Category: Health

{Results from study highlight the promise of mRNA-based vaccines and therapies.}

A new Zika vaccine candidate has the potential to protect against the virus with a single dose, according to a research team led by scientists from the Perelman School of Medicine at the University of Pennsylvania. As reported in Nature this week, preclinical tests showed promising immune responses in both mice and monkeys.

“We observed rapid and durable protective immunity without adverse events, and so we think this candidate vaccine represents a promising strategy for the global fight against Zika virus,” said senior author Drew Weissman, MD, PhD, a professor of Infectious Disease at Penn. “We hope to start clinical trials in 12 to 18 months.”

The research involved a collaboration among Weissman’s laboratory at Penn and several others, including the laboratories of Barton F. Haynes at Duke University and Theodore C. Pierson at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH).

Prompted by the recent Zika virus outbreaks in Latin America and some parts of the United States, scientists around the world have been racing to develop candidate vaccines, and already several have been tested in animals. The new candidate vaccine is the first to show such potent and long-lasting protection without the use of a live virus.

Traditional viral vaccines contain a weakened or killed version of the virus or isolated viral proteins. By contrast, the new Zika candidate vaccine uses tiny strands of RNA that hold the genetic codes for making viral proteins. These RNA molecules are modified versions of the so-called messenger RNAs (mRNAs) that normally carry information from genes and serve as blueprints for the making of proteins within cells. In this case, the mRNAs — produced and purified in a laboratory or biotech production facility — are delivered like a normal vaccine in an injection.

Injected mRNAs normally would be cleared from the body within minutes by a patient’s immune system, but these mRNAs are modified so that they are ignored by the immune system and can easily enter cells. Once inside cells, they are taken up by cellular protein-making machinery and induce the production, over weeks, of the viral proteins they encode.

This extended production of viral proteins mimics what a live virus vaccine would achieve. Live virus vaccines — using slow-replicating versions of the virus they are meant to protect against — tend to induce much more powerful immune protection compared to vaccines that are based on non-replicating versions of a virus or isolated viral proteins. Live virus vaccines have serious potential drawbacks, though, including harmful infection with the virus in people who have weakened immune systems.

Some newer vaccine candidates use harmless viruses such as modified adenoviruses to deliver genes that encode immunizing viral proteins. To date, an adenovirus-based strategy is the only Zika vaccine candidate that has shown strong protection in monkeys with a single dose; however, the immune system tends to attack adenoviruses and in some cases may neutralize them before they can deliver their immunizing payloads.

The mRNA-based strategy has none of these drawbacks.

The new candidate vaccine contains mRNAs encoding two key proteins from a Zika virus strain isolated in a 2013 outbreak. The researchers found that in mice, a single injection of 30 millionths of a gram of these mRNAs — a small fraction of the dose used for a typical vaccine — induced a rapid immune response, which protected mice from intravenous exposure to a separate Zika strain two weeks later. That protection, resulting in zero detectable virus in the bloodstream a few days after exposure, was maintained even when the mice were exposed to Zika virus five months after vaccination.

Tests in macaque monkeys also showed that a single vaccine dose of only 50 micrograms provided strong protection against exposure to Zika virus five weeks later.

In both cases, virus neutralization tests indicated that the vaccine induced high levels of antibodies that block Zika infection — levels that peaked after several weeks and thereafter remained high enough to be protective, potentially for years.

“Our work so far suggests that this new vaccine strategy induces a level of virus neutralization about 25 times greater, after a single dose, than one sees in standard vaccines,” Weissman said.

The powerful, durable protection conferred by the candidate vaccine is due in large part to its strong stimulation of CD4 helper T cells, which are important for maintaining long-term antibody immunity.

The mRNA vaccine approach has other advantages, Weissman added: “If a vaccine is effective after just a single immunization, the infrastructure needed for its administration can be much simpler. Production of an mRNA-based vaccine is also likely to be easier and less expensive compared to traditional virus- or viral protein-based vaccines.”

Weissman and colleagues are also applying their mRNA-based strategy to the development of other vaccines and therapies.

{Tie between collisions, symptoms is even stronger.}

Soccer players who head the ball a lot are three times more likely to have concussion symptoms than players who don’t head the ball often, according to a new study published in the February 1, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Players whose heads were hit in a collision two or more times in a two-week period were six times more likely to have concussion symptoms than players who did not have any unintentional head trauma, such as a ball hitting the back of the head or a head colliding with another player’s knee.

