Living in the Mountains is Great For Your Health

Looking for the secret to a healthier life? According to a recent study, it might be time to ditch the city and head to the mountains. Two million people living at elevations over 4,500 meters appear to have lower rates of metabolic diseases like coronary heart disease and diabetes. While daily mountain hikes could certainly contribute to good health, researchers now believe the key is low oxygen levels caused by high elevation living. This animal study could help find new ways to treat metabolic diseases by exploring the connection between oxygen levels and health.

Our bodies can adapt to a shortage of oxygen, also known as hypoxia. When exposed to low oxygen levels, different organs in our body switch up their energy sources and production pathways to keep us going. This fascinating finding could lead to identifying metabolic receptors that benefit us even in regular oxygen environments. Imagine being able to optimize our metabolism for maximum energy efficiency in any situation. But this adaptation only occurs for people living higher than 4,500 meters, where oxygen levels are only 11% compared to the 21% at sea level.

The researchers explored the effects of long-term hypoxia on the body. By examining the metabolic shifts that occur during adaptation to low oxygen levels, the scientists sought to gain insights into how hypoxia could protect against metabolic diseases. They put adult mice in pressure chambers with varying oxygen levels and monitored their temperature, carbon dioxide, behavior and blood sugar levels for three weeks. Using PET scans, they also tracked nutrient consumption in different organs.

After a few days adjusting to a new pressure chamber, the mice started to display some strange behavior. They were less active and at various times stayed completely still for hours. But, after the third week, things were back to normal. One interesting discovery was the effect of hypoxia on carbon dioxide levels in the blood. The mice breathed at a faster rate for more oxygen, which decreased CO2 levels initially, but this eventually assumed a normal rate. However, one change appeared to stick. The mice’s metabolism seemed to be permanently altered by the hypoxic conditions, with weight and lower blood sugar levels never returning to pre-hypoxia levels. This long-term impact is similar to what doctors notice in people that live at higher elevations.

PET scans revealed interesting changes in the metabolism of the mice in hypoxic conditions. While it was expected for glucose metabolism to increase, the study found that skeletal muscles and brown fat actually reduced their use of sugar. This challenges the assumption that the whole body is more efficient at using oxygen in this environment. Instead, certain organs become glucose savers while others consume more glucose. This suggests that there may be a promising connection between the drop in body weight and glucose levels seen in hypoxic mice and a reduced risk of various diseases such as heart disease.

This study sheds light on the remarkable ability of the body to adapt to low oxygen levels and could have important implications for understanding and treating metabolic diseases. It could lead to a better understanding and treatment of diseases related to oxygen deficiency and information on the potential effects of chronic hypoxia implications for human health.

To view the original scientific study click below:
Organ-specific fuel rewiring in acute and chronic hypoxia redistributes glucose and fatty acid metabolism

Aging Reversed / ABC News

Now researchers have found a way not just to stop, but, reverse the aging process. The key is something called a telomere. We all have them. They are the tips or caps of your chromosomes. They are long and stable in young adults, but, as we age they become shorter, damaged and frayed. When they stop working we start aging and experience things like hearing and memory loss.

In a recent study published in the peer reviewed journal Nature scientists took mice that were prematurely aged to the equivalent of 80-year-old humans, added an enzyme and essentially turned their telomeres back on. After the treatment they were the physiological equivalent of young adults. You can see the before and after pictures in the videos above. Brain function improved, their fertility was restored it was a remarkable reversal of the aging process. In the top video the untreated mouse shows bad skin, gray hair and it is balding. The mouse with it’s telomeres switched back on has a dark coat color, the hair is restored and the coat has a nice healthy sheen to it. Even more dramatic is the change in brain size. Before treatment the aged mice had 75% of a normal size brain like a patient with severe Alzheimers. After the telomeres were reactivated the brain returned to normal size. As for humans while it is just one factor scientists say the longer the telomeres the better the chances for a more graceful aging.

