an autodidact meets a dilettante…

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

women of note 1: Mary Anning, palaeontologist

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She sells sea-shells on the sea-shore,
The shells she sells are sea-shells, I’m sure
For if she sells sea-shells on the sea-shore
Then I’m sure she sells sea-shore shells. 

Terry Sullivan, 1908 – said to be inspired by Mary Anning’s fossickings

Unfortunately, I want to write about everything.

So now I begin an occasional series about women to be celebrated and never forgotten.

Mary Anning was born in the seaside town of Lyme Regis, Devon, in 1799 and died there, too young, of breast cancer in 1847. According to Brian Ford, author of Too big to walk: the new science of dinosaurs, she was ‘the first full-time professional palaeontologist anywhere in the world’. It’s a fair statement; those before her were generalists, given the name ‘naturalists’, and made their livings as pastors or physicians, or were independently wealthy. The term ‘palaeontology’ was just starting to gain traction in the early nineteenth century, replacing the intriguing but probably short-lived ‘oryctology’, though fossil-finding and speculations thereon (mostly infused with religious or mystic beliefs) date back to civilisation’s dawn.

Fossil-hunting had become quite trendy from the late eighteenth century, and Mary’s dad, a cabinet-maker by trade, supplemented his income by selling fossil bits and pieces, discovered himself on the nearby cliffs, to locals and tourists (the region had become something of a haven for those escaping the Napoleonic wars). The cliffs around Lyme Regis on England’s south coast form part of the Blue Lias, alternating sediments of shale and limestone, very rich in fossils from the early Jurassic, around 200 mya.

Richard and Molly, Mary’s parents, had ten children, but only two, Joseph and Mary, survived infancy. Childhood diseases such as measles were often killers, especially among the poor – a reminder of how lucky we are to be living in an economically developed country in the 21st century. The Anning family was never well-off, and Richard died when Mary was just 11 years old. Mary herself just managed to escape death by lightning strike when she was a baby. The strike killed three women, one of whom was tending her at the time. But the family suffered many hardships besides infant mortality. Food shortages and rising prices led to riots in the neighbourhood, and Richard himself was involved in organising protests.

As kids, Joseph and Mary sometimes accompanied their father on fossil-hunting trips on the dangerous cliffs, which were subject to landslides. They would sell their finds, which were mostly of invertebrate fossils such as ammonite and belemnite shells, in front of their home, but clearly life would’ve been a real struggle in the years following Richard’s death, during which time they relied partly on charity. It wasn’t long, though, before Mary’s expertise in finding and identifying fossils and her anatomical know-how came to the attention of well-heeled fossickers in the region. In the early 1820s a professional collector, Thomas Birch, who’d come to know the family and to admire Mary’s skills in particular, decided to auction off his own collection to help support them. This further enhanced their reputation, and Mary became something of a local celebrity, reported on in the local papers:

This persevering female has for years gone daily in search of fossil remains of importance at every tide, for many miles under the hanging cliffs at Lyme, whose fallen masses are her immediate object, as they alone contain these valuable relics of a former world, which must be snatched at the moment of their fall, at the continual risk of being crushed by the half-suspended fragments they leave behind, or be left to be destroyed by the returning tide: – to her exertions we owe nearly all the fine specimens of ichthyosauri of the great collections.

Bristol Mirror, 1823 – quoted in Too big to walk, by Brian Ford, p61

As this article mentions, Mary Anning’s name is often associated with ichthyosaur fossils, but she also discovered the first plesiosaur, the identity of which was confirmed by Georges Cuvier – though he at first accused her of fraud. Amongst other contributions, she was the first to recognise that the conical ‘bezoar stones’ found around the cliffs of Lyme were in fact fossilised faeces of ichthyosaurs and plesiosaurs.

plesiosaur skeleton, beautifully sketched by Mary Anning

For my information, ichthyosaurs were marine reptiles dated from the early Triassic to the late Cretaceous periods (250-90 mya), though most abundant in the early period, after which they were superseded as the top marine predators by the plesiosaurs (approx 204-66 mya).

Anning’s exact contribution to palaeontology is impossible to determine, because so many of her finds were snapped up by professional collectors, in an era when attributions weren’t preserved with much care, and this would have been compounded by her status as an ‘uneducated’ amateur, and a woman. Contemporary commentary about her expertise was often infused with a subtle condescension. There’s little doubt that, had she been male, her admirers would have seen to it that her talents were sufficiently recompensed with scholarships, senior university posts, and membership of the prominent scientific societies. Instead, she remained a fixture at Lyme Regis – there’s no indication that she ever travelled, apart from at least one trip to London, though her expertise was recognised throughout Europe and America. It’s also likely that, coming from a family of Dissenters – a reformist Protestant group – she was regarded with suspicion by the Anglican-dominated scientific hierarchy of the time. Let’s take a look, for comparison, at some of the males she associated with, and who associated with her, and how their professional lives went:

Sir Henry de La Beche – KCB, FRS. That first TLA means ‘Knight Commander of the Bath’ or something similar. I seem to recall bestowing a similar title upon myself while commanding battleships in the bathtub at age six or so. Never received a stipend for it though. FRS means Fellow of the Royal Society of course. Son of a slave-owner who died young, Beche was brought up in Lyme Regis where he became a friend of Anning, sharing her interest in geological strata and what they contained. It’s not unlikely that she was an inspiration for him. He was able to join the male-only London Geological Society at age 21, and later became its President. He became a FRS in 1819 at the still tender age of 24. He was appointed director of the Geological Survey of Great Britain in the 1830s and later the first director of the Museum of Practical Geology in London (now part of the Natural History Museum). He was knighted for his genuine contributions to geology in 1848. Beche was in fact an excellent practical and skeptical scientist who gave support to Anning both financially and in his published work.

William Conybeare – FRS. Born into a family of ‘divines’ (at least on the male side) Conybeare became a vicar himself, and a typical clergyman-naturalist, with particular interests in palaeontology and geology. Educated at the elite (and all-male) Westminster School and at all-male Oxford University, after which he travelled widely through the country and on the Continent (all paid for by ‘a generous inheritance’) in pursuit of geological and palaeontological nourishment. He became an early member of the Geological Society, where he met and advised other notables such as Adam Sedgwick and William Buckland, and contributed papers, including one with Beche which summarised findings about ichthyosaurs and the possibility of another species among them, the plesiosaur. This was confirmed by Anning’s discovery and detailed description of a plesiosaur, which Conybeare later reported to the Geological Society, delighted to be proved correct. He failed to mention Anning’s name. In 1839 Conybeare, together with two other naturalist heavyweights, William Buckland and Richard Owen, joined Mary Anning for a fossil-hunting excursion. Unfortunately we have no smartphone recordings of that intriguing event.

