In The Blood

My leisure reading tonight was about Toxoplasma gondii, a unicellular parasite which infects mammals. It can replicate asexually in any mammal, but can only mate and reproduce sexually inside a cat.

Cats usually become infected by eating a prey animal in which T. gondii has spread into muscle tissue and formed dormant tissue cysts. The parasite then reproduces in the cat and is shed in its feces in the form of oocysts. If another mammal ingests the oocysts, the cycle starts again.

Alternately, non-feline carnivores can become infected directly by eating the tissue cysts.

Humans can acquire the parasite from exposure to cat feces. (Oocytes are shed mainly when the cat has first become infected, for about the first week or two, so kitten poop is more dangerous.) As omnivores, humans can also ingest tissue cysts in the muscle of another infected animal. Pork and lamb have the worst safety record.

But it was the story of an experiment which astounded me. In a Paris orphanage, 10% of the children had detectable T. gondii. After being fed rare steak and horsemeat for a year, the infection rate went up to 50%. Then rare lamb was added to the diet, which brought the infection rate up to 100%. The old, dark days of experimenting on orphans. It was 1965.

In most cases, there are no obvious symptoms of an infection, but sometimes people can have a severe reaction, called toxoplasmosis, which can be like a bad dose of the flu lasting four months.

Heating to 65 celsius will fairly reliably kill the parasites in their tissue cyst state, but cooking a steak “medium rare” or less usually means that the centre stays below 60 celsius. You might as well rub your steak with cat shit.

It has been found that rats with the parasite behave differently to non-infected rats. They have less fear and less aversion to the smell of cat urine. T. gondii achieves this by manipulating the epigenetics of their neurons, obviously an evolutionary adaption which makes the rat more likely to be eaten and the parasite passed on. It hasn’t been shown definitively yet, but some studies indicate that there are psychological effects in humans as well.

Space is Deep

When I first bought my satellite dish over seven years ago, it was a motorized system. You see, television satellites form a ring around the Earth, and the dish must point to the right satellite to receive its broadcasts.

I can’t quite get my head around the excact geometry of it, but my house is attached to the Earth’s surface at a latitude of 53.549 degrees. The satellites are in a ring over the equator, which is zero degrees, while the Earth’s axis of spin is 90.

Anyway, I think how it works out is that the motor has to be aligned at (90 – 53.549) to the horizontal, and then by rotating left or right, it can pick out a satellite.

Well, I got it to work. The wall of the house points a bit West of South, and I could use the motor to point the dish across an arc of satellites. I thought that the Western end might get me some North or South American channels, but that end seemed to be equitorial Africa. In fact, the satellites which serve a particular region don’t sit directly above them. For example, the UK’s Sky and Freesat come from a group of satellites directly overhead 28 degrees East, which is somewhere in the Democratic Republic of the Congo.

But I got the channels I wanted. Freesat for British television, and turning a bit East, Hotbird for Italian, both the state broadcaster RAI and the Berlusconi empire on Mediaset. Going further East, I could get all the way to Khazakstan. Oh, and there were loads of middle-Eastern channels in there, most of them about Allah.

After a year or two though, I became dissatisfied. It took about twenty seconds to turn from UK to Italy, which is a long time in TV. And I hardly ever watched Khazakh television. I took the motor on the dish out of circuit, and put a multiple-LNB bracket on instead.

The LNB is essentially the “receiver” facing a satellite dish. In theory, the dish focusses the beam to one point, which is where you place your LNB, but in reality, it’s not that simple. The beam from a satellite that’s a bit to the left gets focussed, sloppily, more-or-less, to a spot on the right, and vice-versa. If the signal is stong enough or the dish large enough, you can get working television off more than one LNB.

The standard switch for multiple LNBs can handle four. I put up three. One for Freesat, which is a strong signal over the British Isles, and would work even off-centre. About centre, I pointed another at Astra, which has a load of German-language channels (I understand a bit of German) and a few French (my French is a little better than my German). Although the majority of French television seems to be encrypted on the proprietary Canal Plus system, and I can’t receive it. A little bit East, one LNB got Hotbird, with the Italian channels I wanted.

Unfortunately (maybe), after a couple of years, the Italian Mediaset channels on Hotbird went encrypted onto the Tivusat system. If you live in Italy, and have a tax code, you can get a free decoder card. Outside Italy, there are ways and means, but they all cost money. I shrugged and carried on.