The formal study Telomere dysfunction induces metabolic and mitochondrial compromise was published in Nature.

Additional information published by Harvard can be found in the following articles.

Scientists Find Root Molecular Cause of Declining Health in the Old

Decoding Immortality – Smithsonian Channel Video about the Discovery of Telomerase

While scientists are not yet able to accomplish the same results in humans we believe we have developed a nutraceutical to help prolong youth and possibly extend life until age reversal therapy for humans becomes available.

Stem Cell Secret’s of 115 Year Old Woman

New evidence that adult stem cells are critical to human aging has recently been published on a study done on a super-centenarian woman that lived to be 115 years. At death, her circulating stem cell pool had declined to just two active stem cells from stem cell counts that are typically more than a thousand in younger adults. Super-centenarians have survived all the normal diseases that kill 99.9% of us before 100 years of age, so it has been a mystery as to what actually kills these hardy individuals. This recent data suggest that stem cell decline may be the main contributor to aging. If so, stabilizing stem cells may be the best thing one can do to slow your rate of aging.

There are many theories of aging that have been proposed. For example, damage to cells and tissues from oxidative stress has been one of the most popular fundamental theories of aging for more than half a century. Yet antioxidant substances or genes that code antioxidant enzymes have proven largely ineffective in slowing aging when tested in model animals. Thus, interest by scientists has shifted to other hypotheses that might provide a better explanation for the slow declines in function with age.

Stem cells provide one such promising mechanism of aging. Of course, we all know that babies are young and vigorous, independent of the age of their parents. This is because adults have embryonic stem cells that can generate young new cells needed to form a complete young baby. Indeed, these embryonic stem cells are the product of continuously evolving stem cell populations that go back to the beginning of life on earth over 3.5 billion years ago!

In adults, the mostly immortal embryonic stem cells give rise to mortal adult stem cells in all the tissues of the body. These adult stem cells can regenerate your cells and tissues as they wear out and need replacement. Unfortunate, adult stem cells also age, which leads to fewer cells and/or loss of function in cell replacement. As functional stem cells decline, skin and organs decline with age.

Blood from world’s oldest woman suggests life limit

Time Magazine: Long-Life Secrets From The 115-Year-Old Woman

Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis

The somatic mutation burden in healthy white blood cells (WBCs) is not well known. Based on deep whole-genome sequencing, we estimate that approximately 450 somatic mutations accumulated in the nonrepetitive genome within the healthy blood compartment of a 115-yr-old woman. The detected mutations appear to have been harmless passenger mutations: They were enriched in noncoding, AT-rich regions that are not evolutionarily conserved, and they were depleted for genomic elements where mutations might have favorable or adverse effects on cellular fitness, such as regions with actively transcribed genes. The distribution of variant allele frequencies of these mutations suggests that the majority of the peripheral white blood cells were offspring of two related hematopoietic stem cell (HSC) clones. Moreover, telomere lengths of the WBCs were significantly shorter than telomere lengths from other tissues. Together, this suggests that the finite lifespan of HSCs, rather than somatic mutation effects, may lead to hematopoietic clonal evolution at extreme ages.

Walking Fast Can Slow Down Aging

Want to add 16 years to your life? A new study from the University of Leicester says it’s as simple as picking up the pace. Turns out, walking briskly might be the secret to aging gracefully.

Remarkably, engaging in brisk walking throughout one’s life contributes to elongated telomeres, the essential safeguarding “caps” situated at the extremities of our chromosomes. Comparable to the function of the plastic tips on shoelaces, telomeres ensure DNA stability without carrying any genetic data themselves. In order to estimate an individual’s biological age scientists examine the length of these protective caps, with longer telomeres indicating a younger biological profile.

A recent study encompassing 400,000 UK Biobank participants discovered a fascinating correlation. Those participants with a swifter walking tempo appeared biologically 16 years younger by midlife. Remarkably, it seems brisk walking alone, independent of other physical pursuits, contributes to the extension of telomeres – a key component in our biological age determination.