William Buckland, DD [Doctor of Divinity], FRS. Born and raised in Devon, Buckland accompanied his clergyman dad on walks in the region where he collected fossil ammonite shells. He was educated at another elite institution, Winchester College, where he won a scholarship to Oxford. In 1813 he was appointed reader in minerology there, and gave popular lectures with emphasis on geology and palaeontology. He seemed to cultivate eccentricities, including doing field-work in his academic gown and attempting to eat his way though the animal kingdom. His most important association with Mary Anning was his coining of the term ‘coprolite’ based on Anning’s observation that these conical deposits, found in the abdomens of ichthyosaurs, were full of small skeletons. Clearly, Anning knew exactly what they were, but had no real opportunity to expatiate on them in a public forum. Women were often barred from attending meetings of these proliferating scientific societies even as guests, let alone presenting papers at them.

Gideon Mantell, MRCS [Member of the Royal College of Surgeons], FRS. Mantell was himself a rather tragic figure, whose association with Anning was less personal, though he did visit her once at her Lyme Regis shop. He was inspired more by news of her ichthyosaur discoveries, which reinforced an obsession with fossil hunting in his own region of Sussex, where many fossils of the lower Cretaceous were uncovered. Born in Lewes in Sussex, the fifth child of a shoemaker, he was barred from the local schools due to his family’s Methodism. He underwent a period of rather eccentric but obviously effective private tuition before becoming apprenticed to a local surgeon. Though worked very hard, he taught himself anatomy in his free time, and wrote a book on anatomy and the circulation of the blood. He travelled to London for more formal education and obtained a diploma from the Royal College of Surgeons in 1811. Returning to Lewes, he partnered with his former employer in treating victims of cholera, smallpox and typhoid epidemics, and delivering large quantities of babies, building up a thriving practice, but also somehow finding time for fossil-hunting, corresponding with others on fossils and geology, and writing his first paper on the fossils of the region. He started finding large and unusual bones and teeth, which turned out to be those of an Iguanadon, though it took a long time for this to be recognised, and he was mocked for his claims by experts such as William Buckland and Richard Owen. Although he was becoming recognised for his many writings and discoveries, he always remained something of an outsider to the establishment. He later fell on hard times and suffered a serious spinal injury from a horse-and-carriage accident, from which he never really recovered. He apparently died from an overdose of laudanum, used regularly as a pain-killer in those days.

Returning to Mary Anning, we see that class as well as sex was a barrier to intellectual acceptance in early nineteenth century Britain – but sex especially. Mary struggled on in Lyme Regis, recognised and sought out by other experts, but never given her full due. In the 1840s she was occasionally seen to be staggering about, as if drunk. In fact, she too was dosing herself on laudanum, due to the pain of advancing breast cancer. She died in 1847, aged 47.

I should point out that, though Mary Anning’s name is largely unknown to the general public, so are the male names mentioned in this article. We generally don’t fête our scientists very much, though they’re the ones that really change our world, and help us to understand it. Mary was helped out by luminaries such as Beche and Buckland in her later years, and received a small annuity from the British Association for the Advancement of Science. Upon her death, Beche wrote a modest eulogy, which he presented at a Geological Society meeting, which, had she been alive, Anning wouldn’t have been allowed to attend. It was later published in the transactions of the Society. Here’s how it begins:

 I cannot close this notice of our losses by death without adverting to that of one, who though not placed among even the easier classes of society, but one who had to earn her daily bread by her labour, yet contributed by her talents and untiring researches in no small degree to our knowledge of the great Enalio-Saurians [now known as Euryapsida], and other forms of organic life entombed in the vicinity of Lyme Regis ..

Mary Anning by her beloved cliffs, tool in hand, pointing to her not yet dead dog Tray, killed in the line of scientific duty…

References

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

https://ucmp.berkeley.edu/history/anning.html

https://www.nhm.ac.uk/discover/mary-anning-unsung-hero.html

https://www.britannica.com/biography/Mary-Anning

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

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

https://www.bgs.ac.uk/discoveringGeology/time/Fossilfocus/ammonite.html

https://www.bgs.ac.uk/discoveringGeology/time/Fossilfocus/Belemnite.html

https://www.britannica.com/biography/Henry-Thomas-De-La-Beche

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

https://en.wikipedia.org/wiki/William_Conybeare_(geologist)

https://www.strangescience.net/conybeare.htm

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

https://www.theguardian.com/science/2019/feb/03/gideon-mantell-play-fight-over-first-dinosaur

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

Written by stewart henderson

September 24, 2019 at 11:14 am

How statins work 2: atherosclerosis and LDL cholesterol

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Recent studies have revealed that children 8-10 years old are being diagnosed with Type II diabetes, high cholesterol, and high blood pressure at an alarming rate.

Lee Haney

Picture taken from ‘LDL in atherosclerosis and heart disease’ by Axel Sigurdsson, MD, PHD

As I said in my previous post, biochemistry is almost infinitely complex, so bear with me as I crawl towards an understanding of the role of statins in reducing LDL cholesterol in the blood stream, thus reducing atherosclerosis, a major feature of heart disease.

Remembering, first, that cholesterol is a sterol, which is a modified steroid with a hydroxyl (alcohol) group coming off carbon 3. It’s a mostly hydrophobic lipid with this tiny polar hydroxyl group added. It’s carried around in the bloodstream by lipoproteins.

I’ll turn now to atherosclerosis – though I don’t currently know whether statins can perform roles other than reducing the build-up of plaque in the arteries.

