On the morning of May 10, there will be an annular Solar eclipse. In an annular eclipse the Moon does not completely cover the Sun, and the Sun forms a thin ring around the Moon at maximum eclipse depth.

The annular eclipse will be seen from a thin strip in WA, the Northern Territory and remote far north Queensland. Everywhere else will see a partial eclipse of varying depth, the north-east coast of Australia having the best views. The eclipse starts shortly after sunrise. In places along the annular eclipse path, such as Tennant Creek (NT) and Musgrave Roadhouse (QLD), viewers will see a thin rim of Sun around the moon.

Elsewhere viewers will see between 13% (Hobart) – 83% (Cairns) of the Sun covered by the Moon.
A diagram showing eclipse times in Universal Time is here, and an interactive map of the path is here. Click on the map for local timings of the eclipse.

Do NOT look directly at the Sun! Do not use so called filters. Over exposed film, smoked glass etc. used as filters are NOT, repeat NOT safe. Only special solar-rated viewing spectacles from astronomical suppliers should be used (for one example see here), they may cost a bit, but your eyesight is without price. Never use eyepiece filters for telescopes. These can crack at inopportune times and destroy your eyesight. In the annular eclipse path, as there is always some of the solar disk visible, at no time is it safe to view the eclipse with the unaided eye.

The easiest and cheapest way to observe this event is by making a pinhole in a stiff square of cardboard and projecting the image of the Sun onto a flat surface. You are basically making a simple pinhole camera, which will reveal the changes to the Suns outline quite satisfactorily. A card with a 1 mm hole should be projected onto a surface (eg white paper, or a white wall) about 20 cm away, a 5 mm hole should be projected onto a surface 1 to 1.5 meters away.

You need to create a reasonable sized image, so you need a fair distance between the pinhole and the surface you project the image on. This will mean the image is going to be fairly dim, so you also need some sort of sun shield to keep in image in shadow. I use the longest available postpac postal tube, with alfoil over the top (and the pinhole in the alfoil), and wide ring of stiff cardboard to ensure that the image of the sun is projected into a dark area. This link will show you several methods to make pinhole projection systems.

You can also use binocular and telescopic projection systems. This link will show you how to make safe solar viewing and telescope projection systems. Here is my step by step guide to making a binocular projection system, and a guide to aiming your binoculars or telescope when you can’t actually look at the Sun. And this is the projection system I use with my refractor telescope.

Remember, do NOT look directly at the Sun, as irreparable eye damage or blindness can occur (see this video for a graphic demonstration).

City	Eclipse Start	Mid Eclipse	Eclipse End	% Sun covered
Adelaide (ACST)	7:09 am	8:15 am	9:22 am	38
Alice Springs (ACST)	below horizon	8:07 am	9:31 am	79
Brisbane (AEST)	7:41 am	8:58 am	10:28 am	40
Cairns (AEST)	7:28 am	8:49 am	10:27 am	83
Canberra (AEST)	7:50 am	8:55 am	10:10 am	26
Darwin (ACST)	below horizon	8:07 am	9:28 am	68
Hobart (AEST)	8:06 am	8:59 am	9:57 am	13
Melbourne (AEST)	7:50 am	8:52 am	10:02 am	25
Musgrave Roadhouse (AEST)	7:26 am	8:47 am	9:29 am	95 Annular eclipse
Perth (AWST)	below horizon	below horizon	7:45 am	-
Rockhampton (AEST)	7:34 am	8:54 am	10:30 am	56
Sydney (AEST)	7:50 am	8:57 am	10:14 am	27
Tennant Creek (ACST)	6:57 am	8:07 am	9:28 am	95 Annular eclipse
Townsville (AEST)	7:29 am	8:49 am	9:28 am	74

World Homoeopathy Awareness Week has just passed (10 April to 16 April), but I would still like to take this opportunity to make people aware that Homoeopathy is expensive placebo that has been failing clinical trials since 1835.

