Our Body

Environmental Impact on Health

Summary

  • Environmental factors, including pollution and lifestyle choices, significantly influence health outcomes and longevity.
  • Studies indicate that environmental exposures account for approximately 17% of mortality risk, while genetic factors contribute about 2%.
  • Key environmental determinants impacting health include air pollution, socioeconomic status, physical activity, and smoking.
  • Early-life exposures, such as maternal smoking and childhood body weight, can have long-term health implications.
  • Addressing environmental risks offers substantial opportunities for enhancing public health and extending life expectancy.

Introduction

Understanding the determinants of health outcomes and longevity has been a focal point of medical research for decades. While genetic makeup undeniably plays a role, a growing body of evidence underscores the profound impact of environmental exposures on health. This article delves into how environmental factors, encompassing both physical elements like pollution and behavioral aspects such as lifestyle choices, dominate in determining disease risk and lifespan.

The Exposome: A Comprehensive Framework

The term “exposome” refers to the totality of environmental exposures an individual encounters throughout their life, from conception onward. This concept encompasses:

  • External Factors: Air and water quality, chemical exposures, radiation, and socioeconomic conditions.​
  • Internal Factors: Metabolic processes, inflammation, and gut microbiota.​

By considering the exposome, researchers aim to capture the complex interactions between various environmental exposures and their cumulative effects on health.

Environmental Exposures vs. Genetics: Quantifying the Impact

Recent studies have sought to quantify the relative contributions of environmental exposures and genetic factors to health outcomes. Notably:

  • A comprehensive analysis involving over 490,000 individuals revealed that environmental factors accounted for approximately 17% of mortality risk, whereas genetic factors contributed about 2%.

These findings highlight that environmental determinants have a nearly tenfold greater influence on health outcomes compared to genetics.

Key Environmental Determinants Affecting Health

Several environmental factors have been identified as significant determinants of health outcomes:

  • Air Pollution: Long-term exposure to pollutants like nitrogen dioxide (NO₂) has been associated with increased risks of respiratory diseases, cardiovascular conditions, and certain cancers.
  • Socioeconomic Status: Factors such as income, education, and occupation influence access to healthcare, nutrition, and living conditions, thereby impacting overall health. ​
  • Lifestyle Choices: Behaviors including physical activity levels, dietary habits, and smoking have profound effects on health. For instance, smoking is linked to 21 different diseases, while physical inactivity is associated with 17 diseases. ​Time
    Early-Life Exposures and Long-Term Health

Environmental exposures during early life stages can have lasting health implications:

  • Maternal Smoking: Exposure to tobacco smoke in utero is linked to respiratory issues and other health problems in later life.
  • Childhood Body Weight: Early-life obesity is associated with an increased risk of chronic diseases such as diabetes and cardiovascular conditions in adulthood. ​

Implications for Public Health

The dominance of environmental factors in determining health outcomes presents both challenges and opportunities:

  • Policy Development: Implementing policies aimed at reducing pollution, improving socioeconomic conditions, and promoting healthy lifestyles can significantly enhance public health.​
  • Preventive Healthcare: Emphasizing preventive measures that address environmental risks can lead to reductions in disease incidence and healthcare costs.​
    Conclusion

While genetics play a role in health outcomes, environmental exposures are the predominant determinants of disease risk and longevity. By acknowledging and addressing these factors, societies can implement strategies that substantially improve public health and extend healthy lifespans.

References

Understanding Biological Organ Aging: A New Frontier in Disease Prediction

Summary:

  • Organs within the same individual can age at different rates.
  • A simple blood test can determine the biological age of specific organs.
  • Accelerated aging in certain organs predicts higher risk for related diseases.
  • Rapid immune system aging is linked to increased dementia risk.
  • Future healthcare may focus on personalized disease prevention based on organ-specific aging.

Recent research led by University College London (UCL) has unveiled that our organs do not age uniformly; instead, each can age at its own pace. This discovery opens the door to predicting disease risks decades in advance through a straightforward blood test that assesses the biological age of individual organs.

The study, published in The Lancet Digital Health, analyzed data from over 6,200 middle-aged adults participating in the British Whitehall II study. Blood samples collected in the late 1990s were used to determine the biological age of nine organs: heart, blood vessels, liver, immune system, pancreas, kidneys, lungs, intestines, and the brain. The findings revealed that organs often aged at different rates within the same person.

