Archive for the ‘biology’ Category
another look at free will, with thanks to Robert Sapolsky
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has a natural ability to excel at every sport, that one is eternally clumsy and uncoordinated; this girl is shy and withdrawn, that one’s a noisy show-off, etc etc.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/
more about ozone, and the earth’s greatest extinction event
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.
What’s up with Trump’s frontal cortex? – part 1
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.
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.
some stuff about dinosaurs and their relationship to birds
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.
Always chemical: how to reflect upon naturopathic remedies
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:
- Is it absorbed into the body at all?
- Does enough reach the right part of the body to have an effect?
- Does it actually work for the condition?
- Does it have any hazardous, unwanted effects?
- 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.
How do trees transport water such long distances? Part 2: the mechanism remains a mystery (to me)
and I still haven’t found what I’m looking for…
So scientists have learned a lot, though not everything, about water’s travels from soil to leaf in a plant or tree. It’s a fascinating story, and I’m keen to learn more. But the real mystery for me is about energy. As the excellent Nature article, upon which I’m mostly relying, points out, animals have a pump-based circulatory system to distribute nutrients, oxygen and so forth, but plants are another matter, or another form of organised matter.
I actually posed two questions in my last post. How do plants – and I think I should specify trees here, because the massive distance between the soil and their top leaves makes the problem more dramatic – move water such large distances, and how do they know they have to transport that water and how much water to transport?
So let’s look at the Nature Education explanation:
The bulk of water absorbed and transported through plants is moved by negative pressure generated by the evaporation of water from the leaves (i.e., transpiration) — this process is commonly referred to as the Cohesion-Tension (C-T) mechanism. This system is able to function because water is “cohesive” — it sticks to itself through forces generated by hydrogen bonding. These hydrogen bonds allow water columns in the plant to sustain substantial tension (up to 30 MPa when water is contained in the minute capillaries found in plants), and helps explain how water can be transported to tree canopies 100 m above the soil surface.
Notice how we’re again returning to the explanations questioned by Wohlleben – transpiration and capillary action. But we’re introduced to something new – the C-T mechanism. The thesis is that water’s cohesiveness through hydrogen bonding creates a tension (the tension that makes for capillary action) that enables water to be shifted up to 100 metres – all because of the minuteness of capillaries found in plants. And trees? Somehow, I just can’t see it. Perhaps the key is in the phrase ‘helps explain’. There must surely be more to this. The thesis also mentions ‘negative pressure’ generated by transpiration. This is the signalling I wrote about before. Somehow the plant’s chemistry recognises that there’s an imbalance, and of course this happens in all living things, regardless whether they have a complex nervous system. So maybe there’s no need to worry about ‘knowing’. All living organisms respond to their ever-changing environment by altering their internal chemistry, by opening or closing barriers, by selectively adding or subtracting nutrients, and there are unknowns everywhere about precisely how they do that. It’s a kind of organised chemistry that seems like everyday magic from the outside, whether we’re focusing on a beech tree or our own intestines.
The C-T mechanism is only new to me I should add. It can actually be traced back to 1727 and a book by Stephen Hales, in which he pointed out that without what he called perspiration the water in a plant would stagnate, and that it was also required to allow for the capillary movement of water, because ‘the sap-vessels are so curiously adapted by their exceeding fineness, to raise [water] to great heights, in a reciprocal proportion to their very minute diameters’. But this ‘reciprocal proportion’, according to Wohlleben, as quoted in the last post, can only account for a maximum of 3 feet of upward force in ‘even the narrowest of vessels’.
The water transport system, referred to in the last post as the water potential difference or gradient, also has another name, the Soil Plant Atmosphere Continuum (SPAC). I also mentioned something about an ‘apoplastic pathway’. Water enters the tree by the roots, which are divided and subdivided much like branches and twigs above-ground, with the thinnest examples being the fine root hairs. Water enters through the semi-permeable cell walls by osmosis. Cell-to-cell osmosis carries the water deeper into the root system, and thence into an apoplastic pathway. According to this video, this pathway provides an uninterrupted flow of water (no cell wall barriers) which allows a mass flow ‘due to the adhesive and cohesive properties of water’. This is the cohesion-tension theory again. Apparently, due to evaporation, a tension is created in the apoplast’s continuous stream, leading to this ‘mass flow’.