A fascinating cellular investigation reveals that each cellular division causes a progressive shortening of telomeres, leading to a halt in cell division when they become critically short. The accumulation of senescent (elderly and dying) cells contributes to age-related diseases and fragility, although the exact relationship with telomere length remains hazy. By harnessing genetic data and wearable activity trackers, this groundbreaking research solidifies the connection between brisk walking and increased telomere length. This emphasizes the power of habitual physical activity intensity in promoting cellular health.

For the first time, innovative research has emerged linking walking speed to genetic data correlated with extended lifespans. This intriguing discovery builds upon earlier studies that revealed the multifaceted advantages of walking, encompassing physical, mental, and social aspects. Previous investigations into the connection between walking pace, physical activity, and telomere length have faced limitations due to inconsistent results and insufficient data quality. This groundbreaking study prompts further scientific exploration in the field of human longevity.

The intriguing implication that a slower walking pace might indicate a higher risk of chronic illness and poor aging showcases the potential role of activity intensity in optimizing health interventions. To enhance overall well-being, people with higher capabilities could increase the steps they take within a given time frame. Previous studies from Leicester researchers highlight that an engaging ten minutes of brisk walking daily could extend life expectancy by up to two decades compared to those with a more leisurely pace.

The researchers in this investigation observed that there was no connection between a leisurely walking speed and diminishing telomere length. Although past findings have demonstrated that a brisk ambulation pace strongly correlates with an individual’s health condition, evidence that this pace inherently leads to improved health was lacking. By analyzing genetic data, this study revealed that maintaining a faster walking tempo could indeed contribute to a relatively youthful biological age, as indicated by telomere measurements.

To view the original scientific study click below:
Investigation of a UK biobank cohort reveals causal associations of self-reported walking pace with telomere length

The Obesity Paradox

Defying conventional belief, epidemiology studies have frequently uncovered the “obesity paradox,” whereby excess body weight seemingly has marginal impact on mortality risk. Critics argue that such paradox arises from methodological limitations, specifically the usage of body-mass index (BMI) to assess obesity. When accounting for BMI’s inherent drawbacks, recent research unveils the absence of this paradox, underscoring that higher levels of body fat contribute to an increased likelihood of death.

While it’s widely accepted that obesity contributes to numerous health issues, recent studies reveal a fascinating “U” shaped curve, bringing these long-held beliefs into question. This scientific anomaly fuels our curiosity, reshaping our understanding of obesity’s intricate role within the human body.

Unraveling the enigmatic “U” in the relationship between Body-Mass Index (BMI) and mortality risk unfolds some fascinating revelations. Scrutinizing countless epidemiological studies exposes an unexpected twist. Individuals with an “overweight” BMI (25-30) showcase the lowest threat to their mortality, while those deemed “obese” (30-35) exhibit marginal or negligible risk compared to the “healthy” BMI range (18.5-25). However, danger lurks in the extremities of the BMI spectrum, as the “underweight” and extremely obese (35+) populations grapple with increased mortality risks. Moreover, numerous studies suggest that obesity could paradoxically serve as a protective factor for older adults and those affected by chronic illnesses,

The obesity paradox, which emerged from studies reliant on BMI measurements, has recently been contested by critics who argue that BMI is not an accurate measure of obesity. Their concern lies in the fact that BMI does not account for body composition or the distribution of fat in the body. For instance, a highly fit person could be misclassified as obese, while a slender individual with dangerous fat deposits around their organs may be deemed “healthy.” Thus, the reliance on BMI in obesity research raises questions about the validity of the obesity paradox.

A 2020 review article by Italian scientists at Sapienza University suggests a reevaluation of obesity measurement techniques. They recommend utilizing excess body fat as an indicator rather than BMI. Fascinatingly, when researchers in 2018 adjusted BMI to consider muscle mass and its correlation with mortality risk, the typical “U” shaped curve altered into a nearly straight line. This adjustment revealed a drastic increase in death risk – almost 70% – for extremely obese individuals compared to those with healthy body composition.

