Lifeboat Foundation: Safeguarding Humanity
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Category: health – Page 396

Article (2017) about oxygen depletion. “There has been a clear decline in the volume of oxygen in Earth’s atmosphere over the past 20 years. Although the magnitude of this decrease appears small compared to the amount of oxygen in the atmosphere, it is difficult to predict how this process may evolve, due to the brevity of the collected records. A recently proposed model predicts a non-linear decay, which would result in an increasingly rapid fall-off in atmospheric oxygen concentration, with potentially devastating consequences for human health. We discuss the impact that global deoxygenation, over hundreds of generations, might have on human physiology. Exploring the changes between different native high-altitude populations provides a paradigm of how humans might tolerate worsening hypoxia over time. Using this model of atmospheric change, we predict that humans may continue to survive in an unprotected atmosphere for ~3600 years. Accordingly, without dramatic changes to the way in which we interact with our planet, humans may lose their dominance on Earth during the next few millennia.”

There has been a clear decline in the volume of oxygen in Earth’s atmosphere over the past 20 years. Although the magnitude of this decrease appears small compared to the amount of oxygen in the atmosphere, it is difficult to predict how this process may evolve, due to the brevity of the collected records. A recently proposed model predicts a non-linear decay, which would result in an increasingly rapid fall-off in atmospheric oxygen concentration, with potentially devastating consequences for human health. We discuss the impact that global deoxygenation, over hundreds of generations, might have on human physiology. Exploring the changes between different native high-altitude populations provides a paradigm of how humans might tolerate worsening hypoxia over time. Using this model of atmospheric change, we predict that humans may continue to survive in an unprotected atmosphere for ~3600 years. Accordingly, without dramatic changes to the way in which we interact with our planet, humans may lose their dominance on Earth during the next few millennia.

Keywords: Oxygen, Hypoxia, Acclimatization, Physiological adaptation.

Human dominion over planet Earth is driving profound changes that may culminate in extinction. Loss of natural vegetation and the burning of fossil fuels are altering our atmosphere at an alarming rate [1]. Two interconnected themes have received the most attention: the accelerated rise in atmospheric carbon dioxide concentration and the escalation of global temperatures. These changes are accompanied by natural phenomena with potentially catastrophic consequences, such as increasingly unpredictable climate subsystems and rising sea levels from polar ice cap recession [2–4]. If such environmental hazards were not a sufficient threat to the survival of Earth’s 7 billion plus human inhabitants, there is yet another concerning change already underway, global deoxygenation.

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Deep in the rocky earth, in the liquid-filled cracks created by fracking, lives a community of highly interactive microbes—one that could at once have serious implications for energy companies, human health and scientists investigating the potential for life on Mars.

New research has uncovered the genetic details of microbes found in fracking wells. Not only do a wide array of bacteria and viruses thrive in these crevices created by hydraulic fracturing—they also have the power to produce methane, according to a study led by scientists at The Ohio State University and published in the journal Proceedings of the National Academy of Sciences.

That means it’s possible that the tiny life forms could create more energy—and from a different source—than the fracking companies are going after in the first place.

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An international team of researchers have developed a low-cost sensor made from semiconducting plastic that can be used to diagnose or monitor a wide range of health conditions, such as surgical complications or neurodegenerative diseases.

The sensor can measure the amount of critical metabolites, such as lactate or glucose, that are present in sweat, tears, saliva or blood, and, when incorporated into a , could allow to be monitored quickly, cheaply and accurately. The new device has a far simpler design than existing sensors, and opens up a wide range of new possibilities for health monitoring down to the cellular level. The results are reported in the journal Science Advances.

The device was developed by a team led by the University of Cambridge and King Abdullah University of Science and Technology (KAUST) in Saudi Arabia. Semiconducting plastics such as those used in the current work are being developed for use in solar cells and flexible electronics, but have not yet seen widespread use in biological applications.

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A team of researchers from ETH Zurich and the University of Basel in Switzerland and Institut Universitaire de Technologie in France has that found that embryonic kidney cells engineered to produce insulin when exposed to caffeine were able to reduce glucose levels in mouse models. In their paper published in the journal Nature, the group describes their efforts and how well it worked in the mouse models.

People with diabetes suffer from higher than normal levels of glucose in the blood, which can lead to a host of health problems. Current treatments include drugs that make cells more sensitive to insulin, or injection of insulin to make more of it available to cells that need it. In this new effort, the researchers have developed a new way to get more insulin into the body when it is needed most.

Instead of adding externally, the researchers engineered embryonic kidney cells to produce it—but only when they were exposed to caffeine. The team chose caffeine because it has been so extensively studied and because the majority of people consume caffeinated beverages, such as coffee and soft drinks. They point out that caffeine is also a substance that appears very rarely in other foods, making its ingestion easy to regulate. The engineered were covered with a material that protected them from the immune system and were then put into a device that was implanted into the abdomens of mice that had been engineered to have diabetes. The researchers note that tend to spike after people (and mice) eat sugar or food material that the body converts to sucrose. Thus, the optimal time for giving the mice caffeine would be after eating.

