Steviols aging and mitochondria

As the cold weather approached I fancied buying some baked beans to have with a hot breakfast. In the past I had bought the ‘reduced salt and sugar’ version from a well known brand of baked beans. Now I find this product is replaced with a ‘no added sugar’ product.

Suspicious as usual, after reading the label I found that it contains the now ubiquitous steviol sweeteners. Now I admit that I am instinctively suspicious of anything that is basically a ragwort-extract but was not really that bothered until a) it was declared ‘safe’ by the food industry, b) a side effect of its consumption were ‘muscle pain’  and c) it now seems to be in every low sugar ( but still sweet) product.

Having had the ‘shades of statins’ bogey re-awakened I did a bit of digging looking for steviols’ effects on mitochondria. Yep, back in 1985 there was clear evidence that the family of stevia glycosides were  powerful mitochondrial inhibitors. inducing membrane depolarisation.  A few years later I noticed they were being touted as potential chemotherapy compounds for osteo-sarcoma on the grounds of their mitochondrial-mediated apoptotic properties. 

You get it, these compounds have profound effect on mitochondria. Basically that effect is to uncouple/depolarise mitochondria. This may be safe in healthy adults who need to lose a bit of weight but it will be a different story with older folk. Expect to see even more sarcopenia and mental deterioration in this group.

I can see it now, the rise and rise of the living dead. Pharma ‘solutions’ to high blood pressure, high cholesterol and obesity will produce a generation of undead morons. I truly cannot even bring myself to research this topic further; it took me minutes to find the academic papers so presumably this is all well known and will be documented with raging-hindsight in 20 yrs time. 

Mortality figures are not the issue in 21st century UK, morbidity is.

Mitochondria diabetes and cancer

Mitochondria diabetes and cancer

or 'cancerous cell love sugar, what better recommendation can you have?'

How and why do ‘normal’ somatic cells go rogue and become cancers? So much is known of the ‘how’ and in such mind-boggling detail one would have thought that some ‘motive’ would have been uncovered by now.

Of course I don’t really mean to imply  higher levels of heretical motivation to single cells going about their daily tasks as part of a multicellular collective,  or do I?  No-one after all would be embarrassed to speculate as to why say an amoeba did something or another. They might say “ this behaviour is an adaptive response to a chemical diffusing in its environment’ as it duly swims away exhibiting what they would term negative-chemotaxis.

Cells in a multicellular organism could equally  do what they will but they normally don’t. They don’t because:

a) They are physically prevented from moving being as they are part of tissues like liver, muscle kidney and so on.

b)They have stopped dividing, these  are called post-mitotic cells and form the bulk of a multicellular creature’s body like our own.

Cancers rarely form  from cells in these situations, however cells near the outer boundaries of tissues or which form part of the circulating cells ( in blood or lymph) are much more likely to rebel ... being both able to divide and even move. So most cancers are from dividing tissues ( skins or epithelia as called eg: the skin lining the outer shell, the gut, mouth, gullet, womb, cervix, lung, breast ) and mobile tissues ( blood cancers , testicular, ovarian).

More rarely, much more rarely, cells deep within tissues rebel; the common cancers above are called carcinomas the latter sarcomas. Whatever, it looks like opportunity is as always an important factor in transgression from virtue to rogue. Sticking with this the theme of opportunity. What metabolic cue can provide even more opportunity?  I think the answer is sugar. Here’s why.

It is well known that the eukaryote cell is a chimera, albeit an ancient and well integrated one between an anaerobic host and the aerobic symbiont the bacteria-like  mitochondrion.
Biochemically the putative host’s  metabolism is  sugar processing  and the mitochondrion is able to take the host’s sugar waste products as well as their own normal fatty foods and fully oxidise them liberating a lot of energy, enough indeed to build a big complex multicellular creature like us. This is the orthodoxy of student biochemistry, glycolysis followed by oxidative phosphorylation.

Mitochondria are the accidental ‘guests’ that make the miracle of the modern cell.
But, at the end of the day, bacterial-like invasion of a cell,  no matter how ‘beneficial’, is an invasion to be fought … given the opportunity. It is well documented that cancer cells suppress mitochondria, preventing them from dividing and respiring. Sugar metabolism is enough for cancers to get by and divide, albeit normally very slowly. But why suppress mitochondria? Surely more energy is a bonus if you want to grow quickly? The obvious answer is that this is personal. They want mitochondria gone.

