Tag: medicine

New peptide treatment for obese patients suffering from insatiable hunger

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In a new study researchers from the Institute for Experimental Pediatric Endocrinology of the Charité – Universitätsmedizin Berlin have successfully treat patients whose obesity is caused by a genetic defect. Aside from its beneficial effects on the patients, the researchers also provided insights into the fundamental signaling pathways regulating satiety of the new drug. The results of this research have been published in Nature Medicine*.

A mutation in the gene encoding the leptin receptor (LEPR) can cause extreme hunger starting with the first months of life. As a result, affected individuals develop extreme obesity during childhood. Increased exercise and reduced caloric intake are usually insufficient to stabilize body-weight. In many cases, obesity surgery fails to deliver any benefits, meaning that a drug-based treatment approach becomes increasingly important.

Two years ago, Dr. Peter Kühnen and the working group successfully demonstrated that treatment with a peptide, which activates the melanocortin 4 receptor (MC4R) could play a central role in the body’s energy metabolism and body weight regulation. Leptin, which is also known as the satiety (or starvation) hormone, normally binds to the LEPR, triggering a series of steps that leads to the production of melanocyte-stimulating hormone (MSH). The act of MSH by binding to its receptor, the melanocortin 4 receptor (MC4R) which transduce the satiety signal to the body. However, if the LEPR is defective, the signaling cascade is interrupted. The patient’s hunger remains unabated, placing them at greater risk of becoming obese. As part of this current study, researchers used a peptide that binds to the MC4R in the brain, and this activation trigger the normal satiety signal. Working in cooperation with the Clinical Research Unit at the Berlin Institute of Health (BIH), the researchers were able to record significant weight loss in patients with genetic defects affecting the LEPR.

“We also wanted to determine why the used peptide was so effective and why, in contrast to other preparations with a similar mode of action, it did not produce any severe side effects,” explains Dr. Kühnen. “We were able to demonstrate that this treatment leads to the activation of a specific and important signaling pathway, whose significance had previously been underestimated.” Dr. Kühnen’s team is planning to conduct further research to determine whether other patients might benefit from this drug: “It is possible that other groups of patients with dysfunctions affecting the same signaling pathway might be suitable candidates for this treatment.”

*Clément K, et al., MC4R agonism promotes durable weight loss in patients with leptin receptor deficiency, Nature Medicine (2018), doi:10.1038/s41591-018-0015-9.

https://www.charite.de/en/service/press_reports/artikel/detail/den_unstillbaren_hunger_abschalten/

A Simple Treatment May Minimize Hearing Loss Triggered by Loud Noises

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It’s well known that exposure to extremely loud noises — whether it’s an explosion, a firecracker or even a concert — can lead to permanent hearing loss.
But knowing how to treat noise-induced hearing loss, which affects about 15 percent of Americans, has largely remained a mystery. That may eventually change, thanks to new research from the Keck School of Medicine of USC, which sheds light on how noise-induced hearing loss happens and shows how a simple injection of a salt- or sugar-based solution into the middle ear may preserve hearing. The results of the study were published today in PNAS.

Deafening sound
To develop a treatment for noise-induced hearing loss, the researchers first had to understand its mechanisms. They built a tool using novel miniature optics to image inside the cochlea, the hearing portion of the inner ear, and exposed mice to a loud noise similar to that of a roadside bomb.

They discovered that two things happen after exposure to a loud noise: sensory hair cells, which are the cells that detect sound and convert it to neural signals, die, and the inner ear fills with excess fluid, leading to the death of neurons.

“That buildup of fluid pressure in the inner ear is something you might notice if you go to a loud concert,” says the study’s corresponding author John Oghalai, MD, chair and professor of the USC Tina and Rick Caruso Department of Otolaryngology – Head and Neck Surgery and holder of the Leon J. Tiber and David S. Alpert Chair in Medicine. “When you leave the concert, your ears might feel full and you might have ringing in your ears. We were able to see that this buildup of fluid correlates with neuron loss.”

