an autodidact meets a dilettante…

‘Rise above yourself and grasp the world’ Archimedes – attribution

Archive for the ‘biology’ Category

How statins work 1 – stuff about cholesterol, saturated fats and lipoproteins…

leave a comment »

filched from Wikipedia – don’y worry, I don’t understand it either – at least not yet

Statins are HMG-CoA reductase inhibitors, according to Wikipedia’s first sentence on the topic. HMG-CoA reductase is an enzyme – a macromolecule that accelerates or catalyses chemical reactions in cells. The enzyme works in the mevalonate pathway, which produces cholesterol and other terpenoids (terpenoids are very common, varied and useful forms of hydrocarbon).

So what does HMG-CoA stand for, and what’s a reductase?

3 hydroxy -3 methyl-glutaryl coenzyme A, which may be explained later. A reductase is an enzyme which catalyses a reduction reaction, and I’m not sure if that refers to redox reactions, in which case reduction involves the gaining of electrons…

But let’s look at cholesterol, which statins are used against. Sterols are lipid molecules with a polar OH component, and ‘chole’, meaning bile, comes from the liver. So cholesterol is a type of lipid molecule produced largely by the liver or hepatic cells of vertebrate animals. Cholesterol is essential for life, and it’s synthesised in the cell via a complex 37-step process (the mevalonate pathway makes up the first 18 of these). It makes up about 30% of our cell membranes, and its continual production is necessary to maintain cell membrane structure and fluidity. In high food-intake countries such as Australia and the US, we ingest about 300mg of cholesterol a day on average. We also have an intake of phytosterols, produced by plants, which might vary from 200-300mgs. Of course, this is massively dependent on individual diets (increased phytosterol intake may reduce LDL cholesterol, but it comes with its own quite serious problems).

The (very basic) structure of cholesterol is shown below.

The body of the molecule (centre) contains 4 rings of carbon and hydrogen – A, B and C are 6-carbon rings, while D has 5. The bonds between rings A and B, and C and D, represent methyl groups. On the left is a hydroxyl group, which is hydrophilic and polar, though the massive body of the molecule is extremely hydrophobic, which is reinforced by the cholesterol tail connected to the D ring. The hydroxyl polarity creates a binding site, which builds structure as the molecule binds to others.

Interestingly, the need for cholesterol synthesis varies with temperature, or climate. This has to do with fluidity and melting points. People who live in colder climates require less cholesterol production because, in cold weather, solid structure remains intact. Hotter climates cause greater fluidity and increased entropy, so more cholesterol needs to be synthesised to create and maintain structure.

So now to the 18-step mevalonate pathway, by which the liver produces lanosterol, the precursor to cholesterol. Well, on second thoughts, maybe not… It’s fiendishly complex and Nobel Prizes have been deservedly won for working it all out and I’m currently thinking that physics is easy-peasy compared to biochemistry (or maybe not). What I’m coming up against is the interconnectivity of everything and the need to be thorough. For example, in order to understand statins we need to understand cholesterol, and in order to understand cholesterol we need to understand lipids, lipoproteins, the liver, the bloodstream, the digestive system… So I sometimes feel overwhelmed but also annoyed at the misinformation everywhere, with chiropractors or ‘MDs’ announcing the ‘truth’ about statins, cholesterol or whatever in 500-word screeds or 5-minute videos.

Anyway, back to work. Cholesterol is a lipid molecule, and lipids are generally hydrophobic (they don’t mix with water, or to be more exact they’re not very soluble in water), but cholesterol has a hydrophilic hydroxyl side to it. Lipids that have this hydrophilic/hydrophobic mix are called amphipathic. Phospholipids in cell membranes are an example. and they interact with cholesterol in the ‘phospholipid bilayer’. As an indication of the complexity involved, here’s a quote from an abstract of a biochemical paper on this very topic:

Mammalian cell membranes are composed of a complex array of glycerophospholipids and sphingolipids that vary in head-group and acyl-chain composition. In a given cell type, membrane phospholipids may amount to more than a thousand molecular species. The complexity of phospholipid and sphingolipid structures is most likely a consequence of their diverse roles in membrane dynamics, protein regulation, signal transduction and secretion. This review is mainly focused on two of the major classes of membrane phospholipids in eukaryotic organisms, sphingomyelins and phosphatidylcholines. These phospholipid classes constitute more than 50% of membrane phospholipids. Cholesterol is most likely to associate with these lipids in the membranes of the cells.

Anyway, perhaps for now at least I won’t explore the essential role of cholesterol in cell structure and function, but the role of ingested cholesterol, the difference between LDL and HDL cholesterol, and how it relates to saturated fats and heart disease, particularly atherosclerosis. As Gregory Roberts explains it in a Cosmos article, saturated fats (found in butter, meat and palm oil) definitely raise total cholesterol…

But what is saturated fat, as opposed to polyunsaturated or mono-unsaturated fat? Most of us have heard of these terms but do we really know what they mean? Here comes Wikipedia to the rescue (because there’s a lot of bullshit out there):.

saturated fat is a type of fat in which the fatty acid chains have all or predominantly single bonds. A fat is made of two kinds of smaller molecules: glycerol and fatty acids. Fats are made of long chains of carbon (C) atoms. Some carbon atoms are linked by single bonds (-C-C-) and others are linked by double bonds (-C=C-). Double bonds can react with hydrogen to form single bonds. They are called saturated, because the second bond is broken and each half of the bond is attached to (saturated with) a hydrogen atom. Most animal fats are saturated. The fats of plants and fish are generally unsaturated. Saturated fats tend to have higher melting points than their corresponding unsaturated fats, leading to the popular understanding that saturated fats tend to be solids at room temperatures, while unsaturated fats tend to be liquid at room temperature with varying degrees of viscosity (meaning both saturated and unsaturated fats are found to be liquid at body temperature).
Various fats contain different proportions of saturated and unsaturated fat. Examples of foods containing a high proportion of saturated fat include animal fat products such as cream, cheese, butter, other whole milk dairy products and fatty meats which also contain dietary cholesterol. Certain vegetable products have high saturated fat content, such as coconut oil and palm kernel oil. Many prepared foods are high in saturated fat content, such as pizza, dairy desserts, and sausage.
Guidelines released by many medical organizations, including the World Health Organization, have advocated for reduction in the intake of saturated fat to promote health and reduce the risk from cardiovascular diseases. Many review articles also recommend a diet low in saturated fat and argue it will lower risks of cardiovascular diseases, diabetes, or death. A small number of contemporary reviews have challenged these conclusions, though predominant medical opinion is that saturated fat and cardiovascular disease are closely related.