I’ve written about homoeopathy before*, showing that homoeopathic treatments, which either have no trace of active ingredient or levels so low as to be biologically meaningless, have no good evidence of therapeutic benefit.

This video on homoeopathy covers a lot of similar ground to my articles. You may be amused at the sight of me taking an overdose of homoeopathic sleeping pills (around 3:52 into the video). That sequence had a great missed opportunity moment. When Frank Pangallo asks me if I feel sleepy, I should have replied “if this was real medicine, we would be in hospital now”.

There are a number of other discussions relevant to World Homoeopathy week. This article at Science Based Pharmacy about the implications of homoeopathic products for Pharmacists is thought provoking reading. The Guardian’s report that even homoeopaths disavow homoeopathic vaccination should give you pause as well.

There are several relevant videos aside from the one linked above. Here’s Richard Dawkins investigating homoeopathy. James Randi’s TED talk on homoeopathy, and this video from CBC marketplace.

For more general infomation on homoeopathy start at the 10:23 campaign for a good one-stop basic information source. For further detail, over at Science Based Medicine, there is a good, easily readable series on homeopathy.

Then there is the weighty House of Commons Science and Technology Committee (STC) report, Evidence Check 2: Homeopathy, which concludes that there is no evidence that homeopathy works any better than placebos (commentary here). A more general article is the Ars Technica report on homoeopathy.

If you are wondering why people would use homoeopathy when it doesn’t work, this article might help you understand.

For some light relief, a homoeopath explains how physics works, then there’s an amusing poster from the Centre for Inquiry Canada and a song from Australia’s Tim Minchin (warning: rude words).

*My Conversation article ‘Doctors' orders: debunking homeopathy once and for all’, was included in The Best Australian Science Writing 2012 anthology.

It’s very hard to miss that a certain Famous Sports Person has been accused of taking performance enhancing drugs (and is vigorously denying the accusation), splashed as it is throughout all the news media.

While this was a welcome relief from North Korea making yet more histrionic threats of nuclear Armageddon, I was somewhat bemused to see, listed amongst the more serious drugs, that the players received “an extract from pig’s brain used to treat Alzheimer’s, the first milk from a mother cow and a bark extract”

As an Alzhemier’s researcher, I was curious to know what pig’s brain extract it was, and why an alleged anti-Alzheimer’s drug would be given to footballers in the first place. Were they in danger of losing their memories? Forgetting what the ball was for, or what those long poles represented?

It turns out the “pig’s brain extract” is cerebrolysin, a complex mixture of peptides and other substances which have neurotrophic effects. These are hormones which support the survival, development and function of nerve cells. Naturally, hormones which support the survival of nerve cells would be attractive in treating Alzheimer’s disease and vascular dementia, where the central problem is death and dysfunction of elderly nerves in the brain. But for footballers, not so much.

Clinical trials in Alzhemier’s disease shows that cerebrolysin can maintain mental functioning and delay disease progression. However cerebrolysin is about as effective as the currently used drug donepezil. As cerebrolysin has to be injected daily, there is currently no compelling reason to adopt it as a drug. There’s also some evidence that it can help in vascular dementia, although more research is needed.

Still, Alzheimer’s disease is not a significant disease of young, healthy footballers, but a disease of old age. Why would a footballer need cerebrolysin?

Cerebrolysin also has been used in experimental treatment of traumatic brain injury. Traumatic brain injury is something that footballers are likely to be exposed to. Could cerebrolysin be used to as a prophylactic to prevent or limit traumatic brain injury (TBI)?

Pilot studies indicate that people given cerebrolysin recover faster from TBI. This is encouraging, but it is too soon to start using this drug clinically. More importantly there are no studies to show that giving people cerebrolysin before TBI will help them recover or make the damage less.