So, generally, our arteries carry oxygenated blood from the heart to other organs and regions of the body. Atherosclerosis is sometimes called ‘hardening of the arteries’, as sklerosis is from Greek, meaning ‘hardening’, but it’s really a narrowing rather than a hardening, or perhaps it’s better described as both, as we’ll see. Arteriosclerosis is a more general name, while atherosclerosis means blockage or narrowing (stenosis) due to an atheroma, an abnormal accumulation of ‘debris’ or plaque consisting of fat (mostly), calcium and sometimes fibrous tissue in the inner arterial wall (endothelium). These atheroma are difficult to detect before they cause heart attacks or disease, because heart arteries are very small and hidden deep within the chest. They’re also quite mobile and elastic with blood flow. Heart attack and stroke sometimes happen when the atheroma ‘bursts’ – the fibrous cap (of smooth muscles cells, cholesterol-rich foam cells, collagen and elastin) which surrounds the atheroma is ruptured, or breaks free from the arterial wall, causing a blood clot (thrombus). These are sudden events, not easily detected beforehand. Alternatively, major problems arise when the atheroma becomes large enough to defeat arterial flexibility.

There can be symptoms, apart from such major dramas as heart attacks and stroke, which may act as warning signs for atherosclerosis. The narrowing of the arteries means that less blood and oxygen is reaching the cardiovascular system (ischemia), and this may result in vomiting, angina (chest pain), and general feelings of faintness and anxiety. Atherosclerosis of the carotid artery, which feeds the brain, may have different symptoms, including headaches, dyspnea and facial numbness. Atherosclerosis can also affect the function of the liver, kidneys and other organs, and the vascular system.

So what causes atheromas? It seems that these accumulations of plaque are the result of monocyte-macrophage activity. Macrophages are types of white blood cells (leucocytes) that perform immune and cleansing functions. However, we don’t really know why the plaque build-up occurs – though it might be initiated by damage to the endothelium. We do know that atherosclerosis can begin early, and that blood LDL cholesterol is a major factor in the activity that leads to this build-up. That’s why researchers have been rather single-minded about ways of reducing LDL cholesterol, and even on increasing HDL cholesterol levels, though there’s little evidence, apparently, that higher HDL levels are beneficial. Nor, interestingly, is there much evidence that lowering triglycerides has a positive effect on heart disease, while study after study has shown that low LDL cholesterol levels are key to avoiding cardiovascular problems.

Okay, now I’m going to take a few steps back to look more deeply at the role of LDL cholesterol in building atheromas and so causing atherosclerosis. Returning to my vague mention of macrophages and monocytes, here’s a clearer picture, drawn mainly from this excellent video.

  1. Structure of arterial wall

First, we need to know that the arterial walls are layered. The first layer surrounding the lumen (the tunnel space where the blood flows and where you find red blood cells or RBCs, leukocytes and lipoproteins, etc) is the epithelium, a thin layer of squamous cells. This layer is surrounded by the tunica intima (sometimes the epithelium is described as part of the T intima), an elastic layer quite rich in collagen. It also contains structural cells called fibroblasts, and smooth muscle cells (SMCs). Surrounding the T intima is the tunica media (particularly rich in SMCs), which in turn is surrounded by the thicker, tougher tunica adventitia. In general, the arterial wall becomes stiffer and more fibrous as you move from inner to outer. Atherosclerosis is apparently more of a problem in large and middle-sized arteries which contain more of the protein elastin.

2. Plaque formation

Plaque formation begins, it’s believed, when there’s damage to the thin endothelial layer (only one cell thick) as well as an abundance of circulating low density lipoproteins (LDLs). LDLs (mostly lipid with a small amount of protein) can then move through the damaged layer into the T intima where they become oxidised by ‘reactive oxygen species’ (free radicals) and other enzymes such as metallo-proteases, released by the endothelial cells. These oxidised LDLs, which are now ‘trapped’ in the T intima, will activate endothelial cells to express receptors for white blood cells (leukocytes), particularly the largest types of leucocyte, known as monocytes. So we have this accumulation of oxidised LDLs activating endothelial cells to express adhesion molecules for leucocytes, which brings monocytes and T helper cells into the T intima layer. This movement into tissue transforms monocytes into macrophages (not sure how that happens), and these macrophages then ‘take up’ or engulf the oxidised LDLs and form foam cells. By this time the lipid material dumped into the T intima has created something like a lake of fat, known as a ‘fatty streak’. Foam cells are central to the process of plaque formation and atherosclerosis, as they induce more SMCs into the T intima from the T media by means of a released growth factor, IGF-1 (insulin-like growth factor), and this leads to increased synthesis of collagen in the region, which hardens the plaque build-up, a build-up further fostered by foam cell death which releases more lipid material. Foam cells also release pro-inflammatory cytokines and reactive oxygen species as well as chemokines which attract more macrophages to the site. Upon death they also release DNA material that attracts neutrophils, a very common type of white blood cell. All of this will increase inflammation or plaque build-up in the region.

3. Effects

As mentioned, SMCs contribute to the containment of this inflamed lipid area by releasing proteins such as collagen and elastin, which is used to build a fibrous cap around it. They also stiffen the formation, the atheroma as it’s called, by adding calcium. All of this has the effect of enlarging the atheroma and so reducing the diameter of the arterial lumen in the area, which raises blood pressure as the blood tries to maintain an adequate flow. The calcification of the area also considerably reduces the flexibility of the arterial wall, again resulting in increased blood pressure. Rupture of the fibrous cap may result, which may lead to thrombosis.

So where do statins come in here? Let me quote from an abstract of one academic paper: Statins in atherosclerosis: lipid-lowering agents with antioxidant capabilities, published in 2004:

Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are the first-line choice for lowering total and LDL cholesterol levels and they have been proven to reduce the risk of CHD [chronic heart disease]. Recent data suggest that these compounds, in addition to their lipid-lowering ability, can also reduce the production of reactive oxygen species and increase the resistance of LDL to oxidation. It may be that the ability of statins to limit the oxidation of LDL contributes to their effectiveness at preventing atherosclerotic disease.

Note that oxidation of LDL has the effect of fixing it in the T intima, as mentioned above, so if it’s true, as I presume it is, that statins inhibit LDL oxidation, as well as having other benefits, then they can’t be a bad thing, as long as there aren’t serious side-effects. I’ll continue to explore this topic, as it’s teaching me a lot about the blood, the liver and the circulatory system, inter alia – and it’s great fun. Dr Ben Goldacre has written a book Do statins work? the battle for perfect evidence-based medicine, which hasn’t been released yet, but I intend to get my hands on it and devour it, along with more videos and articles. In the meantime I hope it’s not too controversial to go on saying that the best way to reduce that nasty (but not too nasty) LDL cholesterol is to eat a healthy diet and engage in effective exercise.

PS: haha I know this’ll be unreadable to most, but if anybody finds any egregious error in this, let me know.