“These results show that heading the ball is indeed related to concussion symptoms, which is contrary to a recent study that suggested that collisions were responsible for most concussions,” said study author Michael L. Lipton, MD, PhD, of Albert Einstein College of Medicine in Bronx, NY. “The findings raise concerns about the long-term effects from heading the ball, and more research is needed.”

The study involved adult amateur soccer players who played at least six months of the year on leagues or clubs in the New York city area. The players completed an online questionnaire about how often they played soccer during the previous two weeks, how many times they had unintentional head impacts and how many times they headed the ball. The participants were divided into four groups based on how often they headed the ball, with the top group heading the ball an average of 125 times in two weeks and the bottom group heading the ball four times in two weeks.

They were also asked how often they had any symptoms from the head impacts. Moderate impact was defined as moderate pain and some dizziness. Severe impact was defined as feeling dazed, stopping play or needing medical attention. Very severe impact was defined as losing consciousness. Participants could complete the questionnaire again every three months.

A total of 222 players completed 470 questionnaires; 79 percent were men. Men had an average of 44 headers in two weeks and women had an average of 27. One or more unintentional head impacts were reported by 37 percent of men and 43 percent of women.

Of those with head impacts, 20 percent had moderate to severe symptoms. Seven people had very severe symptoms. Of those, six people had two or more unintentional head impacts during the two weeks; four were in the group that headed the ball the most and three were in the group with the second-most headers.

Those in the group with the most headers were three times more likely to have symptoms than those who headed the ball the least. The players with two or more unintentional impacts were six times more likely to have symptoms than those with no unintentional impacts; these results controlled for how often the players headed the ball. Players with one unintentional impact were three times more likely to have symptoms than those with no unintentional impacts. The link between both headers and unintentional impacts stayed the same after researchers adjusted for other factors that could affect concussion risk, such as a history of prior concussions, sex and age.

Lipton said one limitation of the study is that the information was self-reported by the participants, which could introduce errors in recollection. He also noted that the results cannot be generalized to soccer players who are teenagers, children or professional players.

{Americans may be consuming fast food wrapped in paper treated with perfluorinated chemicals (PFCs) — the same chemicals used in stain-resistant products, firefighting materials and nonstick cookware, according to a new study published in the journal Environmental Science & Technology.}

Researchers tested more than 400 samples of packaging materials, including hamburger and sandwich wrappers, pastry bags, beverage cups and French fry containers, and found evidence of fluorinated compounds called per- and polyfluoroalkyl substances (PFASs). Of the materials tested, these chemicals were found in 56 percent of dessert and bread wrappers, 38 percent of sandwich and burger wrappers and 20 percent of paperboard.

Previous studies have shown that these PFASs can migrate, contaminating the food and, when consumed, accumulating in the body.

“This is a really persistent chemical,” said Graham Peaslee, a professor of experimental nuclear physics in the College of Science at the University of Notre Dame, who tested the samples. “It gets in the bloodstream, it stays there and accumulates. There are diseases that correlate to it, so we really don’t want this class of chemicals out there.”

Peaslee used a novel specialized method called particle-induced gamma-ray emission (PIGE) spectroscopy, which he developed to analyze the total fluorine content of each piece of packaging. PIGE is an efficient and cost-effective way to measure the presence of chemicals like fluorine in solid samples.

Previous studies have linked PFASs to kidney and testicular cancers, thyroid disease, low birth weight and immunotoxicity in children, among other health issues. The chemicals have an especially long half-life and take many years before just 50 percent of the intake leaves the human body.

“These chemicals don’t biodegrade. They don’t naturally degrade. They persist in the environment for a very long time,” Peaslee said.

The results are concerning when considering the role of fast food in the American diet. The National Center for Health Statistics reported one-third of U.S. children consume fast food daily.

Samples were collected from a total of 27 fast food restaurant chains including McDonald’s, Burger King, Chipotle, Starbucks, Jimmy Johns, Panera and Chick-Fil-A, in and around Boston, San Francisco, Seattle, Washington, D.C., and Grand Rapids, Michigan. The study did not include takeout containers, such as Chinese food boxes or pizza boxes.