This makes absolutely no sense to me. What I’m so far discovering is that it’s pretty hard to start from scratch as an amateur/dilettante and get my head around all this stuff, and in my reading and video-watching I’ve yet to find a straightforward answer to the how of long distance, fast transport of water in plants/trees – there probably isn’t one.
I’ll try again after a diet of videos – so far I’ve found a large number of videos in Indian English, and their accents defeat me, I’m sad to say. No transcripts available. Meanwhile, I’ve compiled a little glossary (from various sources) to help myself…
apoplast – within plants, the space outside the plasma membrane within which material can diffuse freely. It is interrupted by the Casparian strip in roots, by air spaces between plant cells and by the plant cuticle.
Casparian strip – a band of cell wall material deposited in the radial and transverse walls of the endodermis, which is chemically different from the rest of the cell wall – the cell wall being made of lignin and without suberin – whereas the Casparian strip is made of suberin and sometimes lignin.
cortical cells – in plants, cells of the cortex, the outer layer of the stem or root of a plant, bounded on either side by the epidermis (outer) and the endodermis (inner).
exudation – An exudate is a fluid emitted by an organism through pores or a wound, a process known as exuding.
guttation – water loss, when water or sap collects (at times of low evaporation, dawn & dusk), at tips of grass, herbs (not to be confused with dew, caused by condensation).
hydrostatic pressure – the pressure exerted by a fluid at equilibrium at a given point within the fluid, due to the force of gravity. This increases in proportion to depth measured from the surface because of the increasing weight of fluid exerting downward force from above.
lignin – a class of complex organic polymers that form important structural materials in the support tissues of vascular plants and some algae. Lignins are particularly important in the formation of cell walls, especially in wood and bark, because they lend rigidity and do not rot easily.
osmosis – the movement of water from an area of high to low concentration through a semi-permeable membrane. ‘Pumps’ in the cell membrane transport the specific ions into the cell which means water moves in by osmosis thus maintaining hydrostatic pressure.
phloem – the living tissue that transports the soluble organic compounds made during photosynthesis and known as photosynthates, in particular the sugar sucrose, to parts of the plant where needed. This transport process is called translocation.
plasmodesmata – narrow threads of cytoplasm that pass through the cell walls of adjacent plant cells and allow communication between them.
root pressure – the transverse osmotic pressure within the cells of a root system that causes sap to rise through a plant stem to the leaves. Root pressure occurs in the xylem of some vascular plants when the soil moisture level is high either at night or when transpiration is low during the day
sap – a fluid transported in xylem cells (vessel elements or tracheids) or phloem sieve tube elements of a plant. These cells transport water and nutrients throughout the plant.
suberin – an inert impermeable waxy substance present in the cell walls of corky tissues. Its main function is as a barrier to movement of water and solutes.
symplast – the network of cytoplasm of all cells interconnected by plasmodesmata. The movement of water occurs from one cell to another through plasmodesmata
tracheid – a type of water-conducting cell in the xylem which lacks perforations in the cell wall.
vascular (plants) – also known as tracheophytes and also higher plants, form a large group of plants (over 300,000 accepted known species) that are defined as those land plants that have lignified tissues (the xylem) for conducting water and minerals throughout the plant.
xylem – one of the two types of transport tissue in vascular plants, phloem being the other. The basic function of xylem is to transport water from roots to shoots and leaves, but it also transports some nutrients.
On the Trump’s downfall. What a memo. One wonders if the DoJ is running out of patience with the wannabe dictator and his imbecilities, which may bring things to a head sooner rather than later. But those in the know say that Mueller is always thorough and unlikely to be distracted, so I shouldn’t project my own impatience onto him. Dog give me strength to suffer the horrorshow for a while longer.
How do plants transport water? Part 1: xylem, transpiration and a mysterious water potential difference
roots, xylem, upward flow, transpiration – but how does it work? Find out in the next thrilling episode, maybe.
Stolen from Nature Education, with apologies
This post could fit well in the ‘How Stuff Works’ series, always a useful resource, but I doubt if they’ve done a piece on today’s subject. Maybe I’ll check later.
I’ve been reading a book called The hidden life of trees, by Peter Wohlleben, a Chrissy present from a good friend. One of its shortest chapters is titled ‘The mysteries of moving water’. The reason for its brevity is essentially that there’s as yet no solution to the mystery of how water gets from the soil to the leaves of a tree, or any plant for that matter. At least, according to Wohlleben.