A comprehensive analysis of an extensive 40-year dataset involving around 18,000 participants investigated the correlation between body fat distribution, BMI levels, and mortality risk. This study highlights that the implications of high BMI on health and mortality may not be as binary as previously thought, and instead, could be dependent on the duration spent at a high or low BMI. Consequently, this emerging hypothesis challenges the conventions of generalized categorization, offering fresh insights into understanding the intricacies of BMI’s influence on overall well-being.

In a fascinating revelation, after scrupulously eliminating data biases, it was discovered that obesity elevates the risk of death by an astounding 91%, substantially more than previously thought. The enigmatic U-shaped curve vanished, taking the paradox with it. It was further deduced that excess weight is linked to one in six US fatalities. Public health connoisseurs in a 2017 publication asserted that paradoxes warrant skepticism and that incongruous findings should be deliberated among interdisciplinary professionals. The true “paradox” lies in researchers asserting the existence of such without meticulously examining potential methodological justifications.

To view the original scientific study click below:
Obesity or BMI Paradox? Beneath the Tip of the Iceberg

Farmed Salmon Shown To Have High Toxin Levels

Did you know that the delicious farm-raised salmon on your plate might be hiding a secret? Recent research on over two metric tons of salmon from North America, South America, and Europe revealed some surprising findings. Farm-raised salmon were found with significantly higher levels of PCBs and other toxins when compared to wild salmon. This discovery raises concerns about the potential health risks of indulging in your favorite fish dish.

The production of farmed salmon has skyrocketed by 40 times in just two decades. This astounding leap can be credited to the sprawling salmon farms across Northern Europe, Chile, and North America, which now account for more than half the world’s salmon sales.

Although salmon is known for its numerous health benefits, there’s an untold story about the toxins they potentially accumulate. Salmon, being the fish predators they are, rank high on the food chain, making them prone to build-up of toxins in their bodies.

To gain a better understanding of the lives and diet habits of Pacific salmon, researchers have recently conducted an extensive study involving five wild species from three different regions in North America. For this research project, Chinook, Coho, chum pink and sockeye were all taken into consideration as scientists sought to uncover more information.

After an analysis of salmon samples was done, it revealed a fascinating pattern – farmed Atlantic salmon contained considerably higher amounts of 13 toxins when juxtaposed with their wild Pacific counterparts. Upon dissecting this discovery by geographical regions, it was observed that both European and North American farmed specimens exhibited substantial elevations in all 14 toxin levels in comparison to wild Pacific salmon. Intriguingly, South American farmed salmon only displayed increased levels of 6 toxins, and even demonstrated significantly reduced levels of two toxins (HCB and lindane) compared to wild salmon species.

The team delved into the world of farm-raised salmon and their diet, specifically “salmon chow” – a concoction of pulverized fish and oil. Unveiling a powerful link between the toxicity levels in chow and salmon, the study propounded that these menacing toxins find their way from the feed into the salmon, showing the journey of contaminants.

Farmed salmon carries a higher amount of toxins compared to their wild, open ocean counterparts. So, the next time you’re at the grocery store or your favorite seafood restaurant, pause and ponder. Do you want the economic benefits of farmed salmon or the healthy goodness of their wild counterparts?

To view the original scientific study click below:
Global Assessment of Organic Contaminants in Farmed Salmon

Successful Transformation of Stem Cells into Bone Cells

Scientists recently achieved a breakthrough in stem cell research with the successful transformation of stem cells into bone cells via specifically programmed materials. Using shape-memory polymers and dynamic scaffolds, researchers were able to make this discovery possible.

Stem cells are known to be incredibly malleable, since they have the potential to transform into a variety of different cell types. Scientists have been able to control and direct this transformation process by altering the environment around them. This research is being used in tissue engineering which helps regenerate or repair damaged tissues with substitutes materials mainly via static scaffolds.

