John Hemming's Web Log

Recently another paper was produced which hinted at a link between mitochondrial DNA damage and aging. In fact I have been of the view for some time that the damage to mitochondrial DNA is what drives both aging and development at the lowest level. I have said this before, but thought a summary would be useful. It is worth, however, explaining a few terms first before going into the details of how this happens. It is well known that animals (including people) are made of large number of cells. Within those cells there are little "organelles" called mitochondria that are used to convert nutrients into ATP (Adenosine Tri Phosphate) which is used by cells as a form of energy. There is a hypothesis that is generally believed to be true that this structure of cells arose from some bacteria going into old cells called archea as it created a form of symbiosis where the larger cells provided nutrients to the bacteria for the bacteria to process those. This is called Endosymbio...

The idea that Parkinson's Disease (PD) is an accelerated form of brain aging has been around for quite a long time. However, as with aging more generally any hypothesis as to the mechanisms behind Parkinson's needs to explain all the known research data. I have been discussing PD with a number of people over the past few months. The results from research indicate that Parkinsons is not primarily caused by genetic factors. That is because there are studies where individual twins get Parkinsons, whilst their twin does not. I was wondering, therefore, what might be an alternative cause. This paper is one that substantiates the argument that normally the brain does not age as fast as the rest of the body. What we need to look at is what might cause this to happen. If we start with the assumption from my previous posts that aging results from the mutation of mitochondrial DNA (mtDNA) then we need to find something that prevents the mutation of mtDNA in the brain that does n...

Software Developer and Artifical Intelligence Expert Samuel Collingwood Smith has been working with me on a number of projects for a last few years, mostly in the Artificial Intelligence / AI / bio-hacking space. We entered a number of competitions, some of which were against billion dollar organisations and in one case came in the top-ten with software that runs on a desktop PC, on an nVidia card, against thirty other competitors. As well as using open source AI models hosted in Python, Smith has used his C# and C++ tools to develop his own scratch-written neural network engine, LearnSilver. This is a C# native neural network library that can also execute on CUDA enabled nVidia cards with C/C++, including many gaming graphics cards. It enable significant processing on consumer hardware. It supports training, serialisation of entire models with a single method call and recurrent networks. TALIS is a side, personal project Smith worked on prior to joining me in setting up our new AI c...

The Biohacking Team has withdrawn from XPRIZE Healthspan. We think the prize is a really good idea and the science behind the judging is really good. However, we are not willing to sign the competitors agreement. XPRIZE have asked that the competitors agreement be kept confidential and hence we should not give our reasons as to why we will not sign the competitors agreement. Signing the competitors agreement is a requirement for remaining in the contest, hence we need to withdraw. We wish XPRIZE Healthspan well. Finding out what can be done to increase the proportion of people's lives in good health is a really good idea. We have, however, decided to keep the team together. Although the team was brought together to compete in XPRIZE and we are no longer doing that, we have other things to do. We have already participated in the Biomarkers of Aging contest and the Medical Affairs Olympics. We are also running small scale biohacking coaching sessions on both the Diseases of ...

The Electron Transport Chain has five complexes. These are comprised of a number of subunits. What I find particularly interesting is that some of the proteins are generated via nuclear DNA and some of the proteins are generated via mitochondrial DNA. Most of the ROS (that damages mtDNA) is generated by Complexes 1 and 3. Complex 1 has 45 subunits in humans, but in fact only 7 of those (ND1, ND2, ND3, ND4, ND4L, ND5, ND6) are encoded by the mitochondrial genome. Complex 3, however, has 11 subunits only 1 of which is in mtDNA (MT-CYB) Complex 2 is entirely coded by the nucleus, Complex 4 has 3 (MT-CO1, MT-CO2, and MT-CO3) out of 13 units coded in mtDNA. ATP Synthase also called Complex 5 has 16 units two of which are encoded in the mitochondria. Hence it is clear that complex 1 is perhaps the key complex for mtDNA mutation linked aging and not surprising that this is the complex inhibited in Oocytes. There is an argument that for hydrophobic subunits the energy cost of transferr...

Oxygen is essential for human life. That is well known. However, the level of Oxygen in the atmosphere has interesting effects. I wrote previously about The Hypoxia Inducible Factor (HIF). HIF (particularly 1 alpha) is a molecule which signals cells to create proteins to build in response to stress. This can involve building new mitochondria or recycling old inefficient mitochondria. In essence it is ringing an alarm that calls for cells to get better prepared for stress. Interestingly HIF is switched on by a drop in the oxygen partial pressure (that proportion of air pressure that is oxygen). It is also well known that if brain cells get too little Oxygen then they can get harmed or die. Hence too low an Oxygen level causes brain damage. In fact there is evidence from people living at high altitudes that at a point the oxygen level is too low and this harms health. However, there is another aspect of Oxygen levels that relates to the mitochondria. The mitochondria produc...

There are a number of theoretical debates about aging. One is the question of whether we are "programmed to die". Those who believe this think that at a point creatures get to a stage where the organism at a cellular level starts processes which deliberately set out to end the life of the multicellular organism. Another potentially contradictory view is simply that creatures accumulate damage up the point at which they can no longer survive. It is possible, however, to look at different species and see how their lifespan operates. What is clear is that different species age in different ways. Some species don't age in the same way as others. It is worth having a look at how species vary and to what extent that explains the relationship between evolution and lifespan. Firstly, it is clear that there are species where the adult commits some form of suicide after mating. Octopuses and Pacific Salmon There are, however, also species which have negligible senes...

An interesting paper was published in the week before Christmas. Mitochondrial quality control: the real dawn of intervertebral disc degeneration? The summary states: Intervertebral disc degeneration is the most common disease in chronic musculoskeletal diseases and the main cause of low back pain, which seriously endangers social health level and increases people’s economic burden. Disc degeneration is characterized by NP cell apoptosis, extracellular matrix degradation and disc structure changes. It progresses with age and under the influence of mechanical overload, oxidative stress and genetics. Mitochondria are not only the energy factories of cells, but also participate in a variety of cellular functions such as calcium homeostasis, regulation of cell proliferation, and control of apoptosis. The mitochondrial quality control system involves many mechanisms such as mitochondrial gene regulation, mitochondrial protein import, mitophagy, and mitochondrial dynamics. A large numbe...