Both neurons and sensory hair cells play critical roles in hearing.

“The death of sensory hair cells leads to hearing loss. But even if some sensory hair cells remain and still work, if they’re not connected to a neuron, then the brain won’t hear the sound,” Oghalai says.

The researchers found that sensory hair cell death occurred immediately after exposure to loud noise and was irreversible. Neuron damage, however, had a delayed onset, opening a window of opportunity for treatment.

A simple solution

The buildup of fluid in the inner ear occurred over a period of a few hours after loud noise exposure and contained high concentrations of potassium. To reverse the effects of the potassium and reduce the fluid buildup, salt- and sugar-based solutions were injected into the middle ear, just through the eardrum, three hours after noise exposure. The researchers found that treatment with these solutions prevented 45–64 percent of neuron loss, suggesting that the treatment may offer a way to preserve hearing function.

The treatment could have several potential applications, Oghalai explains.

“I can envision soldiers carrying a small bottle of this solution with them and using it to prevent hearing damage after exposure to blast pressure from a roadside bomb,” he says. “It might also have potential as a treatment for other diseases of the inner ear that are associated with fluid buildup, such as Meniere’s disease.”

Oghalai and his team plan to conduct further research on the exact sequence of steps between fluid buildup in the inner ear and neuron death, followed by clinical trials of their potential treatment for noise-induced hearing loss.

https://www.keckmedicine.org/a-simple-treatment-may-minimize-hearing-loss-triggered-by-loud-noises/

Risk of later developing dementia is doubled after a concussion

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Researchers reported on Monday in the journal JAMA Neurology that dementia was a possible complication following concussion even if the patient did not lose consciousness.

Scientists from the University of California, San Francisco (UCSF) tracked more than one-third of a million American veterans, and found that the likelihood of dementia more than doubled following concussion.

After adjusting for age, sex, race, education and other health conditions, they found that concussion without loss of consciousness led to 2.36 times the risk for dementia.

According to the study, these risks were slightly elevated for those in the loss-of-consciousness bracket (2.51 times) and were nearly four times higher (3.77 times) for those with the more serious moderate-to-severe traumatic brain injury.

In the total of 357,558 participants, whose average age was 49, half had been diagnosed with traumatic brain injury, of which 54 percent had concussion. The study followed participants for an average of 4.2 years, and 91 percent were male and 72 percent were white.

“There are several mechanisms that may explain the association between traumatic brain injury and dementia,” said the study’s senior author Kristine Yaffe, professor with the UCSF departments of neurology, psychiatry, and epidemiology and biostatistics.

“There’s something about trauma that may hasten the development of neurodegenerative conditions. One theory is that brain injury induces or accelerates the accumulation of abnormal proteins that lead to neuronal death associated with conditions like Alzheimer’s disease,” said Yaffe.

“It’s also possible that trauma leaves the brain more vulnerable to other injuries or aging processes,” said Yaffe, “but we need more work in this area.”

http://www.xinhuanet.com/english/2018-05/08/c_137162226.htm

Targeting astrocytes, the brain cells that support neurons, in the brain might help alleviate symptoms of Alzheiemer’s disease

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A study by scientists of the German Center for Neurodegenerative Diseases (DZNE) points to a novel potential approach against Alzheimer’s disease. In studies in mice, the researchers were able to show that blocking a particular receptor located on astrocytes normalized brain function and improved memory performance. Astrocytes are star-shaped, non-neuronal cells involved in the regulation of brain activity and blood flow. The findings are published in the Journal of Experimental Medicine (JEM).

Alzheimer’s disease is a common and currently incurable brain disorder leading to dementia, whose mechanisms remain incompletely understood. The disease appears to be sustained by a combination of factors that include pathological changes in blood flow, neuroinflammation and detrimental changes in brain cell activity.

“The brain contains different types of cells including neurons and astrocytes”, explains Dr. Nicole Reichenbach, a postdoc researcher at the DZNE and first author of the paper published in JEM. “Astrocytes support brain function and shape the communication between neurons, called synaptic transmission, by releasing a variety of messenger proteins. They also provide metabolic and structural support and contribute to the regulation of blood flow in the brain.”