This strikes me as amazing, if true. After all, it’s a simple, everyday scenario for any home gardener. You notice on a hot summer day that the leaves of your capsicum plant are wilting. You apply a two-litre dose of H2O to the base, et voilà, within an hour or two (I don’t know, I’ve never timed it), those leaves have become as turgid as much of my writing. And it just may cross your mind that it’s pretty miraculous how plants can do that. But if it’s true that we don’t know how plants manage such an everyday miracle, surely working it out is Nobel Prizeworthy for any ambitious team of botanico-chemists out there, or whatever.
Of course it’s much more likely that botanists have been trying to solve this mystery for decades – isn’t it? But before I look into it, here’s what Wohlleben says in his book:
…water transport is a relatively simple phenomenon to research – simpler at any rate than investigating whether trees feel pain or how they communicate with one another – and because it appears so uninteresting and obvious, university professors have been offering simplistic explanations for decades… Here are the accepted answers: capillary action and transpiration.
Upon reading this I tried to recall what I knew of these terms. With capillary action I drew a blank, though I feel sure I knew about it once. Transpiration, though, was clear enough: it was like perspiration, the evaporation of water from the leaves, rather than the skin (or is perspiration the secretion of water through the pores rather than the evaporation? Later). So transpiration is only about the movement of water from the surface of a leaf to the atmosphere by means of solar energy; it surely has nothing to do with movement through the stem or trunk, though the loss of water from the leaves is presumably a signal to the plant to draw up more water from the earth, but how can we talk of signals when a plant has no brain or command centre to receive them? And how can water be ‘drawn up’ when it has no muscle power or other obvious energy source?
As to capillary action, Wohlleben explains:
Capillary action is what makes the surface of your coffee stand a few fractions of an inch higher than the edge of your cup. Without this force, the surface of the liquid would be completely flat. The narrower the vessel, the higher the liquid can rise against gravity. And the vessels that transport water in deciduous trees are very narrow indeed: they measure barely 0.02 inches across. Conifers restrict the diameter of their vessels even more, to 0.0008 inches. Narrow vessels, however, are not enough to explain how water reaches the crown of trees that are more than 300 feet tall. In even the narrowest of vessels, there is only enough force to account for a rise of 3 feet at most.
Needless to say, plenty of research has been done on the subject of water transport in plants, but I have to agree with Wohlleben that there’s a lot that’s missing. The key to the process is a material called xylem, a structure made from hollow, dead, reinforced cells. Here’s how a BBC science site tries to explain it:
Transpiration explains how water moves up the plant against gravity in tubes made of dead xylem cells without the use of a pump.
Water on the surface of spongy and palisade cells (inside the leaf) evaporates and then diffuses out of the leaf. This is called transpiration. More water is drawn out of the xylem cells inside the leaf to replace what’s lost.
As the xylem cells make a continuous tube from the leaf, down the stem to the roots, this acts like a drinking straw, producing a flow of water and dissolved minerals from roots to leaves.
Water doesn’t flow upwards, however. It has to be pumped up, or sucked, as we do when we apply our lips and energy to a straw. The BBC also describes the whole process as transpiration, which just seems wrong to me. Obviously much transpires here, but it isn’t just transpiration. What?
What obviously needs explaining is where the energy comes from to draw the water up against gravity, and how the plant ‘knows’ that water needs replenishing.
A more comprehensive, and richly referenced, attempt at an explanation is provided by Nature, the well-known science magazine, on one of its educational websites. There we’re told that ‘plants retain less than 5% of the water absorbed by roots for cell expansion and plant growth’. This is fascinating, as is the reason for the lack of retention – photosynthesis. Water is lost to the atmosphere from the leaves’ stomata, which are like our pores. These stomata are used to absorb CO2 for the photosynthesis of sugars, but their openness to CO2 increases the transpiration rate, so there’s a tricky balance between the two – water loss versus CO2 and sugar gain.
The xylem mentioned above doesn’t reach down all the way to the base of the root system. First the water must pass through several cell layers that act as a filtration system. But how does it do this? What is the force being applied and where does it come from? The Nature article gives this complex explanation:
The relative ease with which water moves through a part of the plant is expressed quantitatively using the following equation:
Flow = Δψ / R,
which is analogous to electron flow in an electrical circuit described by Ohm’s law equation:
i = V / R,
where R is the resistance, i is the current or flow of electrons, and V is the voltage. In the plant system, V is equivalent to the water potential difference driving flow (Δψ) and i is equivalent to the flow of water through/across a plant segment. Using these plant equivalents, the Ohm’s law analogy can be used to quantify the hydraulic conductance (i.e., the inverse of hydraulic R) of individual segments (i.e., roots, stems, leaves) or the whole plant (from soil to atmosphere).