This doesn’t answer the question “why give footballers cerebrolysin”, giving footballers a drug which hasn’t yet been approved before we even know if it can work as a prophylactic doesn’t seem reasonable. Even if cerebrolysin had zero side effects merely repeatedly injecting yourself has risks, risks undertaken for no good reason.

However, cerebrolysin probably wasn’t even being used for this at least plausible reason (reducing damage from TBI).

Cerebrolysin has a wide underground following for boosting mental performance, and on various body building forums* it is claimed to reduce “brain fog”. At least one newspaper report attributes cerebrolysin use to the desire to improve decision making.

There is a world of difference between slowing loss of cognitive ability in elderly people with dementia and improving mental performance in healthy young adults, and there is no research to show that young adults would benefit cognitively from cerebrolysin.

Why would anyone want to regularly inject themselves with a drug that has no evidence of effectiveness beyond anecdotal reports? Especially as placebo responses are rife in sport and the anecdotal, perceived benefits are almost certainly illusory.

Still, sports people have been known to take significant risks for any form of perceived benefit, including taking the poison strychnine to try and enhance performance, even though strychnine was useless.

Given this history, injecting pig brain extracts is one of the less harmful things sportspeople can do to themselves (cerebrolysin has very few side effects), but it suggests that the sports is particularly susceptible to voodoo treatments of no benefit.

*No, I’m not going to link to them, the body-building boards are very scary places.

UPDATE: Here’s a glossary of “Sports Science” drugs to help you navigate some of the weird and wonderful drugs and treatments out there.

This being Easter and all I thought I would revisit a subject dear to all our hearts, chocolate. Or rather, that part of chocolate that we have a love hate relationship with, caffeine.

Have you ever wondered why (some) plants make caffeine? They certainly have not anticipated our desire for alluring chocolate or stimulating coffee. Caffeine is part of the plants defence mechanisms.

Plants can’t run away, so to ward off herbivores they have evolved a range of chemical defences to discourage animals from eating them. This elaborate chemical warfare system is part of the reason that plants such as the common cress have more genes than we humans do.

Ironically, most of humans recreational drugs of choice are these chemical warfare compounds. Nicotine in tobacco, opioids in opium poppies, tetrahydrocannabinol in marijuana are all anti-herbivore defence molecules, either stupefying or killing the animal that tries to munch the plant.

So it is with caffeine, a bitter alkaloid that deters the biter.

But, and you know I’m going to say this yet again “it’s the dose that makes the poison”. All of these compounds at lower doses have effects that humans like (even if they are not actually beneficial). In the case of bees, low doses of caffeine may improve their memory.

Some plants, coffee plants and citrus plants, secrete caffeine in the nectar of their flowers. At a lower level than found in, for example, the tissue around coffee seeds (roughly 1/500th or even less), some some of the concentrations approach that you would find in a cup of instant coffee. If the bitter caffeine is driving off herbivores, what are low levels doing in nectar, which plants use to attract pollinators? Isn’t this counter productive?

A recent paper sheds light on this conundrum.

In humans consumption of low levels of caffeine improves our ability to memorise things (at least short term memory). Could this be happening in bees? The researchers set out to test this idea by training bees to associate a particular scent with a sugary reward. They mixed different concentrations of caffeine in some of the sugar solutions, while others had no caffeine.

Low dose caffeine had a small effect on how fast the bees learnt, but it had a dramatic effect on the bees long term memory. While most control bees forgot the association of sent with sugar after 24 hours, when bees were on caffeine they remembered the association 24 hours later, and there was some memory left after 72 hours.

They did a number of experiments to show that this was not due to having a better sense of smell due to caffeine, and they could show that caffeine affected the section of the bee brain that is involved in memory.

Importantly, the levels of caffeine that increased memory retention in bees is in the range found in the nectar of coffee and citrus flowers, while the level of caffeine seen in the seed tissues of coffee plants is repellent, or even lethal, to them.

So plants can use caffeine to both repel predators and attract pollinators. A rather dramatic demonstration of the dose making the poison (and that evolution is smarter than we are).

