Flabby guts and arteries 2024

 

Flabby guts and arteries 2024

Why we need to look after Smooth Muscle

What is smooth muscle?

We have three distinct types of muscle: skeletal, cardiac and smooth. All three are connected to the nervous system: skeletal muscle is under conscious control, cardiac and smooth muscle are not. The latter two are largely automatic but can and do respond to sensors (receptors) connected to the nervous system. We are conscious of  skeletal and cardiac muscle activity but largely and sometimes entirely, unaware of smooth muscle and its activities.

Where is smooth muscle found?

Smooth muscle is found in the circulatory system particularly arteries; throughout the digestive system; in the urino-genital system; the reproductive organs;  the eyes and lungs. In other words, it’s the most widespread and unappreciated of all our musculature.

Briefly here are some of the functions for different tissues performed automatically by smooth muscle:

Arteries: SM enables the artery to change its internal diameter. When relaxed the artery is wider and vice versa. This has a direct effect on blood pressure and the distribution of blood to organs such as skin, heart, liver as well as  skeletal muscle.

Gut ( alimentary canal): The gut has smooth muscle along its entire length. SM waves of contraction (peristalsis) move food and liquids in a ‘mexican wave’ fashion through the gut from swallow to defecation. It is so effective we can even drink fluids standing on our head! SM provides the no-return valves (sphincters) on entry and exit to the stomach as well as the anus and finally powerful SM allows the stomach to wring and churn food into a liquid digestible state called chyme. 

Eyes: Our eyes have smooth muscle to alter the shape of the lens allowing us to focusnear and far using circular (ciliary) muscles which when relaxed pull the lens into a flatter shape for long distance and when contracted allow the lens to round up enabling closer focus. Muscles in the iris open and reduce the pupil letting more or less light into the eye.

Bladder: the bladder is a sheet of smooth muscle which enables us to empty the bladder when the stretch receptors tell us it is full.

The above is by no means a complete list but it serves to give a sense of the range of vital but unconscious activities on which we depend.

Conditioning Smooth Muscle, can they get flabby ..is it a real thing?

‘Health-aware’ folk take care of their skeletal and cardiac muscle through exercise and diet but they do not, at least do not deliberately, take care of smooth muscle. Does this matter? If smooth muscle can look after itself in pretty much any scenario then the answer is ‘no’; if smooth muscle, like other muscle is vulnerable to the ‘life-style’ of an individual then it does matter. 

Contemporary First World life can be usefully characterised by its environment, activity and diet. For a great many this means living in a largely temperature and light controlled environment; being for the most part sedentary; being medicated for blood pressure and cholesterol levels and finally eating mostly UPF (ultra-processed food). What this means really is that variation (in diet, activity, light, temperature) has been replaced by constant. Unfortunately for us, smooth muscle is conditioned ( or exercised) by variation; variation that was once so normal as to be sufficient to put smooth muscle onto ‘automatic’ and allow us to ignore it. No more I fear is this the case.

Variation versus Constant

This is the point of the post. Smooth muscle has an easy time of it nowadays. 

Consider the gut first: modern food is mostly cooked, processed,  soft, pulped,  predigested, emulsified. The gut has very little work to do compared to working with food of the recent past. IBS, Crohns and reflux are common complaints.

The variation on arterial pressure and diameter is minimised if a life style is sedentary, temperature controlled and  medicated with blood pressure controlling drugs. Atherosclerosis or as it was called, hardening of the arteries, is a classic 21st century pathology.

Eyes too do not get a work out when living in permanent near constant daylight and with focal distances ranging from a computer screen to the office wall. 

Even the bladder does not escape with access to ‘comfort breaks’ being the norm.

My hypothesis is simple. Smooth muscle needs exercise to remain strong and healthy just like any other muscle. Today, for many, it does not get the variation it needs to stay fit. Gut and arterial diseases will have a component that is a direct consequence of flabby smooth muscle.

Addendum:

Smooth muscle cells, like skeletal muscle cells can enter a 'quiescent' phase through disuse and eventually a senescent phase. This is very significant for those cells which line the arterial and venous system. Cell death (apoptosis) of smooth muscle cells in the vascular system can lead to plaque destabilisation in individuals with atherosclerosis. Quiescent cells can however be reactivated by being used again! This has implications also for NIR therapy which is known to cause vascular smooth cell apoptosis.

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.

Longevity, the Holy Grail ... solved!

 

Living forever

Immortality is 'trending'; overly rich Silicon Valley types inevitably want to stay young forever and, as it were ever thus, are creating their own elixirs to do just that. Countless column inches in the popular press document their systems and photos their 'buffed' 50 yr old bodies.