Saturated Fat, Wikipedia. I’ve removed links and notes – they’re just too much of a good thing! Apologies for the lengthy quote but I think this is essential reading in this context.

High density lipoprotein (HDL) cholesterol can be a problem if your levels are low. HDL absorbs cholesterol and carries it back to the liver, from where it’s removed from the body. So generally high levels of HDL will reduce your chances of heart attack and stroke.

As Roberts notes, from the 1950s, heart disease has risen to be a major problem. Heart attack victims have been regularly found to have arteries clogged with ‘waxy plaques filled with cholesterol’. Further proof that cholesterol was to blame came with studies of people with a genetic disease – familial hypercholesterolemia (FH) – which meant that they had some five times the normal levels of blood cholesterol, and suffered heart attacks even as children or teenagers. Also, the rise in blood cholesterol levels and the rise in heart attacks, and heart disease generally, were correlated. This was unlikely to be coincidental.

But what’s a lipoprotein and why the different densities? Here we get into another area of extraordinary complexity. Lipoproteins are vehicles for transporting hydrophobic lipid molecules such as cholesterol, triglycerides and phospholipids through the watery bloodstream or the watery extracellular fluid (blood plasma – the yellowish liquid through which haemoglobin and lipoproteins etc are transported – is a proportion of that fluid). They act as emulsifiers, ‘encapsulating’ the lipids so that they can mix with and move through the fluid. Lipoproteins don’t just come in HD and LD forms – we classify them in terms of their density much as we classify colours in the light (electromagnetic) spectrum. According to that density classification we recognise five major types of lipoprotein in the bloodstream.

Cholesterol arrives in the blood via endogenous (internal) and exogenous (external) pathways. Some 70% of our cholesterol is produced by the liver, so, though diet is an important facet of changing cholesterol levels, finding ways of modifying or blocking liver production was clearly another option. Through studying the way fungi produced chemicals such as penicillin that break down cell walls (a large part of which are cholesterol), Akira Endo was the first to produce a statin from a mould in oranges – mevastatin. That was the beginning of the statin story.

References

https://en.wikipedia.org/wiki/Mevalonate_pathway

https://cosmosmagazine.com/society/will-statin-day-really-keep-doctor-away

Cholesterol metabolism, part one – video by Ben1994 (excellent)

Cholesterol structure, part 1/2, by Catalyst University

https://en.wikipedia.org/wiki/Cholesterol

https://en.wikipedia.org/wiki/Statin

https://en.wikipedia.org/wiki/Lipoprotein

https://en.wikipedia.org/wiki/Saturated_fat

Written by stewart henderson

September 15, 2019 at 10:24 am

kin selection – some fascinating stuff

leave a comment »

meerkats get together for ye olde family snap

Canto: So we’ve done four blogs on Palestine and we’ve barely scratched the surface, but we’re having trouble going forward with that project because, frankly, it’s so depressing and anger-inducing that it’s affecting our well-being.

Jacinta: Yes, an undoubtedly selfish excuse, but we do plan to go on with that project – we’re definitely not abandoning it, and meanwhile we should recommend such books as Tears for Tarshiha by the Palestinian peace activist Olfat Mahmoud, and Goliath by the Jewish American journalist Max Blumenthal, which highlight the sufferings of Palestinian people in diaspora, and the major stresses of trying to exist under zionist monoculturalism. But for now, something completely different, we’re going to delve into the fascinating facts around kin selection, with thanks to Robert Sapolski’s landmark book Behave. 

Canto: The term ‘kin selection’ was first used by John Maynard Smith in the early sixties but it was first mooted by Darwin (who got it right about honey bees), and its mathematics were worked out back in the 1930s. 

Jacinta: What’s immediately interesting to me is that we humans tend to think we alone know who our kin are, especially our extended or most distant kin, because only we know about aunties, uncles and second and third cousins. We have language and writing and record-keeping, so we can keep track of those things as no other creatures can. But it’s our genes that are the key to kin selection, not our brains.

Canto: Yes, and let’s start with distinguishing between kin selection and group selection, which Sapolsky deals with well. Group selection, popularised in the sixties by the evolutionary biologist V C Wynne-Edwards and by the US TV program Wild Kingdom, which I remember well, was the view that individuals behaved, sometimes or often, for the good of the species rather than for themselves as individuals of that species. However, every case that seemed to illustrate group selection behaviour could easily be interpreted otherwise. Take the case of ‘eusocial’ insects such as ants and bees, where most individuals don’t reproduce. This was seen as a prime case of group selection, where individuals sacrifice themselves for the sake of the highly reproductive queen. However, as evolutionary biologists George Williams and W D Hamilton later showed, eusocial insects have a unique genetic system in which they are all more or less equally ‘kin’, so it’s really another form of kin selection. This eusociality exists in some mammals too, such as mole rats. 

Jacinta: The famous primatologist Sarah Hrdy dealt something of a death-blow to group selection in the seventies by observing that male langur monkeys in India commit infanticide with some regularity, and, more importantly, she worked out why. Langurs live in groups with one resident male to a bunch of females, with whom he makes babies. Meanwhile the other males tend to hang around in groups brooding instead of breeding, and infighting. Eventually, one of this male gang feels powerful enough to challenge the resident male. If he wins, he takes over the female group, and their babies. He knows they’re not his, and his time is short before he gets booted out by the next tough guy. Further, the females aren’t ovulating because they’re nursing their kids. The whole aim is to pass on his genes (this is individual rather than kin selection), so his best course of action is to kill the babs, get the females ovulating as quickly as possible, and impregnate them himself. 

Canto: Yes, but it gets more complicated, because the females have just as much interest in passing on their genes as the male, and a bird in the hand is worth two in the bush…

Jacinta: Let me see, a babe in your arms is worth a thousand erections?

Canto: More or less precisely. So they fight the male to protect their infants, and can even go into ‘fake’ estrus, and mate with the male, fooling the dumb cluck into thinking he’s a daddy. 

Jacinta: And since Hrdy’s work, infanticide of this kind has been documented in well over 100 species, even though it can sometimes threaten the species’ survival, as in the case of mountain gorillas. So much for group selection.

Canto: So now to kin selection. Here are some facts. If you have an identical twin your genome is identical with hers. If you have a full sibling you’re sharing 50% and with a half-sibling 25%. As you can see, the mathematics of genes and relatedness can be widened out to great degrees of complexity. And since this is all about passing on all, or most, or some of your genes, it means that ‘in countless species, whom you co-operate with, compete with, or mate with depends on their degree of relatedness to you’, to quote Sapolsky. 