Over a 20-year follow-up period, researchers discovered that accelerated aging in specific organs could predict the risk of 30 different diseases. For instance, a rapidly aging heart indicated a higher likelihood of cardiovascular diseases, while accelerated lung aging was associated with respiratory infections, chronic obstructive pulmonary disease (COPD), and lung cancer.

One surprising outcome was the link between the immune system’s aging and dementia risk. Individuals whose immune systems aged faster were more prone to developing dementia, suggesting that inflammatory processes may play a crucial role in neurodegenerative diseases.

The study also highlighted the interconnectedness of our organs. Accelerated aging in one organ can impair the function of others, leading to multiple age-related diseases across different organs. For example, those with rapidly aging kidneys were more likely to develop vascular disease, type 2 diabetes, and liver diseases.

Advancements in proteomic analyses now allow thousands of proteins to be measured simultaneously from a single blood sample. This technological leap offers a valuable window into monitoring the pace of aging and supports a shift toward more personalized and effective disease prevention. With proteomic signatures of organ aging, risks can be identified earlier, and interventions can be tailored to each person’s unique profile.

Lead author Professor Mika Kivimaki envisions a future where healthcare prioritizes early prevention of age-related diseases, tailoring interventions to individual risk profiles. Such proactive measures could help individuals maintain their health and quality of life as they age.

Source: (sciencedaily.com)

Has The Cellular Aging Master Circuit Been Discovered?

Humans have long searched for the possibility to extend life and some to even become immortal. But when it comes down to it many consider this to just be a flight of fanciful dreams. But according to research this is not necessarily true. In recent years research is indicating that we can take steps to extend our healthspan and in turn longevity. Now University of California researchers have revealed a groundbreaking discovery regarding the intricacies of cellular aging, and in light of their findings the team suggests that the notion of dramatically extended human lifespan is not so far fetched after all.

Each individual’s lifespan and personal rate of aging is determined by the aging of their individual cells. This study set out to investigate different types of cells at different ages, at different speeds based on different causes and stimuli using the budding yeast Saccharomyces cerevisiae which provided a suitable model to track the aging mechanisms of various cell types.

The study published in Science found that two cells made of the exact same genetic material and residing in the same bodily location can age in vastly different ways and cellular/molecular trajectories. Using a variety of complex techniques it was discovered that about half of the cells age due to a slow decline in the stability of their nucleus, while the other cells appear to age primarily due to dysfunctional mitochondria.

At the beginning of their existence cells appear to start aging early on in their nucleolar or mitochondrial path of aging, and they continue to follow the same aging process until they die off. The team claims to have been able to find the master circuit that is in charge of controlling these aging processes and paths among the cells.

“To understand how cells make these decisions, we identified the molecular processes underlying each aging route and the connections among them, revealing a molecular circuit that controls cell aging, analogous to electric circuits that control home appliances,” says senior study author Nan Hao, an associate professor in the Section of Molecular Biology, Division of Biological Sciences.

Their discovery allowed for the construction of a new model of the aging landscape, and the revelation that the team might be able to conceivably manipulate and optimize the aging process. As such using a series of computer simulations the team reprogrammed the master molecular circuit via DNA modifications which resulted in the creation of a novel aging route that offered a much longer lifespan. The team plans to continue testing their model on more complex cells before moving onto human cell testing.

“Our study raises the possibility of rationally designing gene or chemical-based therapies to reprogram how human cells age, with a goal of effectively delaying human aging and extending human healthspan,” Hao says.

“Much of the work featured in this paper benefits from a strong interdisciplinary team that was assembled,” says Biological Sciences Professor of Molecular Biology Lorraine Pillus, a study co-author. “One great aspect of the team is that we not only do the modeling but we then do the experimentation to determine whether the model is correct or not. These iterative processes are critical for the work that we are doing.”

Read the full story.

Source: WorldHealth.net.

Clinical Trial Suggests Pomegranate Molecule Has Anti-Aging Benefits

Supplementation with Urolithin A (“UA”), a pomegranate metabolite is suggested to safely offer anti-aging benefits due to its impact on mitochondrial and cellular health found in the first human double blind, randomized, placebo controlled trial conducted by Amazentis and Swiss Institute of Bioinformatics.