Got that? I may be wrong, but isn’t this just an analogy? Don’t analogies tend to break down with a little bit of analytic pressure? The idea of hydraulic conductance is clearly drawn from electrical conductance, but electrical conductance relies on a power source, doesn’t it? What is the plant’s power source? Yes, I can see that certain parts of the plant have a greater resistance to the water’s mostly upward movement than others, and that this resistance is measurable by examining the time it takes for water to pass through the different parts with their particular structure and chemistry, but it says nothing about the energy source. In Ohm’s law, V, voltage is the amount of power, which comes from a source of that power, such as a battery. In the above analogy, Δψ is described as the water potential difference that drives flow. I’m possibly being dumb, but how does that happen? What’s meant by ‘water potential difference’?
The Nature article, I must say, is very good at telling us about the materials and obstacles negotiated by water molecules on their journey. First they pass through the root’s epidermis, then the cortex and the endodermis and then on to the xylem. They travel by an apoplastic pathway (more of that next time), or else a cell-to-cell pathway (C-C), and the role of ‘water-specific protein channels embedded in cell membranes (i.e., aquaporins)’ is mentioned, but this role is apparently still much of a mystery. Anyway, the xylem continues into the petiole, to which the leaves are attached, and then into the mid-rib, the main central vein of the leaf. From there the water passes into the smaller branching veins of a dicot leaf, which also contain tracheids – elongated xylem cells for the transport of water and mineral salts. It’s from this network of veins that transpiration takes place.
So I’m learning a lot, but the ‘water potential gradient’ and how it pulls or pushes water upwards, that’s still very much a mystery to me. But there’s more to come.
References
Peter Wohlleben, The hidden life of trees, Collins 2017
Ok, the usual update on Trump’s downfall. Some are saying that the Mueller enquiry is winding up (and I’m not talking about GOP hardheads), but I’m hoping not, because I reckon the financial stuff alone will take years to wade through properly. In the meantime though, I’m hoping that more really dramatic developments occur to light a fire under Trump’s capacious backside, sooner rather than later. The latest news is that the Mueller team are looking at the cover-up re Trump Jr’s meeting with Russian agents. So maybe the cover-ups and the endless obstructing will lead to some justice action soon, while the ‘follow the money’ aspect will continue for some time, and hopefully do the really lasting and permanent damage to the Trump horrorshow.
how evolution was proved to be true
The origin of species is a natural phenomenon
Jean-Baptiste Lamarck
The origin of species is an object of inquiry
Charles Darwin
The origin of species is an object of experimental investigation
Hugo de Vries
(quoted in The Gene: an intimate history, by Siddhartha Mukherjee)
Gregor Mendel
I’ve recently read Siddhartha Mukherjee’s monumental book The Gene: an intimate history, a work of literature as well as science, and I don’t know quite where to start with its explorations and insights, but since, as a teacher to international students some of whom come from Arabic countries, I’m occasionally faced with disbelief regarding the Darwin-Wallace theory of natural selection from random variation (usually in some such form as ‘you don’t really believe we come from monkeys do you?’), I think it might be interesting, and useful for me, to trace the connections, in time and ideas, between that theory and the discovery of genes that the theory essentially led to.
One of the problems for Darwin’s theory, as first set down, was how variations could be fixed in subsequent generations. And of course another problem was – how could a variation occur in the first place? How were traits inherited, whether they varied from the parent or not? As Mukherjee points out, heredity needed to be both regular and irregular for the theory to work.
There were few clues in Darwin’s day about inheritance and mutation. Apart from realising that it must have something to do with reproduction, Darwin himself could only half-heartedly suggest an unoriginal notion of blending inheritance, while also leaning at times towards Lamarckian inheritance of acquired characteristics – which he at other times scoffed at.