Then, some months ago, I noticed that there is lots of Italian television on a different satellite, one that is physically above the British Isles at 5 degrees West, but points East to Italy. There is a host of regional RAI stations, and even the Mediaset channels are broadcast unencrypted. But my dish has to be pointing the other direction to see Freesat. (In fact, the Freesat sat is overhead Italy and the Eutelsat one is above the UK. What’s going on?)

There was a slight chance that a fourth LNB could receieve Eutelsat 5 if stuck far enough off centre. They’re only a fiver, so I bought one. And… it didn’t work. After a couple of hours up the ladder (I don’t like heights) I couldn’t get anything, and gave up. I slid the LNB along the bracket until I got a strong signal from an other satellite, any satellite.

This turned out to be Eurobird 9A, with about fifty free television channels on it. Hungarian and Swiss in the majority, but also some Chinese. The People’s Republic of China broadcasts across the world in different languages. I have English, French, Russian and Arabic.

As it happens, there’s an Italian drama tonight on Hungarian television, dubbed into Hungarian, and I don’t understand a word. I can’t even make anything of the programme info. There’s a priest in it but he’s not Don Matteo. Oh wait, I searched on-line for the title — “Rózsák Harca” — and it says “Tuscan Passion”. IMDB reveals: “A story of murder, conspiracy and secrets but above all about a great love story; Tuscan Passion tells the story of an impossible love between Aurora Taviani and Alessandro Monforte. Both belong to enemy families and both are divided by a history of blood and mystery. ”

So just another day in Tuscany. It went out on Mediaset in Italy, and I don’t see that any more.

The Price Of Drink

The British Medical Association in Northern Ireland have jumped on the bandwagon (but certainly not on the wagon) calling for a minimum price per unit of alcohol in drinks. Fifty pence, is what they suggest.

http://www.bbc.co.uk/news/uk-northern-ireland-23574051

The NI Chairman of the BMA, Dr Paul Darragh, is quoted in the BBC report as claiming that there is consistent evidence that alcohol consumption and rates of alcohol-related problems were linked to the cost of drink. Well, that is flat wrong. There is no evidence.

Usually, when pressed on this point, campaigners will refer to a report from the Sheffield Alcohol Research Group (at the University of Sheffield). Sounds impressive, doesn’t it? They must be proper scientists, being at a university and everything. Actually, anything I’ve read from them is absolutely not science. It’s not science to assume first that increased alcohol prices do improve health, and then use circular reasoning and cherry-picked data from other publications to “prove” the original assumption.

A couple of authors from the Adam Smith Institute (an economist and a statistician) published a paper ripping the Sheffield methodology to shreds. It’s worth reading just the executive summary to get a flavour of the arguments. It finishes “We conclude that predictions based on the Sheffield Alcohol Policy Model are entirely speculative and do not deserve the exalted status they have been afforded in the policy debate.”

http://www.adamsmith.org/sites/default/files/research/files/ASI_SAPM.pdf

Excessive alcohol consumption causes both social or health problems. Binge drinking, particularly by young people, is notorious for its effects on society. The television people always find it easy to get footage of late night antics: fighting, falling over, throwing up in the gutter, fornicating in the flowerbeds. People who do that sort of thing are harming their health, of course, but for most of them it’s just a phase they go through. They grow up and become boring.

Those who get hooked on alcohol and can’t give it up are in a different category. It would be compassionate to try to help them, never mind the additional health costs they incur and the impact on our taxes.

What effect would a modest price increase (i.e. one that the politicians could get away with) have on these two classes of problem drinker? Is price a major factor in people’s decision-making? What about the young people staggering home or fighting for taxis; have they all just come out of the cheapest, coarsest drinking dens? Not in my experience. In fact, quite likely they’ve been in a flashy club where the drink prices are substantially inflated.

Allegedly, the youth drinkers start the night by drinking cheap supermarket booze at home, but I’m not sure that this affects the argument. The objective is usually to get hammered, and whether you have nine drinks at home and one in the club or vice versa seems to make no difference.