Glitches in network activity

Similar to neurons, astrocytes are organized into functional networks that may involve thousands of cells. “For normal brain function, it is crucial that networks of brain cells coordinate their firing rates. It’s like in a symphony orchestra where the instruments have to be correctly tuned and the musicians have to stay in synchrony in order to play the right melody”, says Professor Gabor Petzold, a research group leader at the DZNE and supervisor of the current study. “Interestingly, one of the main jobs of astrocytes is very similar to this: to keep neurons healthy and to help maintain neuronal network function. However, in Alzheimer’s disease, there is aberrant activity of these networks. Many cells are hyperactive, including neurons and astrocytes. Hence, understanding the role of astrocytes, and targeting such network dysfunctions, holds a strong potential for treating Alzheimer’s.”

Astrocyte-targeted treatment alleviated memory impairment

Petzold and colleagues tested this approach in an experimental study involving mice. Due to a genetic disposition, these rodents exhibited certain symptoms of Alzheimer’s similar to those that manifest in humans with the disease. In the brain, this included pathological deposits of proteins known as “Amyloid-beta plaques” and aberrant network activity. In addition, the mice showed impaired learning ability and memory.

In their study, the DZNE scientists targeted a cell membrane receptor called P2Y1R, which is predominately expressed by astrocytes. Previous experiments by Petzold and colleagues had revealed that activation of this receptor triggers cellular hyperactivity in mouse models of Alzheimer’s. Therefore, the researchers treated groups of mice with different P2Y1R antagonists. These chemical compounds can bind to the receptor, thus switching it off. The treatment lasted for several weeks.

“We found that long-term treatment with these drugs normalized the brain’s network activity. Furthermore, the mice’s learning ability and memory greatly improved”, Petzold says. On the other hand, in a control group of wild type mice this treatment had no significant effect on astrocyte activity. “This indicates that P2Y1R inhibition acts quite specifically. It does not dampen network activity when pathological hyperactivity is absent.”

New approaches for research and therapies?

Petzold summarizes: “This is an experimental study that is currently not directly applicable to human patients. However, our results suggest that astrocytes, as important safeguards of neuronal health and normal network function, may hold the potential for novel treatment options in Alzheimer’s disease.” In future studies, the scientists intend to identify additional novel pathways in astrocytes and other cells as potential drug targets.

Reference:
Reichenbach, N., Delekate, A., Breithausen, B., Keppler, K., Poll, S., Schulte, T., . . . Petzold, G. C. (2018). P2Y1 receptor blockade normalizes network dysfunction and cognition in an Alzheimer’s disease model. The Journal of Experimental Medicine. doi:10.1084/jem.20171487

https://www.dzne.de/en/news/public-relations/press-releases/press/detail/the-brains-rising-stars-new-options-against-alzheimers/

Disease detectives determine that typhoid killed 12th century Saladin

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Saladin may not be well known in the West, but even 800 years after his death, he remains famous in the Middle East. Born in 1137, he rose to become the Sultan of an enormous area that now includes Egypt, Syria, parts of Iraq, Lebanon, Yemen and other regions of North Africa. He successfully led armies against the invading Crusaders and conquered several kingdoms. Historians have described him as the most famous Kurd ever.

Even today, however, Saladin’s death remains a mystery. The illness began in 1193, when he was 56. After two weeks, the Sultan was dead. Some have speculated that fever was a prominent symptom of the illness.

After closely examining a range of evidence about Saladin’s condition, Stephen J. Gluckman, MD, professor of medicine at the University of Pennsylvania School of Medicine, has developed a diagnosis. Dr. Gluckman theorizes that typhoid, a bacterial disease that was very common in the region at the time, is the most likely culprit. Today of course, antibiotics could have greatly helped Saladin. But in the 12th century these medicines did not exist.