It is now also becoming well known that Type 2 diabetes is strongly associated with cancer.
Unsurprisingly,  diabetic and more significantly perhaps pre-diabetic  conditions are associated with elevated blood glucose levels. Technically I mean elevated fasting glucose levels, that is higher than normal blood sugar when not actually eating sugar. This in my opinion is nothing less than adding another opportunity for a cell ‘wanting’ to return to its origins.

To add motivation to opportunity, how would one eject invaders from your cell? There is no real way to do this directly … but, if you divide repeatedly, and have already prevented the 'invader' from reproducing, then some cells will become free from the infection ...  applying the simple maths of dilution.

In short, cancer could be a defence albeit atavistic in the extreme to the invasion of the host cell by mitochondria. This reaction is effectively and normally comprehensively suppressed in a  multicellular organism and any opportunistic rogue cells  are ruthlessly destroyed by the marauding defensive immune-police.

But what about tipping the balance? Rapidly dividing cells in a sugary environment might just have enough opportunities lined up for one or two to be successful rogue 'start-ups'.

If then time reduces  immune surveillance through old age or stress  then  the ancient 'saccharophile' gts its chance to fight back.

UK Computer Science ... starting over?

This week the British Computer Society (BCS) writing from Roehampton University in South West London came very close to admitting that the introduction of Computer Science into English schools at GCSE and A level has been a bit of a disaster, cock up even.

A few years ago I was blogging for ComputerWorldUK and was one of the fiercest critics of the subject then called ICT and its apologist BECTA a government quango which effectively oversaw the digital revolution in schools at that time.

Long story short, BECTA was abolished, ICT given the chop ( last exams this year 2018 I believe) and Computing re-introduced ostensibly to re-create our pre-eminence in computing following a serious mocking of the current state of the nation by the then head of Google no less.

So enthused was I that I came out of teacher-retirement to teach the new GCSE and A levels in Computer Science. Maybe though I missed some early warning signs. At a educational show I was browsing a stall where the BCS was showcasing a child friendly drag and drop programming interface called Scratch. They ( the stall holders) were an odd bunch, very male very unfriendly and immune to dialogue ( ok criticism)  or interest from a veteran MIndStorms block code user.

In other words very much what you might expect from a certain CompSci stereotype.

Anyway, what transpired was eye-opening

Firstly, CompSci at GCSE and A level is hard. I have taught Chemistry, Physics, Biology, ICT and Computing (c1998) at A level, GCSE and O level during my 38 years in the business. I and my students over the years would vote for Chemistry as the hardest; Physics as impossible without good maths; Biology “easiest but lots of it”; ICT as deeply trivial but useful in the workplace ( MS Office era) and 1990s Computing really quite easy. It’s a long list but it has been a long time albeit punctuated by 10yr back in industry post 2000.

But CompSci 2016--  trumps the lot, and the reason that CompSci is so hard?  … the level of abstraction is very high.

This is a problem. Abstraction is expected to be part of the skill set of A level students but in all honesty some subjects have very little ( Biology and Geography spring to mind). CompSci has a lot. Consequently, only those students who can do this will pass in the subject let alone thrive.
Boys and girls are equally represented with regard to the ability to move from concrete to abstract work. So, from a subset of the school population ( the abstracters) will come the successful CompSci kids.

Boys though are over-represented in their love of computer hardware, computer games, and nefarious activities thus labelling the subject of CompSci as ‘male’. Many of the less successful CompSci students take the subject because of these drivers.

Now we have a double whammy, nay a treble whammy. A hard, ‘boys’ subject suitable for only those few with the best abstract handling abilities that does not deliver the League Table’s best grades. The BCS/Roehampton report here says just that in its very good summary paragraphs at beginning of the report. Worth a read.

Finally another whammy, this time it’s fatal.  Poor uptake of the subject especially at A level means that it is too expensive to keep on a schools portfolio of offerings. Few schools can continue to subsidise a subject in the time of budget squeeze.

What’s to be done? Do we really want computer and programming skills in our upcoming generations?