I don’t know if you’ve ever known someone in the second category, the real alcoholic. Without help, they literally can’t stop drinking. Food, shelter, clothes — everything is secondary to getting the next drink. Do the unit pricers really think that an alcoholic will sit down and rationally decide “Well, with the price increase, alcohol will take a larger proportion of my income, so I must reduce the amount I buy.”?

If I was of a conspiratorial bent, I’d suspect that the whole idea of a legal minimum price per unit was a plot by the supermarkets, who would do very well out of it. Why isn’t anyone arguing for a price increase by increasing the tax and making it depend on the alcohol content? I don’t think that would help either, but at least the additional money could be spent for our benefit, not for fattening shareholders.

But the real thing that narks me about the minimum price idea is the ugly underlying assumption that problem drinking must be a disease of the poor. The proposal is based on the notion that 50 pence per unit will matter to the people with the problem: in order for it to make any difference, it must represent an appreciable percentage of their income. That is, the poor.

As I said at the beginning, the doctors are the latest group to call for a minimum alcohol price. As it happens, out of all employment groups, doctors have one of the highest incidences of alcohol abuse and dependence. But doctors are paid well, very well. Will a minimum price save the alcoholic doctor? I think not.

Walk The Walk

Around the turn of the year, probably a slack news period, a scientific publication got an unusual amount of news coverage. No, it wasn’t the discovery of a new boson, or a habitable planet circling a nearby star. This one was titled “High heels as supernormal stimuli: How wearing high heels affects judgements of female attractiveness” [http://www.sciencedirect.com/science/article/pii/S1090513812001225]

I’m always envious of researchers who can make a living carrying out such work. I remember one study which measured the amount of bare flesh in a nightclub and compared it to the owner’s fertility cycle. That one showed that women do show more skin during the most fertile time of the month, but only if they are in permanent relationships, but out without their partners. You can draw you own conclusions.

Still, you have to be sceptical, particularly if there is a claim of some evolutionary origin of a particular behaviour. That’s almost always stretching the evidence much too far, and anyway, human behaviour is too complicated for a neat just-so story.

That thing about high heels though. It’s an issue which has perplexed and slightly embarrassed me for years. I’d already guessed the same conclusion as the authors of the much-reported paper: that the high heel effects some kind of “supernormal” sexual signal. That is, biological systems seem to work on the basis of “if X is good, then XX is better”. Research (mostly on animals) has shown that exaggerating a stimulus, even well past the point of naturalness, can generate a heightened response.

But it’s not clear exactly what factor is in operation. The research paper was investigating walking, and reported a “shorter stride” and “increased rotation and tilt of the hips” for high-heeled as opposed to flat shoes. From my own observations, I’d add that the static posture is different as well, all the way up to the shoulders; and the silhouette is changed subtly. Which of these things –some? or all? –change our perception?

I say “our” deliberately. In the research, both men and women rated walkers in heels more attractive, even though they were only seeing a pattern of light spots on the joints of the subject. A different set of viewers were found to be twice as likely to guess that the walker in flat shoes was male, even though all subjects were actually female.

So I guess it’s settled. Heels do something to make a woman more feminine and more attractive. It’s not surprising that they are the only item of apparel to be consistently “in fashion” for hundreds of years.

I think it was Sigmund Freud who came up with the concept of “fetishism”, where sexual attraction derives from an object, rather than a person. The liking for high heels was well-known in his time, and his suggested explanation was that we experience our first sexual feelings before we can even walk, when we are crawling around among the ladies’ feet, and henceforth always associate sex with Victorian buttoned boots. But Sigmund was like that: he just made stuff up without a shred of evidence behind it.

I’m not old enough (honest) to have seen high-heeled buttoned boots as a baby, but now I think they can be quite sexy. And other high heels too. That’s the source of the mild embarrassment which I mentioned at the beginning, because if I’m honest with myself I have to admit that some kind of transference has occurred in my brain. The shoe itself, completely separate from the wearer, triggers a response.

I’ll quickly point out that it’s only a little response, only a mild dose of fetishism. I’m sure a brief internet search would reveal sites showing a complete obsession, although I suppose that’s true of practically everything. Anyway, I don’t judge. Sexual attraction is never based on logic or good sense in any of us.

Happy Birthday, Alfred

The name of Charles Darwin is firmly attached to the science of evolution, but if it hadn’t been for one coincidence, maybe someone else would have been more famous.