Dr. Gluckman delivered his diagnosis at the 25th annual Historical Clinicopathological Conference, held Friday, May 4 at the University of Maryland School of Medicine. The conference is devoted to the diagnosis of disorders that afflicted historical figures; in the past, experts have focused on the diseases of luminaries such as Lenin, Darwin, Eleanor Roosevelt and Lincoln.

Dr. Gluckman, an expert on parasitic disorders, has provided care and taught in many countries around the world. He carefully reviewed what is known about the Sultan’s medical history. “Practicing medicine over the centuries required a great deal of thought and imagination,” he says. “The question of what happened to Saladin is a fascinating puzzle.”

Saladin is known for destroying King Guy’s army at the Horns of Hattin in 1187 and reclaiming Jerusalem for Islam after it had been ruled for nearly a century by Christian crusaders. He is also famed for treating his enemies generously.

Typhoid fever is a potentially deadly disease spread by contaminated food and water. Symptoms of typhoid include high fever, weakness, stomach pain, headache, and loss of appetite. It is common in most parts of the world except in industrialized regions such as the United States, western Europe, Australia, and Japan. About 300 people get typhoid fever in the United States each year, and most of them have recently traveled. Globally, typhoid infects about 22 million people a year, and kills 200,000.

‌Also speaking at the conference will be Thomas Asbridge, PhD, is a reader of medieval history at Queen Mary University of London. Dr. Asbridge is an expert on Saladin and the Crusades.

The conference was founded in 1995 by Philip A. Mackowiak, MD, the Carolyn Frenkil and Selvin Passen History of Medicine Scholar-in-Residence at UMSOM. “This is an intriguing piece of medical detecting,” says Dr. Mackowiak. “If antibiotics had been around in the 12th century, history may have been quite different.”

For more information on the conference, visit:
http://medicalalumni.org/historicalcpc/home/

http://www.medschool.umaryland.edu/news/2018/Expert-Disease-Detective-Unravels-Mysterious-Illness-That-Killed-Famed-12th-Century-Sultan.html

Merck study failure may signal doom for a broad group of pivotal Alzheimer’s studies focused on the amyloid theory of treatment.

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by John Carroll

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The BACE theory in Alzheimer’s R&D is simple. Cut off the flow of amyloid beta to the brain and you can eliminate what is widely believed — though not proven — to be a cause of the disease. Do that, and you could bend the course of this devastating illness in millions of people with mild to moderate forms of the disease.

And Merck $MRK just spent a fortune to demonstrate that it may well be completely wrong.

To be sure, Merck ran a clean study for verubecestat, the leading BACE drug in the clinic, and displayed the data on 1,958 patients for all to see today in the New England Journal of Medicine. Investigators carefully tracked amyloid beta flows in cerebrospinal cords and found that the drug did what it was intended to do, with a dramatic reduction of the toxic protein. 

It had no effect, with patients in the two dosage groups tracking in parallel decline on both cognition and function, the two classic measures for Alzheimer’s. 

The conclusion they reached is that the damage already present in the brains of patients with Alzheimer’s may be too extensive to treat with any BACE drug. And they also concede that the amyloid theory itself may be just flat wrong.

This suggests that once dementia is present, disease progression may be independent of Aβ production or, alternatively, that the amyloid hypothesis of Alzheimer’s disease may not be correct. Because Aβ deposition takes place years before clinical symptoms become apparent, it has been proposed that treatments targeting amyloid should be implemented early in the disease process, before the onset of clinical symptoms.

Soon after this study failed, Merck also threw in the towel on their second pivotal trial, noting it too was a flop. Those data are still being evaluated, but it underscores the belief that all of the BACE studies — including those at Eli Lilly $LLY, partnered with AstraZeneca $AZN, or Biogen $BIIB, allied with Eisai — are headed straight to failure.

Biogen is also rolling the dice on aducanumab, which the company has touted as a leading amyloid beta therapy. But with investigators in the field openly wondering whether the amyloid theory has lured a long lineup into a clinical disaster zone, it’s likely to face growing skepticism that it can develop a safe, effective therapy with just one drug.

