism.

Many of the malfunctioning genes were involved in maintaining the circadian rhythm, or "biological clock" -- that is, the timing of biological processes that are supposed to happen at specific times during a 24-hour cycle.

Others were responsible for overall gene regulation, meaning that chronic sleep loss can cause even more negative changes than the ones directly identified in this study.

Sleep deprivation also caused participants to perform more poorly on tests of cognition, memory and attention.

The findings have strong indications for most people living in the industrialized world.

According to the Centers for Disease Control and Prevention (CDC), 30 percent of civilian adults in the United States -- over 40 million workers -- report getting only 6 hours of sleep or less per night.

This means that millions of Americans are susceptible to the long-term changes in metabolism, stress response, and immunity that can put them at risk for disease.

While the ideal length of a good night's sleep varies widely among individuals, studies indicate that most people need somewhere between 7 and 9 hours per night.

Read more at http://www.medicaldaily.com/articles/14142/20130226/one-week-sleep-deprivation-disrupts-gene-expression.htm#7mf4YwcidjPAyJVr.99

Let's Surf! The Torquays "Penetration"

https://www.youtube.com/watch?v=Cg2G8Tx8Mqk

Amazing Spider-Man 121 “The Night Gwen Stacy Died” Original Art Cover Sells For $286,800

From the Bleeding Cool blog

by Mark Seifert

The cover of Amazing Spider-Man #121 has just sold at Heritage Auctions for $286,800.

This 1973 issue by Gerry Conway and Gil Kane, with cover by John Romita Sr. is considered one of the most important comic books of the Bronze Age. As the Heritage Auctions blurb says, “‘This was the end of innocence for comics… it remains one of the most potent stories ever published,’ was Arnold Blumberg’s comment in Comic Book Marketplace.”  Last year, Marvel Studios founder and producer on all the Spider-Man films Avi Arad told Hero Complex, “My favorite cover is “The Night Gwen Stacy Died.” This is a classic story where our hero is doing all the right things, willing to jeopardize himself, and give his life for justice, yet, inevitably, creates a complication and danger to people around him.”

Romita Sr. did (penciled or penciled & inked) approximately 100 Amazing Spider-Man covers in his initial run ranging from #39-169 (1966-1977, though his run on interior art stopped sooner).

By way of comparison, Romita Sr.’s cover for Amazing Spider-Man #49 went for $167,300 in 2011, his Amazing Spider-Man #43 cover sold for $101,700 in 2006, and his cover for Amazing Spider-Man Annual #3 closed at $104,562 in 2012.

The $286,800 sale of this Amazing Spider-Man #121 cover puts it within the top 5 sales of pencil and ink American comic book cover art ever sold publicly.

The highest price ever paid for an American comic book cover is the $675,250 sale of the Todd McFarlane cover of Amazing Spider-Man #328 in 2012.






Don's blog note: That's right. Yours truly, the dandy Dondaroo, penned the peerless Heritage Auction blurb mentioned above:

John Romita Sr. Amazing Spider-Man #121 "The Night Gwen Stacy Died" Cover Original Art (Marvel, 1973).

Some say the death of Gwen Stacy marked the end of the Silver Age of comics. "This was the end of innocence for comics... it remains one of the most potent stories ever published," was Arnold Blumberg's comment in Comic Book Marketplace.

The caption at the lower right crystallizes the theme of the most desirable piece of 1970s comic art we've auctioned to date. "Not a trick! Not an imaginary tale -- but the most startling unexpected turning point in this web-slinger's entire life. How can Spider-Man go on after being faced with this almost unbelievable death?"

It's a story that fans still talk about, and the most sense-shattering deathblow in comics. Letters from outraged fans flooded the Marvel offices, and led to another mini-controversy -- did Stan Lee OK this storyline or not?

The loss of Gwen marked nothing less than an end to the carefree fun and offbeat innocence of the Silver Age era. Spider-Man and the Marvel Age of Heroes were never quite so merry after this story.
This dynamic cover spotlights the taut suspense in an almost unbearable manner -- who among the beloved ASM cast would die? Many a fan thought, "Oh, please let it be Norman Osborn." Any Spider-fan who bought this issue off the spinner-rack has this iconic scene seared into his/her comic consciousness. With this scene, John Romita and Gerry Conway marked a tragic milestone for the world-famous Spider-Man saga launched by Steve Ditko and Stan Lee -- and for Marvelites, landmark issue covers just can't get better than this.