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Only 35 per cent of five- to 17-year-olds and 62 per cent of children ages 3 and 4 are getting the recommended physical-activity levels for their age group (Editor’s note: around 60 minutes of moderate-to-vigorous physical activity daily, including vigorous-intensity activity on at least 3 days per week) and that this may be having an impact on the health of their brains.

___ Getting kids outside and active could help with brain health: Participaction report (The Globe and Mail): The physical benefits of kids leading an active lifestyle, including better heart heal…

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An international team of researchers has discovered evidence of 27 previously unknown viruses in bees. The finding could help scientists design strategies to prevent the spread of viral pathogens among these important pollinators.

“Populations of bees around the world are declining, and viruses are known to contribute to these declines,” said David Galbraith, research scientist at Bristol Myers Squibb and a recent Penn State graduate. “Despite the importance of bees as pollinators of flowering plants in agricultural and natural landscapes and the importance of viruses to bee health, our understanding of bee viruses is surprisingly limited.”

To investigate viruses in bees, the team collected samples of DNA and RNA, which is responsible for the synthesis of proteins, from 12 bee species in nine countries across the world. Next, they developed a novel high-throughput sequencing technique that efficiently detected both previously identified and 27 never-seen-before viruses belonging to at least six new families in a single experiment. The results appear in the June 11, 2018, issue of Scientific Reports.

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Some individuals worry they will discover things about their DNA that will be frightening — namely, the risks they run of contracting various diseases — and not know how to move forward with the information. Professional scientific skeptics contend the information may not even be as accurate as claimed, and lead people to make questionable health decisions. But there’s another type of risk that consumers aren’t focusing on as much, and it’s a big one: privacy. There is nothing more private than your personal genetic information, and sending away for a personal genome kit means sharing your DNA with the testing companies. What do they do with it, beyond providing consumers with genetic and health assessments?

Consumer DNA genetic testing kits are a booming business, and the biggest risk isn’t necessarily uncovering a health scare; it’s what these companies may do, or be forced to do, with your genetic data.

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T he HPV vaccine has almost completely wiped out infections in young women, and if expanded to men could prevent thousands of cancer cases in Britain each year, new figures suggest.

New figures from Public Health England show that the rate of Human Papilloma Virus (HPV) in women aged between 16 to 21 who were vaccinated between 2010 and 2016 has fallen by 86 per cent.

More than 3,000 women are diagnosed with cervical cancer each year, and more than 800 will die from the disease, with most cases caused by the HPV virus.

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Investigators at Harvard Medical School have identified the key cellular mechanisms behind vascular aging and its effects on muscle health, and they have successfully reversed the process in animals.

The scientists used a chemical compound that’s an NAD+ booster called NMN which plays a critical role in repairing cellular DNA as well as maintaining cell vitality to test what would happen.

Could reversing the aging of blood vessels hold the key to restoring youthful vitality? If the old adage “you are as old as your arteries” reigns true then the answer is yes, at least in mice.

According to a new study by Harvard Medical School researchers, they have identified the cellular mechanisms that cause the aging of vascular arteries as well as the effects of such aging on the health of muscles. The Medical team was also able to successfully reverse this aging process.

What these findings seem to indicate is that there’s a glitch in the normal crosswalk between both muscles and blood vessels and keeping both tissues healthy. The scientists were also able reverse the demise of blood vessels and muscle atrophy in the aging mice by using the synthetic precursors of two molecules naturally present in the body. This boosted their exercise endurance in the process.

The Medical team is excited because such a breakthrough will now pave the way to identifying new therapies for humans.

Study senior investigator David Sinclair, professor in the Department of Genetics at Harvard Medical School and co-director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School stated “we’ve discovered a way to reverse vascular aging by boosting the presence of naturally occurring molecules in the body that augment the physiological response to exercise.”

Because there are some very important differences in biology between humans and mice there’s a possibility that this treatment may not have the same effect in humans. Nonetheless, the research team plans to follow through with human clinical trials because the results of this experiment were important enough to prompt the research team in doing so.

Sinclair, who is also a professor at the University of New South Wales School of Medical Sciences in Sydney, Australia stated, “the approach stimulates blood vessel growth and boosts stamina and endurance in mice and sets the stage for therapies in humans to address the spectrum of diseases that arise from vascular aging.”

One of the side effects of aging is reduced blood flow and the compromise of oxygenation of organs and tissue because our tiniest blood vessels began to wither and die. Cardiac and neurologic conditions, muscle loss, impaired wound healing and overall frailty, and among other things are the results of vascular aging. As these blood vessels die there’s a loss of blood flow to organs and tissues which causes toxins build-up and a loss of oxygen.