Doomed to fail? yes of course they will fail, the selfie-mirror always lies until the day it doesn't! The elixirs are always a new take on 'drinking the blood of a young virgin' The pudding's proof won't be visible until they reach over 80, so a way to go.

However, impressive longevity has already been achieved in animals whose ancestors originate in both great animal phyla, namely the dinosoaurs and the mammals. Specifically the improbably long lived  are found among the birds and bats. 

And we know pretty much why they live so long.

Mitochondria and Entropy

At a thermodynamic level the viability of a cell depends on it having low, and in a complex system such as a cell, a highly improbably low value for its entropy. Such a state is achieved only with a substantial input of energy and in energetic terms, entropy at a given temperature, is represented in a form of energy called Gibb's Free Energy ΔG. That energy is supplied for the  most part (by a very long way in fact) ... by mitochondria. Mitochondria are the Free Energy generating machines that make the improbability of complex multicellular life possible. 

Having established above the absolute importance of mitochondria in maintaining the energy requirements for life of a cell and thus in overall terms the whole organism, it is important to take in the fact that mitochondria are also responsible for cell death, or apoptosis as it is called. The suicide death of a cell is initiated by mitochondria in response to its decrepitude, redundancy, infection, or cancerous change. No wonder then that one of the first tasks of a virus or cancer is to shut down mitochondrial reproduction and operation before the cell itself is shut down.

Living with a furnace

Having the dictator's power of life or death is one awesome thing, but what are the downsides of such absolute power? That's easy to answer. Mitochondria produce Reactive Oxygen Species (ROS) as an intrinsic part of their operation. ROS are very destructive free-radicals. It's a measure or their seriously destructive nature that the fastest and most abundant enzymes in a cell are dedicated to ROS neutralisation ( viz catalase and super oxide dismutase) and tellingly, most of the mitochondrial vulnerable genome has been 'outsourced' to the relatively safe environment of the cell's nucleus! No wonder then that ROS damage is cited as a major factor in the deleterious changes in cells that we associate with aging and is by the way, directly responsible for the rise in dietary antioxidant supplements in the hope of mitigating ROS damage. Also by the way these supplements don't work they just mess up the repair signalling pathways.

Mitochondria not only wield the power of life and death of a cell but are aslo at the root of its demise. So the question is begged as to just what can be done to ameliorate the downside and enhance the upside of these amazing structures that once were free living bacteria-like organisms which somehow joined forces with the proto-cells and made complex multicellular life in an oxygen rich environment possible. 

Ideal Mitochondria

Mitochondria in young cells compared to their counterparts in old, senescent cells are in general, smaller, more plentiful and more tightly coupled. Being 'coupled' refers to the ratio between 'food' and oxygen input and chemical energy output. It's a measure of max power output for a given input. An analogy with a car's engine would be along the lines of say both cars delivering a 100 mph output but Car A doing so at 2000rpm and 50mpg wheras Car B does so at 6000 rpm and 25mpg. A fully uncoupled Car C would be stationary, reving away, burning fuel and getting very hot.

Earlier in this article I referred to mitochondria in birds and bats. In these surprisingly long lived animals ( record  examples :birds 60-80 years, bats 30-40 yrs) indeed their mitochondria are small, plentiful and tightly coupled. So no surprises there.

In our own somatic human cells as the cell ages there are fewer of the 'young' mitochondria and more damaged larger mitochondria. It's time to pause here. Clearly when we are old we may not feel so energetic but we are still alive, so enough energy must be being produced to maintain the vital functions of a cell and hence the organs in which they operate. We do not need to use intense amounts of energy to live but birds and bats do ... simply to fly needs huge energetic output.  The point I am making is we can survive carrying 'rubbish' mitochondria but they cannot.

Flat out to stand still

Mitochondria use an electrochemical system to produce the chemical energy the cell needs. It does so by harnessing energy stored in an electrical potential difference ( ie a voltage) across its membranes. This voltage has a threshold below which no energy is prodcued but above that threshold it can make chemical energy in the form of ATP molecules. Aging mitochondria, to keep going, can reduce their total membrane surface area and enlarge to make it easier to reach the voltage threshold but it's at the expense of capacity. Ie the 'battery' has enough power to light the LED but keep it on too long for energy and it fails quickly.

When mitochondria are fully powered up with a high voltage they work well prodcuing energy but generate a lot of ROS. An aging cell has to run its viable mitochondria flat out to meet the cell's minimum demands. In bats however ( and probably birds) the mitochondria are not running flat out, instead they are partially uncoupled, that is they are being a little inefficient. However the pay-back is huge. Vastly fewer ROS species are produced and cell damage is reduced dramatically both to the cell and the mitochondria. Going back to the car analogy it's like my low reving big engined Volvo versus a small commuter car both doing 70mph on the motorway. One engine is at 1800 rpm the other at 4500 rpm. Which one do you expect to reach 200,000 miles intact? 