(I’ve noticed that the religious nuts who deny the occurrence of evolution often use the term “Darwinism” instead of “evolution”, as though it’s easier to dismiss it if it’s the theory of one man. That’s wishful thinking though.)

It’s not entirely unfair that Charles Darwin gets the credit. Some of the ideas on evolution had been discussed for quite some time previously (his own grandfather, Erasmus Darwin, had written a treatise on evolution, The Temple of Nature. In the form of a long poem.) But Charles Darwin was the first to come up with a coherent theory which included natural selection.

The Darwins were rich, and Charles never had to work for a living. He went to the same university as I did, except that I actually got a degree. His famous voyages were paid for by his father. But Charles was a meticulous observer and an intelligent and talented scientist. When he returned from his travels and wrote up a synthesis of his theories, that was pretty much the theory of evolution worked out. It was done by the early 1840s.

He didn’t publish though. Perhaps he was too timid about the possibility of a controversy, perhaps desperate to do more studies to build up the evidence. His close friend, the geologist Charles Lyell, was familiar with Darwin’s ongoing work, and in 1855 spotted a paper published by a young naturalist in Borneo, Alfred Russel Wallace, which showed thinking along the same lines.

Wallace wasn’t rich. He’d had to drop out of grammar school when his family could no longer afford it, but learned surveying and map making as an apprentice under his brother. He worked in various jobs, in surveying, civil engineering and teaching, but at the age of 25, left for Brazil to become a professional collector of natural history specimens to sell to armchair naturalists in England. The business was never very successful, and Wallace was always on the brink of bankruptcy, but he learned a great deal and became a respected scientist. (Or at least, reasonably-well respected, for he was not, of course, a gentleman.)

Wallace sent Darwin his new paper on the theory of evolution in 1858, asking for his advice on whether it was fit for publication. The content was so close to Darwin’s own unpublished theories that it put him in a dilemma. If he did the decent thing and recommended that Wallace’s paper be published (because it was top-class work), then Darwin would lose priority and could not claim to be the discoverer of evolution by natural selection.

If, on the other hand, he now rushed his own theory into print first, the scientific world would never know how much was original and how much had been inspired by Wallace.

At the suggestion of Lyell, a solution was reached where Darwin summarised his own material into a new paper, and both his and Wallace’s were published together as a joint presentation to the Linnean Society.

If Wallace had decided to consult someone other than Darwin, or had submitted his paper for publication directly to one of the scientific journals, then it might have appeared in print before Darwin knew of it. We might today talk of “Wallace’s Theory of Evolution”.

Alfred Russel Wallace, OM, FRS (8th January 1823 – 7th November 1913)

Oh My God

The universe is full of fast-moving sub-atomic particles. Even a staid, middle-class star like our Sun generates a stream of energetic particles which we occasionally see interacting with the Earth’s magnetic field and atmosphere in the form of Auroræ.

Even higher-energy particles arrive from outside the Solar System, and when they crash into our atmosphere they generate a tiny flash of light. The University of Utah operates one telescope system specifically to observe these flashes, because the original particle’s path and identity can be deduced, giving the astronomers information about what is happening out in the universe.

But one night in 1991, the scope detected a flash which could only have been created by a particle with 3.2×10²° electron volts, about forty million times more powerful than the Large Hadron Collider. This particle came to bear a name based on the astronomers’ first reaction. It’s called the “Oh-My-God Particle”.

You’ll know from Special Relativity that nothing (with mass) can be accelerated to the speed of light, but by adding more and more energy, you can edge ever-closer to light speed. Well, the OMG Particle, if it was a proton, would have been doing 0.9999999999999999999999951 of light speed, or to put it another way, in the time light crossed a light year of distance, the OMG would cross a light year less 46 nanometres.

Back to Special Relativity: obviously it takes light a year to travel a light year, and likewise for the OMG (minus 46nm). But for the particle itself, time dilation occurs. Time       actually       slows       down. From the OMG’s point of view, time is slowed so much that the travel time is much shorter. Much, much shorter: 100 microseconds.

If you could accelerate a spacecraft to OMG speeds, you could visit the centre of our galaxy in 3 seconds, or neighbouring galaxies in a few minutes. I can’t see how such speeds will ever be possible for a solid object like a spaceship, but maybe one day we’ll use more modest relativistic effects to make interstellar flight feasible.

