The end of Cholesterol: 35 years of barking up the wrong tree

 

We talk less of paradigms in science and medicine than we did in the 1990s. Then a ‘paradigm shift’ was a phrase not uncommonly heard in a time of rapidly changing tech and science. Think of the advent of mobile phones, personal computers, the internet and the world wide web to get a sense of what was to come. 

AI is generating that same sense of change thirty years on, but this post is about the 1990s cholesterol-busting drugs called statins and the drugs which followed them. These were remedies for cardiovascular diseases that came to rule many lives over the following decades. People knew their cholesterol blood levels with numbers as familiar as their house’s street number. For instance one may hear ‘mine’s 5.5 or 7’ or whatever. Such words would not be unusual to hear at a middle class dinner party. And so a cardiovascular paradigm was born, a paradigm which is now deeply embedded into the medical profession and the general population alike. A paradigm which is collapsing.

Also in the nineties I regularly taught  a class on scientific method. Classics like Karl Popper’s Conjectures and Refutations 1963; The Structure of Scientific Revolutions 1962 by Thomas S Kuhn and Paul Feyeraband’s 1975 Against Method: Outline of an Anarchistic Theory of Knowledge were foundations of the class. What has really stuck in my mind though was Kuhn’s description of the life of a prevailing scientific paradigm 

He asserted that no amount of Popper-esque refutation (e.g. by experimental ‘disproof’) can unseat a powerful embedded way of looking at things, a paradigm. Instead, competing paradigms grow according to the ‘weight of confirmation’ or fade under the ‘weight of disproof’. This is illogical but as he points out we don’t live in a clean cut Popper scientific logical world of conjecture, test, refute ( or not), repeat. Life, even in science, is messier.

The point I am heading towards is that the long lived cholesterol paradigm has had its glory days of ‘confirmations’ and under the weight of refutations is fading. To the medical profession who crave scientific validation this is a sad blow as their cardiovascular remedies default to basic empiricism … if it produces a good result it’s in, otherwise it’s out. 

Below is a summary of this paradigm's story. 

The Beginning 

Arterial plaques are fatty cholesterol-rich deposits which can block arteries and may rupture. They increase with age and start early in life. Some unfortunate individuals produce a lot of cholesterol and have extremely high blood levels of cholesterol lipoproteins and unfortunately also have massive plaque deposition. They usually died young …  until the advent of miracle statin drugs which blocked cholesterol synthesis and saved their lives. 

The ‘paradigm’ really  gets started when these statin drugs were applied to a wider population of people with high but not pathological levels of cholesterol. And behold,  in the newly formed  wake of ‘big data’, positive health outcomes were evident at the population level. And so statin prescription became widespread and millions, no billions, of dollars were poured into the field of lipidology and a lot of knowledge was accumulated.

Not just Cholesterol but ‘Good’ and ‘Bad Cholesterol

It came to pass that the cholesterol-laden lipoproteins were sub-classified according to their density (how big the fatty-droplet bit was) broadly, low-density (big) and high density (small) droplets. We know these as LDL and HDL (the former are large and the latter smaller). LDL is usually ‘bad cholesterol’ and HDL ‘good cholesterol’ to help the public relate to their respective levels.

Actually these droplets circulating in the blood exist in a spectrum of sizes but only the small HDL droplets can penetrate the blood brain barrier and the brain needs a lot of cholesterol to function! Worries about reducing available cholesterol to the brain during a global epidemic of dementia meant a new Holy Grail: the trick would be to make drugs that lowered bad cholesterol and kept decent levels of good cholesterol, maybe even boost it!  

At about the same time a very-bad cholesterol containing very low density lipoprotein called LPa was discovered.  Billions of dollars later, drugs are developed to boost good cholesterol and others to lower bad cholesterol,  and lately even to greatly reduce very-bad cholesterol(LPa). Daily, lifetime-medication with its associated profit beckoned and by the way cardiovascular disease was to be defeated.

The paradigm unravels

As the reader may have guessed some nasty shocks were coming. 