Mukherjee argues here that Darwin’s weakness was impracticality: he was no experimenter, though a keen observer. The trouble was that no amount of observation, in Darwin’s day, would uncover genes. Even Mendel was unable to do that, at least not in the modern DNA sense. But in any case Darwin lacked Mendel’s experimental genius. Still, he did his best to develop a hypothesis of inheritance, knowing it was crucial to his overall theory. He called it pangenesis. It involved the idea of ‘gemmules’ inhabiting every cell of an organism’s body and somehow shaping the varieties of organs, tissues, bones and the like, and then specimens of these varied gemmules were collected into the germ cells to produce ‘mixed’ offspring, with gemmules from each partner. Darwin describes it rather vaguely in his book The Variation of Animals and Plants under Domestication, published in 1868:
They [the gemmules] are collected from all parts of the system to constitute the sexual elements, and their development in the next generation forms the new being; but they are likewise capable of transmission in a dormant state to future generations and may then be developed.
Darwin himself admitted his hypothesis to be ‘rash and crude’, and it was effectively demolished by a very smart Scotsman, Fleeming Jenkin, who pointed out that a trait would be diluted away by successive unions with those who didn’t have it (Jenkin gave as an example the trait of whiteness, i.e. having ‘white gemmules’, but a better example would be that of blue eyes). With an intermingling of sexual unions, specific traits would be blended over time into a kind of uniform grey, like paint pigments (think of Blue Mink’s hit song ‘Melting Pot’).
Darwin was aware of and much troubled by Jenkin’s critique, but he (and the scientific world) wasn’t aware that a paper published in 1866 had provided the solution – though he came tantalisingly close to that awareness. The paper, ‘Experiments in Plant Hybridisation’, by Gregor Mendel, reported carefully controlled experiments in the breeding of pea plants. First Mendel isolated ‘true-bred’ plants, noting seven true-bred traits, each of which had two variants (smooth or wrinkled seeds; yellow or green seeds; white or violet coloured flowers; flowers at the tip or at the branches; green or yellow pods; smooth or crumpled pods; tall or short plants). These variants of a particular trait are now known as alleles.
Next, he began a whole series of painstaking experiments in cross-breeding. He wanted to know what would happen if, say, a green-podded plant was crossed with a yellow-podded one, or if a short plant was crossed with a tall one. Would they blend into an intermediate colour or height, or would one dominate? He was well aware that this was a key question for ‘the history of the evolution of organic forms’, as he put it.
He experimented in this way for some eight years, with thousands of crosses and crosses of crosses, and the more the crosses multiplied, the more clearly he found patterns emerging. The first pattern was clear – there was no blending. With each crossing of true-bred variants, only one variant appeared in the offspring – only tall plants, only round peas and so on. Mendel named them as dominant traits, and the non-appearing ones as recessive. This was already a monumental result, blowing away the blending hypothesis, but as always, the discovery raised as many questions as answers. What had happened to the recessive traits, and why were some traits recessive and others dominant?
Further experimentation revealed that disappeared traits could reappear in toto in further cross-breedings. Mendel had to carefully analyse the relations between different recessive and dominant traits as they were cross-bred in order to construct a mathematical model of the different ‘indivisible, independent particles of information’ and their interactions.
Although Mendel was alert to the importance of his work, he was spectacularly unsuccessful in alerting the biological community to this fact, due partly to his obscurity as a researcher, and partly to the underwhelming style of his landmark paper. Meanwhile others were aware of the centrality of inheritance to Darwin’s evolutionary theory. The German embryologist August Weismann added another nail to the coffin of the ‘gemmule’ hypothesis in 1883, a year after Darwin’s death, by showing that mice with surgically removed tails – thus having their ‘tail gemmules’ removed – never produced tail-less offspring. Weismann presented his own hypothesis, that hereditary information was always and only passed down vertically through the germ-line, that’s to say, through sperm and egg cells. But how could this be so? What was the nature of the information passed down, information that could contain stability and change at the same time?
The Dutch botanist Hugo de Vries, inspired by a meeting with Darwin himself not long before the latter’s death, was possessed by these questions and, though Mendel was completely unknown to him, he too looked for the answer through plant hybridisation, though less systematically and without the good fortune of hitting on true-breeding pea plants as his subjects. However, he gradually became aware of the particulate nature of hereditary information, with these particles (he called them ‘pangenes’, in deference to Darwin’s ‘pangenesis’), passing down information intact through the germ-line. Sperm and egg contributed equally, with no blending. He reported his findings in a paper entitled Hereditary monstrosities in 1897, and continued his work, hoping to develop a more detailed picture of the hereditary process. So imagine his surprise when in 1900 a colleague sent de Vries a paper he’d unearthed, written by ‘a certain Mendel’ from the 1860s, which displayed a clearer understanding of the hereditary process than anyone had so far managed. His response was to rush his own most recent work into press without mentioning Mendel. However, two other botanists, both as it happened working with pea hybrids, also stumbled on Mendel’s work at the same time. Thus, in a three-month period in 1900, three leading botanists wrote papers highly indebted to Mendel after more than three decades of profound silence.