Upon the results of the study, researchers reached out to each of the fast food chains that had been sampled to see if they were aware the packaging being used contained fluorinated chemicals. Only two responded, each stating they believed their packaging was free of PFASs — one went so far as to state they had received verification from their supplier. But the study showed both respondents had tested positive for a substantial amount of fluorinated chemicals, leading researchers to believe that some chains may be unaware of what’s in their packaging.

“This is a wake-up call for those companies and the consumers,” Peaslee said.

Those involved in the study are hopeful the results will encourage fast food restaurants to choose nontoxic alternatives such as plastic coatings, aluminum foil or wax paper.

Peaslee conducted his research as a professor at Hope College. Since joining the University of Notre Dame, he is leading installation of a facility in the Nuclear Science Laboratory at the University to perform PIGE tests routinely on consumer products and environmental samples in the future.

Co-authors include researchers and scientists from the Silent Spring Institute, the California Department of Toxic Substances Control, the Green Science Policy Institute, the Environmental Working Group, the U.S. Environmental Protection Agency and the Oak Ridge Institute for Science and Education, as well as the University of California at Berkeley and Hope College.

{In 2012 this amounted to US$ 1436 billion, nearly 40 percent of which was borne by developing countries.}

Smoking consumes almost 6 per cent of the world’s total spend on healthcare and nearly 2 per cent of global GDP, reveals the first study of its kind, published in the journal Tobacco Control.*

In 2012 the total cost amounted to US$ 1436 billion, with nearly 40 per cent of this sum borne by developing countries, the calculations show.

The detrimental impact of smoking on national health systems and economies has been widely studied since the 1960s, but most of these studies have focused exclusively on high income countries, say the researchers.

They wanted to include low and middle income countries to come up with more accurate estimates of the total global cost. And so they included data from 152 countries representing 97% of the world’s smokers, from Africa, the Americas, the Eastern Mediterranean, Europe, Southeast Asia, and the Western Pacific.

They used the ‘cost of illness’ approach, first devised in 1960. This divides the economic impact of an illness into direct costs, such as hospital admissions and treatment, and indirect costs representing the value of productivity lost to death and disability in current and future years, for a given year.

The direct and indirect costs are then added up to provide the overall societal cost, usually expressed as a percentage of annual gross domestic product (GDP).

The researchers trawled through four leading research databases for relevant studies on direct costs, finding 33, and covering the 44 countries which account for 86% of the world’s total spend on healthcare.

They estimated the indirect costs, using a validated method (HCM) which calculates the current value of productivity lost to illness/disability and death.

And they used data from sources such as the World Health Organization and the World Bank to uncover information on the proportion of ill health and death attributable to smoking, national employment rates, and GDP for each of the 152 countries, to inform their calculations.

These showed that in 2012, diseases caused by smoking accounted for 12% (2.1 million) of all deaths among working age adults aged 30-69 — with the highest proportion in Europe and the Americas. This figure included 1.4 million adults who would have been in the workforce.

The number of working years lost because of smoking related ill health added up to 26.8 million, 18 million of which were lost to death with the remainder lost to disability.

In terms of health spend attributable to smoking, this totalled US$ 422 billion, equivalent to nearly 6% of the global total, with the highest share in Europe and the Americas. In Eastern Europe alone, the calculations indicated that this proportion was 10% of the total healthcare spend for that sub-region.

Based on all these figures, the researchers calculated that the total economic cost of smoking was US$ 1436 billion in 2012, equivalent to 1.8% of the world’s GDP, overall. But there were substantial regional/subregional variations.

The equivalent proportion of the GDP of Canada and the US combined was 3%, and 2.5% in Europe, and 3.6% in Eastern Europe.

Almost 40% of the global economic cost was borne by low and middle income countries; the four BRIC countries — Brazil, Russia, India and China — accounted for 25% of it.

The researchers point out that their calculations did not include the health and economic harms caused by second hand smoke or smokeless forms of tobacco, and that their estimates of lost productivity applied only to those who were economically active.

But they emphasise that in 2015 the UN General Assembly adopted the 2030 Agenda for Sustainable Development. This includes 17 goals that all member states have signed up to achieve by 2030. Goal 3 includes a target to cut by a third early deaths from non-communicable diseases, such as those caused by smoking, and to strengthen national implementation of the WHO Framework Convention on Tobacco Control.