“There are currently no effective solutions to treat age-related decline in muscle function other than months of exercise. This is an important first clinical validation that shows Urolithin A could be a promising solution for the management of healthy muscle function during ageing,” says Professor Roger Fielding, PhD of Tufts University. “The mitophagy activator Urolithin A is safe and induces a molecular signature of improved mitochondrial and cellular health in humans.”

“This positive clinical translation of Urolithin A shows its potential to play an important role in advanced nutritional approaches to improve mitochondrial health through mitophagy and biogenesis, and, as a result, cellular health in humans,” says co-author Professor Johan Auwerx, MD, PhD of Amazentis Ecole Polytechnique Fédérale de Lausanne.

As published in the journal Nature Metabolism 60 healthy but sedentary elderly participants were divided into 4 groups received either a placebo, 250, 500, or 1,000 mg dose of Urolithin A daily over the course of 28 days. Efficacy of UA was determined by examining cellular and mitochondrial health biomarkers in blood and muscle tissue; findings suggest that Urolithin A may help to slow down the aging process by improving the functioning of the mitochondria.

Urolithin A may be the only known compound that can re-establish a cell’s ability to recycle defective mitochondria, this happens naturally in younger people but with age the body loses it ability to do this causing sarcopenia and weakening of other tissues.

Urolithin A is a microflora derived metabolite of ellagitannins, and it is the lead candidate of Amazentis as an oral formulation, the company hopes to build on the promising results to bring a product to market quickly. Nestle Health Science has announced a global partnership with the company to develop products containing UA to develop opportunities in healthcare and medical nutrition.

Check the full story.

Source: WorldHealth.net

Cell Aging Can Be Slowed by Oxidants

At high concentrations, reactive oxygen species – known as oxidants – are harmful to cells in all organisms and have been linked to ageing. But a study from the Chalmers University of Technology has now shown that low levels of the oxidant hydrogen peroxide can stimulate an enzyme that helps slow down the ageing of yeast cells.​

​One benefit of antioxidants, such as vitamins C and E, is that they neutralize reactive oxygen species – known as oxidants – which may otherwise react with important molecules in the body and destroy their biological functions. Larger amounts of oxidants can cause serious damage to DNA, cell membranes and proteins for example. Our cells have therefore developed powerful defence mechanisms to get rid of these oxidants, which are formed in our normal metabolism.

It was previously believed that oxidants were only harmful, but recently we have begun to understand that they also have positive functions. Now, the new research from Chalmers University of Technology shows that the well-known oxidant hydrogen peroxide can actually slow down the ageing of yeast cells. Hydrogen peroxide is a chemical used for hair and tooth whitening, among other things. It is also one of the oxidants formed in our metabolism that is harmful at higher concentrations.

Less food gives longer life

The Chalmers researchers studied the enzyme Tsa1, which is part of a group of antioxidants called peroxiredoxins.

“Previous studies of these enzymes have shown that they participate in yeast cells’ defences against harmful oxidants,” says Mikael Molin, who leads the research group at Chalmers’ Department of Biology and Biological Engineering. “But the peroxiredoxins also help extend the life span of cells when they are subjected to calorie restriction. The mechanisms behind these functions have not yet been fully understood.”

It is already known that reduced calorie intake can significantly extend the life span of a variety of organisms, from yeast to monkeys. Several research groups, including Mikael Molin’s, have also shown that stimulation of peroxiredoxin activity, in particular, is what slows down the ageing of cells, in organisms such as yeast, flies and worms, when they receive fewer calories than normal through their food.

“Now we have found a new function of Tsa1,” says Cecilia Picazo, a postdoctoral researcher at the Division of Systems and Synthetic Biology. “Previously, we thought that this enzyme simply neutralises reactive oxygen species. But now we have shown that Tsa1 actually requires a certain amount of hydrogen peroxide to be triggered to participate in the process of slowing down the ageing of yeast cells.”

Surprisingly, the study shows that Tsa1 does not affect the levels of hydrogen peroxide in aged yeast cells. On the contrary, Tsa1 uses small amounts of hydrogen peroxide to reduce the activity of a central signalling pathway when cells are getting fewer calories. The effects of this ultimately lead to a slowdown in cell division and processes linked to the formation of the cells’ building blocks. The cells’ defences against stress are also stimulated – which causes them to age more slowly.