This doesn’t by any means eliminate work in the area. True, Pfizer recently pulled out after spending hundreds of millions of dollars on their programs. But startups like Denali believe that new and better technology can give them better odds at success, while Celgene is jumping in with its own new pipeline. Others want to see if combination approaches using tau and amyloid beta together could work. 

Merck’s suggestion about going even earlier in the disease process has also prompted a range of studies in pre-symptomatic patients, while the FDA has signaled its interest in coming up with biomarkers to help speed new studies.

After more than 200 R&D projects ended in disaster, though, Alzheimer’s is looking like an increasingly daunting challenge, with no clear path forward that would inspire confidence among patients with the disease.

Merck study may signal doom for a broad group of pivotal Alzheimer’s studies

Personal subjective reports of memory ability may be a reliable early marker of Alzheimer’s disease.

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Psychological sciences doctoral student Marci Horn (left) conducts a name-face memory test as part of a study at the Center for Vital Longevity.

New research from the Center for Vital Longevity (CVL) at The University of Texas at Dallas suggests that subjective complaints about poor memory performance, especially in people over 60, could be a useful early marker for the onset of mild cognitive decline, which sometimes foreshadows Alzheimer’s disease.

Subjective memory is a person’s unscientific self-evaluation of how good his or her memory is, and whether, in that person’s opinion, there has been any worsening of memory through age. While some changes may be undetectable to others and are often too subtle to register on cognitive tests, the person subjectively believes that memory is slipping.

Published recently in Psychology and Aging, the research from Dr. Karen Rodrigue’s lab at CVL examined subjective memory complaints in nearly 200 healthy adults, ages 20 to 94. Previous studies suggest that subjective memory complaints are not necessarily indicative of cognitive decline, and may stem from underlying conditions such as anxiety and depression, which have been shown to impede memory.

The current study measured mood and screened out depressed individuals. Researchers also measured participants for known risk factors for memory loss and Alzheimer’s, such as higher levels of beta-amyloid in the brain and the presence of a gene variant called ApoE4. These factors were taken into account to examine whether subjective memory alone was a reliable correlate of actual memory ability.

The study focused on associative memory — for example, remembering word pairs and name-face pairs. This type of memory is particularly sensitive to age-related decline, and the most common complaint of aging individuals.

The study found that a person’s intuitive or intrinsic assessment of his or her own memory was actually a reliable predictor of performance on the laboratory memory assessment. This result was particularly true for individuals with genetic risk for memory loss.

“Our findings show that subjective memory can be a reliable indicator of memory performance, even in cognitively healthy adults,” said psychological sciences doctoral student Marci Horn, the lead author of the study. “The same people who self-report memory problems may also have other risk factors associated with increased risk of Alzheimer’s disease.”

The researchers also found that men who had higher amyloid levels reported the most subjective memory complaints in the study. Previous studies had not uncovered a sex-specific relationship, nor did they account for the genetic and amyloid risk factors in these associations, the researchers said.

The strongest correlation of subjective memory complaints with actual cognitive performance was in study participants older than 60, when people are generally at greater risk for Alzheimer’s disease.

“It seems that awareness of memory changes may be a reliable indicator of one’s current memory ability, and may serve as another harbinger of future loss, as this relationship was strongest in those with known risk factors for Alzheimer’s disease, namely ApoE4 genotype and beta-amyloid burden in the brain,” said Rodrigue, the senior author of the study and assistant professor in the School of Behavioral and Brain Sciences (BBS). “We are following these individuals over time to further test this idea.”

Dr. Kristen Kennedy, an assistant professor in BBS, also was an author of the study. The research was funded in part by grants from the National Institutes of Health.

https://www.utdallas.edu/news/2018/4/30-32929_Subjective-Memory-May-Play-Role-in-Signaling-Cogni_story-wide.html?WT.mc_id=NewsHomePageCenterColumn

University of Michigan scientists develop a pill that may be superior to mammogram from detecting breast cancer

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As many as one in three women treated for breast cancer undergo unnecessary procedures, but a new method for diagnosing it could do a better job distinguishing between benign and aggressive tumors.