The image area of this eye-popping bombshell, showcasing John Romita Sr. at the height of his talent, measures 10" x 15". The art has some overall paper aging, a horizontal crease in the middle (at the level of the top of Spider-Man's head), a tear on the right side, and scattered staining that has little effect on the overwhelming power of the image; otherwise, the art is in Very Good condition. John Romita signed the page at the lower right. It's not just a classic cover -- it's a priceless piece of Bronze Age Marvel lore.

More Anxiety, Please: Hormone Disrupting Chemicals

'Hormone-disrupting chemical' is becoming an everyday term. But what does it really mean for your health?

by Leah Zerbe

Researchers say it's time to clean up the chemical industry.

It seems like not a week goes by without a study linking a common household product—or its ingredients—to one serious health problem or other. Whether it's BPA in cans causing heart attacks and cancer or fake fragrances in personal care products inducing early puberty in girls, the deluge of what's harming us can be depressing. But all of these studies underline one important fact: Chemicals are introduced onto the market before they're adequately tested for their long-term impacts on human health, and many of them are harmful hormone disruptors.

We turned to expert Laura Vandenberg, PhD, a postdoctoral fellow of biology at the Center for Developmental and Regenerative Biology at Tufts University in Massachusetts. She and her team just published a landmark study in the journal Endocrine Reviews showing that the way we test chemicals for health effects on humans is ineffective and in desperate need of revising. In fact, when it comes to hormone-disrupting chemicals, tiny doses could actually be more harmful than the higher doses commonly tested.

So how can we possibly protect ourselves from the 80,000—often inadequately tested—chemicals on the market? The answer is easy. We need to change testing protocol so that consumers don't have to be chemists to figure out whether or not a bottle of shampoo is safe.

What are hormone disrupting chemicals?

The endocrine system consists of glands located throughout the body whose job is to manufacture hormones that are released into the bloodstream or the fluid of surrounding cells. Different organs contain receptors that recognize and respond to the hormones. It's like members of a symphony working together to create music. Chemicals that interfere with this extremely delicate system cause all sorts of chaos within our bodily systems, kind of like one member of the symphony playing the wrong notes. It throws everything off.

Chemicals commonly found in everyday products are throwing off the endocrine system, causing temporary, and in some cases, possibly permanent, damage. For instance, some chemicals mimic a natural hormone, causing the body to overrespond. Sometimes, the effect is hormones aren't released when they're needed, as in abnormal insulin production. And some hormone-disrupting chemicals block organ receptors that make the endocrine system work properly.

How do hormone-disrupting chemicals affect our health?

The U.S. Centers for Disease Control and Prevention calculates that currently, more than 2 million American women are infertile, with more than 7 million women using infertility services. About 16 million Americans are believed to have diabetes, and more than 20 million are dealing with thyroid disease. All of these ailments have links to hormone disruption. The chemicals in our everyday environment can influence fertility, metabolic syndrome, and thyroid health. These aren't chemicals we are studying just for the sake of science—we are studying them because they can have a serious impact on human health.

Research on hormone-disrupting chemicals has really blossomed over the last decade. Scientists have developed better tools to determine what effects these chemicals might be having on people who are exposed to low levels in their everyday lives. This wealth of knowledge is really coming all at once, which is incredibly exciting to scientists in the field, but can be overwhelming to the general public.

We often hear that the dose makes the poison, but this new research shows small doses could, in fact, be more harmful. How is that possible?

For several years, scientists studying hormone-disrupting chemicals have known that some of these chemicals can have effects at low doses that cannot be predicted based on the effects of high doses. This is because high doses of these chemicals are toxic—they kill animals, or cause serious birth defects.