Researchers engineered a polymer sheet with the remarkable ability to morph in response to temperature changes. By creating grids on its underside and regulating the stretch as temperatures varied, they employed this artificial muscle’s dynamic movement to synchronise signals from two distinct stimuli. These were physical change of temperature and mechanical stimulus which then prompted stem cells to seed onto it into forming bone tissue.

The polymer actuator sheet possesses an incredible shape-memory function that acts like a transducer, allowing it to effectively instruct cells what to do. By combining changes in temperature with the repeated stretching motion of the film, the experiments showed successful differentiation into bone cells from stem cells.

These advanced polymer sheets can be used to treat bones damaged beyond the body’s ability to heal naturally. During an operation, stem cells from a patient’s bone marrow could span across these programmed membranes and wrap around destroyed bones. This would than act as reinforcements while adapting their function like they had been previously trained.

This new development could mean revolutionary advancements in medical treatments.

To view the original scientific study click below:
Polymeric sheet actuators with programmable bioinstructivity

Exciting New Discovery For Stem Cell Therapy

Researchers from The Univ. of Melbourne and the Australian Nat’l Univ. have made a major breakthrough that could revolutionize stem cell delivery. They’ve created a novel ‘hybrid’ hydrogel, which enables clinicians to transport healthy amounts of stem cells directly into the site of brain injuries in mice. This overcomes one of the biggest challenges surrounding this technology since its inception over thirty years ago.

The potential for hydrogel is immense. This water-based gel can not only transport substances into the body, but also provides a nourishing environment that helps stem cells to thrive. It has the ability to deliver oxygen and supply vital nutrients to promote healthy growth. After a stroke or other injury, the brain can suffer from damage to its blood system. To allow cells in that area of the brain to survive until it is repaired, this innovative hydrogel has been developed as an artificial supply of much needed oxygen and nutrients. This has hope for scientists that it will help enhance current treatments involving stem cell therapy and aid in restoring damaged tissues across many areas of medicine.

After five years of intensive study, the team found a breakthrough to ensure stem cells remain viable during delivery. This progress was made possible by utilizing a synthetic protein based on myoglobin from whales and horses. Myoglobin is an oxygen-storing compound commonly found in deep water mammals for extended dives, and galloping equines needing sustainable energy levels over long distances.

This study has achieved incredible progress in healing injured brain tissue. The encouraging results suggest that new, healthy tissue can be created for future therapies. It was discovered that by infusing the delivery hydrogel with myoglobin and oxygen supply, stem cells survive longer and are able to mimic natural responses of regular functioning brain matter. This opens up exciting doors into furthering our understanding of regenerative science.

Researchers and clinicians around the world are brimming with excitement over this recent breakthrough. It has been successfully demonstrated within mice brains, but experts believe it can be generalized to have a broad range of applications. This could be from cell transplantation to drug delivery and even offering 3D versions of diseases in vitro.

No longer bound by traditional limitations, this proof-of-concept discovery offers hope that clinicians may soon have an effective tool to aid the regeneration process. This could pave the way for revolutionary medical treatments using injectable nanomaterials – ushering us into an exciting new era of healthcare.

To view the original scientific study click below:
Hydrogel oxygen reservoirs increase functional integration of neural stem cell grafts by meeting metabolic demands

Muscle Stem Cells Regenerated By Consistent Aerobic Exercise

It’s no secret that getting older can take a toll on the body, with increased risks of heart disease, dementia and reduced immune function. But new research has uncovered evidence that aerobic exercise may combat those effects by actually reversing aging’s impact on essential muscle stem cells involved in tissue regeneration. You don’t have to settle for slowing down as years accumulate. It could be possible to bounce back from workouts or illnesses more easily than before.