The problem that the OMG presented the astronomers — and it still hasn’t been solved — was that when they traced the path back, there was nothing there. Nothing which could plausibly have generated such huge energy in a particle. In fact, because all of space is filled with the Cosmic Microwave Background (CMB) radiation, energetic particles interact with it and are eventually slowed down. The maximum distance that OMG could have travelled is about 50 megaparsecs (160 million light years), which implies that there is a fixed volume of space out there within which it must have originated, but when you investigate: nothing.

Since OMG, there have been about 15 additional detections of its brothers and sisters, but there is still no generally-accepted theory to explain what they are and where they come from. My own favourite is that the universe contains “topological defects”, where the actual geometry of space-time has a discontinuity or flaw. Postulated one-dimensional defects are called “cosmic strings” (nothing to do with string theory) and would be a rippling crack in space-time, the thickness of a proton, but hundreds of light-years long. If a string was to thrash around and loop back on itself, the parts would split off, with a huge release of energy, more than enough to generate OMGs.

Coming Out

Today, 10th October, is World Mental Health Day, a concept instituted 20 years ago “for global mental health education, awareness and advocacy”. This year’s theme is specifically on depression, which, according to the World Health Organization, was ranked as the third leading cause of the global burden of disease in 2004 and will move into the first place by 2030.

So this would be a particularly good time to reveal something which only a few very good friends know about me: I’ve been fighting depression for all of my adult life.

Depression takes two general forms. In the less common type, “bipolar affective disorder”, sufferers have wild mood swings, from deepest depression to crazed mania. Stephen Fry is well-known for being affected by this form of the disease. But more often, there is no manic phase, just recurrent episodes of depression, which can vary in severity. It can be referred to as “unipolar” or “episodic” to distinguish from the bipolar syndrome.

I’ve found that non-sufferers (or let’s call them “normal people”) just don’t understand depression. They’ve been very sad in their lives themselves, or experienced grief, and imagine that depression must be a bit like that. It isn’t at all.

I’m only speaking from my own experience, but depression seems to me to be more like a mental paralysis than any kind of sadness or just feeling low. Doing the simplest things requires a huge effort. A common other symptom is having very low self-esteem, and perhaps feelings of worthlessness, but I’ve never had that. I have two alternate explanations for this difference. One, I wholeheartedly accept that depression is an organic disease, and nothing to do with my self-worth (just as I wouldn’t feel it was my fault if I caught tuberculosis). Or second, maybe I just love myself too much.

The episodic nature of the disease means that I have good times and bad times. During the more severe spells, I cope by cutting down activities and socializing to a minimum. Today, I’m fortunate not to have to get up and go to work every day, but when I did have to do that, I mostly got by, and only rarely invented a physical sickness to cover a day or so off.

So my depression is definitely not the most severe category, because I can continue to function, albeit with some impairment. But some people are hit much harder by it, and practically “shut down” and withdraw from every aspect of normal life. A small percentage decide that they just want it all to stop, and take their own lives.

Friends and relatives can help a lot, but it’s not easy, because depressives are in a state where they interact badly with others. If your friend is depressed, it can help to be gently persistent. They’ll turn down a social event, for example, but might concede after a little encouragement. Or not. Don’t be offended by a refusal, and if you care about someone, don’t give up on them.

Dem Bones

Daniel David Palmer, born in 1845, was the inventor of Chiropractic. Although he had no medical knowledge, he had a small business in Iowa practising “magnetic healing”, which was fashionable in the late nineteenth century.

Palmer then developed a theory about the relationship of spinal alignment to illnesses. In his own words, “A subluxated vertebra … is the cause of 95 percent of all diseases … The other five percent is caused by displaced joints other than those of the vertebral column.”

So, just to be clear, Palmer had decided that all diseases were caused by bone misalignment. Not bacteria, not viruses, not genetic faults; just bones out of line. That’s obviously absurd. Some problems certainly are caused by skeletal issues — back pain, even headaches sometimes — but I’m pretty sure that cholera and malaria aren’t.