Jacinta: Yes, so here’s a term to introduce and then fairly promptly forget about: allomothering. This is when a mother of a newborn enlists the assistance of another female in the process of child-rearing. It’s a commonplace among primate species, but also occurs in many bird species. The mother herself benefits from an occasional rest, and the allomother, more often than not a younger relation such as the mother’s kid sister, gets to practice mothering. 

Canto: So this is part of what is called ‘inclusive fitness’, where, in this case, the kid gets all-day mothering (if of varying quality) the kid sister gets to learn about mothering, thereby increasing her fitness when the time comes, and the mother gets a rest to recharge her batteries for future mothering. It’s hopefully win-win-win. 

Jacinta: Yes, there are negatives and positives to altruistic behaviour, but according to Hamilton’s Rule, r.B > C, kin selection favours altruism when the reproductive success of relatives is greater than the cost to the altruistic individual. 

Canto: To explain that rule, r equals degree of relatedness between the altruist and the beneficiary (aka coefficient of relatedness), B is the benefit (measured in offspring) to the recipient, and C is the cost to the altruist. What interests me most, though, about this kin stuff, is how other, dumb primates know who is their kin. Sapolsky describes experiments with wild vervet monkeys by Dorothy Cheney and Robert Seyfarth which show that if monkey A behaves badly to monkey B, this will adversely affect B’s behaviour towards A’s relatives, as well as B’s relatives’ behaviour to A, as well as B’s relatives’ behaviour to A’s relatives. How do they all know who those relatives are? Good question. The same researchers proved this recognition by playing a recording of a juvenile distress call to a group of monkeys hanging around. The female monkeys all looked at the mother of the owner of that distress call to see what she would do. And there were other experiments of the sort. 

Jacinta: And even when we can’t prove knowledge of kin relations (kin recognition) among the studied animals, we find their actual behaviour tends always to conform to Hamilton’s Rule. Or almost always… In any case there are probably other cues, including odours, which may be unconsciously sensed, which might aid in inclusive fitness and also avoiding inbreeding. 

Canto: Yes and It’s interesting how this closeness, this familiarity, breeds contempt in some ways. Among humans too. Well, maybe not contempt but we tend not to be sexually attracted to those we grow up with and, for example, take baths with as kids, whether or not they’re related to us. But I suppose that has nothing to do with kin selection. And yet…

Jacinta: And yet it’s more often than not siblings or kin that we have baths with. As kids. But getting back to odours, we have more detail about that, as described in Sapolski. Place a mouse in an enclosed space, then introduce two other mice, one unrelated to her, another a full sister from another litter, never encountered before. The mouse will hang out with the sister. This is called innate recognition, and it’s due to olfactory signatures. Pheromones. From proteins which come from genes in the major histocompatibility complex (MHC). 

Canto: Histowhat?

Jacinta: Okay, you know histology is the study of bodily tissues, so think of the compatibility or otherwise of tissues that come into contact. Immunology.  Recognising friend or foe, at the cellular, subcellular level. The MHC, this cluster of genes, kicks off the production of proteins which produce pheromones with a unique odour, and because your relatives have similar MHC genes, they’re treated as friends because they have a similar olfactory signature. Which doesn’t mean the other mouse in the enclosure is treated as a foe. It’s a mouse, after all. But other animals have their own olfactory signatures, and that’s another story. 

Canto: And there are other forms of kin recognition. Get this – birds recognise their parents from the songs sung to them before they were hatched. Birds have distinctive songs, passed down from father to son, since its mostly the males that do the singing. And as you get to more complex species, such as primates – though maybe they’re not all as complex as some bird species – there might even be a bit of reasoning involved, or at least consciousness of what’s going on. 

Jacinta: So that’s kin selection, but can’t we superior humans rise above that sort of thing? Australians marry Japanese, or have close friendships with Nigerians, at least sometimes. 

Canto: Sometimes, and this is the point. Kinship selection is an important factor in shaping behaviour and relations, but it’s one of a multiple of factors, and they all have differential influences in different individuals. It’s just that such influences may go below the level of awareness, and being aware of the factors shaping our behaviour is always the key, if we want to understand ourselves and everyone else, human or non-human.

Jacinta: Good to stop there. As we’ve said, much of our understanding has come from reading Sapolsky’s Behave, because we’re old-fashioned types who still read books, but I’ve just discovered that there’s a whole series of lectures by Sapolsky, about 25, on human behaviour, which employs the same structure as the book (which is clearly based on the lectures), and is available on youtube here. So all that’s highly recommended, and we’ll be watching them.

References

R Sapolski, Behave: the biology of humans at our best and worst. Bodley Head, 2017

https://www.britannica.com/science/animal-behavior/Function#ref1043131

https://en.wikipedia.org/wiki/Kin_selection

https://en.wikipedia.org/wiki/Eusociality

 

 

 

 

 

another look at free will, with thanks to Robert Sapolsky

with 11 comments

Ah poor old Aynnie – from guru to laughing stock within a couple of gens

Having recently had a brief conversation about free will, I’ve decided to look at the matter again. Fact is, it’s been playing on my mind. I know this is a very old chestnut in philosophy, renewed somewhat by neurologists recently, and I know that far more informed minds than mine have devoted oodles of time and energy to it, but my conversation was with someone with no philosophical or neurological background who simply found the idea of our having no free will, no autonomy, no ‘say’ whatever in our lives, frankly ludicrous. Free will, after all, was what made our lives worth living. It gives us our dignity, our self-respect, our pride in our achievements, our sense of shame or disappointment at having made bad or unworthy decisions. To deny us our free will would deny us….  far far too much.

My previous piece on the matter might be worth a look (having just reread it, it’s not bad), but it seems to me the conundrum can be made clear by thinking in two intuitively obvious but entirely contradictory ways. First, of course we have free will, which we demonstrate with a thousand voluntary decisions made every day – what to wear, what to eat, what to watch, what to read, whether to disagree or hold our tongue, whether to turn right or left in our daily walk, etc etc. Second, of course we don’t have free will – student A can’t learn English as quickly and effectively as student B, no matter how well you teach her; this student has a natural ability to excel at every sport, that one is eternally clumsy and uncoordinated; this girl is shy and withdrawn, that one’s a noisy show-off, etc etc.

The first way of thinking comes largely from self-observation, the second comes largely from observing others (if only others were as free to be like us as we are). And it seems to me that most relationship breakdowns come from 1) not allowing the other to be ‘free’ to be themselves, or 2) not recognising the other’s lack of freedom to change. Take your pick.