Low doses do not generally kill or disfigure animals, but that doesn't necessarily mean they are safe. Rather than an immediately obvious effect like death, animals exposed to low doses can experience changes that are harder to detect, such as permanent changes in the development of their organs. That means the brain of a boy animal can look like the brain of a girl animal, or an adult female can stop having regular cycles, and therefore lose the ability to get pregnant earlier in life. Or, an exposed animal may metabolize food differently, so even though it consumes the same number of calories as an unexposed animal, it will become obese later in life.

Scientists studying hormone-disrupting chemicals have known for years that low doses of these chemicals can have serious and permanent effects on animals and people. But most of those studies have focused on single chemicals, such as BPA or phthalates. So the conclusion could be that those chemicals are exceptions. This new research suggests that all hormone-disrupting chemicals have effects at low doses. The analysis of more than 800 peer-reviewed studies suggests that chemicals that mimic or block the actions of hormones will act at low doses—in the range that humans are exposed to. Levels that are currently thought to be "safe."

It's on the store shelf, so it must be safe, right?

The kind of toxicology tests that are done for chemical safety involve giving animals large doses and evaluating whether they die or develop obvious problems like birth defects. Safety testers then use the results of those high-dose tests, plus some mathematical calculations, to predict a safe dose. But the low dose that is thought to be safe for humans is usually not tested. And if it is tested, regulators look to see if animals die or have obvious problems. They don't look at the other sensitive, important endpoints like thyroid health, brain development, lifetime fertility, and other health conditions.

What are some of the most dangerous hormone-disrupting chemicals out there?

There are about 900 identified hormone-disrupting chemicals on the market, and they are commonly found in food packaging, plastics, pesticides, cosmetics, detergents, home and lawn care products, industrial pollutants, and other places.

Studies in the U.S. find more than 100 hormone disruptors in umbilical cord blood samples, indicating that fetuses and neonates are regularly exposed to many. It is hard to say which are the most dangerous, but so far scientific literature has studied BPA, the pesticide atrazine, dioxin, and perchlorate, a component of rocket fuel found in some water sources.

Scientists focused on these chemicals because most humans are exposed to them, and the evidence suggests they aren't safe. There could be worse offenders out there, but the information collected on these well-studied examples can most likely be applied more broadly to other chemicals with similar hormone-disrupting features.

This information may seem overwhelming to someone raising a family. What power does the average consumer have in solving this problem?

It's easy to say, 'This problem is so big, I can't possibly make a difference' and give up. But that simply isn't true. There are small and simple changes that consumers can make to lower exposures to these types of chemicals:

1. Use greener cleaning products.
2. Avoiding plastics whenever possible.
3. Reduce the use of pesticides in their homes and yards.
4. Eat organic.

But this isn't a problem that can be solved simply by smarter shopping. We need regulators to change their ways, and start testing chemicals at low doses (instead of just calculating a safe dose that is never tested).
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In the News: Mediterranean diet 'cuts strokes and heart attacks in at-risk groups'

I would miminimize the grain base of the this food pyramid and rely more on vegetables!

Following a Mediterranean diet rich in either extra-virgin olive oil or nuts reduces the risk of people at risk of a heart attack or stroke suffering either event or dying of a heart condition by 30%, new research reveals.

The findings, published online by the New England Journal of Medicine, offer hope to those in danger of a heart attack or stroke because they smoke, have type 2 diabetes or exhibit other unhealthy characteristics.

They also confirm that the diet common in southern European countries, which involves consuming a lot of fruit, vegetables, fish and wine, and only small amounts of red meat or dairy products, offers protection against heart problems.

For more:

http://www.guardian.co.uk/science/2013/feb/25/mediterranean-diet-strokes-heart-attacks

Gary Marcus: The New Yorker "Obama's Brain" Excerpt

Magnified 400 times, this is a 2-Photon fluorescence image of glial cells in the cerebellum. Glial cells provide support for the brain's neurons. This image was made by Thomas Deerinck of the National Center for Microscopy and Imaging Research, University of California, San Diego.

At some level, the brain is a kind of computer. It takes in information, combines new information with previously acquired information, and performs actions based on the results of those computations.

Yet we know remarkably little about how the brain performs its computations and how those computations relate to behavior, especially in comparison to what we know about computers.