If you are out hiding Easter eggs for the kids Easter egg hunt, maybe you should have a good cup of espresso first, so you can remember where you hid them the next morning.

“Bisphenol A protects against Wheezing” screamed no headline ever, yet that is one of the findings of a paper just published in the Journal of Allergy and Clinical immunology.

I’m sorry, I really was going to talk about the WHO report, and I don’t want this blog to become all BPA all the time, but the press release that comes with the paper (and to some extent the paper itself) highlights significant issues with how science is communicated, and science by press release.

First, some background.

Asthma incidence has been rising in the past 30 years worldwide, except Australia, where the incidence of asthma has actually fallen by 25% in young people over the past 10 years. The reason for these changes is unclear, though environmental influences are likely to be involved. Prenatal exposure to compounds that mimic the sex hormone oestrogen are possible candidates for the increase (the fall in Australia is possibly related to our successful anti-smoking campaigns).

So how can we test this idea. One way is to measure the levels of BPA in pregnant women and their children after birth and see if they develop asthma as the children grow older. There are problems with this approach, but it can be useful and is fairly common.

This is what the authors of the new paper in the Journal of Allergy and Clinical immunology did. They examined perinatal and postnatal exposure to bisphenol A through urinary BPA excretion, and looked at wheezing and various indexes of asthma at 5, 6 and 7 years of age.

And what did they find?

One astonishing finding was that prenatal exposure to the oestrogen mimicking compound bisphenol A reduces the chance of children wheezing at age 5. It also had no effect on overall asthma and wheezing at other ages.

As one of the big worries people have is that prenatal exposure to oestrogen mimics will affect the developing foetus, this finding of no effect (and even a “protective” effect at 5 years of age) is of particular significance.

The “protective” effect of BPA at 5 years of age is quickly passed over in the press release and only briefly discussed in the paper. This should be kept in mind when trying to interpret the variety of results seen when the authors try to correlate post natal exposure to bisphenol A to indexes of asthma and respiratory problems.

When looking at postnatal exposure, the results are inconsistent and contradictory.

Levels of urinary BPA measured at 3 years of age are correlated with wheezing at 5 and 6 years but not at 7 years. But when we look at urinary levels of BPA measured at 5 years, there is only a marginal correlation with wheeze in 5 year old children and not at 6 or 7 years.

The size of the protective effect of prenatal exposure on wheezing, and its statistical significance, was as strong as the positive correlation of postnatal exposure with wheezing at 3 years and stronger than the correlation of postnatal exposure and wheezing at 5 years.

There was a correlation between clinician-diagnosed asthma and BPA exposure. But in stark contrast, there was no correlation between a breath test for asthma (which is equivalent to the standard lung function testing) and BPA at age 3 (which had the best correlation with wheeze) and age 5.

Issues with statistics and interpretation

Keep in mind the correlation does not imply causation (it may waggle its eyebrows suggestively while mouthing “look over there” though). A colleague notes that there is a strong correlation between ice cream sales and drownings.

But ice cream is not causing the drownings, hot weather makes people more likely to eat ice cream and go swimming. You always have to interpret your results with the knowledge that other factors may be involved.

Also keep in mind that to get these correlations, the authors have to apply mathematical calculations to correct for other factors which affect the incidence of asthma (mothers’ history of asthma, and tobacco smoke exposure amongst others).

This is all standard methodology, but again you have be very careful when interpreting the data. If you haven’t correctly identified all the important confounding factors, you can get spurious correlations.

Overall, given the number of tests done (which increases the chance of false positives), the sporadic and inconsistent correlations and the astonishing “protective effect” of prenatal BPA exposure, the results are more likely to be statistical artefacts rather than real associations.

Also, when you look at a number of the confidence intervals that were published alongside the significance values (eg in table IV), the confidence intervals include the no effect value, which is a red flag that the strength of the effects are overestimated.

