Exercise: Good for your mind, body, and telomeres!

Introduction: Telomeres are DNA portions that are located on the two ends of the chromosome. Telomeres play an important role in cellular life. Exercise is one of the factors that contributes to their control. The purpose of the present study was to investigate the effect of 8 weeks of high intensity interval training (HIIT) on telomere length and telomerase activity in non-athletic young men. Materials and methods: 30 inactive students were selected as sample and randomly divided into two groups of exercise (15 people) and control (15 people) in this semi-experimental study. The exercise group performed 8 weeks of HIIT exercise in 3 sessions per week with an intensity of 150 to 175% of their maximum power (Pmax). Control group subjects did not do regular sport activities. To measure telomere length and telomerase activity, 10 ml of blood was taken from the brachial vein of the subjects 24 hours before the first and after the last exercise session. The dependent t was used to analyze intra-group and independent t for within-group differences. Results: The findings of this study showed that 8 weeks of HIIT training in non-athlete young men resulted in a significant increase in telomere length (P = 0.001) and telomerase activity (P = 0.001). Conclusion: It seems that HIIT can alter telomerase activity and telomere length. Therefore, these training may have a positive effect on cell biology.

The SENS Research Foundation has apparently already raised four times its annual income thanks to the PulseChain Airdrop.

The PulseChain airdrop supporting aging research

Richard Heart, the founder of HEX, is about to launch a new cryptocurrency called PulseChain. As part of that launch, he has also arranged an airdrop to give away some of the new cryptocurrency in order to support the SENS Research Foundation (SRF).

Ageing is an incredibly complicated process, so much so that we do not yet understand exactly how complicated it is. It is in fact so complicated, that it could actually be incredibly simple. Confused? Well, imagine if you were a structural engineer who was trying to understand why a building collapsed. From an initial inspection of the rubble, it may be extremely difficult to work out exactly what went wrong. Was the building made from inferior materials? Was it built incorrectly? Was its destruction deliberate? Did it just fall apart due to age? All of these are possible, but what was the true cause for its destruction? Well, that is the same mystery we are trying to solve in longevity research. We can see the damage that is caused by ageing, but what is the cause? Is it a general accumulation of damage, or are there single points of failure which have knock on effects that affect the entire body? A cascade failure if you will.

Of the many different changes that occur during the ageing process, one of the most well-known and understood is the decreased capacity for our body to produced chemical energy, which has a knock-on effect throughout the body. This results in a general decrease in our ability to carry out cellular functions and will therefore effective everything from muscle strength to DNA replication and repair. This decrease in energy output has been linked to defects in our mitochondria, but in addition to these physical defects that occur in these small organisms, we now know that they also suffer a decreased capacity to carry out their function due to lacking a critical coenzyme called Nicotinamide adenine dinucleotide (NAD). Anyone who has taken a high school level biology class will probably recognise this enzyme as part of the electron transport chain in respiration.

The United states army are planning to test NAD+ dietary supplementation experiments next year in hopes of producing a viable method of increasing the viable length of a soldier’s active service.

Did you know that life extension is impossible? I didn’t until the keen minds over at the Guardian informed me as such. Fortunately before I decided to give up my career in regenerative medicine I decided to look into exactly how the Guardian came to such a revelation. What I discovered was so earth shattering that it rocked my very understanding of the world, and made me question everything I thought I knew. That realisation was that, despite their consistent insistence to the contrary, the media lies, a lot.

Ok maybe this was not as shocking as I made it out to be, in fact it’s pretty widely known by now that the media is generally no stranger to the odd lie here and there. If you are not familiar with the story allow me to give you a recap. A recent study was conducted in order to find out if human lifespans have actually increased due to advanced in medicine. To do this, scientists used statistical models to remove non-age related causes of death from historical records (such as murder, death in child birth, plague etc) in order to determine what the uninterrupted human lifespan is, and if it has increased over time. What was found is that our medical science is yet to fundamentally extend human lifespan. This comes as no surprise to anyone in the field of longevity research as we know full well that none of our current medical treatments address causes of ageing. What this study does not conclude however is that life extension is impossible.

AgomAb Therapeutics have announced the successful acquisition of a second round of funding ($74M) for research into the applications of antibodies for use in the field of regenerative medicine. Antibodies have already received a large amount of attention for their ability to positively effect numerous conditions such as inflammation, metabolic disorders, and non-healing wounds.

Antibodies are small protein molecules which are used by the body to ‘tag’ foreign pathogens in order for the immune system to identify and destroy them. What is unique about these antibodies is that due to their structure they will only attach themselves to a particular pathogen (at a particular site known as an antigen). In many cases, the binding of an antibody to a pathogen such as a virus is enough to completely inactive the pathogen, making it effectively harmless.

Where does all the blood for a young blood plasma transfusion come from? Young blood transfusions have been making waves in the media lately, with several different experiments providing exciting evidence that ‘young blood’ can rejuvenate the body and reverse the effects of ageing.

Caenorhabditis elegans is a nematode worm which is commonly utilised in longevity research due to their genetic similarity to humans and their extremely short lifespans (often no more than 4 weeks). Previous research into improving the lifespan of these worms has yielded several interesting results, with modifications to their insulin and rapamycin signalling pathways resulting in a 100% and 30% increase in lifespan respectively. These successes prompted the obvious question, what would happen if both of these pathways were modified at the same time?

Photograph of the Caenorhabditis elegans adult hermaphrodite. Scale bar, 100 μm. Credit: ResearchGate, Nobuyuki Hamada.

A truly shocking revelation has shaken the scientific community to its very core!

The inside of a mitochondria is made up of a folded membrane, which has evolved to produce the greatest surface area possible between two parts of the mitochondria known as the intermembrane space (the outer part) and the mitochondrial matrix (the inner part). To drastically oversimplify this entire process, the mitochondria uses glucose (and ethanol if it’s available) to pump hydrogen ions (with the occasional deuterium and tritium ion) across the membrane which separates these two compartments of the mitochondria (known as the cristae) into the intermembrane space. These hydrogen ions then flow back into the mitochondrial matrix through a very special protein called ATP synthase, which uses the electrostatic potential energy of the hydrogen ion to manufacture ATP.

Unfortunately, as we get older this inner membrane starts to decay and become smaller. As the cristae starts to shrink, there is less space for ATP synthase, which means there is less ATP produced, which ultimately means that our cells do not have enough energy to maintain all of our cellular functions. As you can imagine, this lack of energy is catastrophic for the health of the cell, and will eventually lead to either cell senescent (where the cell essentially becomes dormant), or complete cell death.

Numerous different suggestions have been put forward as to explain why exactly why mitochondria decay in this way, including mutations within the DNA of the mitochondria (they have their own chromosomes), as well as the build up of oxidative agents within the cell itself which cause direct damage to the mitochondria. However, a group of scientists lead by Dr Hazel Szeto have discovered that the decay of the mitochondrial cristae is linked to declining levels of a phospholipid (fat) called cardiolipin. It turns out that as we age, oxidative agents within our body destroy this phospholipid, which is essential for maintaining the folded inner membrane of the mitochondria.