So I’ve just read Robert Sapolsky’s take on free will in his book Behave, and it strengthens me in my ‘free will is a myth’ conviction. Sapolsky somewhat mocks the free will advocates with the notion of an uncaused homunculus inside the brain that does the deciding with more or less good sense. The point is that ‘compatibilism’ can’t possibly make sense. How do you sensibly define ‘free will’ within a determinist framework? Is this compatibilism just a product of the eternal complexity of the human brain? We can’t tease out the chain of causal events, therefore free will? So if at some future date we were able to tease out those connections, free will would evaporate? As Sapolsky points out, we are much further along at understanding the parts of the prefrontal cortex and the neuronal pathways into and out of it, and research increases exponentially. Far enough along to realise how extraordinarily far we have to go. 

One way of thinking of the absurdity of the self-deciding self is to wonder when this decider evolved. Is it in dogs? Is it in mosquitos? The probable response would be that dogs have a partial or diminished free will, mosquitos much less so, if at all. As if free will was an epiphenomen of complexity. But complexity is just complexity, there seems no point in adding free will to it. 

But perhaps we should take a look at the best arguments we can find for compatibilism or any other position that advocates free will. Joachim Krueger presents five arguments on the Psychology Today website, though he’s not convinced by any of them. The second argument relates to consciousness (a fuzzy concept avoided by most neurologists I’ve read) and volition, a tricky concept that Krueger defines as ‘will’ but not free will. Yes, there are decisions we make, which we may weigh up in our minds, to take an overseas holiday or spend a day at the beach, and they are entirely voluntary, not externally coerced – at least to our minds. However, that doesn’t make them free, outside the causal chain. But presumably compatibilists will agree – they are wedded to determinism after all. So they must have to define freedom in a different way. I’ve yet to find any definition that works for the compatibilist.

There’s also a whiff of desperation in trying to connect free will with quantum indeterminacy, as some have done. Having read Life at the edge, by Jim Al-Khalili and Johnjoe McFadden, which examines the possibilities of quantum effects at the biological level, I’m certainly open to the science on this, but I can’t see how it would apply at the macro level of human decision-making. And this macro level is generally far more ‘unconscious’ than we have previously believed, which is another way of saying that, with the growth of neurology (and my previous mention of exponential growth in this field is no exaggeration), the mapping of neurological activity, the research into neurotransmission and general brain chemistry, the concept of ‘consciousness’ has largely been ignored, perhaps because it resembles too much the homunculus that Sapolsky mocks. 

As Sapolsky quite urgently points out, this question of free will and individual responsibility is far from being the fun and almost frolicsome philosophical conundrum that some have seemed to suggest. It has major implications for the law, and for crime and punishment. For example, there are legal discussions in the USA, one of the few ‘civilised’ nations that still execute people, as to the IQ level above which you’re smart enough to be executed, and how that IQ is to be measured. This legal and semi-neurological issue affects a significant percentage of those on death row. A significant percentage of the same people have been shown to have damage to the prefrontal cortex. How much damage? How did this affect the commission of the crime? Neurologists may not be able to answer this question today, but future neurologists might. 

So, for me, the central issue in the free will debate is the term ‘free’. Let’s look at how Marvin Edwards describes it in his blog post ‘Free will skepticism: an incoherent notion’. I’ve had a bit of a to-and-fro with Marvin – check out the comments section on my previous post on the topic, referenced below. His definition is very basic. For a will, or perhaps I should say a decision, to be free it has to be void of ‘undue influences’. That’s it. And yet he’s an out and out determinist, agreeing that if we could account for all the ‘influences’, or causal operants, affecting a person’s decision, we could perfectly predict that decision in advance. So it is obvious to Marvin that free will and determinism are perfectly compatible.

That’s it, I say again. That’s the entire substance of the argument. It all hangs on this idea of ‘undue influence’, an idea apparently taken from standard philosophical definitions of free will. Presumably a ‘due influence’ is one that comes from ‘the self’ and so is ‘free’. But this is an incoherent notion, to borrow Marvin’s phrase. Again it runs up against Sapolsky’s homunculus, an uncaused decider living inside the brain, aka ‘the self’. Here’s what Sapolsky has to say about the kind of compatibilism Marvin is advocating for, which he (Sapolsky) calls ‘mitigated free will’, a term taken from his colleague Joshua Greene. It’s a long quote, but well worth transcribing, as it captures my own skepticism as exactly as anything I’ve read:

Here’s how I’ve always pictured mitigated free will:

There’s the brain – neurons, synapses, neurotransmitters, receptors, brain-specific transcription factors, epigenetic effects, gene transpositions during neurogenesis. Aspects of brain function can be influenced by someone’s prenatal environment, genes, and hormones, whether their parents were authoritarian or their culture egalitarian, whether they witnessed violence in childhood, when they had breakfast. It’s the whole shebang, all of this book.

And then, separate from that, in a concrete bunker tucked away in the brain, sits a little man (or woman, or agendered individual), a homunculus at a control panel. The homunculus is made of a mixture of nanochips, old vacuum tubes, crinkly ancient parchment, stalactites of your mother’s admonishing voice, streaks of brimstone, rivets made out of gumption. In other words, not squishy biological brain yuck.

And the homunculus sits there controlling behaviour. There are some things outside its purview – seizures blow the homunculus’s fuses, requiring it to reboot the system and check for damaged files. Same with alcohol, Alzheimer’s disease, a severed spinal cord, hypoglycaemic shock. 

There are domains where the homunculus and that biology stuff have worked out a détente – for example, biology is usually automatically regulating your respiration, unless you must take a deep breath before singing an aria, in which case the homunculus briefly overrides the automatic pilot.

But other than that, the homunculus makes decisions. Sure, it takes careful note of all the inputs and information from the brain, checks your hormone levels, skims the neurobiology journals, takes it all under advisement, and then, after reflecting and deliberating, decides what you do. A homunculus in your brain, but not of it, operating independently of the material rules of the universe that constitute modern science.

This captures perfectly, to me, the dilemma of those sorts of compatibilists who insist on determinism but. They seem more than reluctant to recognise the implications of that determinist commitment. It’s an amusing description – I love the bit about the aria – But it seems to me just right. As to the implications for our cherished sense of freedom, we can at least reflect that it has ever been thus, and it hasn’t stopped us thriving in our selfish, selfless ways. But as to the implications for those of us less fortunate in the forces that have moved us since childhood and before, that’s another story.

