Social Media's evolution was inevitable-repost from 2018

Please stop teaching psychology

…  or why Darwin and Dawkins are always right.

This article from 8 years ago seems more relevant now and introduces the

idea of a psyhcological-niche obeying the laws of natural selection evolution.

It could also be titled 'don't blame the techies for your mess'

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”. 

Statins and Mitochondria update.

 

I've posted about the effect of the cholesterol synthesis blockers known as statins on mitochondria before. This week though a couple of updates on the national news seem worthy of comment.

The first was a a publication from the University of Columbia detailing the source of the muscle pain side-effect associated with statin use. The work was very detailed at the molecular level and demonstrated clearly that the pain was associated with in infux of calcium ions into muscle cells. 

The second was a finding that  most of the very many side effects of statins as described on the crib-sheet supplied with the drugs were actually not attrubutable statins at all. The muscle pain side effect though was.

The above findings are interesting at the scientific, the linguistic and legal levels equally. The first finding regarding the influx of calcium ions is important because it is well known that mitochondria rapidly and unselectively absorb these ions, swell and may burst as the outer membrane gives way. 

Nearly fifty years ago my first paper showed that mitochondria became more fragile to swelling with age. Then we did not know so well that their rupture and release of weakly bound Cytochrome C ( this binds less tightly with age) triggers cell death ... we know it well now and it is the source of muscle wastage (sarcopenia) in old age. So, Columbia's research shows why a side effect of statins is muscle pain but it's findings infer that all mitochondria  will swell as a result of the drug. It's just that it is not always fatal to the cell! Do this to damaged, senescent mitochondria in aged cells and the cell will die as the mitochindria rupture.

The second finding's announcement was laughably 'straw-man' and linguistically manipulative.  The imaginary side effects listed on the drug sheet turn out to be, well, imaginary so can be crossed off,  and the confirmed side-effect (see above) is very rare so please ignore

... so the authors conlclude that the drugs are actually 'safer' than we thought and their role in tackling 'bad-cholesterol' is an even better option for now reassured people. 

Outrageous, my dim GP will no doubt be persuaded by this Pharma's ChatGtp bot generated blurb but this week's message is actualy the opposite. It's that statins cause severe change in calcium flux in muscle cell and this side effect is confirmed as real, ...  and the reasearch provides a clear causal path to sarcopenia in the vulnerable populations prescribed the wonder drug.

To get the message above though you will need at least a PhD in mitochondrial biochemistry and a working ability detecting thematic meme reasoning. 

Or in the opposite scenario, to be reassured, you will need a) a trust in big Pharma struggling to sell its wares, b) faith in your GP's scientific knowledge and c) an admiration for the Mandelson level of manipulation reached by generative AI

Fibre: my 30g per day

High Fibre food is all the rage replacing 'high protein' on every label as it in turn had replaced 'low fat' and 'no added sugar'. 

The recommendation is to eat about 30g of fibre by dry weight each day for optimum gut health mixing soluble and insoluble fibre found in plant based foods. The fibre content is found on all manufactured food labels and AI will get the rest for you using your search engine of choice.

It's actually quite hard to manage 30g of fibre a day and experts estimate 96% of us don't make the target.

Yesterday I did, This is how I did it:

Breakfast: Full english ( sausage, egg, tomato, black pudding, baked beans, mushroom, bacon and two slices of toast) Total 7g Fibre

Lunch: a banana, a packet of peanuts, a bag of crisps washed down with a glass of red wine.              Total 10g.

Supper and evening:

Fish in batter and medium chips with mushy peas and two pints of beer.

Total 14g

Grand total 31g!!  

Plus, this diet was very low in sugar and cholesterol and high in protein, vitamins and minerals.

In all the perfect diet. 

Don't suppose the nutritionalists would approve though. 

Mitochondria: how they interact with the world.

 
Mitochondria can and do 'see' our world.

The effects of electromagnetic radiation (EM) on the bodies of animals and their cells has been investigated
and studied for over a century. From low frequencies to high, the penetration and absorption of EM radiation
in tissues has been of potential concern. This is more so now that we are not only ‘bathed’ in the traditional
frequencies of EM from the slow pulses of the geo-magnetic earth itself and the light from the sun but to the all
pervasive microwave waves of the connected world. 