Could lead to drugs that mimic the positive effects of calorie restriction

“Signal pathways which are affected by calorie intake may play a central role in ageing by sensing the status of many cellular processes and controlling them,” says Mikael Molin. “By studying this, we hope to understand the molecular causes behind why the occurrence of many common diseases such as cancer, Alzheimer’s disease, and diabetes shows a sharp increase with age.”

The fact that researchers have now come a step closer to understanding the mechanisms behind how oxidants can actually slow down ageing could lead to new studies, for example looking for peroxiredoxin-stimulating drugs, or testing whether age-related diseases can be slowed by other drugs that enhance the positive effects of oxidants in the body.

The Chalmers researchers have shown a mechanism for how the peroxiredoxin enzyme Tsa1 directly controls a central signalling pathway. It slows down ageing by oxidizing an amino acid in another enzyme, protein kinase A, which is important for metabolic regulation. The oxidation reduces the activity of protein kinase A by destabilizing a portion of the enzyme that binds to other molecules. Thus, nutrient signalling via protein kinase A is reduced, which in turn downregulates the division of cells and stimulates their defence against stress.

Other studies have also shown that low levels of reactive oxygen species can be linked to several positive health effects. These oxidants are formed in the mitochondria, the ‘powerhouse’ of a cell, and the process, called mitohormesis, can be observed in many organisms, from yeast to mice. In mice, tumour growth is slowed by mitohormesis, while in roundworms it has been possible to link both peroxiredoxins and mitohormesis to the ability of the type 2 diabetes drug metformin to slow cellular ageing.

Read the full story.

Source: WorldHealth.net

What Makes Hard Workouts So Effective

High-intensity interval training strengthens the heart even more than moderate exercise does. Now researchers have found several answers to what makes hard workouts so effective.

“Our research on rats with heart failure shows that exercise reduces the severity of the disease, improves heart function and increases work capacity. And the intensity of the training is really importance to achieve this effect,” says Thomas Stølen, a researcher at the Norwegian University of Science and Technology (NTNU).

Stølen and his colleague Morten Høydal are the main authors of a comprehensive study published in the Journal of Molecular and Cellular Cardiology. The researchers went to great lengths to investigate what happens inside tiny heart muscle cells after regular exercise.

“We found that exercise improves important properties both in the way heart muscle cells handle calcium and in conducting electrical signals in the heart. These improvements enable the heart to beat more vigorously and can counteract life-threatening heart rhythm disorders,” says Stølen.

For a heart to be able to beat powerfully, regularly and synchronously, a lot of functions have to work together. Each time the heart beats, the sinus node – the heart’s own pacemaker – sends out electrical impulses to the rest of the heart. These electrical impulses are called action potentials. All the heart muscle cells are enclosed by a membrane. At rest, the electrical voltage on the inside of the cell membrane is negative compared to the voltage on the outside. The difference between the voltage on the outside and the inside of the cell membrane is called the resting membrane potential.

When the action potentials reach the heart muscle cells, they need to overcome the resting membrane potential of each cell to depolarize the cell wall. When this happens, calcium can flow into the cell through channels in the cell membrane.

Calcium initiates the actual contraction of the heart muscle cells. When this process is complete, calcium is transported out of the cell or back to its storage site inside each heart muscle cell. From there, the calcium is ready to contribute to a new contraction the next time an action potential comes rushing by. If the heart’s electrical conduction or calcium management system fails, the risk is that fewer heart muscle cells will contract, the contraction in each cell will be weak, and the electrical signals will become chaotic so that the heart chambers begin to flutter.

“All these processes are dysfunctional when someone has heart failure. The action potentials last too long, the resting potential of the cells is too high, and the transport function of the calcium channels in the cell wall is disturbed. Calcium then constantly leaks from its storage places inside every heart muscle cell,” Stølen says.

Before Stølen gives us the rest of the good news, he notes, “Our results show that intensive training can completely or partially reverse all these dysfunctions.”

Normally, the sinus node causes a human heart to beat between 50 and 80 beats every minute when at rest. This is enough to supply all the organ systems and cells in the body with as much oxygen-rich blood as they need to function properly.

When we get up to take a walk, our heart automatically starts beating a little faster and pumping a little harder so that the blood supply is adapted to the increased level of activity. The higher the intensity of the activity, the harder the heart has to work.

Exercise strengthens the heart so it can pump more blood out to the rest of the body with each beat. Thus, the sinus node can take it a little easier, and well-trained people have a lower resting heart rate than people who have not done regular endurance training.