As well, there are some inconsistencies in the data in the figures given for urinary bisphenol A. The urinary BPA levels in table IV are not the same as the BPA levels In table I. One table gives median values and the other mean values to be sure, but it is hard to interpret the values when they can’t be directly compared.

This is important as the table IV values means that these kids exposure to BPA is in the top 10% of concentrations seen in America according to the Fourth National Report on Human Exposure to Environmental Chemicals (2012), and the 3 year olds in the top 5% (ie 95% of the under-15 population have lower exposure to BPA than these kids do).

This means that these are not ordinary levels of exposure as claimed in the press release. It also suggests that these children have been exposed to unusually high levels of BPA (and possibly other environmental chemicals that were not controlled for).

The press release does not indicate any of these complexities, but is headlined “BPA raises risk for childhood asthma”. Since most people will read the press release and articles derived from it, rather than the actual study, once again we see that science by press release serves us poorly.

I’m going to take a break from my planned blogging of the WHO Endocrine Disrupting Chemicals Report to talk about this paper “Bisphenol A delays the perinatal chloride shift in cortical neurons by epigenetic effects on the Kcc2 promoter”, just published in the Proceedings of the National Academy of Sciences.

Why? The paper illustrates some of the issues with the WHO report, and the perils of trying to make otherwise valid scientific research “relevant”. Let’s start with the press release.

“DURHAM, N.C. — Environmental exposure to bisphenol A (BPA), a widespread chemical found in plastics and resins, may suppress a gene vital to nerve cell function and to the development of the central nervous system, according to a study led by researchers at Duke Medicine”

We have met bisphenol A before. It is an endocrine disrupting chemical, which mimics the structure of the hormone oestrogen.

However, it’s a very weak mimic, and is rapidly broken down in the environment and in our bodies. While BPA is used to make plastics that are used for drink bottles and food storage, our exposure to this chemical is minuscule.

Now, back to the paper. Will environmental exposure to BPA do what the press release says?

This is a very interesting study, unfortunately, it’s linkage to environmental exposure to bisphenol A is misleading, in that the concentrations used in this study are hundreds to thousands of times higher than humans would be exposed to that the maximal permissible level of BPA in food. Thus, this study, while it throws light on aspects of gene regulation, is not relevant to human exposure to this chemical.

In the first part of the study, cultured nerve cells were exposed to “relatively” low levels of BPA. When I say relatively, these levels are inn the nanomolar range (ie very tiny). But even these tiny levels are around 100 times greater than the blood levels expected from exposure to the highest permitted levels of BPA.

Also, direct exposure of these cells to BPA does not reflect the levels (or conditions) that brain cells in the body would be exposed to.

In the second part of the study female mice were fed BPA containing food and the effects on the brain of the offspring were studied. In terms of human exposure, the concentrations of BPA fed were 1000 times higher than the maximal permitted level of human exposure, so again not relevant to human exposure.

Put it this way, for a pregnant woman to get the same dose BPA the pregnant mice were getting, they would have to eat well over 2000 cans a day, every day, for months, of the foods Choice found to have the highest levels of BPA in them. This would be a heroic feat under any circumstances, and you would have other issues just from consumption of this much food alone.

While the study establishes that it’s possible to manipulate how genes are switched on in the developing brain, and that some of these genes may have a significant effect on processes relevant to brain function, the concentrations of BPA in this study are well beyond that which would be experienced by humans.

Trying to pitch the study as being environmentally relevant distorts the actual research and creates unnecessary panic. The authors should have a severe talk to their PR department.

Yesterday the World Health Organisation released a report entitled “State of the science of endocrine disrupting chemicals – 2012”

Endocrine disrupting chemicals are a broad range of substances that can interfere with how our hormonal systems work, by either mimicking natural hormones such as oestrogen, or altering their production and breakdown.