Exercise has long been known to promote health and extend life, but this new research takes it one step further. It indicates that aerobic activities like jogging, swimming or cycling can help older individuals recover faster than they would naturally. In the future these results might form a basis for creating de-ageing drugs meant specifically for muscle stem cells. Exercise isn’t just about adding years to your lifespan anymore. It now could potentially reverse age related diseases as well.

This research uncovered a promising result. Aerobic exercise can demonstrate anti-aging benefits on cells, encouraging them to behave with renewed youth. To confirm this outcome, two groups of mice were observed. One group was given the ability to run up to 10km each night for three weeks while the other group had no opportunity for physical activity. Sure enough, after only seven days both older and younger mice had established an active nightly routine.

Regular aerobic exercise like swimming, running or cycling may be the human equivalent to mice voluntarily turning a wheel for three weeks. In this study, it was found that muscle stem cells from older exercising mice were just as effective at regenerating fibers in injured tissue compared with younger counterparts. Thus, indicating physical activity’s positive effect on aging muscles.

The research indicates that sustained aerobic exercise can have an overall rejuvenating effect and improve muscle stem cell function in older animals. This was observed even when there wasn’t an increase in the number of cells present. Rather, it facilitated tissue repair so effectively that it seemed as though those aging cells were turned back into young ones. However, the benefit is fleeting if activity levels taper off after one week post-exercise causing the effects to dissipate.

Many of the researchers were surprised when they found that running a wheel did not improve muscle repair in young mice. Young mice saw no improvement to muscle repair despite running on the wheel – as if they had already reached peak efficiency.

Through the study, scientists have unlocked the potential of aerobic exercise to restore and accelerate regeneration in muscle stem cells. Exercise has the potential to reverse age-related decline in stem cells, thanks to a tiny protein called cyclin D1. This exciting discovery means scientists can now target this critical component of tissue repair with drug therapies or prescribed exercise regimens. However, before any anti-aging advances can come into full effect further research is necessary within human studies.

The findings suggest voluntary physical activity on a consistent basis will help us live our best lives by combating age related illnesses while also allowing us to stay functionally younger longer.

To view the original scientific study click below:
Exercise rejuvenates quiescent skeletal muscle stem cells in old mice through restoration of Cyclin D1

Research Shows You Can Reactivate Aging Brain Stem Cells

Our brain is capable of generating new neurons even late in life, an ability which plays a vital role in memory processes. Unfortunately, age and Alzheimer’s can severely impede this regenerative capacity, weakening the hippocampus’ efficiency to remember.

A team of researchers from the University of Zurich recently discovered that a decrease in the number of newly generated neurons is linked with aging. This occurs due to faulty distribution of proteins between daughter cells, caused by an imbalance of nucleic protein structures within neural stem cells.

With aging comes a decline in the production of lamin B1, an essential nuclear protein. Rresearchers conducting experiments on mice were able to reverse this process and revitalize stem cells by increasing levels of lamin B1. Utilizing genetic engineering and advanced microscope techniques allowed doctoral candidate Khadeesh bin Imtiaz to identify a direct connection between these processes. This could lead us closer towards unlocking our body’s full potential throughout every part of life.

The research team is working diligently to combat the effects of aging on stem cells through a variety of projects. As we age, many important regenerative processes become impaired throughout our bodies, including in brain stem cells. While this study was specific to their role, similar mechanisms likely play an influential part when it comes to other types of stem cell deterioration with age as well.

From this research, a vital leap forward has been taken in comprehending how age influences the behavior of stem cells. We’ve discovered that we can rekindle aging brain stem cells, bringing us closer to potentially boosting levels of neurogenesis. This is especially important for elderly individuals or those grappling with degenerative diseases like Alzheimer’s.

With this new knowledge, it may be possible for scientists to create solutions and therapies aimed at preserving or even re-establishing healthy neuron formation as we age.

To view the original scientific study click below:
Declining lamin B1 expression mediates age-dependent decreases of hippocampal stem cell activity