References

Atherosclerosis video – Nucleus Medical Media (2009)

Atherosclerosis – pathophysiology, video by Armando Hasudungen (2014)

Atherosclerosis – part 1, Khan Academy video

https://www.ncbi.nlm.nih.gov/pubmed/15177118

https://training.seer.cancer.gov/anatomy/cardiovascular/blood/classification.html

Cholesterol metabolism part 1, video by Ben1994 (2015)

Cholesterol metabolism part 2, video by Ben1994 (2015)

Cholesterol metabolism part 3, video by Ben1994 (2015)

Written by stewart henderson

September 21, 2019 at 5:20 pm

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

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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

The statin controversy

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Never edit your own writing! Brian J Ford.

one thing thing you can be sure of – this claim (posted by a British chiropractor) is meaningless bullshit

I read Ben Goldacre’s quite demanding book Bad pharma some years ago, and that’s where I learned about statins, but I don’t recall much. I do recall that, not long after I read the book, I was at a skeptics meet-up when Dr Goldacre’s name came up. The man next to me started literally spitting chips at the mention – he was eating a massive bowl of chips and was grossly overweight (not that I’m assuming anything from this – just saying, haha). He roolly didn’t like Dr Goldacre. What went through my head was – some people may be really invested in having a magic pill that allows them to live forever and a day no matter what their diet or lifestyle.

I’ve just discovered that Goldacre has a new book out, entirely on this topic, which I intend to read, but my current decision to explore the issue is based on listening to Dr Maryanne Demasi’s talk, ‘statin wars – have we been misled by the evidence?’, available on YouTube. I very much recall the massive Catalyst controversy a few years ago, when a two-part special they did on statins led finally to the demise of the program. Without knowing any details, I thought this was a bit OTT, but when I heard Dr Norman Swann, a valued health professional and presenter of the ABC’s Health report, railing about the irresponsibility of the statin special, I frankly didn’t know what to think.

So statins are lipid-lowering medications that come in various flavours, including atorvastatin, fluvastatin, lovastatin and rosuvastatin. Lipitor, a brand name for atorvastatin manufactured by Pfizer, is the most profitable drug in the history of medicine. I’ve never taken statins myself, and I’m starting this piece as a more or less total beginner on the topic. I’ve read the Wikipedia entry on statins, which is quite comprehensive, with a very long reference list. Of course it’s not entirely comprehensible to a lay person, but that’s not a criticism – immunobiology and related research fields are complex. It’s also clearly pro-statin. It includes this interesting sentence:

 A systematic review co-authored by Ben Goldacre concluded that only a small fraction of side effects reported by people on statins are actually attributable to the statin.[63]

It’s interesting that Goldacre, and nobody else, is mentioned here as a co-author. It makes me wonder…

My only quibble, as a lay person, is that the positive effects of these statins, and their relatively few side-effects, seems almost too good to be true. I speak, admittedly, as a person who’s always been ultra-skeptical of ‘magic bullets’.

Which brings me to issues raised in Dr Demasi’s talk, and not addressed in the Wikipedia article. They include the idea, promoted by an ‘influential group’, that statin use should be prescribed for everyone over 50, regardless of cholesterol levels. Children with high cholesterol levels are being screened for statin use and Pfizer has apparently designed fruit-flavoured statis for use by children and adolescents. Others have suggested using statins as condiments in fast-food burgers, and even adding statins to the public water supply. It’s easy to see how such ‘innovations’ involve making scads of money, but this isn’t to deny that statins are effective in many if not most instances, and we should undoubtedly celebrate the work of the Japanese biochemist Akiro Endo, who pioneered the work on enzyme inhibitors that led to the discovery of mevastatin, produced by the fungus Penicillium citrinum.

But Demasi made some other interesting points, firstly about how drug companies like Pfizer might seek to maximise their profits. One obvious way is to widen the market – for example by lobbying for a lowering of the standard level of cholesterol in the blood considered dangerous. From the early 2000s in the US, ‘high cholesterol’ was officially shifted down from as high as 6.5 down to below 5, moving vast numbers of people onto having a ‘need’ for these cholesterol-lowering drugs. Demasi points out that this lowering wasn’t based on any new science, and that the body responsible for these decisions, the National Cholesterol Education Program (NCEP), was loaded with people with financial ties to the statin industry. To be fair, though, one might expect that doctors and specialists concerned with cholesterol to be invested, financially or otherwise, in ways of lowering it. They might also have felt, for purely scientific reasons, that the level of cholesterol considered dangerous was long overdue for adjustment.

Another change occurred in 2013 when two major heart health associations in the US decided to abandon a single number in terms of risk factors for heart disease/failure. Instead they looked at cholesterol, blood pressure, weight, diabetes and other factors to calculate ‘percentage risk’ of cardiovascular problems. They evaluated this risk so that if it was over 7.5% in the next 10 years, you should be prescribed a statin. A similar percentage risk system was used in the UK, but the statin prescription started at 20%. Why the huge discrepancy? Six months later, the Brits brought their threshold down to 10%. The US change brought almost 13 million people, mostly elderly, onto the radar for immediate statin prescription. The method of calculation in the US was independently analysed, and it was found that they over-estimated the risk, sometimes by over 100%. Erring on the side of caution? Or was there a lot of self-interest involved? It could fairly be a combination. The term for all this is ‘statinisation’, apparently. It’s attributed to John Ioannidis, a Stanford professor of medicine and a noted ‘scourge of sloppy science’. If you look up statinisation, you’ll find a storm of online articles of varying quality and temper on the issue – though most, I notice, are five years old or more. I’m not sure what that signifies, but I will say that, while we’ll always get the anti-science crowd baying against big pharma, vaccinations and GM poison, there’s a clear issue here about vested interests, and the need to, as Demasi says, ‘follow the money’.