The focus of interest has been, firstly one of penetration, ie how deep into tissue the EM goes and secondly one of absorption/blocking: does the EM just cause heat ( molecules vibrate more) or does it cause damage (molecules suffer broken bonds)? For example we know about skin damage from UV  light radiation, tissue damage from X rays and the heating effects of microwaves in a microwave oven. So from our perspective of investigation we have EM categorised into:  block; reflect  and absorb with heat and damage being the salient associated words that link with the EM that surrounds us.

This post though is not about the long list of research findings from the above, it is about the interaction of environmental EM with mitochondria. Why mitochondria? Because,  if you have chanced upon these posts before you will know that I regard mitochondria principally as electrical devices; specifically oscillating organic capacitors that use stored charge as the electromotive force to drive biosynthesis.

To an electronic engineer a device of this ilk that holds charge, a charge which varies in magnitude, amplitude and period, is something to be reckoned with. It has an oscillating electromagnetic field so it will inevitably be subject to interaction with EM radiation in complex ways. Terms like field induction, tuned resonances, field switching and so on familiar to the engineer will apply to mitochondria.

Mitochondria are known to interact with penetrating EM radiation at a variety of frequencies.

These are:  
Fields in the 1–8 Hz range have been shown to induce mitophagy (removal of damaged mitochondria) and promote rejuvenation, influencing the electron transport chain (ETC).  the Schumann Resonance at approximately 7.83 Hz, and higher harmonics at around 14.3 Hz, 20.8 Hz, 27.3 Hz;  
An oscillation period of 25 kHz is shown for superoxide; 
Some models suggest cells, including mitochondria, might have resonant frequencies in the 10–30 kHz and 150–180 kHz ranges, though these are less studied.
~125 Hz:

Linked to increased mitochondrial numbers, higher reactive oxygen species (ROS), and changes in

nerve size in some tissues;
 ~250 Hz: A prominent resonant frequency affecting peripheral nerves, leading to inflammation and injury indicators,

and potentially influencing mitochondria indirectly.
120THz  Black Light NIR therapy, absorbed by mitochondria in the 800nm wavelengths

All of the above frequencies are of penetrating EM radiation and its interactions with mitochondria are well documented. Of particular note is the fact that the low frequencies and the high NIR frequency both have their origins in the earth's diurnal rhythms. 
The nature of the mitochondrion has been on a steady journey in the last 50 years.

Lynn Margolis’ persistence and brave insight liberated the mitochondrion from being an

innate structure of the eukaryote cell to that of a once free living organism to now a symbiont working with the cell.

Even so the mitochondrion’s paucity of genetic material kept it in its place subservient to the nucleus’ control.

Even that has changed as the mitochondrion’s ability to retrograde signal with its outsourced nuclear  genes has

become apparent.

Finally, on this journey, i would like to point out that the mitochondrion is not incarcerated,

blind to the outside world. To us we look solid as visible light bounces off our skins but penetrating EM

does not suffer this illusion. Mitochondria within the  body can ‘see’ the environment and due to their electrical

nature they can and do interact with it.

Time to rest, the sun is setting and my mitochondria are signalling time to sleep.  

Silo knowledge and AI

 

Hopefully this post does not come over merely as the grumbling of an old scientist but grumbling it is. My research field was, and my current scientific interest remains in the ageing of mitochondria and their role in senescence.

Anyone who has chanced on my blog posts will know that my focus has always been on the electrical nature of mitochondria and on the entropic nature of the Free Energy they generate. Now, to understand this post you must first understand that mitochondria ‘belong’ to the biochemists,  the molecular biologists, the geneticists (and molecular geneticists), the cell biologists,  the physiologists and even the medics: they all have their particular ‘take’ on mitochondria. All, pretty much nowadays, agree that mitochondria play a central, even THE role in the ageing of an organism. None have any idea what to do about the ageing of mitochondria … and that is despite phenomenal advances in all of their fields in the last 40 years.

At the start of the paragraph above I used words like capacitance and entropy. The former, capacitance,  belongs to the world of wires, charges, voltages, resistance, amps and coulombs. In other words, the world of the electronic engineer. The second word entropy belongs to the world of the physical chemist: enthalpy, entropy, equilibria, Gibbs free energy, joules and statistics (maths!). There is virtually no substantial research on mitochondria as physical chemical electronic devices despite their having trans membrane potentials ( voltages); electron flow (amps);  and capacitance ( farads). That is despite mitochondria initiating cell death when they depolarise ( ie short out to earth ) and losing membrane density as they age (capacitance). There is just as little about the energy mitochondria generate. It is blithely written as Free Energy but unthought of as a hybrid concept embodying enthalpy and entropy. Cholesterol is not mentioned for its ability to increase the dielectric of a membrane; of course not, what’s ‘dielectric’ to a protein molecular cluster specialist?