Researchers at the University of Michigan are developing a pill that makes tumors light up when exposed to infrared light, and they have demonstrated that the concept works in mice.

Mammography is an imprecise tool. About a third of breast cancer patients treated with surgery or chemotherapy have tumors that are benign or so slow-growing that they would never have become life-threatening, according to a study out of Denmark last year. In other women, dense breast tissue hides the presence of lumps and results in deaths from treatable cancers. All that, and mammograms are notoriously uncomfortable.

“We overspend $4 billion per year on the diagnosis and treatment of cancers that women would never die from,” said Greg Thurber, U-M assistant professor of chemical engineering and biomedical engineering, who led the team. “If we go to molecular imaging, we can see which tumors need to be treated.”

The move could also catch cancers that would have gone undetected. Thurber’s team uses a dye that responds to infrared light to tag a molecule commonly found on tumor cells, in the blood vessels that feed tumors and in inflamed tissue. By providing specific information on the types of molecules on the surface of the tumor cells, physicians can better distinguish a malignant cancer from a benign tumor.

Compared to visible light, infrared light penetrates the body easily—it can get to all depths of the breast without an X-ray’s tiny risk of disrupting DNA and seeding a new tumor. Using a dye delivered orally rather than directly into a vein also improves the safety of screening, as a few patients in 10,000 can have severe reactions to intravenous dyes. These small risks turn out to be significant when tens of millions of women are screened every year in the U.S. alone.

But it’s not easy to design a pill that can carry the dye to the tumor.

“To get a molecule absorbed into the bloodstream, it needs to be small and greasy. But an imaging agent needs to be larger and water-soluble. So you need exact opposite properties,” Thurber said.

Fortunately, they weren’t the only people looking for a molecule that could get from the digestive system to a tumor. The pharmaceutical company Merck was working on a new treatment for cancer and related diseases. They got as far as phase II clinical trials demonstrating its safety, but unfortunately, it wasn’t effective.

“It’s actually based on a failed drug,” Thurber said. “It binds to the target, but it doesn’t do anything, which makes it perfect for imaging.”

The targeting molecule has already been shown to make it through the stomach unscathed, and the liver also gives it a pass, so it can travel through the bloodstream. The team attached a molecule that fluoresces when it is struck with infrared light to this drug. Then, they gave the drug to mice that had breast cancer, and they saw the tumors light up.

The research is described in a study in the journal Molecular Pharmaceutics, titled, “Oral administration and detection of a near-infrared molecular imaging agent in an orthotopic mouse model for breast cancer screening.”

This work was done in collaboration with David Smith, the John G. Wagner Collegiate Professor of Pharmaceutical Sciences at the U-M College of Pharmacy. It was supported by the Foundation for Studying and Combating Cancer and the National Institutes of Health.
Bhatnagar, S., Verma, K. D., Hu, Y., Khera, E., Priluck, A., Smith, D., & Thurber, G. M. (2018). Oral Administration and Detection of a Near-Infrared Molecular Imaging Agent in an Orthotopic Mouse Model for Breast Cancer Screening. Molecular Pharmaceutics. doi:10.1021/acs.molpharmaceut.7b00994

New research suggests that these 5 healthy habits could help you live a decade longer: eating healthy, exercising, keeping a healthy BMI, not smoking and not drinking too much.

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Want to prolong your life expectancy by more than a decade? A new study suggests that you can do just that by following these five healthy habits: never smoke, maintain a healthy body-mass index, keep up moderate to vigorous exercise, don’t drink too much alcohol, and eat a healthy diet.

Adhering to those five lifestyle factors at age 50, compared with not adhering to any of them, was associated with 14 additional years of life expectancy among women and 12.2 additional years among men in the study, published in the journal Circulation on Monday.