At the other end of the continuum are people with heart failure. Here the pumping capacity of the heart is so weak that the organs no longer receive enough blood to maintain good functioning. People with heart failure have a low tolerance for exercise and often get out of breath with minimal effort.

In other words, increasing the pumping power to the heart is absolutely crucial for the quality of life and health of people with heart failure.

Many of the more than 100,000 Norwegians who live with heart failure have developed the condition after suffering a major heart attack – just like the rats in Stølen and Høydal’s study.

In the healthy rats, the heart pumped 75 percent of the blood with each contraction. In rats with heart failure, this measure of pump capacity, called ejection fraction, was reduced to 20 per cent, Stølen says.

The ejection fraction increased to 35 percent after six to eight weeks with almost daily interval training sessions on a treadmill. The rats did four-minute intervals at about 90 percent of their maximum capacity, quite similar to the 4 × 4 method that has been advocated by several research groups at NTNU for many years.

“The interval training also significantly improved the rats’ conditioning. After the training period, their fitness level was actually better than that of the untrained rats that hadn’t had a heart attack,” says Stølen.

Impaired calcium handling in a heart muscle cell not only causes the cell to contract with reduced force every time there is an action potential. It also causes the calcium to accumulate inside the fluid-filled area of the cell – the cytosol – where each contraction begins.

The calcium stores inside the cells are only supposed to release calcium when the heart is preparing to beat. Heart failure, however, causes a constant leakage of calcium out of these stores. After each contraction, calcium needs to be efficiently transported back into the calcium stores – or out of the heart muscle cell – via specialized pumps. In heart failure patients, these pumps work poorly.

When a lot of calcium builds up inside the cytosol, the heart muscle cells can initiate new contractions when they’re actually supposed to be at rest. An electrical gradient develops which causes the heart to send electrical signals when it shouldn’t. This can cause fibrillation in the heart chambers. This ventricular fibrillation is fatal and a common cause of cardiac arrest.

“We found that interval training improves a number of mechanisms that allow calcium to be pumped out of the cells and stored more efficiently inside the cells. The leakage from the calcium stores inside the cells also stopped in the interval-trained rats,” says Stølen.

The effect was clear when the researchers tried to induce ventricular fibrillation in the diseased rat hearts: they only succeeded at this in one of nine animals that had completed interval training. By comparison, they had no problems inducing fibrillation in all the rats with heart failure who had not exercised.

Read the full story.

Source: ScienceDaily.

 

Self Tracking Is Easy and an Effective Way to Lose Weight

Being overweight or obese is associated with several risks such as developing type 2 diabetes, high blood pressure, cardiovascular disease, cancer, and even mortality. Despite these well documented risks federal statistics indicate that obesity in America has increased from 35% in 2007-08 to being 40% in 2015-16 and that number is still climbing.

This doesn’t mean that Americans are not making an effort to lose weight as a report by the Boston Medical Center suggests around 45 million embark on diets every year, spending over $33 billion annually on the pursuit of dropping extra weight. The sad reality is that only a small portion of those dieters will reach their goals, as for many the process is too difficult and what they can and can’t eat proves to be too much of a struggle for them to sustain long term.

Weight loss doesn’t have to be unsustainable and an unachievable dream, research is showing that self tracking methods such as an app or diary are the most effective ways to successfully lose weight. Some may feel that self tracking is time consuming, but research from the University of Vermont has found that it can be quick and easy, taking about 15 minutes a day.

As published in the journal Obesity results were examined from 142 self tracking participants. The most successful participants spent on average 14.6 minutes per day online based on their logged in activity in the behavioral weight loss program in which they recorded calories, fat, portion sizes, and preparation methods for all food and beverages consumed; and met weekly for 14 weeks in an online group session with a trained dietician.

The most successful dieters were determined to be those that lost at least 10% of their body weight, who spent 23.2 minutes a day logged in for the first 6 months, then on average 14.6 minutes logged in afterwards. Successfulness was not revolved around how much time was spent logged in, rather it was the number of times they logged in to report what they ate.

“Those who self-monitored three or more times per day, and were consistent day after day, were the most successful,” explained lead author Jean Harvey, chair of the Nutrition and Food Sciences Department at the University of Vermont. “It seems to be the act of self-monitoring itself that makes the difference — not the time spent or the details included.”