What to do

Finally then going back to the start of this post. What should our potential 'immortals' be doing? Answer: to become more bat-like.

Here's my list:

To encourage lots of small, well coupled mitochondria:

    periodic intense demand for energy

    Near-infra red radiation ( see previous posts)

To give mitochondria 'spare' capacity:

    stimulate mitochondrial energy cycle with intermediates like malate

    facilitate transport into mitochondria with B vitamins and CoQ10

    facilitate acetyl unit uptake with acyl carnitine

These steps won't make them immortal but just maybe will keep them young and live longer active lives. The selfies and death certificates will judge the outcome.

    

,

NIR: Why do bats fly at dawn?

Why do bats fly at dawn? 

Bats, ounce for ounce are the longest lived of all mammals. A two year old mouse is already a geriatric whereas it takes ten years for a tiny Pipistrel to start to conk out with age and outrageously, it takes 40 years for a 7 gramme Brand's bat to do the same. Even the incredibly tiny Kitti's Hog Nosed bat at 2g (!) lives for 5 years. 

We have a good idea why bats live so long; it's the same reason as do pidgeons and parrots ... they have very good mitochondria. In both (very diverse) genera the mitochondria are smaller, more prolific, energy efficient and produce fewer damaging free radicals than do their counterparts in mice and indeed humans.

In recent time mitochondrial well-being has become the focus of a multitude of anti-aging strategies and increasingly photo-therapy using near infra-red radiation (NIR) has gained in popularity.

This is because NIR can penetrate through the skin ( and clothes or fur) and stimulate mitochondrial proliferation. The mechanism is proposed to involve cytochrome c oxidise acting as the NIR photo-receptor  absorbing it at around 800-850nm and from there a path of retrograde signalling informs the cell about what to do for the best.

In effect, new mitochondria potentially 'rejuvenate' an old cell which will have a significant population of damaged mitochondria. As a result of this knowledge and availability of cheap LEDs there is a good, even an over-supply, of NIR lamps for sale for personal as well as professional use.

If NIR, is truly beneficial to mitochondria ( as seems it is)  then the source of NIR and the mechanism of action must be rather more ancient than NIR LED lamps! Fortunately 54% of incident light on the earth is NIR ( 34% is our 'visible' light th erest UV). This gives animals every chance to soak NIR up. 

The whole 'NIR is good for you' edifice however looked like falling becasue our long-lived super mitochondrial bats are, as everyone knows,  are nocturnal. Worse, they like dark caves and  famously, belfries, during the day.

A quick bit of on-line research turned up two facts One I should have known, the other was new to me. The latter is that the most ( by far) NIR during the day occurs at dawn follwed by the light at dusk.  Bats swarm or just fly about feeding a lot at dawn and dusk. Some like the tiny Kitti's bat only fly at dawn and dusk.

NIR causes apoptosis of vascular smooth muscle cells. This appears to be a good and a bad thing. Remodelling of blood vessels littered with quiescent ( unused ) smooth muscle cells benefit from a clear-out and remodelling. However for diseased vessels and atherosclerotic vessels there can be adverse effects including plaque rupture. 

Fructose makes you very Fat

 Fuctose makes you very Fat

High fructose corn syrups are the principle cause of the First World's obesity epidemic. Many scientists, medics and nutritionalists given a basic understanding of biochemistry have known this for years. 

It's one thing though  to know something and quite another to go up against the food industry whose 'counter-clout' or more explicitly, their ability to destroy you, rivals that of big pharma or, as in the past, the tobacco industry*.

After all isn't obesity caused by taking in too many calories, especially calories 'hidden' in liquid or pre-masticated, semi-digested food products in which lurk fats and sugars? It's simple, isn't it?  And so accordingly foodstuffs are now labelled clearly with nutritional information listing fats, sugars and of course calories to help us controll our intake.

Usually fat in obesity debates gets the lion share of the blame on account of the energy density per gram that fats have. Then comes generic sugars as the new popular villain while more specific types of sugar; like fructose, lactose and oligi sacharrides usually escape scrutiny.

Finally there is a dawning awareness that all calories from whatever source are not equivalent. That is, maybe calories from sugars are not 'one to one 'equivalent to calories from proteins and fats. How can this be? 

Whatever, the situation is multifactorial, complex and a full understanding requires biochemical knowledge of intermediary metabolism outside the scope of nutritionalists and medics in general. 

So, given the above, how can we say fructose, a single sugar, abundant in fruits is alone as the chief driver of obesity?

The answer is simple. 

Anyone with a basic knowledge of intracellular glycolysis and oxidative phosphorylation will tell you that fructose is handled differently to other simple sugars like glucose and galactose. 