For quite some time scientists have known the essential role that endothelial cells, which line blood vessels, play in the health and growth of blood vessels that supply oxygen-rich and nutrient-loaded blood to organs and tissues. Unfortunately, as with all things on the human body, these endothelial cells age having a detrimental effect on the body. New blood vessels fail to form, blood vessels atrophy, and the overall blood flow to most parts of the body diminishes. This has a powerful impact on muscles, which heavily rely on robust blood supply to function because they’re heavily vascularized.

Typically we exercise in hopes of slowing down sarcopenia, but unfortunately even that doesn’t last forever. Gradually our muscles grow weaker and begin to shrivel as part of the aging process.

What precisely curtails the blood flow and precipitates this unavoidable decline? Why does even exercise lose its protective power to sustain muscle vitality? Is this process reversible? There were some of the leading questions Sinclair and team had.

The Experiment/Results:

Sinclair and his team discovered through a series of experiments that the flow of blood is reduced as endothelial cells start to lose a critical protein known as sirtuin1, or SIRT1. SIRT1 delays aging and extends life in yeast and mice as shown in previous studies.

Research done previously by Sinclair and others has shown that NAD+ boosts the activity of SIRT1. SIRT1 loss is a result of the loss of NAD+, which is a key regulator of protein interactions and DNA repair that was identified more than a century ago. As NAD+ declines with age so does the protein SIRT1.

The results showed that the critical interface that enables the conversation between endothelial cells in the walls of blood vessels and muscle cells is provided by NAD+ and SIRT1.

SIRT1 signaling is activated and generates new capillaries, the tiniest blood vessels in the body that supply oxygen and nutrients to tissues and organs in young mice muscles. As the mice aged, however, the study found that muscle tissue was left nutrient-deprived and oxygen-starved as a result in the diminishment of NAD+ and SIRT1.

The researchers hope that their findings may pave the way to therapeutic advances that hold promise for the millions of older people for whom regular physical activity is not an option.

Abhirup Das, the studies first author, who conducted the work as a post-doctoral fellow in Sinclair’s lab, currently a visiting scholar in genetics at Harvard Medical School and a post-doctoral research fellow at the University of South New Wales School of Medical Sciences, said that “we reasoned that declining NAD+ levels reduce SIRT1 activity and thus interfere with aging mice’s ability to grow new blood vessels.”

The researchers then set their sights on the NAD+, which is a critical coenzyme for enzymes that fuel reduction-oxidation reactions, carrying electrons from one reaction to another, and as a cosubstrate for other enzymes such as the sirtuins and poly(adenosine diphosphate-ribose) polymerases.

The scientists used a chemical compound that’s an NAD+ booster called NMN (no not m&m!) which plays a critical role in repairing cellular DNA as well as maintaining cell vitality to test what would happen.

One of the results showed that treatment from NMN caused endothelial cells from humans and mice to have strong growth capacity and reduced cell death.

The team then wondered what would happen to a group of mice that were 20 months old—the rough equivalent of 70 in human years given NMN. After a 2 month time span the results showed that NMN treatment restored the number of blood capillaries and capillary density to those seen in younger mice. Blood flow to the muscles also increased and was significantly higher than blood supply to the muscles seen in same-age mice that didn’t receive NMN.

That wasn’t the most surprising result to the researchers however. What they discovered was that the aging mice showed in comparison to the entreated mice that they regained the capacity to exercise by 56 and 80% more. The untreated mice could only run 240 meters, or 780 feet, on average whereas the mice treated with NMN could run 430 meters, or about 1,400 feet, on average. This treatment could be an answer to humans who have lost the capacity to exercise due to other disabilities or age-related diseases.

The next step for the researchers was to explore methods for boosting the activity of SIRT1. To do this the researchers added a second compound NaHS, sodium hydrosulfide, which is known to be a precursor of SIRT1.

For four weeks a group of mice that were 32-month-old mice—the rough equivalent to 90 in human years—receiving the combo treatment. The results were significant! Not only were the mice able to run longer and faster but they were able to outperform the untreated mice by a longshot. The treated mice ran 1.6 times further than the untreated mice.

Study co-author James Mitchell, associate professor of genetics and complex diseases at the Harvard T. H. Chan School of Public Health stated that “these are really old mice so our finding that the combo treatment doubles their running capacity is nothing short of intriguing.”

“This observation underscores the notion that age plays a critical role in the crosstalk between blood vessels and muscles and points to a loss of NAD+ and SIRT1 as the reason behind loss of exercise effectiveness after middle age,” Das said.

One of the ultimate goals for the team is to eventually move forward in developing small-molecule, NMN-based drugs that mimic the effects of exercise—enhanced blood flow and oxygenation of muscles and other tissues. Though they must first replicate their findings first. Such therapies could potentially help with new vessel growth of organs that suffer tissue-damaging loss of blood supply and oxygen, a common scenario in heart attacks and ischemic strokes, the team said.

Harvard Medical School Report