Firstly, in first line ( i.e. well run, large and validated) medical trials, drugs which boosted good cholesterol whilst lowering bad cholesterol made no improvements in cardiovascular outcomes. The drugs were withdrawn not least due to unfortunate side effects.

Secondly, and shockingly to the scientists involved, lowering very bad cholesterol (LPa) which the industry was convinced was causal for plaque formation, had absolutely no effect on cardiovascular outcomes.

Finally, an awkward epidemiological fact was emerging. It is called the ‘cholesterol paradox’. For people under sixty, lower levels of cholesterol in the blood, especially the bad cholesterol (LDL) and the very bad cholesterol ( LPa) do associate with what the medical profession call a protective effect. But, above 65 yrs old,  in the 64-74 group and for all of the octo- and nonagenarians the opposite is true. Low bad cholesterol is strongly associated with poor cardiovascular outcomes and vice versa. You may need to read this again.

The end of an era.

So it’s over. Drugs to prevent cardiovascular disease are now only judged on one criterion: ‘do they work?’. Gone are the mad metrics of your cholesterol numbers; gone are the theoretical scientific assumptions underpinning medical research in this area and gone is the confidence of big pharma. All that is left is a ‘suck it and see’ strategy. 

It’s devastating for the scientists whose careers have been built on these sands and schadenfreude for the biochemists who were baffled from the start at the claims of the medical industry. I take some comfort though in being privileged to witness Kuhn’s philosophy of science actually happening in my own era.

Hopefully this news will trickle down to the GPs but as with all paradigms says Kuhn, they never actually disappear.

Mitochondria are Intelligent

It seems an age since Lynn Margulis and her supporters fought bitterly for the notion that mitochondria were once free living organisms now engulfed and residing as organelles in every eukaryote cell

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In the past, fifty years ago until quite recently, mitochondria were perceived as ‘enslaved’, de-individualised, genetically stripped out, aerobic power houses of a cell under the master control of the genetic hegemony … namely the nucleus. This picture is taught to students worldwide and invariably biological  articles and text books referring to mitochondria usually begin with a weak entree:  ‘these tiny structures are the power house of the cell’ or some such thing and ends there. The tiny batteries have a job and carry it out under the auspices of the nucleus.

Mitochondria traditionally pay second fiddle to the nucleus in the cell which is regarded as containing the blueprints for all life stored in DNA-based code. The tyranny of this mega-repository of genetic information, has  been reinforced in our minds over the years by Dawkins’ notion of the ‘selfish-gene’. The survival of the replicating ‘gene’ units being the uber-determinant of the variety of creatures ( or gene-depositories) we see today. I have no quarrel with the logic of this thesis, save that emotionally, irrationally some will say, on my part the model’s lack of intelligence is uninspiring. I am no creationist apostle of ‘intelligent design’ , on the contrary, but even so the gnostic in me seeks more!

In the current world of AI though, we are coming to understand a wider notion of intelligence ( including an ironic thumbs up for machine intelligence from Dawkins himself). So this is where I wish to start this essay: mitochondrial intelligence.

In 1995 Hideak Sena published a sci-fi horror book, in Japanese, that had as its conceit that mitochondria were intelligent parasites living in an intracellular ecosystem who controlled the fate of its organism ( in the book humans are the organism) and which could communicate with the outside world. Amongst other things they could coordinate death of the organism, influence its longevity and even, by collective synchronous discharge of electrical potential, cause spontaneous combustion!  I really like that idea.

Far fetched? Yes quite a bit but, less so today.

Mitochondria are not the slave ‘batteries’ of the cell. They may have only a few genes inside the free-radical furnace that is the interior of the mitochondrion, but they do have an active intracellular retrograde-signalling life, communicating with their legacy and adopted genes in the nucleus, as well as modifying the epigenetic profile of the cell: the latter being in response to environmental ( ie outside the cell) cues. And of the latter comes communication. Mitochondria we now know, can ‘see-feel’ and react directly to the world outside of the body as the result of penetrating NIR radiation and additionally host of penetration electromagnetic frequencies from low to high. By ‘react’ I mean power up, power down, divide, die, and modify epigenes.