I am not trying to show what a great polymath I am. Having specialised early in physical biochemistry and later worked as a software programmer and later still worked in the micro-electronics world, all of the above ‘insights’ are obvious to me. No, my point is that if you are a young researcher and mitochondria are what you are looking at then you will be in a silo of one of the areas above in which mitochondria ‘belong’. It is pointless for you  even to know what the electronics engineer or the physical chemist would think as their world is closed to you.

This is a then a grumble about specialisation leading to silo knowledge and research. Nothing new here, but maybe with AI there is a chance that at least the walls of the silos will become visible. Just AI lookup ‘the role of electrical capacitance on the aging of mitochondria’ and you’ll get the picture. 

AI will let you know what you don’t know.

Entropy and Ageing

 

Entropy and Ageing

When I took up my PhD work on the biochemistry of liver mitochondria from old and young rats, my supervisor to be and his senior post-doc both said ‘when we get old we run out of energy so it must be the mitochondria’. They did not actually say ‘duh’ but you felt it.

50 years on, very little progress has been made when it comes to extending our life span: that’s despite astonishing progress in genetic analysis and manipulation. I think (as anyone who reads my posts knows already) that the key to aging is with the mitochondria. The reason is compellingly simple: entropy. 

Entropy is not just another word that simply replaces ‘energy’; it isn’t that simple.

Mitochondria, ultimately generate the vast majority of the chemical-‘energy’ molecule known as ATP, (adenosine tri-phosphate) which can be hydrolysed to form ADP {adenosine di-phosphate) and phosphate ions. The mechanism by which mitochondria do this and the full nature and stoichiometry of the ATP/ADP chemical equation are elaborated to students in details that correspond to whether they are A level students, undergraduate biologists, biochemists, chemists or medical students. What they are not, invariably are engineers or chemists which is a shame as they see things differently.

When you look up the energy yield of ATP hydrolysis it is -7.3 kJ.mol-1,  

That’s usually enough information for most people. It’s energy, end of story. But this is actually a change in energy called Gibbs’ Free Energy and under standard conditions ( pressure temp) it has the symbol  deltaG0

It is a particular form of energy and was ‘discovered’ empirically and formulated explicitly during the steam age, 1873, by Josiah Gibbs. Put simply it was the energy ‘available to do work’ Quite simply engineers and calorimetric chemists noticed that the heat energy released by burning coal never fully translated into work ( eg ‘work’ as in lifting things up)  that a heat engine could do. After fruitless hunting for this energy allowing for heat losses, friction and so on it became a mysterious but fixed fact of life.   Today we know why and all chemistry students are versed in the difference between heat energy, electrochemical energy  and Gibbs Free Energy ( deltaG0) 

I do not have the slightest intention of typing an exposition of dreaded thermodynamics, just to point out that the energy term used above  -7.3 kJ.mol-1, is free energy, and as such contains the term entropy according to the equation: 

ΔG=ΔH−TΔS

In words: Gibbs free energy change is the enthalpy change ( ΔH heat change) minus the change in entropy ( ΔS) at a given temperature(T)

More words: because of this equation,  the key way of looking at mitochondria is less as energy producing organisms but as entropy reducing organisms.

Entropy is a mathematical probability concept, and according to the Second Law of Thermodynamics no spontaneous change occurs without a net increase in entropy. A complex system with a high degree of organisation is in an improbably low entropic state and without a lot of energy input will naturally and completely disorganise itself over time and entropy of that system will increase. 

.

An organism like ourselves, with a vast array of physiological structures and huge storage of complex information from the cellular-genetic to the electronic storage of the brain, requires vast amounts of energy to maintain such local levels of improbability. And as soon as we die, well ‘dust to dust’ springs to mind.

As we age our mitochondria do a sterling job of maintaining a stance against the Second Law but as they fade, if even a little, our system entropy increases and senescence, non-viability of the organism beckons. Tumours have a higher entropy than organ tissue, a demented brain has a higher entropy than a fully functioning one, an arthritic joint has a higher entropy than a healthy joint. The list is endless.

Back to the beginning of this essay: 

The key to understanding aging must be within mitochondria. Its own internal DNA plus that is which it outsourced to the nucleus (for safe keeping from the oxidative furnace that is a mitochondrion) contain the answers. For with Gibbs free energy in abundance they can maintain our low entropy, without it they can't.

As we get old we increase in entropy.