Hugo de Vries
The next step of course, was to move beyond Mendel. De Vries, who soon corrected his unfair treatment of his predecessor, sought to answer the question ‘How do variants arise in the first place?’ He soon found the answer, and another solid proof of Darwin’s natural selection. The ‘random variation’ from which nature selected, according to the theory, could be replaced by a term of de Vries’ coinage, ‘mutation’. The Dutchman had collected many thousands of seeds from a wild primrose patch during his country rambles, which he planted in his garden. He identified some some 800 new variants, many of them strikingly original. These random ‘spontaneous mutants’, he realised, could be combined with natural selection to create the engine of evolution, the variety of all living things. And key to this variety wasn’t the living organisms themselves but their units of inheritance, units which either benefitted or handicapped their offspring under particular conditions of nature.
The era of genetics had begun. The tough-minded English biologist William Bateson became transfixed on reading a later paper of de Vries, citing Mendel, and henceforth became ‘Mendel’s bulldog’. In 1905 he coined the word ‘genetics’ for the study of heredity and variation, and successfully promoted that study at his home base, Cambridge. And just as Darwin’s idea of random variation sparked a search for the source of that variation, the idea of genetics and those particles of information known as ‘genes’ led to a worldwide explosion of research and inquiry into the nature of genes and how they worked – chromosomes, haploid and diploid cells, DNA, RNA, gene expression, genomics, the whole damn thing. We now see natural selection operating everywhere we’re prepared to look, as well as the principles of ‘artificial’ or human selection, in almost all the food we eat, the pets we fondle, and the superbugs we try so desperately to contain or eradicate. But of course there’s so much more to learn….
William Bateson
bonobo society, sex and females
sexual dimorphism – a difference on average, but massive individual variation
Men are bigger than women, slightly. That’s how things evolved. It’s called sexual dimorphism. It happens with many species, the genders are different in size, shape, coloration, whatever. With humans there’s a size difference, and something of a shape difference, in breasts and hips, but really these aren’t significant. Compare, say, the deep-water triplewort seadevil, a type of anglerfish, in which the female is around 30 cms long, and the male a little over a centimetre. The difference in mass would be too embarrassing to relate.
Among our primate cousins the greatest sexual dimorphism, in size as well as other features, is found in the mandrills, with the male being two to three times the size of the females. In some gorillas there’s a substantial size difference too in favour of the males, and in fact in all of the primate species the male has a size advantage. But size isn’t everything, and the bigger doesn’t have to always dominate.
Female bonobos are smaller than the males, even more so than in humans, yet they enjoy a higher social status than in any other primate society, probably including humans, though it’s hard to compare, since humanity’s many societies vary considerably on the roles and status of women. So how have females attained this exalted status within one of the most highly socialised primate species?
Bonobos and chimpanzees are equally our closest living relatives. It isn’t clear when exactly they separated from each other, but some experts claim it may have been less than a million years ago. Enough time for them to become quite distinct physically, according to the ethologist Franz De Waal. Bonobos are more gracile with longer limbs and a smaller head, and they have a distinctive hairstyle, with a neat parting down the middle. They’re also more easily individuated by their facial features, being in this sense more like humans. And there are also major differences in their social behaviour. Male chimps are dominant in the troupe, often brutally so, whereas bonobo society is less clearly hierarchical, and considerably less violent overall. De Waal, one of the world’s foremost experts on both primates, became interested in bonobos primarily through studies on aggression. He noted that sometimes, after a violent clash, two chimps would come together to hug and kiss. Being interested in such apparent reconciliations and their implications, he decided to look at reconciling behaviours in other primates. What he discovered in bonobos (at San Diego Zoo, which in 1983 housed the world’s largest captive colony) was rather ‘shocking’; their social life was profoundly mediated by sex. Not that he was the first to discover this; other primatologists had written about it, noting also that bonobo sex was far more human-like than chimp sex, but their observations were obscurely worded and not well disseminated. There are other aspects of the physical nature of sexual relations in bonobos that favour females, such as female sexual receptivity, indicated by swelling and a reddening of the genital area, which pertains for a much longer period than in chimps. Female bonobos, like humans and unlike other primates, are sexually receptive more or less all the time.