Easy, drop Computer Science from GCSE and GCE. It belongs with the technical qualifications.
With technical qualifications the abstract can be balanced with meaningful applied skills, (something not achievable in traditional schools). More girls will be attracted just for the reason that an employable skill is an employable skill and they are as pragmatic as boys. Place this subject in large institutions ( 1000+) so that class sizes can be viable.

In conclusion, the re-introduction of Computing to schools has been botched  by geeks who thought everyone was like them. By the way developing ‘Scratch’ was not a solution to accessing programming. It was a distracting dead end.

Mitochondrial morphology: aging and capacitance 2

Mitochondrial morphology is critical to understanding how energy demands are managed by cells. The key to understanding how this is regulated lays in an electrochemical capacitance model. 

In a 2016 article from the Salk Institute, the importance of mitochondrial morphology was presented in its clearest form1. Essentially the team shows that mitochondria respond withregard to their size and shape, to  AMPK* enzymes. These are in effect part of a signalling system that monitors cellular ATP levels.

A drop in ATP levels ( in response to exertion-demand or toxins/poisons ) causes the mitochondria population to shatter in as much as they don’t burst but divide into a collection of a much smaller spheroid population. This is in contrast to some of the large, sometimes exotic, reticulate and tubular confections that mitochondria can form.

Mitochondrial fusion and fission was the subject of the conjectures in the paper and such musings have been mine for many years. In my PhD thesis and observed many times subsequently sged, senescent cells often show ‘mega-mitochondria’ with spherical shape and few cristae. I have speculated on the meaning of this change at length in a previous blog2.

My conclusions were that this was a phenomenon driven by electrical capacitance and the maintenance of a critical threshold membrane potential.

The question then, in light of the research and evidence of a variation in morphology from Salk, is what is the significance of such an astonishing range of shape and size?

My thesis has always been that it concerns the  electronic capacitance of a mitochondrion.
The free energy needed to drive the synthesis of ATP occurs at membrane potentials of 120+ mv. A mitochondrion with a large surface area, ie one with a great deal of inner membrane folding, must of course, meet the 120mv condition but will, by virtue of its larger internal surface area, have a greater capacitance.

This means, as in regular electronics, that it can store more energy than its counterparts with smaller capacitances. It is ‘easier’ to fully charge ( ie reach the critical threshold potential to produce ATP) an individual  mitochondrion with a smaller capacitance than one with the higher values simply because it requires less charge. However TOTAL CAPACITANCE within a cell will the sum of the individual capacitances of the mitochondria.

 It is also clear from ageing studies and the work illustrated by Salk that mitochondrial morphology (and hence capacitance) appears highly adaptive  …  but why?

In a very energetic high output cells ( say a bird or bat’s muscle cells ) you find many many very small tightly coupled ( ie low charge-leaking) mitochondria. In failing, senescent cells you see a few large swollen mitochondria with very little internal folding. In dividing cells, you can see an amazing network, a reticulum of fused and branching mitochondria wrapped around the nucleus undergoing division.

I think there are enough clues here to speculate on the role of mitochondrial morphology.
If I stick to the capacitance-charge model then it is possible to outline different scenarios.

Scenario 1: Small, high cristae level spheroids. 

Each mitochondrion has a relatively small capacitance so will reach the ‘ATP charge level’ quickly. A population of small spheroids has a much larger external surface area, as delineated by the outer membrane, than do the equivalent super-reticulate structures. This ratio aids rapid transport of charge (supplied by food) to the mitochondrion. So although in time of high demand, individual mitochondria could discharge below their threshold easily, they can also  be re-supplied very quickly.

This is consistent with finding of lots of small mitos as a result of high energy demands or even poisoning where resultant charge leakage across the membrane can be accommodated by ( using electronics analogy) drawing more current. High collective capacitance, high external surface area to maximise 'food' supply.


Scenario 2: Large reticulated structures.

A super-net of mitochondria, fully charged, stores a lot of energy within the inner-membrane folds but presents a relatively low external surface area in contrast with the spheroid extreme describe above.

In the extreme case of a dividing cell, the opportunity to ‘feed’ the mito-structures is lower than normal as the cell itself is otherwise engaged. However the free energy to power cell division (which requires a predictable and a modest amount of ATP) can be stored in the ‘giant capacitor’ that surrounds the nucleus. High capacitance and relatively low external surface.