This brings up the issue of how trials of these drugs are conducted, who pays for them, and who reviews them. According to Demasi, the vast majority of statin trials are funded by manufacturers. Clearly this is a vested interest, so trial results would need to be independently verified. But, again according to Demasi (and others such as Ioannidis and Peter Gotzsche, founder of the nordic Cochrane Collaboration) this is not happening, and ‘the raw data on statin side-effects has never been released to the public’ (Demasi, 2018). This data is held by the Cholesterol Treatment Triallists’ (CTT) collaboration, under the Clinical Trial Service Unit (CTSU) at Oxford Uni. According to Demasi, who takes a dim view of the CTT collaboration, they regularly release meta-analyses of data on statins which advocate for a widening of their use, and they’ve signed agreements with drug companies to prevent independent examination of research findings. All of this is described as egregious, which might seem fair enough, but Elizabeth Finkel, in a long-form article for Cosmos magazine in December 2014, takes a different view:

.. [the CTT] are a collaboration of academics and they do have access to the raw data. It is true that they do not share that data outside their collaboration and are criticised by other researchers who would like to be able to check their calculations. But the trialists fear mischief, especially from drug companies seeking to discredit the data of their rivals or from other people with vested interests. Explains [Professor Anthony] Keech, “the problem with ad hoc analyses are that they can use methods to produce a particular result. The most reliable analyses are the ones done using the methods we published in 1995. The rules were set out before we started.” And he points out these analyses are cross-checked by the academic collaborators: “Everything is replicated.”

As a regular reader of Cosmos I’m familiar with Finkel’s writings and find her eminently reliable, which of course leaves me more nonplussed than ever. I’m particularly disturbed that anyone would seriously claim that everyone over fifty (and will it be over forty in the future?) should be on these medications. I’m 63 and I take no medications at all, which I find a great relief, especially when I look at others my age who have mini-pharmacies in their homes. But then I’m one of those males who doesn’t visit doctors much and I have little idea about my cholesterol levels (well yes, they’ve been checked and doctors haven’t raised them to me as an issue). When you get examined, they usually find something wrong….

In her talk, Demasi made a comparison with the research on Tamiflu a few years ago, when Cochrane Collaboration researchers lobbied hard to be allowed to review trial data, and it was finally revealed, apparently, that it was certainly not as effective and side-effect free as its makers, Roche, claimed it to be. The jury is still out on Tamiflu, apparently. Whether it’s fair to compare the Tamiflu issue with the statin issue is a matter I can’t really adjudicate on, but if Finkel is to be believed, the CTT data is more solid.

There’s also an issue about more side effects being complained of by general users of statins – complaints made to their doctors – than side effects found in trials. This has already been referred to above, and is also described in Finkel’s article. Many of these complaints of side-effects haven’t been able to be sheeted home to statins, which suggests there’s possibly/probably a nocebo effect at play here. But Demasi suggests something more disturbing – that many subjects are eliminated from trials during a run-in period precisely because the drug disagrees with them, and so the trial proper begins only when many people suffering from side-effects are excluded. She also notes, I think effectively, that there is a lot of play with statistics in the advertising of statins (and other drugs of course) – for example a study which found that the risk of having a heart attack on statins was about 2% compared to 3% on placebos was being advertised as proving that your heart-attack risk on statins is reduced by a third. This appears to be dodgy – the absolute percentage difference is very small, and how is risk actually assessed? By the number of actual heart attacks over period x? I don’t know. And how many subjects were in the study? Were there other side-effects? But of course we shouldn’t judge the value of statins by advertising guff.

Another interesting attack on those expressing doubts about the mass prescription of statins has been to call them grossly irresponsible and even murderers. This seems strange to me. Of course doctors should be all about saving lives, but they should first of all be looking at prevention before cure as the best way of saving lives. Exercise (mental and physical) really is a great form of medicine, though of course not a cure-all, and diet comes second after exercise. Why the rush to medicalise? And none of the writers and clinicians supporting statins are willing to mention the financial bonanza accruing to their manufacturers and those who invest in them. Skepticism is the lifeblood of science, and the cheerleaders for statins should be willing to accept that.

Having said that, consider all the life-saving medications and procedures that have preceded statins, from antibiotics to vaccines to all the procedures that have made childbirth vastly safer for women – who cares now about the pharmaceutical and other companies and patentees who’ve made their fortunes from them? They’re surely more deserving of their wealth than the Donnie Trumps of the world.

So, that’s my initial foray into statins, and I’m sure the story has a way to go. In my next post I want to look at how statins work. I’ve read a couple of pieces on the subject, and they’ve made my head hurt, so in order to prevent Alzheimer’s I’m going to try an explanation in my own words – to teach myself. George Bernard Shaw wrote ‘those who can, do, those who can’t teach (it’s in Man and Superman). It’s one of those irritating memes, but I prefer the idea that people teach to learn, and learn to teach. That’s why I love teaching, and learning…

By the way, the quote at the top of this post seems irrelevant, but I keep meaning to begin my posts with quotes (it looks cool), so I’m starting now. To explain the quote – it was from a semi-rant by Ford in his introduction to the controversial dinosaur book Too big to walk (I’ve just started reading it), about writers not getting their work edited, peer reviewed and the like, and being proud or happy about this situation. This, he argues, helps account for all the rubbish on the net. It tickled me. I, of course, have no editor. It’s hard enough getting readers, let alone anyone willing to trawl through my dribblings for faults of fact or expression. Of course, I’m acutely aware of this, being at least as aware of my ignorance as Socrates, so I’ve tried to highlight my dilettantism and my indebtedness to others. I’m only here to learn. So Mr Ford, guilty as charged.

References

Dr Maryanne Demasi – Statin wars: Have we been misled by the evidence?

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

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

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

https://www.smithsonianmag.com/science-nature/what-is-the-nocebo-effect-5451823/

http://www.center4research.org/tamiflu-not-tamiflu/

Written by stewart henderson

September 9, 2019 at 9:44 pm

the Palestinian/Israeli tragedy – a timeline 1

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of course, this map was not created in the time of Jesus, when there would have been no marked boundaries and no clear agreements about territories

Every time I start writing about something I feel vaguely guilty that I’m not writing about something else. Pretty silly but there you go. I hope to get back to sciency stuff after this….