This isn’t to say that bonobos are oversexed, whatever that may mean. Sexual relations are far from constant, they are casual, sporadic and quickly done with. Often they’re associated with finding food, and it seems likely that sexual relations are used to reconcile tensions related to food availability and other potential causes of conflict.
So how does this use of sex relate to the status of females in bonobo society. I’ll explore this further in the next post.
bonobo relations – more than just sex
Abiogenesis – LUCA, gradients, amino acids, chemical evolution, ATP and the RNA world
Jacinta: So now we’re thinking of the Earth 4 billion years BP, with an atmosphere we’re not quite sure of, and we want to explore the what and when of the first life forms. Haven’t we talked about this before?
Canto: Yeah we talked about the RNA world and viroids and abiogenesis, the gap between chemistry and biology, inter alia. This time we’re going to look more closely at the hunt for the earliest living things, and the environments they might’ve lived in.
Jacinta: And it started with one, it must have. LUA, or LUCA, the last universal common ancestor. Or the first, after a number of not-quite LUCAs, failed or only partially successful attempts. And finding LUCA would be much tougher than finding a viroid in a haystack, because you’re searching through an immensity of space and time.
Canto: But we’re much closer to finding it than in the past because we know so much more about what is common to all life forms.
Jacinta: Yes so are we looking definitely at the first DNA-based life form or are we probing the RNA world again?
Canto: I think we’ll set aside the world of viroids and viruses for now, because we want to look at the ancestor of all independently-existing life forms, and they’re all DNA-based. And we also know that LUCA used ATP. So now I’m going to quote from an essay by Michael Le Page in the volume of the New Scientist Collection called ‘Origin, Evolution, Extinction’:
How did LUCA make its ATP? Anyone designing life from scratch would probably make ATP using chemical reactions inside the cell. But that’s not how it is done. Instead energy from food or sunlight is used to power a protein ‘pump’ that shunts hydrogen ions – protons – out of the cell. This creates a difference in proton concentration, or a gradient, across the cell membrane. Protons then flow back into the cell through another protein embedded in the membrane, which uses the energy to produce ATP.
Jacinta: You understand that?
Canto: Sort of.
Jacinta: ‘Energy from food or sunlight is used..’ that’s a bit of a leap. What food? The food we eat is organic, made from living or formerly living stuff, but LUCA is the first living thing, its food must be purely chemical, not biological.
Canto: Of course, not a problem. I believe the microbes at hydrothermal vents live largely on hydrogen sulphide, and of course sunlight is energy for photosynthesising oganisms such as cyanobacteria.
Jacinta: Okay, so your simplest living organisms, or the simplest ones we know, get their energy by chemosynthesis, or photosynthesis. Its energy, or fuel, not food.
Canto: Semantics.
Jacinta: But there are other problems with this quote re abiogenesis. For example, it’s talking about pre-existent cells and cell membranes. So assuming that cells had to precede ATP.
Canto: No, he’s telling us how cells make ATP today. So we have to find, or synthesise, all the essential ingredients that make up the most basic life forms that we know – cell membranes, proteins, ATP and the like. And people are working towards this.
Jacinta: Yes and first of all they created these ‘building blocks of life’, as they always like to call them, amino acids, in the Miller-Urey experiments, since replicated many times over, but what exactly are nucleic acids? Are they the same things as nucleic acids?
Canto: Amino acids are about the simplest forms of organic compounds. It’s probably better to call them the building blocks of proteins. There are many different kinds, but generally each contain amine and carboxyl groups, that’s -NH2 and -COOH, together with a side chain, called an R group, which determines the type of amino acid. There’s a whole complicated lot of them and you could easily spend a whole lifetime fruitfully studying them. They’re important in cell structure and transport, all sorts of things. We’ve not only been able to create amino acids, but to combine them together into longer peptide chains. And we’ve also found large quantities of amino acids in meteorites such as the Murchison – as well as simple sugars and nitrogenous bases. In fact I think we’re gradually firming up the life-came from-space hypothesis.
