Homo Algorithmicus II...life after Sapiens

Homo sapiens, the planet's last  surviving species of the once diverse* genus Homo, currently numbers about 80 billion souls. Sapiens has multiplied to cover the globe in a way that its recent** cousins, the Neanderthals and the Denisovans failed to do. The latter two, to all intents and purposes were modern humans possesing culture and tools. They interbred with sapiens and their echos are seen in the DNA of the present human populations. Broadly, Neanderthal in the west, Denisovan in the east and neither in Africa.

The reasons that individual Homo species died out are of course speculative and range from ( in no particular order): killed by Sapiens; out-competed by Sapiens; out-adapted by smarter more flexible Sapiens; assimilated genetically by Sapiens and inevitably climate-change. But basically no-one knows.

What is sure, and this applied to Sapiens also, that numbers matter. Smaller isolated populations are in any species not just Homo, vulnerable to poplation collapse. In-breeding leads to a smaller less diverse gene pool with the risk of accumlating genetic faults and in addition anihilation by novel dieases. It may be that by chance alone that Sapiens escaped that fate and lived to spread its genes globally, hitting basically a virtuous cirlce of diversity which even the black death could not beat into extinction***

But no more, Homo sapiens in  the 21st Century  is very reluctant to pro-create  causing alarm from London to Bejiing. Global population has already levelled off and is about to crash. Developed countries are maintaining economic viability only through mass immigration (which itself  is causing unrest) and technological development of automation and AI.

The decline in birth rates especially in developed countries is spectacular. For example, today in Afghanistan birth rates are similar to those of Ireland and Italy a mere 35 years ago. that is a figure between 4 and 5. Ireland and Italy today are at 1 or below. 2.2 is the replacement figure for reference. Immigrants from countries with birth rates similar to Afghanistan into developed countries reduce their birth rate to the cultural norm within a generation.

The question now arises as to whether reproduction in sapiens like in other mammals is  responding  to extrinsic or intrinsic factors. This is an important question. We, that is Us, are very good at proposing extrinsic factors that affect our behaviour and very poor at proposing intrinsic factors. 

Extrinsic factors to reduce reprodcution are: 

1) Capitalist/consumerist economic models of society where increasing family size is inversely correlated with wealth and therefore limiting full participation in the 'good life'.

2) Access to the means to control births, that is to say female access to chemical contraception and/or abortion.

Intrinsic factors are less tangible. Mammals, specifically female mammals of course, can regulate their reprodcution intrinsically; they can re-absorb their embryos. There is no hint by the way that male mammals have any role to play in the regulation of reproduction. Re-absorbtion is common in rat populations kept in laboratory conditions. In fact in my own work as a  PhD student I went an entire year with a colony of rats 'refusing' to reproduce!

Why female mammals intrinsically regulate their reproductive roles is again a matter of speculation. Such speculation inlcudes obvious perceived ( by the animal)  extrinsic factors such as food availability, food quality and the current climate as all being restrictors on a successful outcome regarding their infants' chances of reaching maturity. 

It's all about signalling.  That is to say extrinsic signals are preceived as funadamentally meaninful and which bring about profound changes in reproductive behaviour. P D James' book The Children of Men in 1992 described a future where for unknown reasons human reproduction had stopped. It reminded me of my lab rats. In fact 'lab-rat' is also a good descriptor of humans in advanced societies; temperature and light controlled, well-fed, good access to sexual mates and under-exercised. So I do wonder if in such an environment a signal is being recieved, the nature of which is unknown which says 'stop' to reprodcution. 

What could this signal be? Is it a misreading of an ancient extrinsic signal? Is it existential, a form of self-conscious despair?  Did a similar fate befall the Neanderthals/Denisovans  20,000-50,000 years ago?

Loads to speculate about but there surely will not be Sapiens around to speculate in 20,000 years time at the rate of depopulation emerging. What may remain is the logical descendant of the long journey of Homo, yes Homo Algorithmicus our AI progeny.

As a footnote, a falling population will have a powerful effect on the relationship between labour and capital, or indeed between serfs and their feudal lords. The aftermath of the Great Plague which destroyed so much of the population of europe, saw wages and life conditions improve radically for the survivors. Even with AI  robot labour on the rise human labour will increase in value under any economic system. One day it may be priceless!

* 12 and counting

** 20-50, 000 years ago

*** 50 million deaths in Europe alone with 50-80% mortality, 

Saturated fat is still not 'bad' in 2024

 

This post has been prompted by an article about diet in a respectable journal and repeated in respectable papers. In a nutshell, the claim is 'dietary saturated fat' is bad for you because it is associated with increased risk of cardio vascular disease (CVD) especially atherosclerosis ( aka 'hardening of the arteries through accumulation of fatty plaques).