References

https://ussromantics.com/2018/05/15/is-free-will-a-thing-apparently-not/

R Sapolsky, Behave: the biology of humans at our best and worst, Bodley Head 2017. Note especially Chapter 16, ‘Biology, the criminal justice system and free will’. 

https://plato.stanford.edu/entries/compatibilism/#FreWil

https://www.psychologytoday.com/au/blog/one-among-many/201803/five-arguments-free-will

https://www.theatlantic.com/notes/2016/06/free-will-exists-and-is-measurable/486551/

Written by stewart henderson

October 27, 2018 at 1:25 pm

more about ozone, and the earth’s greatest extinction event

leave a comment »

the Siberian Traps are layers of flood basalt covering an area of 2 million square kilometres

Ozone, or trioxygen (O3), an unstable molecule which is regularly produced and destroyed by the action of sunlight on O2, is a vital feature in our atmosphere. It protects life on earth from the harmful effects of too much UV radiation, which can contribute to skin cancers in humans, and genetic abnormalities in plant life. In a previous post I wrote about the discovery of the ozone shield, and the hole above Antarctica, which we seem to be reducing – a credit to human global co-operation. In this post I’m going to try and get my head around whether or not ozone depletion played a role in the so-called end-Permian extinction of some 250 mya. 

I first read of this theory in David Beerling’s 2009 book The emerald planet, but recent research appears to have backed up Beerling’s scientific speculations – though speculation is too weak a word. Beerling is a world-renowned geobiologist and expert on historical global climate change. He’s also a historian of science, and in ‘An ancient ozone catastrophe?’, chapter 4 of The emerald planet, he describes the discovery and understanding of ozone through the research of Robert Strutt, Christian Schönbein, Marie Alfred Cornu, Walter Hartley, George Dobson, Sidney Chapman and Paul Crutzen, among others. He goes on to describe the ozone hole discovery in the 70s and 80s, before focusing on research into the possible effects of previous events – the Tunguska asteroid strike of 1908, the Mount Pinatubo eruption of 1991 and others – on atmospheric ozone levels, and then homes in on the greatest extinction event in the history of our planet – the end-Permian mass extinction, ‘the Great Dying’, which wiped out some 95% of all species then existing.

According to Beerling, it was an international team of palaeontologists led by Henk Visscher at the University of Utrecht who first made the claim that stratospheric ozone had substantially reduced in the end-Permian. They hypothesised that, due to the greatest volcanic eruptions in Earth history, which created the Siberian Traps (layers of solidified basalt covering a huge area of northern Russia), huge deposits of coal and salt, the largest on Earth, were disrupted:


The widespread heating of these sediments and the action of hot groundwater dissolving the ancient salts, was a subterranean pressure cooker synthesising a class of halogenated compounds called organohalogens, reactive chemicals that can participate in ozone destruction. And in less than half a million years, this chemical reactor is envisaged to have synthesised and churned out sufficiently large amounts of organohalogens to damage the ozone layer worldwide to create an intense increased flux of UV radiation.

However, Beerling questions this hypothesis and considers that it may have been the eruptions themselves, which lasted 2 million years and occurred at the Permian-Triassic boundary 250-252 mya, rather than their impact on salt deposits, that did the damage. There’s evidence that many of the eruptions originated from as deep as 10 kilometres below the surface, injected explosively enough to reach the stratosphere, and that these plumes contained substantial amounts of chlorine. 

More recent research, published this year, has further substantiated Visscher’s team’s finding regarding genetic mutations in ancient conifers and lycopsids, and their probable connection with UV radiation enabled by ozone destruction. The mutations were global and dated to the same period. Laboratory experiments exposing related modern plants to bursts of UV radiation have produced more or less identical spore mutations.

The exact chain of events linking the eruptions to the ozone destruction have yet to be worked out, and naturally there’s a lot of scientific argy-bargy going on, but the whole story, even considering that it occurred so far in the past is a reminder of the fragility of that part of our planet that most concerns us – the biosphere. The eruptions clearly altered atmospheric chemistry and temperature. Isotopic measurements of oxygen in sea water suggest that equatorial waters reached more than 40°C. As can be imagined, this had killer effects on multiple species. 

So, we’re continuing to gain knowledge on the ozone shield and its importance, and fragility. I don’t know that there are too many ozone hole skeptics around (I don’t want to look too hard), but if we could only get the same kind of apparent near-unanimity with regard to anthropogenic global warming, that would be great progress. 

Written by stewart henderson

October 10, 2018 at 3:15 pm

What’s up with Trump’s frontal cortex? – part 1

with one comment

He is fitful, irreverent, indulging at times in the grossest profanity… manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operations, which are no sooner arranged than they are abandoned in turn for others appearing more feasible. 

Trump, when asked who he consults with on foreign policy

You might be forgiven for thinking the above description is of the current US President, but in fact it’s a 19th century account of the change wrought upon Phineas Gage after his tragically explosive encounter with a railway tamping rod in 1848. It’s taken from neurobiologist Robert Sapolsky’s book Behave. A more fulsome analysis is provided in Antonio Demasio’s landmark work Descartes’ Error. The 19th century account is provided by Gage’s doctor.

Due to an accident with blasting powder the iron tamping rod blew a large hole through a part of Gage’s brain, exited through the top of his skull and landed some eighty feet away ‘along with much of his left frontal cortex’ (Sapolsky). Amazingly, Gage survived, though with great changes to his behaviour, as described above . Before the accident he had earned a reputation as a highly skilled, disciplined and reliable railway team foreman.

I was quite happy to be reacquainted with Gage’s story this morning, because in a recent conversation I was expounding upon Trump’s pre-adolescent nature, his tantrums, his solipsism, his childish name-calling, his limited language skills, his short attention span, his more or less complete ethical delinquency and so forth, about which my companion readily agreed, but when I suggested that this was all about a profoundly underdeveloped frontal cortex, she demurred, feeling I’d gone a bit too far.

Of course, I’m not a neurologist, but…

Any full description of Trump’s apparently missing or severely reduced frontal cortex needs to be evidence-based, but Trump is as likely to submit to any kind of brain scan or analysis as he is to present his tax returns. So the best we can do is compare his behaviour to those we know to have frontal lobe impairment.

Sapolsky tells us about the importance of the frontal lobe in making the tough decisions, the kinds of decisions that separate us from other primates. These are decisions in which our emotions and drives are activated, as well as higher order thinking involving a full understanding of the impact upon others of our actions.

Interestingly, in the case of Gage, his personality transformation meant that he couldn’t continue in his former occupation, so for a time he suffered the humiliation of being an exhibit in P T Barnum’s American Museum. I find this particularly intriguing because Trump has often been compared to Barnum – a showman, a con-man, a self-promoter and so forth. So in some ways – for example in Trump’s rallies, which he clearly loves to engage in – Trump has a dual role, as exhibitor and exhibit.