I’m going to try writing a timeline of events and data leading up to the current situation in Palestine/Israel, which will never be comprehensive but…

  • c9000 years ago the region we may now call Palestine or Israel didn’t have a clear name. It was inhabited by agricultural communities practising various religions. There was at least one concentrated centre, Jericho, regarded as one of the world’s oldest towns, successively inhabited for the past 11000 years.
  • c7000 years ago – evidence has recently been discovered that Jerusalem was inhabited at this time (the Chalcolithic era). The Israeli press made much of this, but there’s no evidence of course that Judaism dates back that far. I should add that, in considering the history of the people of the region, I make the reasonable assumption that ‘holy texts’ are propagandist and of extremely limited reliability.
  • c6000 years ago – the region from this time is generally known as Canaan, at least by historians and archaeologists – though the first known use of the term comes much later (we’re at the very beginnings of rudimentary writing). The inhabitants spoke a variety of Semitic languages and dialects. We’re talking here about a large region encompassing much of modern Israel, Lebanon, Syria and Jordan.
  • c4500 – 4000 years ago – the region’s population grew – it benefitted from but was also threatened by surrounding civilisations, such as the Egyptians to the south, the Sumerians and Akkadians in Mesopotamia, and later the Assyrians, Babylonians and other peoples. These infiltrating groups also influenced religious beliefs.
  • c3500 – 3000 years ago – small city states had developed, and the region, particularly in the south, came under increasing control of Egypt. one of the principal languages was Eblaite, in the north. The Hittites of Anatolia were another major influence. During this period, a number of towns and cities still known today came into being, or into prominence, including Sidon, Tyre, Haifa, Jaffa, Beirut and Hebron. The Canaanite religion, from which the Israelite religion essentially derived, was polytheistic but hierarchical, and among the many deities worshipped in a very diverse and volatile region were Dagon, Ba’al Hadad, Anat, Astarte, El Elyon and Moloch.
  • c2800 years ago – by this time there were a number of distinct kingdoms in the region, including Israel/Samaria, whose principal god was Yahweh, Judah (also Yahweh), Moab (Chemosh), Edom or Idumea (Qaus), and Ammon (Moloch). Each of these gods headed a pantheon of lesser gods.
  • c2700 years ago – around this time the Judaic religion began to take full form. Israel and Judah had become vassals of the Assyrian empire. Israel rebelled and its kingdom was destroyed. Refugees who fled to Judah, particularly the elite, promoted Yahweh as a supreme god, the only one to be worshipped. The sudden collapse of the Assyrian empire and the support of a new king of Judah (Josiah) helped the ‘reform’ to succeed. The old covenant, or treaty, between Judah and Assyria was replaced by a covenant with its new overlord, Yahweh. However, we cannot know how many people in the kingdom adhered to the new monotheism.
  • 586 BCE – the Babylonians sacked Judah’s capital, Jerusalem, and the elite were taken captive. It’s impossible to know how many lives were lost. It’s claimed that the ‘first temple’, supposedly built under the reign of Solomon, was destroyed at this time, but there is no evidence of the existence of this fabulous structure.
  • 539 BCE – the Persians under Cyrus the Great captured Babylon and many exiles returned to Judah. They regained control of the kingdom (now called Yehud) and brought with them a more ascetic, exclusivist form of the religion, very probably influenced by Zoroastrianism, a Persian form of monotheism. It was at this time that the Torah or Pentateuch was written. However, Yehud/Judah was now a part of the Persian Achaemenid empire, and remained so for over 200 years. The region was considerably smaller and less populated than suggested in Judaic holy texts – it was situated south of Samaria, bordering the Dead Sea to the east, but not quite stretching to the Mediterranean in the west.
  • 332 BCE – Alexander the Great conquered the region, but died shortly thereafter. The Ptolemies, descendants of one of Alexander’s generals, gained control of the region.
  • c 200BCE – another Greek dynasty, the Seleucids, based in Syria, gained control of the region. Clearly the people of the southern Levant region, among whom were people we might now call the Jews, had never really experienced autonomy, which might explain something of the modern situation. The Seleucids were keen to either suppress Judaism or to Hellenise it, leading to increased tensions with the ruling powers, and between traditional and ‘modernising’ Jews.
  • 167-160 BCE – This was the Period of the ‘Maccabean Revolt’, involving a series of battles which eventually led to a semi-autonomous Jewish state, the Hasmonean dynasty.
  • c110 BCE – with the weakening of the Seleucids, the Hasmonean dynasty became autonomous and expanded its territory into Samaria and Galilee in the north, Idumea to the south, and Perea and Iturea to the west. It should be noted however that this was a kingdom, not a religious state. The state was always reliant on more powerful states, such as the Roman Republic and the Parthian empire.
  • 63 BCE – the region became a client state of Rome after invasion, and the Jewish territory was again reduced. The Hasmonean dynasty came to an end in 37 BCE when Herod, an Idumean, took over the throne. The Hasmonean period has been used for propaganda purposes by Zionist nationalists to claim modern rights to the land governed by the Hasmoneans before the Roman invasion.
  • 6 CE – the first Roman governor/prefect of Judea – a Roman province – was appointed. The region was still a kingdom, but most power was in Roman hands.
  • 66-73 CE – during these years a major rebellion broke out against Roman rule. The second temple was destroyed by the forces of the future Roman Emperor, Titus, and the first major diaspora of Jews occurred – though Jews were already starting to migrate to Egypt, Anatolia and Mesopotamia.

Okay, this first part of the timeline, taking us to the beginnings of the Christian era, has clearly more information about the Jews and Judaism than about the other peoples of the region. That’s largely because there’s more information out there about the Jews than the other cultures/religions. It’s virtually impossible to get reliable information about the population of the region in toto, let alone the proportions of different peoples, their range of occupations, the number and sizes of towns, the degree of co-operation and rancour between disparate groups etc etc. In any case, we’ve now covered the period which the most hardline Zionist nationalists say is the basis of their claim to a Zionist monocultural state. From this point on, the Jewish diaspora will be a feature, as well as the ever-changing situation in and around the southern Levant, or Palestine.

Written by stewart henderson

September 4, 2019 at 10:50 am

random thoughts on human rights

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Over the years I’ve had arguments and discussions with people, and semi-disputes online, about the status of human rights, and rights in general. Some have been quite dismissive of their ‘mythical’ nature, others like Scott Attran have described them as a crazy, transcendental idea invented by a handful of Enlightenment figures back in the day, and boosted by the reaction to world wars in the 20th century. There have been objections by certain states claiming they don’t give sufficient cognisance to ‘Asian values’, and Moslem countries have argued that they need to be amended in accordance with Shar’ia Law.

The first point I would make is that, granted that rights are a human invention, that doesn’t make them ‘unreal’ or in some sense nugatory. Tables, chairs, buildings, computers, bombs, democracy and totalitarianism are all human inventions, but very real, if not all of equal value. To describe human rights as a form of transcendentalism also doesn’t make sense to me. Certainly if you say ‘God has granted certain inalienable rights…’ you’re using transcendental language, but that language is, I think, superfluous to the idea of rights, which, I would argue, is grounded in both empiricism and pragmatism.