The key to weight loss success may well be to start a food journal or download a self monitoring app in which to briefly, but no less than 3 times a day report the details of the food and beverages which have been consumed. 

Check the full story.

Source: WorldHealth.net

Study Links Junk Food To Age Marker In Chromosomes

According to a study recently published in the peer-reviewed American Journal of Clinical Nutrition, presented at an online medical conference, those who consume a lot of industrially processed junk foods are more likely to exhibit a change in their chromosome that is linked to ageing.

Scientists at the European and International Conference on Obesity reported that those who consumed three or more ultra-processed foods per day were found to have doubled their odds of their DNA and telomere proteins being shorter when compared to those from people who rarely consume such foods.

Shorter telomeres are a proven marker of biological ageing at the cellular level, this study suggests that diet is a factor in driving cells to age faster. It was noted that although the correlation is very strong, the causal relationship between consuming highly processed foods and shrinking telomeres is speculative, additional research is required.

Every human has 23 pairs of chromosomes that house our genetic code. While telomeres don’t carry any genetic information, these are the protective end caps that are vital for preserving the stability and integrity of our chromosomes, and the DNA that all the cells within the body rely on to function. With age, telomeres shorten naturally as each time a cell divides a part of the telomere is lost, and this reduction in length is recognized as a marker of biological age.

Scientists from the University of Navarra Spain wanted to investigate the suspected connection between shrinking telomeres and regular consumption of highly processed junk food. Previous studies pointed to a possible link, but the findings were inconclusive.

Ultra-processed junk foods are industrially manufactured substances that are composed of some mix of oils, fats, sugars, starch, and proteins that contain very little if any whole or natural foods. The items will typically include artificial flavourings, emulsifiers, preservatives, colourings, and other additives to increase shelf life and profit margins. But these same compounds also mean that these types of foods are very nutritionally poor compared to less-processed options.

Previous studies have shown strong correlations between ultra-processed foods and obesity, type 2 diabetes, hypertension, depression, and some types of cancer. Such conditions are often age-related as they are linked to oxidative stress and inflammation which are both known to influence the length of telomeres.

In this study health data for nearly 900 people who were 55 years of age or older were involved in this study who provided DNA samples in 2008 and provided detailed data about the eating habits at that time as well as every two years after. Participants were equally divided into 4 groups depending on their consumption of ultra-processed foods from low to high.

Those in the high intake of ultra-processed foods group were found to be more likely to have a family history of cardiovascular disease, diabetes, abnormal blood fats, and snacked more in between meals. This group also consumed more fats, saturated fats, polyunsaturated fats, sodium, cholesterols, SSBs, fast food, and processed meats while intaking fewer carbs, protein, fibre, olive oil, fruits, vegetables, and other micronutrients. Those who consumed more ultra-processed foods were observed to be less likely to adhere to a Mediterranean style diet.

As the consumption of ultra-processed foods increased the likelihood of having shortened telomeres increased dramatically with each quartile above the lowest having a risk increase of 29% for the medium-low group, 40% for the medium to high group, and 82% for the high consumption of ultra-processed food group for having shortened telomeres. Consumption of ultra-processed foods was also associated with the risk of depression, hypertension, being overweight, obesity, and all-cause mortality, especially in those with low levels of physical activity.

“In this cross-sectional study of elderly Spanish subjects, we showed a robust strong association between ultra-processed food consumption and telomere length. Further research in larger longitudinal studies with baseline and repeated measures of TL is needed to confirm these observations,” concluded the authors.

Read the full story.

Source: WorldHealth.net.

Why You Should Consider Chia Seeds

Chia seeds may be small, but they are loaded with a wealth of important nutrients that can help to support a healthy and nutritious diet.

These versatile and nutritious tiny seeds are commonly ground, stirred, or sprinkled into smoothies, yogurt, pudding, salads, and oatmeal making them great for those on the go. The gel produced from the ground seeds can even be used as an egg substitute in pancakes and bake goodies.

One of the big pluses to chia seed is that although they are rich in nutrients they are very low in calories. Just two tablespoons contain 18% of the daily recommended value of calcium, 137 calories, 30% of the RDV for manganese and magnesium, as well as 27% of the RDV for phosphorus. They are also rich sources of zinc, potassium, and vitamin B, for all of these reasons, it makes them an extremely efficient source of nutrients.