More importantly though, and this story is I think far more important than his injury and humiliation, Gage recovered almost completely over time – a testament to the brain plasticity which has recently been highlighted. On reflection, this shouldn’t be so surprising. Gage had been a person of rectitude and responsibility for decades before the disaster, and the neuronal pathways that his habitual behaviour had laid down, perhaps since early childhood, had only to be recovered through memory. It’s astonishing how this can happen even with subjects with less brain matter than ‘normal’ humans. Different parts of the brain can apparently be harnessed to rebuild the old networks.

The case of Trump, though, is different, as these higher order networks may never have been laid down. This isn’t to say there isn’t something there – it’s not as if there’s just a great hole where his frontal cortex should be. It’s more that his responses would map onto the responses of someone – a teenager or pre-teenager – who reliably behaves in a certain way because of the lack of full development of the frontal cortex, which we know isn’t fully developed in normal adults until their mid-twenties. And when we talk of the frontal cortex, we’re of course talking of something immensely complex with many interacting parts, which respond with great variability to different stimuli among different people.

But before delving into the neurological issues, a few points about the recent New York Times revelations regarding Fred Trump’s businesses, his treatment of young Donald and vice versa. The Hall & Oates refrain keeps playing in my head as I write, and as I read the Times article. What it suggests is a gilded, cosseted life – a millionaire, by current financial standards, at age eight. It seems that right until the end, Fred Trump covered up for his son’s business incompetence by bailing him out time and time again. This adds to a coherent narrative of a spoilt little brat who was rarely ever put in a position where he could learn from his mistakes, or think through complex solutions to complex problems. Trump senior clearly over-indulged his chosen heir-apparent with the near-inevitable result that the spoilt brat heartlessly exploited him in his final years. Fred Trump was a business-obsessed workaholic who lived frugally in a modest home and funnelled masses of money to his children, especially Donald, who basically hoodwinked the old man into thinking he was a chip off the old block. In the usual sibling battle for the parents’ affection and regard, Donald, the second son, saw that his older bother, Fred junior, was exasperating his dad due to his easy-going, unambitious nature (he later became an alcoholic, and died at 42), so Donald presented himself as the opposite – a ruthless, abstemious, hard-driving deal-maker. It worked, and Donald became his pretend right-hand man: his manager, his banker, his advisor, etc. In fact Donald was none of these things – underlings did all the work. Donald was able to talk the talk, but he couldn’t walk the walk – he had none of his father’s business acumen, as the Times article amply proves. In the late eighties, with the stock market crashing and the economy in free-fall, Trump made stupid decision after stupid decision, but his ever-reliable and always-praising dad kept him afloat. He also bequeathed to his son a strong belief in dodging taxes, crushing opposition and exaggerating his assets. The father even encouraged the son’s story that he was a ‘self-made billionaire’, and it’s not surprising that the over-indulged Donald and his siblings eventually took advantage of their ailing father – enriching themselves at his expense through a variety of business dodges described in the Times article. By the time of his death, Fred Trump had been stripped of almost all of his assets, a large swathe of it going to Donald, who was by this time having books ghost-written about how to succeed in business.

Of course it can be argued that Trump has one real talent – for self-promotion. This surely proves that he’s more than just a spoilt, over-grown pre-teen. Or maybe not. It doesn’t take much effort to big-note yourself, especially when, due to the luck of your family background, you can appear to walk the walk, especially in those rallies full of uncritical people desperate to believe in the American Business Hero. Indeed, Trump’s adolescent antics at those rallies tend to convince his base that they too can become rich and successful idiots. You don’t actually have to know anything  or to make much sense. Confidence is the trick.

It’s not likely we’ll ever know about the connections within Trump’s frontal and prefrontal cortices, but we can learn some general things about under-development or pre-development in those regions, and the typical behaviour this produces, and in my next post – because this one’s gone on too long  – I’ll utilise the chapter on adolescence in Sapolsky’s Behave, and perhaps other texts and sources – apparently Michelle Obama brought Trump’s inchoate frontal cortex to the public’s attention during the election – to explore further the confident incompetence of the American president.

Written by stewart henderson

October 7, 2018 at 5:38 pm

some stuff about dinosaurs and their relationship to birds

leave a comment »

Archaeopteryx lithographica with its long bony tail – I took this pic myself at London’s Natural History Museum

Jacinta: Let’s talk about dinosaurs. Are they a thing?

Canto: Of course they are, what are you talking about?

Jacinta: Well I read recently in a New Scientist article that for quite some time in the recent past dinosaur experts didn’t really think ‘dinosaur’ existed as a scientific classification. A new way of classifying was needed because some dinosaurs were bird-hipped and some were lizard-hipped, though they were neither birds nor lizards. So, new names were required.

Canto: Right, so some had hips like lizards, but were clearly not lizards because they had anatomical features that set them apart, and the same went for those that had hips like birds?

Jacinta: Yes I think that’s right. Let’s talk as we learn. Bird-hipped dinos are ornithischians – think ornithology – and the lizardy ones are called saurischians. It was Harry Seeley who shook up the dinosaur-loving world back in 1887 when he argued, before the Royal Society, that what they’d thought were dinosaurs (a term coined by Richard Owen) were really two separate groups, based on those hip bones. Seeley was right about the two groups, but the term ‘dinosaur’, which of course has never disappeared in popular writing, has been rescued over time for science by agreement on other features which bespeak ‘dinosaur’. This has much to do with cladistics, which we may or may not discuss later.

Canto: So the first dinos appeared some 235 mya in the late triassic period, but interestingly they flourished between two major extinction events, the Triassic-Jurassic extinction event about 201 mya, a very sudden event that allowed dinosaurs to fill vacated ecological niches on land, and the Cretaceous-Paleogene (or Cretaceous-Teriary, or K-T) extinction event of 66 mya, which wiped out all the non-avian dinos.

Jacinta: And it should be mentioned that birds are now considered feathered avian dinosaurs, descended from earlier therapods, which strangely are saurischians (lizard-hipped), though a very recent and still controversial paper has reclassified them as ornithischians. I should also mention that dinosaur researchers are a notoriously feisty and bickering tribe, from what I’ve heard.

Canto: I’ve started ploughing through a course on dinosaurs via youtube – The Natural History of Dinosaurs – and I’ve already learned some words, just as background: lithify, diagenesis and coprolite. I’ll let you know if anything exciting crops up, but tell me more about birds being the only remaining dinosaurs and how we know that.