These chemicals have a wide range of applications, from pesticides to plastics. As we use plastics ubiquitously, from drinking from plastic containers to storing food in plastic containers to handling things like plastic credit cards, people are worried that these exposure may be harmful to our health.

The WHO report is a wide ranging survey of our understanding of endocrine disruptors, and builds on a previous 2002 WHO report.

The main report is nearly 300 pages long, and the Summary for Decision Makers is still substantial at 30 pages. I’m going to bet that it is the Summary the everyone reads, and I’m ready for a new round of Chemophobia from hasty reading of the Summary.

I’ll talk about some particular issues that arise from this report in the coming week, but before I start there is an issue that I thinks needs consideration

The main theme of the report is that more research is needed, and we have a lack of understanding of how these various chemicals impact on human health.

One of the people who talked to me about the report today asked a simple but important question that requires a complex answer.

If we are we are uncertain that these chemicals have particular health effects, why should we have any exposure to these chemicals in the face of this uncertainty.

It depends on the kind of uncertainly we are talking about. If we are uncertain that concentrations of chemical X cause diabetes for example, but the contentious concentrations are 100 times the existing maximum permitted intake of this chemical, there is sufficient margin of error to keep our current thresholds.

Especially if most people will never approach this maximum threshold of chemical X, it is acceptable to keep our current threshold levels until we have better data (we might revise them down a bit for an extra margin of safety).

An example is Soy products (okay these are natural products, not industrial chemicals, but the issues are identical).

There are a whole range of phytoestrogens in Soy, which might be protective against some forms of cancer, or might produce other cancers or interfere with male reproduction, and has even been linked to obesity.

Given that modest consumption of soy is unlikely to be involved with serious side effects, it makes sense not to prohibit soy products until we have firm evidence that particular levels are a risk.

That’s the general question out of the way.

Unfortunately, because of it’s very breadth of scope, covering so many chemicals, some issues are clearly differentiated.

The Summary for Decision Makers (the one most people will read) in particular often does not distinguish high-risk chemicals from low risk chemicals, or those where the evidence base is less complete. I’ll deal with some of these particular issues in the coming week.

So should you lick your credit cards? So long as you don’t make a habit of it, it should be fine.

The discovery that certain overseas processed meat products contained, Quelle Horreur, meat that was not exactly the promised beef has generated a fair degree of shock and outrage.

There’s a number of elements in this story, from the damage to the trust in our regulators and markets, to the ick factor of eating an animal many consider to be an intelligent friend to the reports that the meat may be contaminated with pharmaceuticals.

It doesn’t help when you have newspaper accounts breathlessly reporting that the meaty treats in question have “cancer causing chemicals” in them. So, what is going on?

The chemicals in question are phenylbutazone, also known as bute) and its breakdown products (mostly oxyphenylbutazone).

Phenylbutazone is a Non-Steroidal Anti-inflammatory, one of a large class of structurally diverse compounds that reduce inflammation and are, well, not steroids. Other compounds in this class are things like aspirin, indomethacin and ibuprofen. They all work by inhibiting the enzyme that makes the signalling molecules that result in inflammation (steroids, such as prednisone, switch off the gene that makes this enzyme).

Phenylbutazone was a reasonably effective anti-inflammatory, which was often used in Ankylosing spondylitis when other anti-inflammatories failed. Unfortunately, it had a high rate of side effects. The most important were aplastic anaemia and agranulocytosis, where the patients bone marrow failed.

The blood disorders side effect was rare, about 14-22 people contracting them per million prescriptions, but considering this side effects severity the drug was pulled from the human market.

However, phenylbutazone is a very effective veterinary anti-inflammatory, especially in horses (I can find no reports of aplastic anaemia in horses, although it occurs in dogs). When phenylbutazone was banned, it was banned not only from human use but also from being present in all food producing animals, which created a bit of a problem with horses.