Furthermore, mitochondria can be ‘conditioned’ intracellularly through oxidative hermeneutic stresses created by the larger organism.  Examples of this would be extreme activity or response to acute infection.

In short, mitochondria are genetically active, well connected to the data-base and ‘know’ what’s going on outside their cellular prison and can react accordingly.

Mitochondria have the power of life and death of their host cell. Killing their host is routine and necessary. The process is called apoptosis. A cascade of events initiated by mitochondria kills a cell when variously: the cell is senescent and damaged; when viruses have invaded and threaten to reproduce within the cell and when a cell goes rogue, transforming  into a cancer cell. As an aside it is no surprise then that the first job of a invading virus or emerging cancerous cell is to switch off the mitochondria … if they can.

Mitochondria: age; die; reproduce by fission; fuse together (for collective electrolytic capacity and power storage  during cell division when feeding is not possible); split apart and can move rapidly throughout the cell on the cytoskeleton gel/sol highways to sites of high energy demand, or even to meet foreign-body intruders … a busy life.

But are mitochondria intelligent? 

Here we need to move to more modern concepts of intelligence. Artificial Intelligence development has taught us a few fundamentals. Call these: storage, comms, and computing.. Do mitochondria and their intracellular ecosystem infrastructure have these fundamentals?

Yes they do. Firstly, the DNA of the nucleus and epigenetic loops store decent amounts of information, upwards of IGb in conventional computing language. Secondly mitochondria oscillate at approx 10-100 MHz ( the so called New Agers’ frequencies) and are capable of resonant interaction with the electromagnetic spectrum right through to the kilo, mega and terra hertz. In other word ‘communication’ is quite possible. Oscillators are communicators .. think anything from a drum to a loudspeaker for an analogy.

Thirdly, what about computing power? Mitochondria are electrical devices analogous to capacitors which enable charge separation ( high- low states, ie binary) and transport electrons through proteins capable of quantum tunnelling or in computer speak: very fast data buses and quantum wires.. Superposition quantum states are possible too according to Roger Penrose in 1998, maintained within the cytoskeleton using tubulin proteins to stabilise them. 

To cut a long theory short, the intracellular ecosystem contains the wherewithal to maintain a non-algorithmic, quantum computing state of consciousness, fully  integrated with the ‘world’ of electromagnetism and gravity i.e. Wiitengstein's the ‘World’.

In summary, in this essay the cell is a conscious entity, and conscious because a dumb legacy infrastructure was leveraged by energetic, entropy-defying guests, the mitochondria.

The intelligence and consciousness of the cell is innate and, to  multicellular creatures with algorithmic-driven nervous systems, it is inaccessible. Maybe the next generation of machine intelligence will give us insights into this world but for now only the minds of cosmic physicists  such as Professor Pensose can think with a level of abstraction denied to the likes of me.

To finish, my picture of the cell  puts the  engulfing adoption and subjugation of mitochondria by a larger phagocytic host rather into reverse … as an invasion. Free living, cell penetrating, bacteria-like infectors, invaders, coming to stay, liking what they found and steadily building a super-creature we know as the eukaryote cell. Pure science fiction as Margulis was told way back.

Neoteny, the man-child

Neoteny is the retention of juvenile traits into adulthood. Humans, homo sapiens, that is to say have extreme neotenous traits when compared to their great ape cousins and homo ancestors. They are well known, but just to restate some of them: hairless bodies ( or nearly so); flat faces; large head to body proportions; large eyes ( again relative to head and body); a lower degree of  sexual dimorphism; an extended childhood with traits like explorative behaviour conserved into adulthood (even for life); increased brain plasticity … and many many others. Finally, observable to even the most casual looker, neoteny is ongoing. Adolescent behavioral traits are often maintained into early thirties and pre-adolescent gender fluidity is increasing accompanied with falling birth rates as pre-reproductive phases encroach on post-reproductive phases of life.