But in fact, Palmer’s information came from a medical source, Doctor Jim Atkinson. Doctor Jim was unfortunately dead at the time, but apparently he had communicated the first information to Palmer during the Mississippi Valley Spiritualists Camp at Clinton, Iowa. Subsequently, Palmer developed his theories himself under the unspoken “inspiration” of Atkinson. Or, to be more cynical, he simply made stuff up.

The degree of Palmer’s delusions are indicated by the fact that he explicitly compared himself to Jesus and Mohammed (and also Joseph Smith, Mary Baker Eddy and Martin Luther). He was a prophet and had founded the new belief system of Chiropractic. It was religious and spiritual.

In spite of the ludicrous background and lack of medical rationale, Chiropractic didn’t disappear with the credulous nineteenth century. Quite the reverse: it’s one of the biggest and most profitable types of non-scientific medical practice today.

Although the Chiropractic organizations generally still make claims like Palmer’s to be able to treat many and various illnesses — or, to use Simon Singh’s words “happily promote bogus treatments” — the majority of people who attend a practitioner do so because of back pain. In a way, that’s understandable, because in a small proportion of cases, real medicine can’t help, and sufferers are desperate for relief.

Well, the placebo effect ensures that some will find relief, but there’s one thing you can be absolutely certain that Chiropractic will relieve you of: the contents of your wallet.

Pig Flu

The Swine Flu of 2009 was officially a pandemic. It spread widely enough and killed enough people to qualify, even though vaccination campaigns successfully reduced its potential impact. Some people have questioned the medical investment to counter the virus on the basis that it didn’t turn out to be as bad as predicted. That misses the whole point. The expense was worth it because it worked.

That year’s Influenza A virus subtype H1N1 is a beautiful thing. In an engineering sense, I mean. You can admire the way nature has put together an efficient and elegant machine. (The name comes from the variety of Hemagglutinin and Neuraminidase proteins in the outer shell. There are 16 H and 9 N subtypes, and this one has version 1 for both.)

Flu viruses have a genome consisting of eight separate sections of genetic information. The 2009 H1N1 has three genes from North American swine flu, two from Eurasian swine flu, two from North American bird flu, and one from human flu, the latter being specifically from the H3N2 strain that came from South East Asia in the 1993 flu season.

So H1N1 is a custom virus, the swine flu genes code for its outer shell, and the human and avian flu genes for its replication abilities. I’m not suggesting that it was put together in a laboratory: it almost certainly put itself together in a pig. Probably a North American pig. Because when a cell gets infected with two different flu viruses at once, the viral replication almost inevitably creates mixed offspring.

The famous flu pandemic of 1918 was also caused by a type of H1N1 which had acquired alternative genes, although the exact specifics are still being researched. In that case, the outer protein shell was of avian flu origin; inside there was at least one human flu gene; and possibly a swine flu gene.

H1N1 of 1918 is estimated to have killed about 20% of humans that it infected, or about 5% of the world’s population: maybe about 100 million people. Initially though, it was not very lethal. There was a first wave of infections in the Northern Hemisphere Spring which was similar to an ordinary flu outbreak. But by Autumn, the virus had evolved, either by random mutation or by acquiring a new, swapped gene from another sister virus.

In the second wave, the virus had acquired the ability to over-drive the victim’s immune system. almost like a massive allergy attack. Most people actually died from secondary infections in their lungs caused by excess fluid as their immune systems overwhelmed their bodies, but there were other interesting symptoms, such as bleeding from the nose, ears, stomach, and intestine. Unusually, the majority of fatalities all round the world were in young, healthy people, because their vigorous immune systems were powerful enough to kill them when turned loose by the virus.

Because the second wave virus was a mutated descendant of the first, the people who had suffered “normal” flu in the first wave were immune to the second, but as you probably know, the virus mutates so swiftly that you need a new vaccination every year.

Swine flu is still circulating, and still mutating. This year, 297 Americans contracted the H3N2 strain from pigs, mostly at agricultural fairs. One person died. In a separate outbreak, three people in Minnesota were infected with H1N2. Interestingly, both strains of the virus carry the same human gene which made the 2009 pandemic so infectious. So does a different variety of H1N2 found in Korea.

So far, most research has taken place on the Korean virus, and it has turned out to be unusually infectious and virulent. It is likely that the two American ones are as well, but it has been claimed that testing has been hindered by the reluctance of the American agricultural industry to accept that there is a problem and to engage with it.