Between the two extremes above must lay ‘normal’, ‘poisoned and senescent scenarios.

I would guess that in stable low ATP demand tissues mitochondrial fusion would be favoured, as if ‘stockpiling’ energy if the demand suddenly arose or if feeding was suspended for a while.. On the other hand in very high output tissues then small low capacitance mitochondria would favour fission.

In poisoned or senescent scenarios, charge-leakage across the inner mitochondrial membrane would demand an adaptive change to reduce capacitance. There are two ways of achieving this: small mitochondria with normal cristae or large mitochondria with fewer cristae.

My conjecture is that in a low-economy cell for example, a semi-senescent cell (in limbo like an underused muscle cell, parked and marked for death), a large medium capacity mitochondrion is superior to many smaller versions (with overall similar total capacity) because the risk of local depolarisation is reduced. That is, one small mitochondrion, although requiring less to charge it, a demand ( an energy draw) is much more likely to cause it to depolarise if it is already is leaking. This is critical because depolarisation could trigger the cascade leading to apoptosis.

The larger single mitochondrion is less likely to simply locally fail. It still might fail but not as in the case above have inevitable mini- failures. It is a case of all eggs in fewer baskets.

The Ageing Mitochondria Scenario

With age mitochondria lose the ability to divide (or fuse) and they leak more charge. This means that to meet the energy demands of a cell they cannot divide and regenerate in response to AMPK signalling even if it is still working. In order to maintain minimum capacitance to supply enough energy for the cell they need to enlarge. Hence the appearance of mega-mitochondria. After this response any failure in the supply side of 'food' or further leaking will spell the end.



*AMPK a collection of protein kinases activated by AMP (adenosine monophosphate) a marker for ATP levels ( adenosine triphosphate).




1) https://www.sciencedaily.com/releases/2016/01/160114152323.htm
2) https://www.blogger.com/blogger.g?blogID=3906287940044842441#editor/target=post;postID=5246291255183981633;onPublishedMenu=allposts;onClosedMenu=allposts;postNum=28;src=postname

Microsoft's AI for NHS?

Many years ago I would blog under the auspices of ComputerWorld.uk about UK educational computing. I was an open source apologist and enjoyed the collective outrage we felt when the money that the then UK government spent on Microsoft operating systems and Office software was made public.

Schools and public bodies were basically being ripped off as each upgrade iteration was released until suddenly all all came to a screeching halt. The school’s advisory quango BECTA was abolished and  schools stopped upgrading.

What happened was that an awful lot of public sector computers ended up still using Windows XP ( just ask the NHS ) though most schools and public sector businesses now use Win7; MS Office became relatively cheap and outsourcing giants such as Capita kept a fierce lid on spending.

Ah, those were the days.

Microsoft changed tack realising that the Cloud and Big Data would be the future but knowing that selling Office365 off their Azure cloud would not be a runner against Google’s ‘free’ doc suite. They got wise and made a  move on a new cash cow, aka medicine.

Put simply, medics collect data, always have, always will. Nowadays there are lots of data sitting in databases just waiting to be ‘mined’.  Big data mining is all the rage, sophisticated (you might suppose) algorithms honed by maths genii look for pattern and correlation in order to discover the meaning of life or whatever they are selling. Yes I am a skeptic but medics and economists love this stuff.

Some countries have diverse medical systems but one country has a monolithic, cradle to grave system. That’s BIGLY population data. So bigly that these data now form the basis of what goes for post grad research ( no more pesky experiments for the millennials ). Oh sorry forgot to mention the country …it’s the UK. And we have the NHS.

Today, Mrs May the UK Prime Minister has just announced that she will use (ie  fund) AI ( artificial intelligence) to save ‘thousands of lives’ and cure cancer by mining all that data.
She will need help to do this of course. Luckily Cara McGoogan reported in The Telegraph last September about Microsoft’s new Cambridge-based Health Care AI research unit!

Maybe I’m too skeptical, too untrusting, too suspicious: maybe the words Cambridge and data-harvesting are not the best combo at present, thanks to London based Cambridge Analytica’s Facebook misbehaviour. But I’m sure nothing will happen to the NHS’s data in Microsoft’s hands. Maybe even it’s not Microsoft being awarded this work but my gut-data says otherwise.