“Smoking imposes a heavy economic burden throughout the world, particularly in Europe and North America where the tobacco epidemic is most advanced,” they conclude.

They add: “These findings highlight the urgent need for all countries to implement comprehensive tobacco control measures to address these economic costs, while also helping to achieve the Sustainable Development Goals of the member states.”

{Brains of mice with autism-like symptoms develop neural defects when first circuits take shape.}

Autism is not a single condition, but a spectrum of disorders that affect the brain’s ability to perceive and process information. Recent research suggests that too many connections in the brain could be at least partially responsible for the symptoms of autism, from communication deficits to unusual talents.

New research from the University of Maryland suggests that this overload of connections begins early in mammalian development, when key neurons in the brain region known as the cerebral cortex begin to form their first circuits. By pinpointing where and when autism-related neural defects first emerge in mice, the study results could lead to a stronger understanding of autism in humans — including possible early intervention strategies.

The researchers outline their findings in a research paper published January 31, 2017 in the journal Cell Reports.

“Our work suggests that the neural pathology of autism manifests in the earliest cortical circuits, formed by a cell type called subplate neurons,” said UMD Biology Professor and senior study author Patrick Kanold. “Nobody has looked at developing circuits this early, in this level of detail, in the context of autism before. This is truly a new discovery and potentially represents a new paradigm for autism research.”

Subplate neurons form the first connections in the developing cerebral cortex — the outer part of the mammalian brain that controls perception, memory and, in humans, higher functions such as language and abstract reasoning. As the brain develops, the interconnected subplate neurons build a network of scaffolding thought to support other neurons that grow later in development.

“The cortex is a very important region in the adult human brain that undergoes a complex, multi-stage development process,” said Daniel Nagode, a former postdoctoral researcher at UMD and lead author of the study. “Because our findings implicate the earliest stages of cortex circuit formation in a mouse model, they suggest that the pathological changes leading to autism might start before birth in humans.”

To study the relationship between autism and subplate neuron development in mice, Kanold, Nagode and their collaborators began with a well-established mouse model of autism. The model involves dosing mouse embryos with valproic acid (VPA) on day 12 of their 20-day gestation period by injecting the drug into the mother mouse.

VPA has a known link to autism in humans and also induces autism-like cognitive and behavioral abnormalities in mice. For example, normal newborn mouse pups will emit frequent, high-pitched noises when they are separated from their littermates, but VPA-treated pups do not.

The researchers used a technique called laser scanning photostimulation to map the connections between individual subplate neuron cells in the brains of the mouse pups. Within the first week after birth, the VPA-dosed mice showed some patches of “hyperconnected” subplate neurons. In contrast, control mouse pups dosed with plain saline solution showed normal connections throughout their cortical tissue.

Ten days after birth, the patches of hyperconnected subplate neurons had grown more widespread and homogeneous in the VPA-dosed pups compared with the control pups. Because subplate neurons help lay the foundation for cortical development in all mammalian brains, a thicket of hyperconnected subplate neurons in the developing cortex could result in permanent hyperconnections.

“Subplate neurons form critical developmental structures. If their early progress is impaired, later development of the cortex is also impaired,” Kanold explained. “In a developing human fetus, this stage is a critical gateway, when subplate neuron circuits are the most abundant.”

If the same dynamic plays out in human brains, hyperconnections in the developing cortex could result in the neural pathologies observed in human autism, Kanold said. In mice as well as in humans, the critical window of time when subplate neurons develop is very short.

“The timing of the effects is important. The hyperconnectivity in VPA pups occurs only in small patches a few days after birth,” Nagode said. “But after 10 days, the hyperconnectivity becomes much more widespread.”

In mice, subplate neuron development takes place mostly after birth. Eventually, the subplate neurons die off and disappear, their job done, as other neural circuits take their place. In humans, however, the first subplate neuron connections form in the second trimester. By the time humans are born, most of their subplate neurons have already disappeared.

“Our results suggest that we might have to interfere quite early to address autism,” Kanold said. “The fetal brain is not just a small adult brain, and these subplate neurons are the major difference. There may, in fact, be other developmental disorders we can tackle using this information.”