Ok, no alarm bells raised with me so far; demonising saturated fat is an old trope harking back to the days when the food industry (which sold plant oils), was making saturated fats by saturating unsaturated fats (plant oils)  with hydrogen. Or, in plainer english, they were turning oils (unsuitable for baking) into hard fats (suitable for baking); unfortunately they were also producing novel, almost-saturated fats called trans-fats. Trans-fats it turned out were indeed harmful to the heart and were eventually banned.

So why are foods high in saturated fats, chiefly hard fat from pork (lard) beef (dripping) and butter back in the 'bad for you' news? 

The answer is probably commercial.

The food industry sells plant oils including the ubiquitous palm oil as well as rapeseed oil, sunflower oil, corn oil and coconut oil. Palm oil is the only one of these that can be used 'hard-enough' for baking but there is currently push-back from consumers unhappy with the ecological devastation caused by palm oil plantations. Consequently 'margarines' which have many oil-like ingredients, have been re-invented as an ingredient term. This slight of hand partially covers up/obscures the use of palm oil as a major ingredient in margarine.

Worse though for industry is the increasing use by consumers of animal fats, especially from the dairy industry, as people shy away from UPF ( ultra-processed foods). So call me cynical, but the industrial drive is on to demonise animal fats once again. Called to the rescue, on time and updated, is our old friend cholesterol. Cholesterol the ultimate food demon which was so successful in the past at destroying the animal fat business.

Imagine my surprise ( this is ironic in tone)  to find then a 'top-nutrionalist' stating that a diet high in saturated fat raises the levels of our newest villain  'bad-cholesterol' ( LDL or low-density lipoprotein) in the blood. Better still, a mechanism is presented that states that saturated fat lowers the number of LDL receptors in the liver, receptors whose function is to remove LDL from the blood ...  and as we all know LDL is associated with increased risk of CVD. Job done as they say.

This actually did get my full attention, for as a bicochemist I would struggle to ascribe such a signalling or biologically active role to a set of molecules as chemically inert as saturated fats.

 A little bit of research showed much more expectedly that 'the LDL receptor is a highly conserved cell membrane glycoprotein' which is regulated by a  'kexin type 9 (PCSK9)  protein that promotes degradation of cell surface LDL receptors'.  So, PCSK9, a complex hormone-like metabolicly-potent signal controls LDL receptor levels ... not saturated fat!

I did find that very ill people with high levels of disilpdidemia (plasma fats in  pathological levels and ratios) got worse with high levels of dietary saturated fat and had higher levels of PCSK and hence fewer LDL receptors. This is hardly, as in improbably remote, a paper saying dietary saturated fat lowers LDL receptors in the liver in a wider context.

There are a few technical terms in the paragraph above, and this may seem patronising, but it's all but unintelligable to a nutritionalist or a medical profressional, let alone the general educated and interested public;a public that is being re-fed a simplified version of the non-logic:  'fat makes you fat, and being fat is bad and so fat is bad'. 

What the techical paragraph actually says is 'nuts to the assertion that saturated fat increases LDL by decreasing the LDL receptors.

More delving into the latest LDL literature was actually surprising ( I should keep up to date more). It looks like the science world is getting closer to unravelling the underlying mechanisms of a predisposure to CVD ...still the biggest killer in the developed world. Modern drugs can affect LDL (bad cholesterol) and HDL (good cholesterol) levels and ratios differentially: specifically, some drugs selectively lower LDL. 

However data from such drug induced manipultion of lipoprotein levels and ratios has shown pretty unequivocably that high HDL is not 'good' per se neither is low LDL 'good' pe se  with regard to CVD either. 

Ah, now that is surprising, sorry Doc, here is my prescription back.

Lipoproteins in the blood are a complex heterogeneous bunch of entities but one is coming to the fore: Apolipoprotein-C3. The gene involved in the expression of this regulatory protein is coming into focus as a causal agent in disposition to CVD as APOC3 is powerfully assocaited with atherosclerosis. 

So to summarsise to date: CVD is something to do with the regulation of bio-active plasma lipoproteins but  it's now unlikely to be the two cholesterol-conjugated ( ie a cholestrol molecule is part of the structure) lipoproteins LDL and HDL.  Dietary cholesterol and dietary saturated fat unequivocably  are not  part of the story. 

This post was difficult to write because it is so steeped in technical molecular concepts. In an academic paper it would be easy but almost entirely inaccessible, whereas to simplfy the story risks falling into serious error. 

The risk of error is compounded when one suspects sophisticated bad actors with deep pockets and research funds are happy to confuse the living daylights out of any one casually encountering their self-serving nonsense.

Saturated fat is not bad for you.