A study conducted at Brigham Young University by exercise scientists has found that people who consume low fat milk experience several years less biological aging when compared to those who drink high fat milk, both 2% and whole milk. This supports existing dietary guidelines which do not recommend high fat milk as part of a healthy diet.

The study assessed 5,834 adults and included data from the National Health and Nutrition Examination Survey as well as questionnaires for the participants. They looked at the relationship between telomere length along with milk intake frequency (daily drinkers vs. weekly drinkers or less) and the milk fat content that was consumed (whole vs. 2% vs. 1% vs. skim).

Telomeres are the end caps of human chromosomes and act like biological clocks. They are correlated with age. As people get older, their telomeres get shorter. People who consumed more high fat milk showed telomeres that were significantly shorter.

For every 1% increase in milk fat consumed (drinking 2% vs. 1% milk), telomeres were 69 base pairs shorter in the adults in the study. This translates into more than four years in biological aging. In the very extreme milk drinkers, the adults who drank whole milk had telomeres that were a striking 145 base pairs shorter.

Half of the adult participants in the study consumed milk on a daily basis with another quarter consuming milk at least weekly. Less than a third of the adults consumed full fat milk and an additional 30% reported drinking 2% milk. Approximately 10% consumed 1% milk and another 17% consumed non fat milk. 13% did not drink any cow milk.

Surprisingly, the study found that people who did not consume milk at all had shorter telomeres than adults who drank low fat milk meaning they aged quicker than skimmed milk drinkers. This suggests that there may be some anti aging benefits to consuming milk, but there is sweet spot to be found.

The study suggests that the milk fat and subsequent link with cellular aging was most likely due at least in part to increases inflammation and oxidative stress caused by the increase in saturated fat consumption. The team believes that this saturated fat in high fat milk is the culprit that causes the damage and contributes to the death of tissues in the human body.

Milk is one of the most controversial foods in the U. S. Current dietary guidelines for Americans encourage adults to consume low fat milk, both 1% and non-fat, and avoid high fat milk altogether. It isn’t necessarily a bad thing to drink milk, but according to the study, the type of milk matters.

To view the original scientific study click below

Milk Fat Intake and Telomere Length in U.S. Women and Men: The Role of the Milk Fat Fraction

Scientists have identified pathways that could enable humans to live for well over 100 healthy years according to one of the scientists who participated in the research. The synergistic cellular pathways for longevity that increase the lifespan five fold were discovered in C. elegans which are a nematode worm used as models in aging research. This translates to extending human lifespan by about 50%.

C. elegans are popular models for aging research because they share many of its genes with humans and due to its short lifespan of three to four weeks, scientists can quickly assess the effects of genetic and environmental interventions for extending healthy lifespan.

The discovery of two major pathways governing aging in C. elegans has created intensive research. These pathways are conserved which means they have been passed down to humans through the evolutionary process. A variety of drugs that can extend healthy lifespan through altering these pathways are currently under development. The discovery of the synergistic effect has opened the door to more effective therapies aimed at anti aging.

The recent research used a double mutant in which the insulin signaling IIS and TOR pathways were genetically altered. Because an alteration of the IIS pathways will yield a 100% increase in lifespan and an alteration of the TOR pathway yields a 30% increase, the double mutant would be expected to live 130% longer. However, its lifespan was amplified by 500%.

Despite this discovery in C. elegans of cellular pathways that govern aging, it wasn’t clear how these pathways interact with each other. Through helping to characterize these interactions, the research team is paving the way for needed therapies to increase healthy lifespan for the rapidly aging population.

The synergistic extension is something the team calls “wild”. The effect wasn’t one plus one equals two. It was one plus one equals five. The findings demonstrate that nothing throughout nature exists in a vacuum. To develop the most effective treatments for anti aging, longevity networks rather than individual pathways needs to be looked at.

This discovery of the synergistic interaction might lead to the use of combination therapies with each affecting a different pathway to extending human healthy lifespan. The synergistic interaction might also explain why researchers have not be able to identify a single gene that is responsible for the ability of some humans to live to very old ages free of major diseases.

To view the original scientific study click below

Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity.

New research has revealed how a high level of exercise can slow one type of aging. This is the kind of aging that occurs within our cells. We just have to be willing to put in some sweat equity!

Researchers at Brigham Young University have found that people who consistently perform physical activity at a high level have significantly longer telomeres when compared to those have live a sedentary lifestyle as well as those who are moderately active.

Telomeres are protein end caps on our chromosomes. The are like our biological clock and are strongly tied to aging. Every time a cell replicates, it loses a tiny bit of the end caps. As a result, the process of aging gradually shrinks or shortens our telomeres.

The team analyzed data from 5,823 adults who participated in the CDC’s National Health and Nutrition Examination Survey. This survey is one of the few indexes that includes telomere length values for the study participants. The index also includes data for 62 activities participants may have participated in over a 30 day period. This data was analyzed to calculate the participant’s levels of physical activity.