The 2009 pandemic probably started in North America. The 2012/13 one probably will as well.

Iran and the Bomb

It must be obvious to everyone now that Iran is attempting to produce a nuclear weapon. The claim of peaceful pursuit of nuclear power is rendered implausible by the concentrated efforts to increase the enrichment of uranium — far beyond what might be required for nuclear fuel. In fact, Iran probably has enough medium-enriched uranium to make a crude bomb already, even though it has not developed the technology to produce technically “weapons-grade” uranium.

I used to think that plutonium presented the biggest risk of nuclear weapons proliferation, because there’s so much of it lying about. Plutonium doesn’t exist naturally, but it’s a by-product of the nuclear power industry. Some reactors are designed to “burn” plutonium, but for the most part it’s just stockpiled. The UK alone has over 100 tonnes, or 17,000 times the amount that went into the atomic bomb dropped on Nagasaki.

The Manhattan Project — the Allied programme to develop nuclear weapons in the Second World War — began working on three separate atomic bomb designs. In the end, one was abandoned during development, and the other two were used in the Trinity test in New Mexico and the attacks on Hiroshima and Nagasaki in Japan.

The two working designs were code-named “Fat Man” and “Little Boy”. The former was the type detonated in Trinity and then dropped on Nagasaki. It was the more complex bomb, consisting of a spherical arrangement of plutonium which was “imploded” inwards by explosives. “Little Boy”, on the other hand, was a so-called “gun” bomb, where two pieces of nuclear material, this time uranium, were shot together like a bullet hitting a target. The design was judged to be so simple that a test was unnecessary: the device was dropped immediately on Hiroshima.

The one which didn’t get made — it was called “Thin Man” — was also a gun design, but a plutonium gun. The Manhattan Project found that plutonium for bombs was in much better supply than uranium, even though plutonium is an artificial element, not found in nature. Plutonium was created by irradiating natural uranium, and then separating out the plutonium product by chemical means (different elements react differently). To make weapons-grade uranium, however, uranium-235 had to be separated out from uranium-238. These are the same element, differing only in nuclear properties, and can’t be separated by chemistry. Separation was very difficult with the technology of the time.

However, calculations showed that plutonium was too reactive to be used in a gun-type bomb, unless the “gun barrel” was made impractically long. The basis for all atomic bombs is assembling a critical mass of nuclear material, in which a rapid chain reaction takes place, releasing a large amount of energy. However, a chain reaction can begin before the critical mass is properly squeezed together, in which case it will blow the nuclear material apart, terminating the reaction. In the case of the plutonium gun, the scientists couldn’t work out how to get the two sub-critical pieces of plutonium to contact quickly enough in a weapon which could feasibly be put on a bomber aircraft.

The Fat Man design separated the plutonium into more, smaller pieces, so that the chance of a premature chain reaction was avoided. However, the engineering of the imploding explosive device was very precise and complicated, requiring major industrial resources and the best work of some exceptional scientists and engineers.

The difficulty of making an implosion bomb makes it a challenge, even given the resources of a state government, and it is likely that in most cases the simpler, gun-type design will be chosen. Since a plutonium gun is also impractical, enriched, weapons-grade uranium must be acquired. For uranium enriched to 85% or more of uranium-235, you need about 60kg (preferably in several pieces) for a critical mass for a simple weapon. (The comparable figure for plutonium is just 11kg, and lots of plutonium is stockpiled, since it’s a by-product of nuclear power generation). But if you have a lot of uranium, you can make a bomb with material enriched to only 20%.

According to the International Atomic Energy Authority, Iran is researching multi-point explosive capabilities, the technology for an implosion plutonium bomb. However, the scale of their uranium enrichment programme is evidence that they are pursuing the simpler uranium gun bomb first. This would enable them to detonate a static nuclear “test”, long before they had the ability to make a weapon.

Yesterday, a resolution was introduced jointly by China, France, Germany, Russia, the United States, and the United Kingdom to the IAEA Board of Governors. It criticized Iran for defying UN Security Council resolutions to suspend uranium enrichment, and called on Iran to allow inspections of evidence that it is pursuing weapons technology. The resolution was passed, with 31 votes for, 1 against and 3 abstentions. In light of previous events, it seems unlikely that Iran will comply.