I would also argue, no doubt more controversially, that human rights make little sense if based entirely on the individual. They are principally about human relations, and so imply that each individual is part of a larger social entity, within which they may be accorded ‘freedoms from’ and ‘freedoms to’. Aristotle puts the point well in his Politics:

the individual, when isolated, is not self-sufficing; and therefore he is like a part in relation to the whole. But he who is unable to live in society, or who has no need because he is sufficient for himself, must be either a beast or a god: he is no part of a state.

It follows that rights must be under the guardianship of states and enshrined in and upheld by their laws. This is vital because individuals often have competing interests, and it’s sometimes the case that particular individuals don’t recognise or understand that there’s a common, social interest beyond their own. This is the difficulty with rights – because we often think of them as my rights or my freedoms, we fail to understand that these rights, though granted in some sense to individuals, must be based on the thriving of the wider social sector, whether we’re referring to village, tribe or state. And it is to these larger social entities – states, or civilisations – that we owe our phenomenal success as a species, for better or worse.

This raises a question of whether the best human rights should flow from the best states, or vice versa. Interestingly, Aristotle and his students collected some 150 constitutions from the world of Greek poleis or city-states in order to devise the best, most ‘thriving’ city-state possible, which of course should have involved comparing the constitutions with the situation on the ground in those city-states. We don’t know if any such comparison was made (it’s very doubtful), but it does suggest that Aristotle thought that the state, via its constitution, was the engine of a thriving citizenry rather than the other way around.

Turning to rights in the modern world, the unfortunate claim by Tom Paine in his Rights of man (1791) that ‘rights are inherently in all the inhabitants’ of a state, has helped to create the confusion about rights being ‘natural’ to humans, like having two legs and a complex prefrontal cortex (the latter being largely the result of living in increasingly complex and organised society). If we’re to take human rights seriously, we need to be honest about their a posteriori nature. They need to be seen as the result of our understanding of how to create an environment that best suits us, as the most socially constructed mammals on the planet. In that respect, we’ve come a long way, not only from Aristotle (who excluded women and slaves from his citizenry), but also from the the late eighteenth century revolutionaries (who executed Olympe de Gouges for daring to even suggest adding women to the rights-owning citizenry of her own nation). Indeed, examining the issue of rights historically should remind us that they need to be updated on the basis of our ongoing advances in knowledge. The 1948 Universal Declaration of Human Rights, by this understanding, should certainly not be fixed in stone.

My views, of course clash with ‘natural law’ notions of human rights, which tend to be based on the individual an sich, and have claims to be outside of social or temporal considerations.

If we try to think of rights as ‘natural’ or self-evident, rather than something we construct to help us understand what we owe to, and might expect from, the best of civil states, we might well agree with Alasdair McIntyre’s view that there’s nothing natural or self-evident, say, about allowing people, by right, the freedom to express or live by their religious views. Many religious views are notoriously idiosyncratic and sometimes offensive from an outsider’s perspective, and adding the ‘no harm’ principle doesn’t suffice to smooth things over. The jury is very much out as to whether religion is, or has been, a benefit to society, but it’s well known that some religions have, in the past, engaged in human sacrifices. And even today new religions might crop up which may involve practices that the majority would find inimical both to individual and social well-being. And of course the very definition of religion is far from being self-evident. Article 18 of the Universal Declaration of Human Rights, states:

Everyone has the right to freedom of thought, conscience and religion; this right includes freedom to change his religion or belief, and freedom, either alone or in community with others and in public or private, to manifest his religion or belief in teaching, practice, worship and observance.

However, it makes no attempt to define religion, and in the same Article it claims the right of all to ‘manifest his… belief…in practice and observance’. This, if taken literally, is absurd, as a person might hold a belief that slave-owning is okay, and is given the green light by this Article to ‘manifest that belief in practice.. and observance’. No doubt my criticism doesn’t capture the liberal ‘spirit’ of the Article, but it does highlight an obvious problem. People do act on beliefs, and many actions, based on those beliefs, can be harmful, and subject to criminal prosecution. The law, of course, prosecutes acts, not thoughts, so we know that we’re free to think what we want – we don’t need a ‘right’ to protect this. I won’t try to define religion, but at least it seems to involve both beliefs and actions. Actions will be subject to civil and criminal law, so it might be argued that rights don’t find a place there. Beliefs are private unless and until they’re acted on, in which case they’ll be subject to law. So there’s a question whether rights have a place there also.

The more I look at human rights, the more difficulties I see. Let me take, more or less at random, Article 21 of the UDHR:

(1) Everyone has the right to take part in the government of his country, directly or through freely chosen representatives.
(2) Everyone has the right of equal access to public service in his country.
(3) The will of the people shall be the basis of the authority of government; this will shall be expressed in periodic and genuine elections which shall be by universal and equal suffrage and shall be held by secret vote or by equivalent free voting procedures.

Section 3 here reads like a directive, but I agree that every member of a state should be allowed at least the opportunity to cast a vote for government. In Australia, voting is compulsory for eligible parties, as it is in some 22 countries (though enforced in only 11). It’s questionable whether compulsion accords with human rights and freedoms, but given the socially constructed nature of humanity, voting should definitely be encouraged as a duty, at the very least. The ideal, of course, would be that everybody is aware of what they owe to the state, and their interest in creating and maintaining a state that is beneficial to the whole and so to themselves as a part.

There is no doubt in my mind that participatory democracies make for better states than any alternatives, and if this can be bolstered by human rights language that is fine, though I think that interest and duty (what we owe to ourselves and others) makes more sense as an argument. The ‘Asian values’ objection here (revisited recently by the Chinese oligarchy) is bogus and self-serving, as evidenced by the success of democratic nations such as Japan, South Korea and Taiwan. There is a tendency in Asian nations to be more collectivist in thinking and behaviour than in many European nations, and especially the USA, but this would make them more attracted to participatory democracy, not less.

Concluding remarks – the more I look at rights, the more questionable I find them. I would rather encourage a neo-Aristotelian way of thinking. We’re now political animals more than ever, in a wider sense than Aristotle saw it, because civilisation itself is political, and civilisation is hardly something we can opt out of. I don’t advocate world government – that was an impossible if admirable ideal – but I certainly advocate intergovernmental co-operation as opposed to zero sum nationalism. We need to make an all-out effort to improve our state structures and understanding between them for the sake of all their members (and the rest of the biosphere).