Glucose dominates the simple sugars being derived from starches, maltodextrins and other oligosacharrides as well as from 'sugar' sucrose and 'milk-sugar' lactose {sucrose = glucose+fructose, lactose = glucose+galactose}. Unsuprisingly glucose is carefully regulated both outside and inside the cell whether by the insulin system or enzymatic control. Fructose is not.

A paper published in the journal Obesity, elegantly and triumphantly spotted something simple and profound.  They studied animals preparing for hibernation. Naturally animals that do hibernate need to maximise fat reserves for the winter sleep. In order to do this the calories you take in must exceed that calories you expend but what is the best way to prioritise fat storage in the autumnal feeding phase?

The animal is active during this phase, very active foraging, so it does not want to use a gramme of its fat reserves as energy. Fortunately at this time sugars but especially fructose in fruit is abundant. They found that fructose did two jobs, these were, a) putting on fat and b) conserving exsiting fat deposits.

The biochemical explanations were not in the scope of the paper but they are very clear from a metabolic control point of view. Fructose 'screams' unregulated through the pathway known as glycolysis. Glycolysis is used to break down glucose to provide the simple molecular 'food' for mitochondria which they then fully oxidise to generate energy and biosynthetic power.

The problem is that mitcondria cannot handle unlimited amounts of their molecular food known as 'acetyl' a simple two carbon atom molecule combined with hydrogen and oxygen. They can only process a limited amount and even this depends on the level of demand created by activity of the cell and the animal that it belongs to. In order to stop a catastrophic build up of acetyl it is turned into fat which can be safely ( from a biochemical perspective) stored in adipose tissue. 

Clearly in a fructose rich environment one can easily visualise evey last gram of ingested fructose going straight to fat.

So, what of humans rather than hiberanting mammals? Well, due to our lifetsyles being so inactive many of the mitochondria especially in muscle will already be down-regulated, some will be nearly dormant. Now, add a fructose rich diet, eg high-fructose syrups in biscuits, cakes, candy and fruit-rich products like juices and yoghurts and the mitochondria will be 'maxed out' quite quickly. 

Now, and here's the key, and the one made clear by the authors in Obesity: add a modest amount of any other foodstuff to the diet: lean meat, fish, bread, whatever and the calories are not going anywhere .. except as fat storage.

This means that with high fructose diets, the total calorie count means less than the composition of the diet. You can reduce your calorie intake substantially and yet get very much fatter ... how cruel but how obvious when you look around you.

1) The fructose survival hypothesis as a mechanism for unifying the various obesity hypotheses

Richard J. Johnson, Laura G. Sánchez-Lozada, Miguel A. Lanaspa

First published: 17 October 2023 https://doi.org/10.1002/oby.23920

*the vape nicotine comeback is pretty impressive so don't count themm out.

The most unhealthy meal ever?

 

It’s holiday time and so to explore the most unhealthy meal ever?

Forget UPFs this is serious.

(in case anyone reads this I am being ironic..the food IS healthy)

 

Imagine you are in a nice holiday restaurant,

say on one of the countries bordering the Mediterranean sea.

On the table are some fresh olives and wild mushrooms in an extra-virgin olive oil

vinegar, garlic and thyme vinaigrette and some fresh cod-roe taramasalata too.

You choose the clams in white wine and parsley as a starter  and the grilled sardine for your main meal

All served with fresh flatbreads and ad-libitum green salad .. and of course, naturally, some wine to wash it down.

OMG! ( does anyone say that nowadays?) are you mad? You are signing your own death warrant, think about your cholesterol levels, after all that's why you are on statins.

Yes, I choose this particular meal for a reason:

Firstly it is an exemplar of the ‘healthy’ med-diet and it is a meal that I could plausibly present as an exemplar. It has oily fish, extra virgin olive oil, is high in protein and low in carbs. No animal fats and no processed foods. Plus green veg and wine!

Secondly I choose it as a meal as high in cholesterol and cholesterogenic foodstuffs that I could imagine without becoming taste-wise implausible.

Basically, oily fish, fish eggs and seafood such as prawns, mussels, clams, calamari are  the top three foods for the levels of cholesterol. Also, (sorry vegans) extra virgin olive oil and mushrooms contain squalene and ergosterol respectively which are quickly converted to cholesterol by the body  ( = cholesterogenic) .

So, healthy or deadly?

Luckily you are on holiday somewhere sunny so some of this circulating cholesterol in your bloodstream is being converted to vitamin D by the action of sunlight on your reddening skin and equally luckily you take statins to lower blood cholesterol.

Pity those poor locals who don’t know what risks they are taking.Enjoy

ps Don't get me started on that lamb's liver and wild mushroom casserole on the Autumn menu.