I just hope HM Gov got a good price or it’ll look like deja-vu all over again.

I can feel a Freedom of Info request coming on.

Ban psychology teaching - it leads to Social Media

Please stop teaching psychology …  or why Richard Dawkins is always right.

In my role as a Computer Science teacher I needed to prepare some classes for my students about social media. It’s in the syllabus, it was in the news; Facebook and data harvesting being the media’s ‘mot du jour’ . So I ‘did’ SnapChat, Instagram, Twitter, WhatsApp and Facebook. But what struck me was I hadn’t got much to teach my students. The computing stuff was old and simple; TCP/IP comms, a bit of up to date compression and optional encryption; it was a bit all 1990. As a techie, its core was of little/no interest.

So who is interested in this stuff? I don’t mean the users of social media, obviously they are interested, but which ‘gods’ are watching over these applications?

A few years ago I looked at the UK graduate stats by subject. Without too much dissection it is safe to say that psychology graduates rather outnumber computer graduates by a factor over tenfold and much more than that if you only count females. Psychology is now rather hidden in the official stats as it is bundled into a category ‘subjects allied to medicine’. I suspect it was becoming embarrassing to discover how many budding ‘shrinks’ were in the pipeline.

So, take a bit of simple tech ( remember MS Instant Messaging, Skype?) add a generation of business and psychology graduates and what do you get?  Social Media, the love child of a million psychology graduates looking for a job in selling anything from plastic frogs to conspiracy theories.

What does psychology qualify you for with regards to selling? … manipulation is the obvious answer. However to manipulate effectively you have to know your target. To know your target as an individual does not scale well, so called micro- targeting works really not on individuals but  on quasi-homogeneous groups. It’s so much more than your browsing history and postcode

Here is how it’s done. Below is a homage to the great Richard Dawkins, author of the Selfish Gene and creator of the gene’s abstract replicator, the meme.

Social media platforms have something in common, the ability for a communication to be approved by a group or deprecated; more familiarly ‘liked’ or ‘disliked’. This is profound and if we borrow the logic and terms of evolutionary biology we can do the following steps:

A post, (maybe a picture/movie or an opinion) gains in value if it is liked and loses value if disliked. The direct analogy is with a selection pressure deriving from an environment. So an ecological niche corresponds to the social media group ( It may be big or small and highly specialised or less so just like nature). Being ‘liked’ is a bit like having the right beak to open the local nuts.

If we regard a post not just as one post, destined to survive or die, think of it as an instance of the user themselves; an abstract organism that is made manifest via it’s posting-phenotype. A subsequent post is actually a reproduction from that user. It’s not the same post obviously, but it inherits properties from earlier posts. ‘Liking’ a post makes it fitter to survive in its environment and subsequent posts will then inherit characteristics that caused it to be liked. Ideally being ‘liked’ even more becoming a more valuable property of the organism.

Vice-versa for dislikes you may think but not quite so. Consider a group of say 20 folk, a given post you notice is liked by 15+ on average, but consistently 1-3 dislike it. They do not have a selection pressure, they simply get ‘unfriended’ or whatever the term is in the software. If 15+ quite often don’t like your post then you must change or migrate out of the group. The latency built into the system increases with the size of the group but the principle remains true.

However you do it within your ecological nice ... psychological niche is the right phrase, ‘fitness’ to survive reflects an accretion of adaptations. And as in Nature, the drive is towards homogeneity, but without sex to stir the pot or an unyielding indifferent environment to provide external limits to change. A psychological niche is user-defined and so has no limits only homogeneity.

Now we have it, a group occupying a psychological niche can be characterised by the watching ‘gods’ through a process called data-harvesting. Once you know the psycho-nice well enough you can manipulate it, sell to it.

So that is where all those psychology graduates went. All they demand from the techies are more tools to harvest data from daft quizzes, geospatial data, face recognition and so on. Then it’s back to the ‘how the brain works’ books on behaviour and job done.

Micro-targeting bad examples: don’t try to sell ex-Nazi era thermal underwear to folk living in sunny Israel nor books on liberal democracy to an ISIS whatsapp group. They won’t buy.