{In a bold and very challenging move, thoracic surgeons at Toronto General Hospital, University Health Network removed severely infected lungs from a dying mom, keeping her alive without lungs for six days, so that she could recover enough to receive a life-saving lung transplant.}

This is believed to be the first such procedure in the world, made possible by advanced life support technology, a dedicated and diverse surgical, respirology, intensive care and perfusion team, as well as the grit and gumption of the patient and her close-knit family.

“This was bold and very challenging, but Melissa was dying before our eyes,” recalls Dr. Shaf Keshavjee, Surgeon-in-Chief, Sprott Department of Surgery at University Health Network (UHN), one of three thoracic surgeons who operated together on Melissa to remove both her lungs. “We had to make a decision because Melissa was going to die that night. Melissa gave us the courage to go ahead.”

Melissa Benoit, then 32, was brought into Toronto General Hospital’s (TGH) Medical Surgical Intensive Care Unit (MSICU) in early April 2016, sedated and on a ventilator to help her laboured breathing. For the past three years, Melissa, who has cystic fibrosis, had been prescribed antibiotics to fight off increasingly frequent chest infections.

A recent bout of influenza just before her hospital admission had left Melissa gasping for air, with coughing fits so harsh that she fractured her ribs. Her inflamed lungs began to fill with blood, pus and mucous, decreasing the amount of air entering her lungs, similar to a person drowning.

As Dr. Niall Ferguson, Head of Critical Care Medicine at the University Health Network (UHN) and Mount Sinai, describes it, the influenza “tipped her over the edge into respiratory failure. She got into a spiral from which her lungs were not going to recover. Her only hope of recovery was a lung transplant.”

Melissa’s oxygen levels dipped so low, conventional ventilation was no longer enough. To help her breathe, and to gain more time until donor lungs became available, physicians placed her on Extra-Corporeal Lung Support (ECLS), a temporary life-support medical device that supports the work of the lungs and heart. Despite this, Melissa’s condition worsened.

The bacteria in her lungs developed resistance to most antibiotics, and spread throughout her body. Her blood pressure dropped. She slid into septic shock, triggering inflammation, leaky blood vessels and reduced blood flow. One by one, her organs began to shut down. She had to have kidney dialysis.

Melissa was now on maximum doses of three medications to maintain her blood pressure, along with the most advanced respiratory support, and on last-line powerful antibiotics, the last option for patients resistant to other available antibiotics. The team was still waiting for donor lungs but, by this time, Melissa was too sick to have a lung transplant.

Dr. Marcelo Cypel, the thoracic surgeon on call that late April weekend, kept a careful watch on Melissa. On a Sunday afternoon, with the clock ticking, he kept weighing her risk of death versus the risk of trying something which had never been done before.

It was bold, but scientifically sound. Removing both her lungs — the source of bacterial infection — could save her life.

Dr. Cypel gathered his colleagues, calling in Dr. Shaf Keshavjee, Dr. Tom Waddell, Head of Thoracic Surgery at UHN, Dr. Niall Ferguson, and respirologist Dr. Mathew Binnie — all seasoned and well-known for their skills in navigating complex cases, along with Melissa’s husband, mom and dad.

The surgical team had been discussing the concept of this procedure for several years. They had observed patients with cystic fibrosis, waiting for a lung transplant, who developed severe lung infections. These infections spread through the bloodstream into their bodies, resulting in septic shock and death, despite maximum support on the ECLS device.

While the team faced many unknowns — risk of bleeding into an empty chest cavity, whether her blood pressure and oxygen levels could be supported afterwards, and if she would even survive the operation — they agreed that Melissa was a possible candidate, and that it was her only chance, although a slim one.

As Dr. Keshavjee explained, she likely still had enough strength to withstand the procedure and get better afterwards, the source of the infection was clear-cut and difficult to control in current circumstances, the family understood the risks and explained that Melissa had often told them she would want to try everything possible to live for her husband Christopher and two-year-old daughter, Olivia.

“Things were so bad for so long, we needed something to go right,” remembers, Chris, “and this new procedure was the first piece of good news in a long time. We needed this chance.”

As Melissa tells it, Chris was the one who “held my life in his hands…He had to trust in himself, knowing me, relying on past conversations, and he chose exactly what I would have told him to.”