Computers are, for all practical purposes, entirely understood. We know what they’re made of, we know how electrons move inside of them, and we know how their basic logical functions (such as “and,” “or,” and “not”) combine to form more complex operations, such as arithmetic and control (e.g., performing process X if a password is entered correctly and process Y if the password is entered incorrectly).

 In turn, programming languages relate machine language to more abstract sets of instructions that are more readily understood by human beings. An unbroken chain of inference connects the plans of the programmer to the actions of the electrons that ultimately implement them.

When it comes to the brain, we know comparatively little, in part because the brain is considerably less straightforward. By some counts (though the exact number remains elusive), there are hundreds of different kinds of neurons, each with different physical properties and ways of interacting with other neurons.

We don’t, for example, even know whether the basic unit of computational currency in the brain is digital (e.g., a set of zeroes and ones, like in virtually all modern computers) or analog (like the continuously moving second hand in an old-fashioned clock, an approach that was commonly used in some pre-Second World War computers).

Likewise, although we know something about which brain regions participate in the processing and storage of memories, we still don’t understand how the brain encodes those memories. And we know very little about how the brain’s basic units organize into larger-scale circuits, and how those circuits, often in physically disparate parts of the brain, work together to produce unified behavior.

Modern biology was launched in large part by three discoveries: Oswald Avery’s discovery of DNA; Watson and Crick’s deciphering of the physical structure of the DNA; and the discovery, by several researchers in the early nineteen sixties, of the code by which different triples of RNA nucleotides are turned into amino acids. All three of these discoveries were made possible in part by Mendel’s experiments with peas, in which he identified what we now know as genes.

The brain will finally give up its secrets when we do something similar, by constructing an inventory of the brain’s basic elements—the neural analogs to transistors, logic gates, and microprocessors — and relating those basic elements to broader-scale cognitive computations.

To connect brain to behavior, we don’t need to build a whole brain, as the E.U. aims to do; we need to understand how the brain’s parts work together.

And new techniques, like optogenetics (which allow experimenters to control brain activity—and hence an animal’s behavior—by exposing neurons to light) and fluorescent imaging (which makes it possible to monitor the responses of thousands of neurons simultaneously in awake, behaving animals), make addressing such questions potentially feasible for the first time.

Read more: http://www.newyorker.com/online/blogs/newsdesk/2013/02/obamas-brain.html#ixzz2LwNwZm7I

Bobby Moore and The Rhythm Aces Reaching Out. .

Robert "Bobby" Moore (1930-2006) was a tenor saxophonist and bandleader. He was born in New Orleans, Louisiana, and joined the US Army in his teens. While stationed at Fort Benning in Georgia in 1952, he formed the first line-up of the Rhythm Aces with members of the Fort Benning marching band; they toured the south playing at military events and clubs for a few years. When he moved to Montgomery, Alabama after being demobbed in 1961, Moore put together a new group, featuring his brother, Larry Moore (saxophone), Chico Jenkins (vocals, guitar), Marion Sledge (guitar), Joe Frank (bass), Clifford Laws (keyboards), and John Baldwin, Jr. (drums). They did local Alabama gigs and played behind national touring acts such as Sam Cooke and Ray Charles.

https://www.youtube.com/watch?v=M5wBvx6OMTs

Ready to Overthink?: Neurophilosophy (Yow!)

Neuronal circuits, feedback, and vector space -- the complexities of the evolved mind/brain are difficult to model.

Just because inquiring meta-minds want (?) to know.

From the intro on yee Wiki:

Neurophilosophy or philosophy of neuroscience is the interdisciplinary study of neuroscience and philosophy that explores the relevance of neuroscientific studies to the arguments traditionally categorized as philosophy of mind. The philosophy of neuroscience attempts to clarify neuroscientific methods and results using the conceptual rigor and methods of philosophy of science.

While the issue of brain-mind is still open for debate, from the perspective of neurophilosophy, an understanding of the philosophical applications of neuroscience discoveries is nevertheless relevant.