So don’t blame the computer scientists for the evils of social media, the tech is not rocket science or even new. Blame an army of psychology graduates looking for a job who took our IP protocol and made a monster. All of this by the way is fully predicted by Scott Adams in his 1999 book The Dilbert Future: “Thriving on Stupidity in the 21st Century”.

Cancer cell division and leaky mitochondria: a trigger?

Recently, reading a fascinating paper from a young researcher on the suppression of mitochondrial activity (both respiration and division)  in cancer tumours.1, That cancer cells largely rely on sugar and the anaerobic pathway called glycolysis alone to produce energy, rather than oxidative phosphorylation, was well known, but the mechanism of suppression of mitochondria and the therapeutic possibility of reversal was unknown to me.

 In my own work so many years ago we induced tumours in old and young rats and isolated the mitochondria in the conventional way. We found as others did that there were few mitochondria to be had and that there were no differences in the so called respiratory quotient (RC) between tumours from old and young rats.We concluded, wrongly I now think, that ‘no difference’ meant the tumour mitochondria had been ‘rejuvenated’ … even though their RCs were pretty average (3-4) in any case. More about this latter observation later.

 In any case, cell division in tumours does not need the energy provided by mitochondria.. Multicellular creatures are traditionally described as being able to emerge through evolutionary time due to the energy bounty provided by mitochondria; they need it to ‘fund’ a highly organised low entropy matrix of differentiated cells movement and nervous communication..

 Tumors are by definition multicellular but their internal organisation is minimal which due to the much lower thermodynamic pressures needed for low entropy states  presumably enables them to divide and grow on the low energy yields from glycolysis without the ability to differentiate, move and ‘think’.

 But why divide at all? There is no future after death, no chance of persistence over time, in other words no driver to run this show. Traditionally cancer cell division is studied in incredible depth for obvious reasons but at the ‘why?’ level there is a fall back to saying ‘rogue cells, out of control etc’.

 In previous blogs2 I have referred to the junction between the ancient glycolysis pathway of the cell’s cytoplasm and the TCA oxidative respiration cycle of the mitochondria. My suspicion always has been that it is a kludge. Its kludgy symbiont origins show as we age; we become less able to handle carbohydrates and get fat on them instead of burning them in mitochondria (which are essentially fat burners).

 I suspect that cell division in cancers is the echo of an atavistic response by unicellular anaerobes to ‘infection’ by mitochondria/bacteria. A two pronged response would be effective:

 1) inhibit mitochondrial division and
2) divide, by what is called binary fission in Amoeba but is really mitosis by definition for eukaryote cells.

 Imagine you have 10 invaders evenly distributed, two fissions and you have 2-3 in each, three divisions and it’s possible statistically that one cell is free of infection. Four divisions and this likelihood increases. I will never forget first seeing mitochondria using light microscopy whizzing through the cytoskeleton as if on a  complex motorway system. Selective cytokinesis could enhance the effectiveness of a division strategy by streaming and compartmentalising invading bacteria.

 But I can’t yet find evidence for stimulation of cell division in anaerobes or even single celled organisms such as protist. by ‘intruders’ there is some ‘old but good’3 stuff on the intruders such as bacteria as they evade the lysosomes. Outcomes range from relationships with intruders form obligate symbiont to outright killers. Lots on the response of bacteria to phagocyte predation ( for obvious reasons since that’s what our killer white blood cells do to bacteria) but on the ‘host’ cell’s response … nothing. So I am on my own here. A host response is pure speculation.

 However, there’s more speculation to follow.

 When I used to prepare mitochondrial isolates from the livers of old and young rats it took a long time get to the point where the mitochondria showed good respiratory control ratios (RC) indicating that they were in good shape. Typically ratios 4-5 would be ‘good’. I found small age related difference between old and young preparations ( old had lower RCs) as expected. However sometimes I prepared mitochondria from young animals that had ratios 10 and more. This never lasted for half an hour and never did I get this from old preparations.

My feeling today is that we ended up comparing young damaged mitos with old slightly more damaged mitos and the reason was leakage of Cytochrome C which I already knew was happening in older mitochondria4.