In the UK and Ireland, horses are not seen as a food animal, whereas in many parts of Europe they are seen as food animals. Faced with the possible loss of an effective anti-inflammatory agent, veterinarians negotiated a system in the European Union where animals (usually racehorses) that were treated with phenylbutazone were issued with certification (a “passport”) that they would not enter the human food chain.

This would all be well if all the traders adhered to this certification, but it’s is now clear that the meat trading system is not as accountable as one would wish.

It is not yet clear that any of the horse meat in the suspect meat products actually comes from animals treated with phenylbutazone. While some animals sent for slaughter have had traces of phenylbutazone, it has not been found in any meat products yet.

While Woolworths has announced it will conduct DNA tests on its home-brand meals, what is the risk from potential contamination with horse meat?

Not much. Phenylbutazone is relatively rapidly removed from a horses system, if your meals were made 100% from horses that had been injected with phenylbutazone just before slaughter, you would need to eat about a kilo of that meat a day every day for over a week to get the kinds of concentrations needed to see serious side effects.

That is not going to happen, any realistic level of phenylbutazone will be much, much lower than the scenario I outlined above, and the overall risks are minute.

But the low risks are beside the point, the fact is that the surveillance and tracing systems failed big time. Good food policy needs reasoned debate, which can’t happen when people are hyperventilating about a minimal risk.

This weekend the asteroid 2012 DA14 will zoom across our skies, just below the geostationary satellite orbits. While Australians are fortunate in that they have a chance to view this otherworldly rock, there is a deeper Australian connection.

On the 13th of January, a month ago, nearly 10 years since the Mount Stromlo observatory was destroyed in the Canberra fires, fire ripped through the iconic Siding Spring Observatory. Through a combination of good planning in the wake of the Mount Stromlo fire and the heroic work of the New South Wales fireies, none of the telescopes were seriously damaged. However, some of the infrastructure and some of the astronomers homes were destroyed. One of the homes that were destroyed belonged to Rob McNaught.

You may not know the name, but many of you will have seen one of his comets. In January and February of 2007, comet McNaught was a spectacular sight as its tail arched across the south-eastern sky. Rob is the worlds premier comet hunter, and an inspiration to amateur astronomers like myself. One of my prized possessions is a signed poster of his iconic comet.

Losing your home to fire is a devastating experience, one shared by many Australians this fire season (although Rob has reacted with characteristic good humor). However, this personal tragedy has obscured another important loss. Rob McNaught has failed to gain funding for his work at the SSO.

For Rob is not just a comet finder, he also helps protect our planet from death from the skies. He’s the man who searches the southern skies for asteroids that might hit the Earth. For years Rob has toiled to locate these objects before they pose a danger to us. Or was, as Rob has failed to gain funding, since January 2013 there is no dedicated survey of the southern skies for potentially hazardous Near Earth Objects.

Now Rob is just one of a legion of deserving people who failed to be funded, but this particular case has special implications. If most of you have thought of hazardous Near Earth Objects, you may have thought of them in terms of the movies Armageddon or Deep Impact. Large planet killers that we can do nothing about. Or maybe you think that these impactors are so rare that we don’t need to worry about them (after all, the last planet-killer was 65 million years ago).

But planet-killers are not the only worry. The 50 meter Tunguska impactor flattened 2,150 square kilometres of empty Siberian forest, but would have been devastating if it hit a populated area. Even relatively small asteroids, say the size of a house, would cause serious damage if they hit a city. These events are still relatively rare, but at a likelihood of one every 5 years, they need to be taken seriously (luckily most of these 10 metre ones disintegrate in the upper atmosphere and/or impact over water).

Importantly, these small ones can easily sneak up on us, often we have no more than 24 hours notice before they swing by. Rob has been instrumental in finding some of these. We can’t stop them, but 24 hours is enough time to evacuate a potential target area and prevent great loss of life if these sneaky rocks are headed for impact.

But now our eye on the southern sky is going blind.