Humans are changing, we could say ‘evolving’ but we need to update our school-age Darwinian play-book to make sense of this. When I taught ‘evolution’ in senior biology classes I relied on a paradigm that was and is ‘true’ but as one would expect not the whole picture. Evolution according to this paradigm and runs like this:

Our genes (genotype) control our appearance (phenotype) and by extension all our physical and mental attributes. Variation in our genes either through random mutation or the natural pack-shuffling of sexual reproduction produces  variation in the next generation. Interaction of these offspring with the ever changing environment determines how well they thrive and live to successfully reproduce. This is the fate of the  ‘survival of those most fitted to their world’ and by extension so  their genes will be passed on.

Two major discoveries nuance this piece of well tested logic. The first is the fact that most genes are highly conserved. That means they don’t change. For example the gene for a fly’s eye is the same as that of an octopus as that of a human. But these creatures have very different eyes! 

The second fact is that epigenetic changes ( DNA outside of the nucleus not in theory passed on in reproduction) authored by interaction with the environment can and do get incorporated into the genome which is then passed on. This is called neo-Lamarkianism after the soviet agronomist who believed ( disastrously in this case) that the effects of the environment directly shaped the genome.

What we now appreciate is that it is the activation and temporal expression of control genes that created the bewildering variety of life, not the library itself. This brings me to the central point of this post. We are now led not to the library of genes but to the importance of the interface of the organism and the world. The interface is where the integration and communication with the world happens.

The Descartian dualism of the past has always been a hindrance to modern science where we are special creatures observing objectively a world which we can interrogate. Physicists have long overcome this illusion but environmentalism is a newer discipline and is only just catching up.

We interact with our environment. We have senses ( which misleadingly can enhance dualistic approaches ) just for that purpose; we acquire epi- genetic material from a kaleidoscope of viruses and vaccines that infect us and even, deep within bodies, our mitochondria inside cells sense and react to NIR (near infra red) light from the dawn and dusk sunlight.

It’s not rocket science to realise that if our interaction with our world results in a small change in control genes then our own phenotype will change too … and rapidly, not Darwinian generationally. Anyone who has seen a now old video of young late-adolescent orangutans will not forget the recording of the favored youth among many candidates ( selected by the female on whatever grounds)  metamorphose into an adult challenger complete with cheek pouches, just on a high-level environment signal aka the females’ approval. 

It is possible (and it is my opinion) that the neotenous tendency of our control genes, the very genes that produced the man-child that propelled Sapiens to its technical tool making dominance, are on the march again. The signals from the environment ( maybe TV/Smart Phones) have awoken them. This time this peculiar trait may well bring about our reproductive end and explain a reverse coin of neoteny that is early onset cancer. On the upside the boost in creativity may give birth to a very different version of ourselves, know colloquially as AI.

NAD+ solves the aging puzzle

 

It’s fifty years since I completed my PhD on the biochemistry of mitochondrial aging. At that time, interest in the subject of aging was minimal. Fast forward to today and the biochemistry of aging and the role of mitochondria is centre stage. One can feel the breakthroughs coming very swiftly as pennies are dropping.

In the 1970’s, the centrality of mitochondria in the process of aging was based on a very simple premise: in senescence you run out of energy and it’s mitochondrial bioenergetics that generate that energy.  Mitochondrial dysfunction in aged cells reduces the availability of chemical energy changes (Gibbs energy (∆G)), which means that the low entropic state that is a healthy living cell gradually increases until it fails.

Today, the fundamental truth above is fully appreciated

and can be integrated with many of the puzzles of aging..

Fifty years of results from genetic activity (genomics) ,

free radical theories of aging and metabolic signalling

can be reconciled into a bigger picture.

In addition, the disparate macro effects of obesity,

lifestyle, and diet on aging now all slot into place.

The key link is the new darling of the anti-aging world

… NAD+ and its aging-linked nemesis NADH + H+.

It’ll be tricky to explain in readable prose,  but I will try. 

The small molecule NAD+  decreases within cells with age. It is the oxidised form of a class of molecules called nucleotides. NAD+ is used up, consumed, in various biochemical processes and with age decreases despite being synthesised from scratch and carefully scavenged and recycled. It is also not easily supplemented.