The research found that adults with high physical activity levels have telomeres with a biological aging boost of nine years when compared to those who live comparably idle lifestyles. They also have a 7 year advantage compared to those who engage in moderate levels of physical activity.

In order to be considered to be a highly active person, men must engage in 40 minutes of jogging 5 days per week and women must engage in 30 minutes of jogging 5 days per week. To see a significant difference in slowing biological aging, a little exercise won’t make it. People have to work out regularly and at high levels.

The study showed that the shortest telomeres came from people who were considered sedentary. They had 140 base pairs of DNA less at the endpoints of their telomeres compared to the highly active participants. Surprisingly, the study showed that there was no significant or meaningful difference in telomere length between the participants who were sedentary and those who engaged in low or moderate physical activity.

The exact mechanism responsible for how exercise preserves the telomeres is unknown. The team believes the mechanism may be tied to the combination of oxidative stress and inflammation. Earlier studies have determined telomere length is closely tied to those two factors. And it is well known that physical activity can suppress both these factors over time.

It is well known that regular physical activity can help reduce mortality and prolong life. Now it is known that part of that advantage might be related to the preservation of telomeres that occurs with high physical activity.

To view the original scientific study click below

Physical activity and telomere length in U.S. men and women: An NHANES investigation.

Due to the buildup of scar tissue from a variety of tendon injuries such as jumper’s knee and rotator cuffs, secondary tendon ruptures along with painful and challenging recoveries can occur. New research has shown that the existence of stem cells in tendons can potentially be harnessed to not only improve the healing of tendons but also even avoid surgery.

Tendons are the connective tissue that tethers our muscles to our bones. These tendons improve not only our stability but also facilitate the transfer of force which allows us to move. However, they are particularly susceptible to damage and injury.

Once tendons are injured they rarely fully recover. This can result in mobility limitations and often times requires long term pain management and even surgery. The problem is the fibrous scars which disrupt the tissue structure of the tendons.

The research which was conducted at the Carnegie Institution for Science, revealed all of the cell types which are found to be present in the Patellar Tendon which is found below the kneecap. This included previously undefined tendon stem cells.

Because injuries to the tendons rarely heal completely, it has been thought that tendon stem cells did not even exist. Many researchers have searched for them but to no avail until the recent work which defined them for the first time.

Stem cells are blank cells which are associated with nearly even tissue type which have not fully differentiated into a specific function. They can self renew which creates a pool from which newly differentiated types of cells can form to support a particular tissue’s function. Muscle stem cells for example differentiate into muscle cells.

The research team showed that both tendon stem cells and fibrous scar tissue cells originate in the identical space which is the protection cells that surround our tendons. Additionally, the tendon stem cells are part of a competitive system with precursors of fibrous scars. This explains why healing of injured tendons is so challenging.

The researchers demonstrated that both scar tissue precursor cells and tendon stem cells are stimulated into action by a protein known as platelet derived growth factor A. When tendon stem cells become altered so they do not respond to this particular growth factor, then only scar tissue and no new tendon cells form following an injury.

Tendon stem cells must outcompete scar tissue precursors so they can prevent the formation of difficult fibrous scars. Discovering a therapeutic way to block these scar forming cells and instead enhance the tendon stem cells could be a huge game changer for treating tendon injuries.

To view the original scientific study click below

A Tppp3+Pdgfra+ tendon stem cell population contributes to regeneration and reveals a shared role for PDGF signalling in regeneration and fibrosis.

Typically for many people a New Year is the perfect time to adopt new habits both in the gym and at the grocery store. People can be eager to try out new diets, but does scientific evidence actually support claims made for these diets?

Mark Mattson, Ph. D., a neuroscientist at John Hopkins Medicine, has studied intermittent fasting for 25 years and adopted it himself about 20 years ago. He concludes that intermittent fasting does live up to the claims that it can be a part of a healthy lifestyle.

Generally, intermittent fasting diets fall into two categories: 5:2 intermittent fasting in which people will limit themselves to one moderate sized meal two days each week, and daily time restricted eating which narrows eating times to 6 to 8 hours per day.

A variety of animal and human studies have shown that alternating between eating and fasting supports cellular health. The thought is that most likely this happens by triggering an age old adaptation to periods of food scarcity referred to as metabolic switching. This switch occurs when cells use up stores of rapidly accessible sugar based fuel and begin converting fat into energy which occurs in a slower metabolic process.

Studies have shown that this metabolic switch improves the regulation of blood sugar, suppresses inflammation, and increases the resistance to stress. Most Americans consume three meals in addition to snacks every day so they do not experience the switch and the suggested benefits.