To go along with the nutrient profile, chia seeds are a good source of fibre-containing 11 grams in that same 2 tablespoons. As most people don’t reach the DRV of 30 grams, adding chia seeds to your diet is a good option to help reduce the risk of heart disease, type 2 diabetes, colorectal cancer, and regulate blood sugar levels.

Those looking to up intake of anti-ageing antioxidants that can help to prevent or delay certain types of cell damage may want to consider chia seeds as well as they are a rich source of antioxidants due to the presence of chlorogenic acid, caffeic acid, myricetin, quercetin, and kaempferol which are believed to help protect the heart and liver as well as having anti-ageing and anti-carcinogenic characteristics.

Those looking to add more plant-based protein to their diet may find chia seeds to be a good option as they are approximately 14% protein, and they are a complete protein containing all of the essential amino acids that are required for human nutrition including isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, histidine, and valine which help build proteins, grow muscle, and transport nutrients.

Another plus is that gram for gram chia seeds contain more omega-3 fatty acids than salmon does which has various anti-inflammatory properties and may also help to support better brain and heart health as well as improve stress response.

The rich calcium, magnesium and protein content will also help to support healthy bones which again is good news for those looking to increase intake of more plant-based options as 25 grams of chia seeds contains 157 grams of calcium which is more than the content of 100 ml of dairy milk.

Studies suggest that regular consumption of chia seeds could significantly reduce blood pressure for those with hypertension, and the rich omega-3 content can work as a blood thinner reducing overall blood pressure. The reductions can support overall heart health and may help to reduce the risk of cardiovascular disease and all-cause mortality. It is worth noting that those taking medications should consult with their physician as very large quantities of chia seeds could potentially interact with certain blood pressure or blood sugar medications.

The body digests chia seeds slowly which will provide slow-release energy and help to keep blood sugar levels stable throughout the day, while the fibre content can slow the absorption of sugar into the blood and decrease overall blood sugar levels.

Additionally, the high concentration of soluble fibre makes chia seeds expand in the stomach which can help to keep you feeling fuller for longer and reduce snacking which can help to support healthy weight loss as part of a healthy diet when combined with exercise.

Read the full story.

Source: WorldHealth.net.

AKG Supplement Promoted Healthy Aging & Longevity In Animal Study

Mice given alpha-ketoglutarate (AKG) supplements were reported to be healthier as they aged, and female mice lived longer than those not given the supplement, according to the researchers at the Buck Institute for Research on Aging.

“The big thing about this is that its safety profile is so good,” says the University of North Dakota aging researcher Holly Brown-Borg, who was not involved with the study. “It has potential and should be explored further, for sure.”

AKG is naturally made in both mice and human bodies, and it is already considered to be safe by regulators. It is part of the metabolic cycle that cells use to make energy from food; sometimes it is used to treat osteoporosis and kidney disease, along with some bodybuilders to bulk up.

In 2014 researchers discovered that this molecule may have an anti-ageing possibility when a study published in Nature reported that it helped to extend the lifespan of C.elegans by more than 50%; and other studies showed it improving lifespan in fruit flies.

AKG levels will gradually decline with age, as such the researchers are looking for ways to restore levels to those seen in younger years. In this study published in Cell Metabolism 18-month-old mice, which is the equivalent of around 55 human years, were given AKG as 2% of their daily feed until they died or for up to 21 months, recording all changes.

Within a few months: “They looked much blacker, shinier, and younger” than control mice, says Azar Asadi Shahmirzadi, a postdoc at the Buck Institute who did the experiments as a graduate student. Animals in the AKG group also scored on average 40% better on tests of frailty as measured by 31 physiological attributes including walking gait, grip strength hearing, and hair colour. Additionally, female mice in the AKG group lived a median of 8-20% longer than the controls. It was noted that the mice in the AKG group did not perform better in tests for heart function or treadmill endurance, and they did not test for cognitive improvement.

Female mice in the AKG group were found to produce higher levels of a molecule that fights inflammation. Although these effects on health and longevity were smaller for AKG than for some other anti-ageing compounds, some of the other compounds have had safety issues, for example, rapamycin can suppress the immune system and may promote diabetes.

The researchers plan to test AKG in human volunteers in the near future, possibly in a group of people between the ages of 45-65 to investigate whether the molecule will improve ageing-related biomarkers such as inflammation, arterial hardening, and chemical signatures on DNA that are associated with ageing.

Read the full story.

Source: WorldHealth.net.