The  important thing about NAD+ is that it is able to accept electrons from hydrogen (H). These electrons come from the metabolism of food such as fats, proteins and sugars. NAD+  then becomes NADH + H+ and this molecule feeds electrons into the mitochondrion’s complex system of enzymes to produce chemical energy. It’s the ratio of NADH/NAD which is creating excitement in the aging world. Basically if NADH is much higher than NAD, ie the ratio is bigger than it should be, this is a very bad thing in terms of aging. 

The reason why a high NADH/NAD is bad is because the mitochondria, unless very active energetically, cannot handle the amount of electrons that can be provided by excess NADH. Long story short, depending on how much the oversupply of electrons is,  a burst of highly damaging free radicals is produced. Reactive oxygen species (ROS) as they are properly called, are known to increase with age and to be responsible for a lot of the cellular damage associated with aging. And, as is well known, we are urged to eat healthy foods high in anti-oxidants to prevent such damage.

Clearly then, since NAD+ reduces with age any increase in the size of the pool of NADH will make things worse. This is where 21st Century humanity come unstuck.

It’s a fact: modern humans in the developed countries are largely physically inactive, well fed and graze feeders.

This means that they have no spare capacity to store dietary sugar as glycogen. Sugar which is not needed for activity, cannot be stored because the stores are already full. Modern diets high in glucose syrups, maltodextrins, lactose, fructose and potato starch are effectively diets of sugar. The sugars must be metabolised within cells. They cannot hang around in the blood. The metabolised sugars are then either stored safely as fat or broken down further and their hydrogen passed to the mitochondria for oxidation. Here is the first source of hydrogen over supply together with the link to diet and obesity. Inactive bodies have inactive mitochondria. The stimulation of mitochondrial metabolic activity from baseline tickover is signalled in an array of ways, foremost amongst which is physical activity. The mitochondria are not ready to receive hydrogen/electrons, ie not powered up. They will however accept the electrons, but with accompanying disastrous free radical production as the electrons react in an uncontrolled way with oxygen. Here is the second driver of oversupply of hydrogen.

As a consequence of the above, ( viz UPF rich diets, grazing eating and sedentary living) the ratios of NADH to NAD become high; too high. This state risks massive spikes in free-radical damage which lead to premature aging and early cancers. 

As I said at the start of this post, the biochemists now know what is going on. What will be the result? A new pill? Or a lifestyle change? Your guess, but at least we are close to knowing aging now.

Creatine Supplementation and Aging Mitochondria

Creatine and aging mitochondria.

Creatine supplementation and aging mitochondria.

Implications of the capacitance hypothesis in aging mitochondria.

As we age we run out of energy. An everyday colloquial, universal refrain which brooks no exceptions. What exactly we run out of is more difficult to pin down. This post hopefully will give clear picture of what it is. It is inspired by a couple of contemporary trends: batteries and creatine supplements. Or put another way, energy storage.

A while ago I described in a previous post (Mitochondria, oscillators and broadcasters?) an electrical model of a mitochondrion. 

It was very simple: electrons were supplied in variable amounts to a capacitor which then discharged through a solenoid coil when it reached a threshold voltage.

The supply of electrons was regulated by a light dependent variable resistor; the capacitance of the ‘mitochondrion’ could  be varied; the activation of the solenoid in reaction to the discharge of the capacitor represented a transduction of energy into a form that could do work and finally a ‘bleed’ variable resistor simulated the loss of charge by a ‘leaking’ aged mitochondrial membrane.

All of the above is meant to be an analogy, in purely electrical terms, of a real mitochondrion receiving electrons from its substrates, charging the inner mitochondrial membrane and transducing its energy into the likes of ATP. 

 

As described previously, what shocked me after I chose to output to a sound file in Sonic.py, was the thumping beat of the oscillating charge and discharge, and how this sound changed its period as the ‘leak’ was increased until it collapsed into a single tone. 

Recently I sketched these results which are shown below as how I imagine it occurs in actual mitochondria.

It can be seen that as a mitochondrion becomes more prone to losing charge, leakier’, as is well known to happen in senescent mammalian cells, then the charging curve takes longer.

Clearly the next ‘dump’ of energy cannot happen until the threshold voltage for the individual as been reached. 