Jacinta: Well, it’s been known since at least the discovery of Archaeopteryx, the type specimen of which was found just two years after Darwin published The Origin of Species, that there are clear anatomical similarities between birds and non-avian dinosaurs. Feathers and hollow bones, for example. There’s also evidence that they share nesting and brooding behaviour. There are also relations with non-avian dinosaurs, some species of which also had feathers, and these discoveries are raising fascinating questions about the origin of flight in these creatures. Of course it’s all very controversial and some researchers are still holding out on the dinosaur-bird link, suggesting other archosaurs were the ancestors.

Canto: What’s an archosaur?

Jacinta: It means ‘ruling reptile’ and these are creatures which first emerged some 300 mya, and they’re the ancestors of living reptiles today. They’re also the ancestors of birds, and dinosaurs. So they’re a larger and older group. Presumably the hold-outs have reason to think birds emerged out of some reptilian line that was distinct from theropod dinosaurs. But that’s nothing to the arguments about the evolutionary steps that led from maniraptoran theropods (perhaps) to modern birds, or the arguments about the origin of flight. Now let me point out that theropods are a suborder of dinosaurs with hollow bones and three-toed limbs, which have long been classed as saurischians until this very recent paper discussed in the New Scientist article, which reclassifies them as ornithiscians. And this seems to be another step – if it holds – towards our understanding of the relationship between birds and their ancestral dinosaurs. An earlier but still pretty recent step were the discoveries, particularly out of China, of a number of fossilised dinosaurs with evidence of feathers, or proto-feathers, and all this, together with advances in analysing and categorising existing specimens using cladistics described in Wikipedia as ‘a method of arranging species based strictly on their evolutionary relationships, using a statistical analysis of their anatomical characteristics’.

Canto: I get very confused about all this. Weren’t there flying dinosaurs – we used to call them pterodactyls – and did they have feathers, or were their means of flight completely different? I seem to remember them depicted like gliders – I mean of the animal kind, with great flaps of skin to catch the wind… Of course that was long before any talk of feathered dinos.

Jacinta: Well hopefully I’ll get to that. Let me talk first about Archaeopteryx, which they reckon dates back to about 150 million years ago. It was probably about the size of a magpie, though there may have been different species of different size (only 11 fossil specimens have been discovered so far). They had feathers, but it’s not known whether they flew like modern birds (flapping flight) or merely glided. A recent study (which I’ve not read) has argued that their flight capabilities were quite limited. They had long, bony tails, which I’m assuming would’ve hampered long-term flight. Interestingly, complex and, for me, impossible-to-verify coloration analyses have presented evidence that the feathers of these critters were a matte black, at least predominantly. Of course it’s hard to prove all this conclusively with 150 million-year-old animals, but speculation and analyses continue, for example on the brain-case of one Archaeopteryx specimen, to determine whether it had a brain for flight (e.g. adequate eyesight, hearing and muscle manipulation). Most of this converges on a limited flight ability, but just how limited will be endlessly argued. And concerning the evolution of birds and flight, there’s a ‘trees-down’ theory (think of sugar gliders etc) and a ‘ground up’ theory. Where does Archaeopteryx fit with those alternatives? That’s still up for grabs.

Canto: Okay, so what about pterodactyls, are they still a thing? Dactyl means digit or finger, doesn’t it?

Jacinta: Winged finger. Yes, they’re a species of pterosaur, with thirty known specimens. They presumably achieved fame among the children of the world as the first-known flying dinosaurs – but they’re not dinosaurs. It’s confusing because ‘saur’ means ‘lizard’, and ‘dinosaur’ means ‘terrible lizard’ and ‘pterosaur’ means ‘winged  lizard’ and they all seem to be connected…

Canto: So what about their relation to birds? Any sign of feathers?

Jacinta: They may have had downy feathers here and there, but not for flight. Their wings were more like those of bats, and they were originally classified as an archaic type of bat. In fact, in the early days of taxonomy, many fossils that had vague similarities to the first pterodactyl fossils discovered in the late 18th century were wrongly designated as pterodactyls, which probably explains their general popularity. It has taken years and many improvements in analysis and dating to sort out the mess, and apparently it still hasn’t been sorted. Anyway, they’re not seen as ancestral to birds. But I may be wrong.

Canto: Wow. Disappointing.

Jacinta: So getting back to the origin of birds, the question of clavicles (collar bones) is important. Birds have wishbones (furculae), which are fused clavicles. The question of bird ancestry has hung on these clavicle bones to a large degree. They’re delicate bones, not easily preserved, and it was long thought that they didn’t exist in dinosaurs. This view has been completely overturned, and in fact most of our understanding about the relationship between birds and earlier dinosaurs come from skeletal studies, or re-examinations, as well as studies of musculature and internal organs, though of course it’s feathers that capture the public’s imagination. But of course there’s a lot of controversy about the how and when of bird evolution, and the evolution of flight, which you’d expect from such scant solid evidence together with intense scientific and public interest.

Canto: Well, I’ve learned something more than the little I knew before about dinosaurs. And their hips. I’ll watch the rest of The Natural History of Dinosaurs’, and we’ll speculate some more in a later post.

Written by stewart henderson

September 4, 2018 at 1:03 pm

Always chemical: how to reflect upon naturopathic remedies

leave a comment »

most efficacious in every case

So here’s an interesting story. When I was laid up with a bronchial virus (RSV) a few weeks ago, coughing my lungs up and having difficulty breathing, with a distinct, audible wheeze, I was offered advice, as you do, by a very well-meaning person about a really effective treatment – oregano oil. This person explained that, on two occasions, he’d come down with a bad cough and oregano oil had done the trick perfectly where nothing else worked.

I didn’t try the oregano oil. I followed my doctor’s recommendation and used the symptom-relieving medications described in a previous post, and I’m much better now. What I did do was look up what the science-based medicine site had to say about the treatment (I’d never heard of oregano oil, though I’ve had many other plant-based cures suggested to me, such as echinacea, marshmallow root and slippery elm – well ok I lied, I found the last two on a herbal medicine website).

I highly recommend the science-based medicine website, which has been run by the impressively-credentialed Drs David Gorski and Steve Novella and their collaborators for years now, and which thusly has a vast database of debunked or questionable treatments to explore. It’s the best port of call when you’re offered anecdotal advice about any treatment whatsoever by well-wishers. Not that they’re the only people performing this service to the public. Quackwatch, SkepDoc, and Neurologica are just some of the websites doing great work, but they’re outnumbered vastly by sites spreading misinformation and bogus cures, unfortunately. It’s almost a catch-22 of the internet that you have to be informed enough to use it to get the best information out of it.