Melissa’s mom, Sue, was so eager to save her daughter’s life, she urged the team to go ahead: “Melissa always volunteers for any study or clinical trial. She would want to do this. Let’s not waste any more time and get her into the OR.”

At 9:00 pm that Sunday evening in mid-April, a team of 13 operating room staff, including three thoracic surgeons — Drs. Cypel, Keshavjee and Waddell — removed Melissa’s lungs, one at a time, in a nine-hour procedure. Her lungs had become so engorged with mucous and pus that they were as hard as footballs, recalls Dr. Keshavjee. “Technically, it was difficult to get them out of her chest.”

But within hours of removing her lungs, Melissa improved dramatically. She did not need blood pressure medication, and most of her organs began to improve.

To keep Melissa alive, she was placed on the most sophisticated support possible for her heart and lungs. Two external life support circuits were connected to her heart via tubes placed through her chest.

A Novalung device, a small portable artificial lung, was connected by arteries and veins to her heart to function as the missing lungs. Working with the pumping heart, the device added oxygen to her blood, removed carbon dioxide, while helping to maintain continuous blood flow. At the same time, another external device, extracorporeal membrane oxygenation (ECMO), which has an external pump, circuit and oxygenator for the gas exchange of oxygen and carbon dioxide, also helped to circulate oxygen-rich blood throughout her body.

TGH is a leader in using these technologies, with the largest such program in Canada, performing up to 100 ECLS cases per year. ECLS specialists or perfusionists and MSICU nurses are specially trained in caring for patients on various ECLS devices. Six days later, a pair of donor lungs became available and Melissa was stable enough to receive a lung transplant in late April 2016.

“The transplant procedure was not complicated because half of it was done already,” noted Dr. Cypel, “Her new lungs functioned beautifully and inflated easily. Perfect.” For the past several months, Melissa has been steadily improving. Her previously thick hair is growing back, she can play with her daughter for whole days without getting tired, and she has not needed a walker or cane for the past month. She is still on kidney dialysis.

“It’s the simple things I missed the most,” she said, “I want to be there for Chris and Olivia, even through her temper tantrums! I want to hear Olivia’s voice, play with her and read her stories.”

The medical team is developing criteria for the select types of patients who could be candidates for this novel procedure while waiting for a lung transplantation. The report of this case by Drs. Marcelo Cypel, Shaf Keshavjee, Tom Waddell, Lianne Singer, Lorenzo del Sorbo, Eddy Fan, Mathew Binnie and Niall Ferguson on Melissa Benoit entitled, “Bilateral pneumonectomy to treat uncontrolled sepsis in a patient awaiting lung transplantation” is published online in The Journal of Thoracic Cardiovascular Surgery, November, 2016.

{Pregnancy comes with certain signs. If you pay enough attention, there’s no way you wouldn’t know. Here are a few of those signs to watch for.}

{{Shortness of breath}}

It’s common and normal to suffer shortened breath during pregnancy. The reason this happens is because your body wants to divert some air to the foetus. If you notice this, you may want to check with your doctor.

{{Cramps and mood swings }}

Due to hormonal changes that would have occurred, or that are happening in your body, you may experience stomach cramps and annoying mood swings.

{{Aches in your body }}

Headaches, back aches, you may experience it all. You’re carrying more than just your bodily weight now, remember!

{{You feel nauseated}}

You wake up in the morning, and you feel uncomfortable, and next, you’re throwing up in the toilet… Typical pregnancy symptom.

{{Fatigue }}

All of a sudden, you’re tired for most of the time, without doing much? Well, it can happen for a host of reasons, and pregnancy is one of them.

{{Your boobs feel sore}}

Some hormonal changes occur with pregnancy, and they’ll affect your breasts too. So if for any reason, you feel soreness in your breasts, it may be that you’re pregnant.

Remember, that these are just signs. You’re not sure until you check with a doctor.

{Study one of first conducted outside of sleep lab}

Many people report getting sick when they don’t get enough sleep. A new study helps explain why.

Researchers took blood samples from 11 pairs of identical twins with different sleep patterns and discovered that the twin with shorter sleep duration had a depressed immune system, compared with his or her sibling. The findings were published Jan. 25 in the journal Sleep.