Written by stewart henderson

August 31, 2019 at 8:44 am

Bayesian probability, sans maths (mostly)

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Bayesian stuff – it gets more complicated, apparently

Okay time to get back to sciency stuff, to try to get my head around things I should know more about. Bayesian statistics and probability have been brought to the periphery of my attention many times over the years, but my current slow reading of Daniel Kahneman’s Thinking fast and slow has challenged me to master it once and for all (and then doubtless to forget about it forevermore).

I’ve started a couple of pieces on this topic in the past week or so, and abandoned them along with all hope of making sense of what is no doubt a doddle for the cognoscenti, so I clearly need to keep it simple for my own sake. The reason I’m interested is because critics and analysts of both scientific research and political policy-making often complain that Bayesian reasoning is insufficiently utilised, to the detriment of such activities. I can’t pretend that I’ll be able to help out though!

So Thomas Bayes was an 18th century English statistician who left a theorem behind in his unpublished papers, apparently underestimating its significance. The person most responsible for utilising and popularising Bayes’ work was the French polymath Pierre-Simon Laplace. The theorem, or rule, is captured mathematically thusly:

{\displaystyle P(A\mid B)={\frac {P(B\mid A)P(A)}{P(B)}}}

where A and B are events, and P(B), that is, the probability of event B, is not equal to zero. In statistics, the probability of an event’s occurrence ranges from 0 to 1 – meaning zero probability to total certainty.

I do, at least, understand the above equation, which, wordwise, means that the probability of A occurring, given that B has occurred, is equal to the probability of B occurring, given that A has occurred, multiplied by the probability of A’s occurrence, all divided by the probability of B’s occurrence. However, after tackling a few video mini-lectures on the topic I’ve decided to give up and focus on Kahneman’s largely non-mathematical treatment with regard to decision-making. The theorem, or rule, presents, as Kahneman puts it, ‘the logic of how people should change their mind in the light of evidence’. Here’s how Kahneman first describes it:

Bayes’ rule specifies how prior beliefs… should be combined with the diagnosticity of the evidence, the degree to which it favours the hypothesis over the alternative.

D Kahneman, Thinking fast and slow, p154

In the most simple example – if you believe that there’s a 65% chance of rain tomorrow, you really need to believe that there’s a 35% chance of no rain tomorrow, rather than any alternative figure. That seems logical enough, but take this example re US Presidential elections:

… if you believe there’s a 30% chance that candidate x will be elected President, and an 80% chance that he’ll be re-elected if he wins first time, then you must believe that the chances that he will be elected twice in a row are 24%.

This is also logical, but not obvious to a surprisingly large percentage of people. What appears to ‘throw’ people is a story, a causal narrative. They imagine a candidate winning, somewhat against the odds, then proving her worth in office and winning easily next time round – this story deceives them into defying logic and imagining that the chance of her winning twice in a row is greater than that of winning first time around – which is a logical impossibility. Kahneman places this kind of irrationalism within the frame of system 1 v system 2 thinking – roughly equivalent to intuition v concentrated reasoning. His solution to the problem of this kind of suasion-by-story is to step back and take greater stock of the ‘diagnosticity’ of what you already know, or what you have predicted, and how it affects any further related predictions. We’re apparently very bad at this.

There are many examples throughout the book of failure to reason effectively from information about base rates, often described as ‘base-rate neglect’. A base rate is a statistical fact which should be taken into account when considering a further probability. For example, when given information about the character of a a fictional person T, information that was deliberately designed to suggest he was stereotypical of a librarian, research participants gave the person a much higher probability of being a librarian rather than a farmer, even though they knew, or should have known, that the number of persons employed as farmers was higher by a large factor than those employed as librarians (the base rate of librarians in the workforce). Of course the degree to which the base rate was made salient to participants affected their predictions.

Here’s a delicious example of the application, or failure to apply, Bayes’ rule:

A cab was involved in a hit-and-run at night. Two cab companies, Green Cabs and Blue Cabs, operate in the city. You’re given the following data:

– 85% of the cabs in the city are Green, 15% are Blue.

– A witness identified the cab as Blue. The court tested the reliability of the witness under the circumstances that existed on the night of the accident and concluded that the witness correctly identified each one of the two colours 80% of the time and failed 20% of the time.

What is the probability that the car involved in the accident was Blue rather than Green?

D Kahneman, Thinking fast and slow, p166

It’s an artificial scenario, granted, but if we accept the accuracy of those probabilities, we can say this: given that the base rate of Blue cars is 15%, and the probability of the witness identifying the car accurately is 80%, we have this figure for the dividend – (.15/.85) x (.8/.2) =.706. Dividing this by the range of probabilities plus the dividend (1.706) gives approximately 41%.

So how close were the research participants to this figure? Most participants ignored the statistical data – the base rates – and gave the figure of 80%. They were more convinced by the witness. However, when the problem was framed differently, by providing causal rather than statistical data, participants’ guesses were more accurate. Here’s the alternative presentation of the scenario:

You’re given the following data:

– the two companies operate the same number of cabs, but Green cabs are involved in 85% of accidents

– the information about the witness is the same as previously presented

The mathematical result is the same, but this time the guesses were much closer to the correct figure. The difference lay in the framing. Green cabs cause accidents. That was the fact that jumped out, whereas in the first scenario, the fact that most clearly jumped out was that the witness identified the offending car as Blue. The statistical data in scenario 1 was largely ignored. In the second scenario, the witness’s identification of the Blue car moderated the tendency to blame the Green cars, whereas in scenario 1 there was no ‘story’ about Green cars causing accidents and the blame shifted almost entirely to the Blue cars, based on the witness’s story. Kahneman named his chapter about this tendency ‘Causes trump statistics’.

So there are causal and statistical base rates, and the lesson is that in much of our intuitive understanding of probability, we simply pay far more attention to causal base rates, largely to our detriment. Also, our causal inferences tend to be stereotyped, so that only if we are faced with surprising causal rates, in particular cases and not presented statistically, are we liable to adjust our probabilistic assessments. Kahneman presents some striking illustrations of this in the research literature. Causal information creates bias in other areas of behaviour assessment too, of course, as in the phenomenon of regression to the mean, but that’s for another day, perhaps.

Written by stewart henderson

August 27, 2019 at 2:52 pm