Mattson also notes that four different studies in both people and animals found intermittent fasting also decreases blood pressure, resting heart rates, and blood lipid levels. There is also mounting evidence that this type of fasting can modify risk factors which that are associated with diabetes and obesity.

Two studies conducted at the University Hospital of South Manchester NHS Foundation Trust which involved 100 overweight women showed that the women on the 5:2 intermittent fasting diet lost the same amount of weight as women who restricted their calories. Additionally they did better with insulin sensitivity and reduced belly fat when compared to those in the reduced calorie group.

Recently, Mattson says preliminary studies have suggested that intermittent fasting could also benefit brain health. A multi center clinical trial at the University of Toronto found that 220 healthy and non obese adults who maintained a calorie restricted diet for a period of two years showed evidence of improved memory in a variety of cognitive tests. If further studies show the proof that fasting can improve learning and memory, interventions may be developed that can stave off dementia and neurodegeneration.

Mattson believes we are at a point where medical school curricula alongside advice and healthy diets and exercise may be developed. Although he recognizes that researchers do not completely understand the specific mechanisms of metabolic switching and that there are some people who or unwilling or unable to adhere to a fasting program.

With guidance and patience, most people are able to incorporate fasting regimes into their lives. It does take the body some time to adjust to intermittent fasting and to get past some of the initial hunger pangs and irritability that can accompany it. These symptoms typically pass after two weeks to a month as the brain and body become accustomed to this new habit.

To manage that hurdle, Mattson suggests that health care professionals advise patients to gradually increase the frequency and duration of the fasting periods over the course of several months, instead of going cold turkey.

To view the original scientific study click below

Effects of Intermittent Fasting on Health, Aging, and Disease.

Researchers from the University of Illinois have conducted a new study on rats that suggests caffeine may offset some of the health risks associated with diets high in sugar and fat. What they found was that rats who consumed caffeine which was extracted from mate tea gained 16% less weight and accumulated 22% less body fat compared to rats who consumed decaffeinated mate tea.

Mate tea is an herbal beverage high in flavonoids, phytochemicals, and amino acids. It is consumed as a stimulant by people living in southeastern Latin American countries. The amount of caffeine in a serving of mate tea ranges from 65 to 130 milligrams. The caffeine in coffee ranges from 30 to 300 milligrams per one cup.

The rats in the study ate a diet that contained 40% fat, 15% protein and 45% carbohydrates for four weeks. They also consumed one of the forms of caffeine equivalent to someone who drinks four cups of coffee daily.

At the end of the study period, the percentage of lean body mass in the different groups of the rats differed significantly. The rats that consumed caffeine from the mate tea, coffee, or synthetic sources accumulated less body fat compared to the rats in the other groups.

The accumulation of lipids in the adipocytes in the rats was significantly associated with increased body fat and greater body weight gain. To understand the mechanism of this action, the team performed cell culture studies where they exposed adipose cells from mice to synthetic caffeine or the mate or coffee extracts.

They discovered that regardless of the source, caffeine decreased the accumulation of lipids in adipose cells by 20% to 41%. The team also tracked the expression of a variety of genes that are associated with obesity and lipid metabolism. This included the fatty acid synthase gene (Fasn) which is an enzyme compound involved in the synthesis of fatty acids from glucose, and also the lipoprotein lipase gene (Lpl) which codes for an enzyme which breaks down triglycerides.

All caffeine treatments regardless of the origin significantly down regulated the expression of both Fasn and Lpl. Within the cell cultures, Fasn expression diminished by 31% to 39% and the Lpl expression diminished by 51% to 69% among cells that had been treated with synthetic caffeine or the caffeine derived from coffee or mate tea.

In the rats that were given the mate tea caffeine, expression of Fasn decreased by 39% in their fat tissue and decreased by 37% in their livers. Additionally, the decreased expression of the Fasn gene and two other genes in the liver evoked a lower production of low density lipoprotein cholesterol and triglycerides in the liver.

The study adds to a growing body of research which suggests mate tea might help fight obesity. It also provides other beneficial health effects associated with the vitamins, flavonoids, and phenolic compounds it contains.

Based on the studies findings, caffeine can be considered an anti obesity agent. The consumption of caffeine from mate and other sources alleviates the negative impact of a high sucrose and high fat diet on body composition due to the modulation of certain lipogenic enzymes in the liver and adipose tissue. The diminished expression of Lpl and Fasn brought about the lower synthesis and accumulation of triglycerides in the andipose tissue.

The findings of the study could be scaled to people to understand the roles of caffeine and mate tea as possible strategies in preventing overweight and obesity in addition to subsequent metabolic disorders which are associated with these conditions.

To view the original scientific study click below

Caffeine, but not other phytochemicals, in mate tea (Ilex paraguariensis St. Hilaire) attenuates high-fat-high-sucrose-diet-driven lipogenesis and body fat accumulation.