 So consider this; from the host cells point of view, are mitochondria friends or foes? I think that the relationship between glycolysis ( host cell) and oxidative respiration (symbiont visitor) becomes strained as we age. We know that mitochondria are cell killers. Their ability to destroy a cell (apoptosis) is used by the body to clear out zombie  or damaged cells. They do this with increasingly with age ruthlessly decommissioning under used muscle cells (sarcopena).They do so by releasing Cytochrome C setting off a cascade of reactions leading cell death!
We know also that mitochondrial division reduces with age and they enlarge to compensate5.

 So finally, in the aging cell do leaky mitochondria activate an atavistic defence response from the host cell leading to suppression of mitochondrial division and setting off unregulated ‘defence’ mitosis?


https://www.ncbi.nlm.nih.gov/pubmed/20849810

  G Solaini - ‎2011

 2)  DECLINE IN RESPIRATORY CONTROL RATIO OF RAT-LIVER MITOCHONDRIA IN OLD-AGE
Author(s): HORTON, AA; SPENCER, JA Source: MECHANISMS OF AGEING AND DEVELOPMENT  Volume: 17   Issue: 3   Pages: 253-259   DOI: 10.1016/0047-6374(81)90062-2   Published: 1981



3)Protozoa and Protists Michael A Sleigh Cambridge Press 1973: https://books.google.co.uk/books?id=K2Y4AAAAIAAJ&pg=PA281&lpg=PA281&dq=bacterial+infection+of+anaerobic+protists&source=bl&ots=BwLasl4cJs&sig=Zm4ozp8HKwa2SYOuTVaNfjZtLpU&hl=en&sa=X&ved=0ahUKEwiTitCAw9XZAhVUGsAKHV-bBfgQ6AEIUDAE#v=onepage&q=bacterial%20infection%20of%20anaerobic%20protists&f=false4

 4) Implication of mitochondria in apoptosis. Detection of Mitochondrial Diseases, Developments in Molecular and Cellular Biochemistry Volume 21, 1997, pp 185-188 Patrice Xavier Petit, Naoufal Zamzami, Jean-Luc Vayssière, Bernard Mignotte, Guido Kroemer, Maria Castedo
4 BARJA, G. (1998), Mitochondrial Free Radical Production and Aging in Mammals and Birds. Annals of the New York Academy of Sciences, 854: 224–238. doi: 10.1111/j.1749-6632.1998.tb09905.x


5) Release of Cytochrome C by osmotic swelling. J.A Spencer and Alan A Horton 1979

Steroid use and Roid Rage

Forty years ago I was a half-decent weightlifter (olympic weightlifting, British student team ) and very proud of my strength and speed. Back then, as is well known now, anabolic steroid use was widespread in the strength sports and one of the reasons for me giving up was a personal unwillingness to use the steroids to improve my performance.

The Guardian today (22nd January) ran an article by Steven Morris describing the abuse of anabolic steroids by a million UK ‘gym-bunnies’ of all ages from too young to too old. They are not taking them for a competition advantage ( it’s actually quite hard to do this as drug monitoring makes it a bit tricky) they are doing it for narcissistic reasons.

Personally, I am not in the least surprised by the article, mere anecdotal observation as a school teacher has had me saying “goodness is he steroid pumped?” or for females “ that’s looks like a steroid rash not acne” on far too many occasions. You see, I recognise the effects of steroids at a glance from years of training in the weightlifting world.

So far, so good, ‘bully for me” you might say, “what observation skill!”. But this is serious, steroids are serious. We were very used to steroid rage, “roiders” they were called. It was well known that one of the world’s greatest lifters needed a team of minders with him during competition in case he exploded. Trashed hotel rooms were common. Even at my college we knew not to get across an olympic field athlete and who became a lot safer when he retired!

Over the past years, when a brutal attack has taken place which is featured on the media, the first thing I look for is to see if he is ( in my observation, a ‘roider’). Explosive, sudden, often unheralded violence usually accompanies  descriptions of the perpetrators who range from baby-sitters to gang-enforcers to terrorists. Tip, check out the neck first.

The point of this short blog is to highlight the the psychotropic dangers of steroid use. You might be very proud of your physique and power but be unaware of the unexploded bomb that is you. Or indeed the Tony Soprano image  may be why you are taking steroids in the first place. Either way if Steven Morris’s million users is anyway near the mark this is a serious problem and personally I would ask for anabolic steroids to be classified as a Class A drug.