Jacinta: But amino acids and proteins aren’t living entities, no matter how significant they are to living entities. We’ve never found living entities in space or beyond Earth. Your quote above suggests some of what we need. A boundary between outside and inside, a lipid or phospho-lipid boundary as I’ve heard it called, which must be semi-permeable to allow chemicals in on a very selective basis, as food or fuel.
Canto: I believe fatty acids formed the first membranes, not phospho-lipids. That’s important because we’ve found that fatty acids, which are made up of carbon, hydrogen and oxygen atoms joined together in a regular way, aren’t just built inside cells. There’s a very interesting video called What is Chemical Evolution?, produced by the Center for Chemical Evolution in the USA, that tells about this. Experimenters have heated up carbon monoxide and hydrogen along with many minerals common in the Earth’s crust and produced various carbon compounds including fatty acids. Obviously this could have and can still happen naturally on Earth, for example in the hot regions maybe below or certainly within the crust. It’s been found that large concentrations of fatty acids aggregate in warm water, creating a stable, ball-like configuration. This has to do with the attraction between the oxygen-carrying heads of fatty acids and the water molecules, and the repulsion of the carbon-carrying tails. The tails are forced together into a ball due to this repulsion, as the video shows.
fatty acids, with hydrophobic and hydrophilic ends, aggregating in solution
Jacinta: Yes it’s an intriguing video, and I’m almost feeling converted, especially as it goes further than aggregation due to these essentially electrical forces, but tries to find ways in which chemical structures evolve, so it tries to create a bridge between one type of evolution and another – the natural-selection type of evolution that operates upon reproducing organisms via mutation and selection, and the type of evolution that builds more complex and varied chemical structures from simpler compounds.
Canto: Yes but it’s not just the video that’s doing it, it’s the whole discipline or sub-branch of science called chemical evolution.
Jacinta: That’s right, it’s opening a window into that grey area between life and non-life and showing there’s a kind of space in our knowledge there that it would be exciting to try and fill, through observation and experimentation and testable hypotheses and the like. So the video, or the discipline, suggests that in chemical evolution, the highly complex process of reproduction through mitosis in eukaryotic cells or binary fission in prokaryotes is replaced by repetitive production, a simpler process that only takes place under certain limited conditions.
Canto: So under the right conditions the balls of fatty acids grow in number and themselves accumulate to form skins, and further forces – I think they’re hydrostatic forces – can cause the edges of these skins to fuse together to create ‘containers’, like vesicles inside cells.
Jacinta: So we’re talking about the creation of membranes, impermeable or semi-permeable, that can provide a safe haven for, whatever…
Canto: Yes, and at the end of the video, other self-assembling systems, such as proto-RNA, are intriguingly mentioned, so we might want to find out what’s known about that.
Jacinta: I think we’ll be doing a lot of reading and posting on this subject. I find it really fascinating. These limited conditions I mentioned – limited on today’s Earth surface, but not so much four billion years ago, include a reducing atmosphere lacking in free oxygen, and high temperatures, as well as a gradient – both a temperature gradient and a sort of molecular or chemical gradient, from more reducing to more oxidising you might say. These conditions exist today at hydrothermal vents, where archaebacteria are found, so researchers are naturally very interested in such environments, and in trying to replicate or simulate them.
Canto: And they’re interested in the boundary between chemical and biological evolution, and reproduction. There are so many interesting lines of inquiry, with RNA, with cell membranes….
Jacinta: Researchers are particularly interested in alkaline thermal vents, where alkaline fluids well up from beneath the sea floor at high temperatures. When this fluid hits the ocean water, minerals precipitate out and gradually create porous chimneys up to 60 metres high. They would’ve been rich in iron and sulphide, good for catalysing complex organic reactions, according to Le Page. The temperature gradients created would’ve favoured organic compounds and would’ve likely encouraged the building of complexity, so they may have been the sites in which the RNA world began, if it ever did.
a hydrothermal vent off the coast of New Zealand. Image from NOAA
Canto: So I think we should pursue this further. There are a lot of researchers homing in on this area, so I suspect further progress will be made soon.
Jacinta: Yes, we need to explore the exploitation of proton gradients, the development of proton pumps and the production of ATP, leaky membranes and a whole lot of other fun stuff.
Canto: I think we need to get our heads around ATP and its production too, because that looks pretty damn complex.
Jacinta: Next time maybe.