(In a cell containing thousands of mitochondria we are not looking at an individual but a population but nevertheless the principle will be the same for old and young mitochondrial subpopulations within a cell.)

Running out of puff = running out of Power

The power output of the mitochondria is the rate at which free energy can be drawn off, the unit is Joules per second,  commonly known as Watts. ATP the ‘free energy molecule’ can provide about 58,000 joules per mole of ATP.

From the graph you can easily see that although a fully charged mitochondrion can provide the same energy whether old or young, the longer it takes to recharge, the lower the power output.

Creatine and Batteries

Creatine is a very popular food supplement. It has been used by strength athletes foe many years but now is finding great favour as a sleep aid and calmative. Creatine stores are like batteries. Many homes nowadays have batteries to store energy in off peak times to charge their EVs for action later or indeed their heating systems. Creatine stores are analogous in that they are able to store chemical energy from ATP as Creatine phosphate which they can very rapidly give back to the ATP on demand.

Aged humans often have sleep problems. The brain needs a lot of ATP energy, 24/7. This is provided classically from glucose and ultimately by mitochondria. If the baseline power output of mitochondria in the brain is low then they will not be able to stay in sleep-mode. They will have to up their output to the minimum required by the brain. However if you have invested in a battery, then they can be supported. In fact although most creatine phosphate is stored in the muscles for instant action, five percent is stored in the brain.

It is likely that creatine supplementation in general is a good ‘battery’ support for aging mitochondria in many active tissues. Natural sources are fish, meat and dairy ( herring being foremost) but to get large amounts you need the white powder supplement. Given the above post it will be interesting to see how supplementation pans out long term.

 

The Wagyu Generation, Gen W

The Wagyu Generation

This post could be also titled GenW or ‘Ways the USA’s agro-biz makes us sick’ but that latter remark would be to invite the inevitable lawyers’ letters … so Wagyu it is.

I have for a good while now noticed that a lot of folk under 25, especially adolescents and children look oddly ‘inflated’.  Not fat in the way older people have a protruding abdomen and various mounds and flaps of subcutaneous adipose tissue, but softly pneumatic. Additionally, also noticeable is that sexual dimorphism is less evident thus adding to their unique appearance. 

If we were cannibals (or if they were cattle) they would, I think , be good to eat with tender, heavily fat-marbled meat and pale fatty soft livers. Yum. Wagyu.

(as an aside, quite possibly if they were actually cattle, EU regulations may have something to say about how they are kept cooped up in small rooms an overfed on high calorie junk food)

The ‘wagyu’ generation as I will refer to them is real. In previous posts I explained already how we know UPFs increase intramuscular fat ( ‘UPFs give you Wagyu Thighs’), why fructose excels at creating fat deposits even if you exercise (‘Fructose makes you very fat’) and why Soya’s phyto-estrogens contribute to declining birth rates in all  developed countries (‘The Future is Trans’). Read them if you want more details. Below is my conclusion in the simplest terms:

This largely sedentary generation’s diet has been fatally corrupted through its levels of fructose, soya  and CLAs ( conjugated linoleic acids).

1. Fructose (or fruit sugar as it is often called) bingeing started with the availability of fruit juice concentrates. Overproduction of citrus in the US plus good marketing leveraged its Vitamin C content and the rest is history. Now fruit derived concentrates are everywhere. Later, as a result of an analogous overproduction of corn in the US, we have high fructose corn syrup as the main sweetener in nearly all cakes and baked goods.

2. Soya is in so many products I will not enumerate them.Soya milk is ever popular and, finally, the marketeers have struck gold with the high protein fad leveraging soya’s high protein content. Overproduction and reliance on soya beans in the US has.. oh we’ve done this before!

3. Finally, Conjugated Linoleic Acids used by farmers to make wagyu beef are plentiful in wheat and dairy ( think Latte and Pizza) leading to a plethora of coffee shops and pizza outlets. Overproduction of wheat and milk in the US ...

So there you have it. The wagyu generation. Fed on food no one needed or wanted, marketed brilliantly to unsuspecting dupes.

At least the farmers made a profit but at your cost/

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”.