“What we show is that the immune system functions best when it gets enough sleep. Seven or more hours of sleep is recommended for optimal health,” said lead author Dr. Nathaniel Watson, co-director of the UW Medicine Sleep Center at Harborview Medical Center.

A unique feature of this study was to employ identical twins in order to control for the large genetic determinant to humans’ sleep duration. Researchers say genetics account for 31 to 55 percent of sleep duration and behavior and environment account for the remainder.

Dr. Sina Gharib, director of UW Medicine’s Computational Medicine Core at the Center for Lung Biology, and the paper’s senior author, explained that a lot of existing data shows that curtailing sleep — for a limited time in the laboratory setting — can increase inflammatory markers and activate immune cells. Little is known, though, about the effects of longstanding short sleep duration under natural conditions. This study employed “real world” conditions, he said, and showed for the first time that chronic short sleep shuts down programs involved in immune response of circulating white blood cells.

“The results are consistent with studies that show when sleep deprived people are given a vaccine, there is a lower antibody response and if you expose sleep deprived people to a rhinovirus they are more likely to get the virus,” Watson said. “This study provides further evidence of sleep to overall health and well-being particularly to immune health.

The researchers, citing data from the Centers for Disease Control, said that over the past century people in the United States are sleeping an estimated 1.5 to two hours less, and about one-third of the working population sleeps less than six hours per night.

“Modern society, with its control of light, omnipresent technology and countless competing interests for time, along with the zeitgeist de-emphasizing sleep’s importance, has resulted in the widespread deprioritization of sleep,” they wrote.

{Biologists at The Scripps Research Institute (TSRI) have identified a brain hormone that appears to trigger fat burning in the gut. Their findings in animal models could have implications for future pharmaceutical development.}

“This was basic science that unlocked an interesting mystery,” said TSRI Assistant Professor Supriya Srinivasan, senior author of the new study, published in the journal Nature Communications.

Previous studies had shown that the neurotransmitter serotonin can drive fat loss. Yet no one was sure exactly how. To answer that question, Srinivasan and her colleagues experimented with roundworms called C. elegans, which are often used as model organisms in biology. These worms have simpler metabolic systems than humans, but their brains produce many of the same signaling molecules, leading many researchers to believe that findings in C. elegans may be relevant for humans.

The researchers deleted genes in C. elegans to see if they could interrupt the path between brain serotonin and fat burning. By testing one gene after another, they hoped to find the gene without which fat burning wouldn’t occur. This process of elimination led them to a gene that codes for a neuropeptide hormone they named FLP-7 (pronounced “flip 7”).

Interestingly, they found that the mammalian version of FLP-7 (called Tachykinin) had been identified 80 years ago as a peptide that triggered muscle contractions when dribbled on pig intestines. Scientists back then believed this was a hormone that connected the brain to the gut, but no one had linked the neuropeptide to fat metabolism in the time since.

The next step in the new study was to determine if FLP-7 was directly linked to serotonin levels in the brain. Study first author Lavinia Palamiuc, a TSRI research associate, spearheaded this effort by tagging FLP-7 with a fluorescent red protein so that it could be visualized in living animals, possible because the roundworm body is transparent. Her work revealed that FLP-7 was indeed secreted from neurons in the brain in response to elevated serotonin levels. FLP-7 then traveled through the circulatory system to start the fat burning process in the gut.

“That was a big moment for us,” said Srinivasan. For the first time, researchers had found a brain hormone that specifically and selectively stimulates fat metabolism, without any effect on food intake.

Altogether, the newly discovered fat-burning pathway works like this: a neural circuit in the brain produces serotonin in response to sensory cues, such as food availability. This signals another set of neurons to begin producing FLP-7. FLP-7 then activates a receptor in intestinal cells, and the intestines begin turning fat into energy.

Next, the researchers investigated the consequences of manipulating FLP-7 levels. While increasing serotonin itself can have a broad impact on an animal’s food intake, movement and reproductive behavior, the researchers found that increasing FLP-7 levels farther downstream didn’t come with any obvious side effects. The worms continued to function normally while simply burning more fat.

Srinivasan said this finding could encourage future studies into how FLP-7 levels could be regulated without causing the side effects often experienced when manipulating overall serotonin levels.