Even if neuroscience eventually found that there is no casual relationship between brain and mind, the mind would still remain an epiphenomenon of the brain, and as such neuroscience would still be relevant for the philosophy of the mind. At the other end of the spectrum, if neuroscience will eventually demonstrate a perfect overlap between brain and mind phenomena, neuroscience would become indispensable for the study of the mind. Clearly, regardless of the status of the brain-mind debate, the study of neuroscience is relevant for philosophy.

Huh? For (much, much) more, go to:

http://en.wikipedia.org/wiki/Neurophilosophy

Jack Lemmon as Ensign Pulver in "Mister Roberts"

"What's all this crud about no movie tonight?"

http://www.youtube.com/watch?v=ASOLrKsyrFU

"All right, who did it? Whhhoooooooo diiid ittt?"

Samuel J. Mann, M. D. Blogs: Is There a Mind/Body Connection in Hypertension?

The mind/body connection in health and illness has been the subject of a tremendous amount of research and public interest. Studies and articles receive considerable attention in the medical, psychology and lay press because of the popular belief in such a connection, and in mind/body interventions as a means to prevent or cure conditions such as hypertension.

Over decades, thousands of studies funded by hundreds of millions of National Institutes of Health dollars have been performed. It is long past time to ask: What has this enormous body of research taught us regarding the understanding or treatment of hypertension? Should further money be poured into mind/body research in hypertension? In this two-part blog, I will address these questions, based on what research tells us, and based on my own research and clinical experience.

Part I:

http://www.huffingtonpost.com/samuel-j-mann-md/stress-and-hypertension_b_2517600.html

Part II:

http://www.huffingtonpost.com/samuel-j-mann-md/hypertension_b_2738014.html?utm_hp_ref=health-news&ir=Health%20News

Remembering the Magnificent Marvin (1924-2009)



You can already see the rigid, mask-like countenance caused by PD on dad's face in this newspaper photo portrait.



It's hard to believe that it's been four years since my dad, Alaskan artist and arctic geologist, Marvin Mangus, passed away from complications from his Parkinson's Disease.

http://www.adn.com/2009/02/24/701522/marvin-mangus-artist-and-geologist.html

Since then, my mother has let me know in no uncertain terms that she  doesn't like it at all when I post dad's paintings on the internet, because of  copyright protection concerns. I don't entirely agree with this internet ban philosophy, but hey, it's my mom -- so I don't. What a good son, right? What I do instead, as a legitimate work-around, is grab images already posted on the web by others. This small painting is showcased on the  2 friends a most unusual gallery blog/website, with this caption.

September 29, 2012
"We received an absolutely beautiful Marvin Mangus painting yesterday. It is already hanging on the wall with two new Henne’s (note from Don: Ellen Henne Goodale, a family friend), a Robertson, and a Scott McDaniel. You will feel like you are in a museum but you can actually buy the art."

Here's a plug for the 2 friends:

Gallery Hours and Contact Info

Tuesday - Friday: 11 a.m. - 6 p.m.
Saturday: 10 a.m. - 5 p.m.
Sunday: 12 p.m. - 5 p.m.
Closed Monday

341 E. Benson Blvd., Anchorage, AK, 99503

(907) 277-0404

2friendsgallery@gmail.com

In the News: Study Disputes Long-Term Medical Savings from Bariatric Surgery

I personally replace the whole grain portion with yet more veggies.

by Melissa Healy, Los Angeles Times, February 20, 2013
In the span of 15 years, the number of bariatric surgeries performed in the United States has grown more than 16-fold to roughly 220,000 per year, gaining cachet as a near-panacea for obesity.

Despite the daunting price tag, mounting research has boosted hopes that the stomach-stapling operations could reduce the nation's healthcare bill by weaning patients off the costly drugs and frequent doctor visits that come with chronic obesity-related diseases like diabetes and arthritis.

But a new study has found that the surgery does not reduce patients' medical costs over the six years after they are wheeled out of the operating room.

The  study, published Wednesday in the journal JAMA Surgery, tracked the expenses of nearly 30,000 Americans who got one of two forms of bariatric surgery, and compared their long-term health costs with those of similar patients who were obese but did not go under the knife to lose weight. Even when the initial $20,000-$25,000 cost of the procedure was taken out of the equation, the ongoing expenses for the patients who had surgery were roughly the same as for those who did not.