Each of those factors is significantly associated with a reduced risk of dying from the top two killers in the United States, cardiovascular disease and cancer, according to the study.
About 610,000 people die of heart disease in the US each year, which is about one in every four deaths, according to the US Centers for Disease Control and Prevention.
About 609,640 Americans are expected to die of cancer this year, according to the American Cancer Society.

“These are some of the leading causes of premature death, so by preventing or reducing the incidence of those diseases, it promotes longevity, and it also improves survival after diagnosis of those diseases,” said Dr. Meir Stampfer, a professor of medicine at Harvard Medical School and professor of epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, who was a co-author of the study.

“We can do so much better for having a long healthy life by pretty simple minimal changes in our behavior, and only 8% of adults in our country are adhering to these,” he said. “The main take-home message is that there’s huge gains in health and longevity to be had just by simple changes in our behavior pattern, and as a country, I think we need to make it easier for ourselves to do this by promoting tobacco cessation, by providing better environments for physical activity and so on.”

Globally, the US ranks 43rd when it comes to life expectancy at birth, with an average life expectancy of 80, according to 2017 data from the Central Intelligence Agency’s World Factbook.
The three countries ranked highest for life expectancy at birth are Monaco, with 89.4 years; Japan, with 85.3 years; and Singapore, with 85.2 years, according to those data.

The countries with the lowest life expectancy at birth, based on that data, are Chad, with 50.6 years; Guinea-Bissau, with 51 years; and Afghanistan, with 51.7 years.

The ‘surprising’ impact of behaviors on longevity

For the new study, researchers measured the association between those five lifestyle factors and premature death using data from the national Nurses’ Health Study and the Health Professionals Follow-Up Study. The data came from 1980 to 2014 and included more than 122,000 people combined.

Then, the researchers used data from the National Health and Nutrition Examination Surveys to estimate the distribution of those modifiable lifestyle factors among adults in the United States. Those data, from 2013 to 2014, consisted of 2,128 adults, 50 to 80 years old.

The researchers also derived death rates of US adults using the CDC’s Wide-Ranging Online Data for Epidemiologic Research database.

After analyzing the data, the researchers found that, in 2014, the overall projected life expectancy at age 50 was to live 33.3 more years for women and 29.8 more years for men.

Yet among the adults who reported that they adopted all five healthy lifestyle factors, the researchers found, they lived 43.1 more years among women and 37.6 more years among men.

Among those adults who reported that they adhered to none of the five healthy lifestyle factors, the researchers found that they lived only 29 additional years among women and 25.5 additional years among men.

“To me, the surprising outcome was how strong it was: what a big impact these simple behaviors could have on life expectancy,” Stampfer said. “I was surprised that it was that pronounced.”

Among the women, on average, about 30.8% of the life expectancy at age 50 that they gained from adopting five, versus zero, of those lifestyle factors was attributed to a reduced risk of cardiovascular disease death; 21.2% was attributed to a reduced risk of cancer and 48% to other causes of death.

Among the men, those percentages were 34.1% attributed to a reduced risk of cardiovascular disease death, 22.8% attributed to a reduced risk of cancer and 43.1% to other causes.

The study had some limitations, including that the data on adherence to the five lifestyle factors were all self-reported, making outcome vulnerable to measurement errors.

Also, the data analysis did not include measures of certain health conditions that are risk factors for a shorter life expectancy, such as diabetes or high blood pressure.

That limitation, however, “is both a strength and a limitation, in a way … because what we’re estimating here is the prolongation of life expectancy just based on behaviors,” Stampfer said.
“Obviously, it’s much better to do these healthy behaviors from childhood, really, but if you’re beyond age 50, beyond age 60, beyond age 70, it’s not too late,” he added.

The factor that was seen as more ‘powerful’

The findings should encourage and motivate people to adopt a healthier lifestyle, said Dr. Douglas Vaughan, chairman of the department of medicine in Northwestern University’s Feinberg School of Medicine, who was not involved in the study.

Though the study highlighted how the combination of all five lifestyle factors could help prolong life expectancy, Vaughan pointed out how each individual factor also was tied to a reduced risk of premature death.