As to oregano oil specifically, Scott Gavura at science-based medicine proves a detailed account. I will summarise here, while also providing my own take. Firstly people need to know that when a substance, any substance –  a herb or a plant, an oil extracted therefrom, or a tablet, capsule or mixture,something injectable or applied to the skin, whatever – is suggested as a treatment for a condition, they should consider this simple mantra – always chemical. That’s to say, a treatment will only work because it has the right chemistry to act against the treated condition. In other words you need to know something (or rather a lot) about the chemistry of the treating substance and the chemistry of the condition being treated. It’s no good saying ‘x is great for getting rid of coughs – it got rid of mine,’ because your cough may not have the same chemical cause as mine, and your cough in February 2007 may not have the same chemical cause as your cough in August 2017. My recent cough was caused by a virus (and perhaps I should change the mantra – always biochemical – but still it’s the chemistry of the bug that’s causing the problem), but no questions were asked about the cause before the advice was given. And you’ll notice when you look at naturopathic websites that chemistry is very rarely mentioned. And I’m not talking about toxins.

Gavura gives this five-point test for an effective treatment:

When we contemplate administering a chemical to deliver a medicinal effect, we need to ask the following:

  1. Is it absorbed into the body at all?
  2. Does enough reach the right part of the body to have an effect?
  3. Does it actually work for the condition?
  4. Does it have any hazardous, unwanted effects?
  5. Can it be safely eliminated from the body?

The answer to Q1 is that oregano oil contains a wide variety of chemical compounds, particularly phenolic compounds (71%). It’s these phenolic compounds that are touted as having the principal beneficial effects. However, though we know that there’s some absorption, we don’t have a chemical breakdown. We just don’t know which phenolic compounds are being absorbed or how much.

Q2 – No research on this, or on absorption generally. Topical effects (ie effects on the skin) are more likely to be beneficial than ingested effects, as the oil can maintain high concentration. This would have no effect on a cough.

Q3 – According to one manufacturer the oil has ‘scientifically proven results against almost every virus, bacteria, parasite, and fungi…’ (etc, etc, but shouldn’t that be bacterium and fungus?). In fact, no serious scientific research has ever been conducted on oregano oil and its effectiveness for any condition whatsoever. So the answer to this question is  – no evidence, beyond anecdote.

Q4 – There have been reports of allergic reactions and gastro-intestinal upsets, but the naturopathy industry is more or less completely unregulated so you can never be sure what you’re getting with any bottle of pills or ‘essential oils’. As Gavura points out, the lack of research on possible adverse effects, for this and other ‘natural’ treatments, is of concern for vulnerable consumers, such as pregnant women, young or unborn children, and those with pre-existing conditions.

Q5 – At low doses, there’s surely no concern, but nobody has done any research about dosing up on carvacrol, the most prominent component of oregano oil, which gives the plant its characteristic odour. Other organic components are thymol and cymene.

 

So there’s no solid evidence about oregano oil, or about the mechanism for its supposed efficacy. But what if my well-wisher was correct, and something in the oregano oil cleared up his cough – twice? And did so really really well? Better than several other treatments he tried?

Well, then we might be onto something. Surely a potential billion-dollar gold-mine, considering how debilitating your common-or-garden cough can be. And how, if not cleared up, it can leading to something way more serious.

So how would a person who is sure that oregano oil has fantastic curative properties (because it sure worked for him) go about capitalising on this potential gold-mine? Well, first he would need evidence. His own circle of friends would not be enough – perhaps he could harness social media to see if there were sufficient people willing to testify to oregano oil curing their cough, where other treatments failed. Then , if he had sufficient numbers, he might try to find out the causes of these coughs. Bacterial, viral, something else, cause unknown? It’s likely he wouldn’t make much headway there (most people with common-or-garden coughs don’t go to the doctor or submit to biochemical testing, they just try to ride it out), but no matter, that might just be evidence that the manufacturer was right – it’s effective against a multitude of conditions. And yet, it seems that oregano oil is a well-kept secret, only known to naturopathic companies and health food store owners. Doctors don’t seem to be prescribing it. Why not?

Clearly it’s because Big Pharma doesn’t support the stuff. Doctors are in cahoots with Big Pharma to sell attractive pills with long pharmacological names and precise dosages and complex directions for use. Together they like to own the narrative, and a multi-billion dollar industry is unlikely to be had from an oil you can extract from a backyard plant.

Unless

Our hero’s investment of time and energy has convinced him there’s heaps of money to be made from oregano oil’s miraculous properties, but that same investment has also convinced him that it’s the chemical properties that are key, and that if the correct chemical formula can be isolated, refined and commercialised, not only will he be able to spend the rest of his life in luxury hotels around the globe, but he will have actually saved lives and contributed handsomely to the betterment of society. So he will join Big Pharma rather than trying to beat it. Yes, there would have to be a massive upfront outlay to perform tests, presumably on rats or mice at first, to find out which chemical components or combinations thereof do the best job of curing the animals, who would have to be artificially infected with various bugs affecting the respiratory system, or any other bodily system, since there are claims that the oil, like Lily the Pink’s Medicinal Compound™, is ‘most efficacious in every case’.

But of course it would be difficult for any average bloke like our hero to scratch up the funds to build or hire labs testing and purifying a cure-all chemical extract of oregano oil. Crowdsourcing maybe, considering all the testimonials? Or just find an ambitious and forward-thinking wealthy entrepreneur?

Is that the only problem with the lack of acceptance, by the medical community, of all the much-touted naturopathic cures out there? Lack of funds to go through the painstaking process of getting a purefied product to pass through a system which ends with double-blind, randomised, placebo-controlled human studies with large sample sizes?

Permit me to be sceptical. It’s not as if the chemical components of most herbal remedies are unknown. It’s highly unlikely that pharmacologists, who are in the business of examining the chemistry of substances and their effects for good or ill on the human body, haven’t considered the claimed cornucopia of naturopathic treatments and the possibility of bringing them into the mainstream of science-based medicine to the benefit of all. Yes, it’s possible that they’ve missed something, but it’s also possible, indeed more likely, that people underestimate the capacity of our fabulous immune system, the product of millions of years of evolution, to bring us back to health when we’re struck down by the odd harmful bug. When we’re struck down like this, we either recover or we die, and if we don’t die, we tend to attribute our recovery to any treatment applied. Sometimes we might be right, but it pays to be skeptical and to do research into a treatment, and into what ails us, before making such attributions. And to do so with the help of a good science-based medical practitioner. And remember again that motto: always chemical. 

 

Written by stewart henderson

August 24, 2018 at 10:18 am