In an editorial accompanying the study, Dr. Edward H. Livingston wrote that "bariatric surgery does not provide an overall societal benefit." Though acknowledging that such surgery has "dramatic short-term results," he added that its longer-term effects — including on longevity — have been disappointing.

"In this era of tight finances and inevitable rationing of healthcare resources, bariatric surgery should be viewed as an expensive resource" that should only be offered to patients "if there is an overwhelming probability of long-term success," he wrote.

Obesity, which affects 1 in 3 American adults, is proving a tough and expensive challenge for the nation's healthcare system. The annual cost of treating obesity-related diseases — including stroke, heart disease and certain cancers — is now $190 billion. With no decline in U.S. obesity rates, that surcharge is projected to reach $550 billion by 2030.

The finding that bariatric surgery does not save money is sure to be disappointing to public health officials seeking to "bend the cost curve" downward. Despite high upfront costs that range from $10,000 to $43,000, broadening access to bariatric procedures might help drive down healthcare costs in the longer run, the thinking went.

"We were so hopeful," said Dr. David Goodman of Dartmouth College medical school, who was not involved with the new study.

Bariatric procedures foster rapid weight loss by surgically reshaping the intestinal tract. To varying degrees, they aim to reduce the stomach's capacity, decrease the calories and nutrients absorbed from food, and change the chemical signals of fullness that are passed between the brain, the gut and the endocrine system.

The new study considered two such procedures: Roux-en-Y gastric bypass, in which the path of food is rerouted around a large portion of the stomach and the upper intestine; and gastric banding, which constricts the stomach to create a smaller pouch for food.

Several studies have suggested that bariatric surgery might indeed be cost-saving. At a minimum, it could be seen as paying for itself when improvements in patients' quality of life were given a monetary value.

But the new analysis, which compared nearly 60,000 patients covered by Blue Cross Blue Shield health plans, showed that those who had bariatric surgery incurred an average of $29,517 in costs in the first 30 days after their procedures. The average costs for the control patients were $1,004 during the equivalent period.

That huge surgical bill was not recouped during the course of the study, since costs for patients in both groups were roughly the same. In the sixth and last year examined, the average medical expenses for a surgery patient were $9,259; for a patient in the control group, they were $8,714.

"We need to know better not just what works, but what gets us the best bang for the buck," said John Cawley, a Cornell University health economist who praised the study's design and ambition.

Dr. Philip Schauer, a bariatric surgeon at the Cleveland Clinic, said the benefits of surgery might have looked better if the study tracked patients for longer than six years and included indirect cost savings to employers and insurers, such as reduced absenteeism and fewer disability claims. For many patients, the cardiovascular benefits of bariatric surgery — and resulting savings in hospital care — may not be realized for at least 10 years, he said.

Among a dozen or so studies on the topic in the last decade or so, "theirs is kind of an outlier," Schauer said.

Study leader Jonathan P. Weiner of the Johns Hopkins Bloomberg School of Public Health said his team did not try to figure out whether some of the costs incurred by patients in the surgery group reflected underlying improvements in their health. For instance, patients who lost weight might have an easier time getting pregnant and could wind up in the hospital to give birth. Others might attempt knee or hip replacements that would have been too risky when they were obese.

If it turns out that bariatric surgery doesn't save money, public health officials will have to hope they can find cost savings with medications and lifestyle interventions, neither of which has shown consistent evidence of long-term success in helping patients maintain weight loss or head off obesity-related disease.

Kenneth Thorpe, chairman of health policy and management at Emory University's School of Public Health, said there's reason to believe that drug and behavioral therapies are a better investment than surgeries.

For patients considered pre-diabetic, studies have shown that a 16-week course called the Diabetes Prevention Program staves off the disease in 58% of those under 60 and 71% of patients over 60. And the Food and Drug Administration last year approved two new weight-loss medications, Qsymia and Belviq, that could bring similar health benefits.

The cost of these treatments are "a pittance compared with what we're doing with bariatric surgery," Thorpe said.