“It looks like cigarette smoking has a more powerful effect than the other lifestyle changes or behaviors. Certainly, maintaining a reasonable body-mass index is a great way to protect oneself against the development of diabetes,” Vaughan said.

Body-mass index, a calculation derived from a person’s weight and height, is used as a screening tool for body fatness. A normal or healthy body-mass index is typically said to be between 18.5 and 24.9.

“So, in aggregate, we see the effect on longevity, but you can imagine it’s largely through effects on cardiovascular risk and metabolic risk,” Vaughan said. “It suggests potentially at a defined point in life, say age 50, if you adhere to a healthy paradigm like this, you can have an impact on your longevity and on your health span.”

Dr. Jack Der-Sarkissian, a family medicine physician and assistant area medical director of Kaiser Permanente Los Angeles Medical Center, called smoking “the least-debated health risk factor.”

“Beyond cancer risk, smoking contributes to lung disease, heart disease and diabetes. The study shows that even minimal smoking — from one to 14 cigarettes a day — is associated with increased death due to cancer and heart disease,” said Der-Sarkissian, who was not involved in the new study.

As for some of the other lifestyle factors, “getting weight below a BMI of 30 appears to help considerably, according to the study. A higher body weight is linked to increased risk of diabetes and cancer, among other obesity-related conditions,” he said. “The study suggests physical activity of at least 30 minutes a day of moderate or vigorous activities, including brisk walking.”

https://www.cnn.com/2018/04/30/health/life-expectancy-habits-study/index.html

Scientists discover a new human organ – the insterstitium

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A newfound organ, the interstitium, resides beneath the top layer of skin, and in tissue layers lining the gut, lungs, blood vessels, and muscles. The organ is a body-wide network of interconnected, fluid-filled compartments supported by a meshwork of strong, flexible proteins.

Using a new way of visualising anatomy, scientists have just discovered a vast new structure in the human body that could be considered an organ in its own right.

The finding, published in the journal Scientific Reports, has important implications for our understanding of how all organs and tissues function, and could reveal previously unknown mechanisms driving diseases such as fibrosis and cancer.

But how could something so significant have gone unnoticed all this time?

It was well known that a layer of tissue lies just below the surface of the skin, and also lines the lungs, the digestive and urinary tracts, and much of the circulatory system. But it was thought this comprised little more than dense, connective tissue.

The new research reveals that it is actually a vast, interconnected system of fluid-filled compartments that extends all over the body.

That contents is extra-cellular, or “interstitial”, fluid. Accordingly, the structure has been dubbed “the interstitium”.

Until now, the interstitium had been hidden in plain sight because the traditional method of preparing microscope slides involves draining away fluid. This had caused the sacs to collapse, leaving only the supportive connective tissue visible.

But recently, researchers led by Neil Theise at New York University in the US began using probe-based confocal laser endomicroscopy, which aims laser light at living tissue and detects reflected fluorescent patterns, providing a different sort of microscopic image. While examining the bile duct of a cancer patient, they found a network of fluid-filled sacks that had never been seen before.

They soon found this network everywhere tissues are distended or compressed as part of normal function — which is quite a lot of the body — and propose that the interstitium may function as a shock absorber.

Its physical structure is certainly quite unusual: the fluid-filled spaces are supported by an extensive lattice of collagen bundles that are lined on only one side by what appear to be a type of stem cell.

These cells may help make collagen, and could aid in wound healing. Similarly, they could contribute to conditions associated with inflammation and ageing.

In addition to cushioning, the interstitium may have another important job. While it was known that interstitial fluid is the major source of lymph fluid, which carries immune cells throughout the body, just how it reaches the lymphatic system was unclear. The new research shows that the interstitium drains directly into the lymph nodes.

The study also shows that cancers, such as melanoma, are able to spread via the interstitium.

“This finding has potential to drive dramatic advances in medicine, including the possibility that the direct sampling of interstitial fluid may become a powerful diagnostic tool,” says Theise.

https://cosmosmagazine.com/biology/meet-your-interstitium