And it’s not just about loss of life, although that gets the most headlines. Last year a couple of these rocks barrelled through just above where our satellites orbit. As I mentioned above this Saturday the NEO 2012 DA14 will pass through the region of space where our satellites are. An asteroid smashing into a working satellite could potentially disrupt communications or vital earth sensing operations and will generate hazardous debris threatening even more satellites. The chance that a sizable rock can zoom through our satellite band is far and away higher than one hitting us.

Again, while these things can creep up on us, even 24 hours notice could give us time to move some satellites. But with half of the sky now being free from dedicated surveillance, that chance that these rocks can sneak through is much higher.

Previously on the Conversation a series highlighted the free ride Australia gets in space in terms of satellite access, yet again Australia is abrogating it’s responsibilities in space, but this time our lack of responsibility could have a much higher impact.

Some more background on the importance of Rob’s work and the funding situation is here.

PS. If you want to contribute to the Coonabarabran and Siding Spring fire relief funds go here.

This Australia Day, you might be feeling a little nervous as you slap your slightly carbonised sausages or lamb chops on a melamine plate if you have read news coverage of research just published in the Journal of the American Medical Association. Will you get more than the tomato sauce covered treat you have been looking forward to? Will you get an extra helping of melamine?

Melamine is the base chemical which makes the robust melamine plastic tableware we so love because of its durability. Melamine (the base chemical) is also infamous as an illegal adulterant in pet food and children’s milk formulas. The milk contamination event resulted in the deaths of six children and kidney problems in many more.

The levels of melamine that caused these problems was enormously higher than that we are likely to consume from our normal diet. However, long term consumption of lower levels of melamine may be associated with an increased risk of kidney stones (although the falling incidence of kidney stones in women is evidence against this idea).

Where would we get melamine from in the first place? Some research has found that placing very hot fluids (distilled water and acetic acid) in melamine plastic tableware for 30 minutes can cause melamine to leach into those fluids.

However, the effect is only really significant at temperatures from 60 degrees centigrade and up, with the highest levels found when fluids are kept at 90 degrees centigrade for 30 minutes. The relevance of this to standard food serving is unclear.

The new paper by Wu et al provides a more relevant study of melamine exposure from food. Wu et al show that hot (90 degree) soup will leach melamine from melamine plastic soup bowls and this melamine is absorbed by the body and excreted in the urine.

They showed that the melamine is very rapidly excreted. Importantly, the total levels of melamine excreted suggest an exposure to melamine over 600 times lower than the most stringent exposure limit[*]. This is despite the researchers using a brand of melamine ware with the highest melamine leaching on contact with hot fluids.

What we don’t know from this report is whether the contact time with the soup was representative of standard household or restaurant use (how many families will serve soup at 90 degrees C, not that far from boiling) and if, like the leaching experiments, the soup was held at 90 degrees centigrade for 30 minutes.

If anything, it is likely the risk from standard household use is even less than this study indicates.

The Wu et al study suggests that even with a melamine ware that has a very high level of melamine leaching, under conditions that favour melamine leaching, the level of melamine exposure that results are extremely unlikely to have any health impacts.

However, the fact that even small amounts of melamine can leach from these ubiquitous food containers at high temperatures should make us cautious.

It may be useful to test melamine tableware for melamine leaching, and only permit the sale of low leachant tableware. It may also be prudent to avoid keeping very hot foods in melamine bowls for extended periods of time.

What about your Australia Day chops? The surface of hot meat hitting your plate cools down very rapidly, and there is very much less surface area in contact with the plate (unlike fluids which evenly spread on the plastic surface), so you can bite into your chops and snags with confidence.

[*] The US FDA uses a limit of 0.063 milligrams melamine per kilogram of body weight to be the safe limit consumed daily, the WHO uses a limit of 0.2 milligrams melamine per kilogram of body weight daily

If you have been reenacting a crossing of the Simpson desert for the past two years, or are a recently returned hermit, they you are probably unaware of the forthcoming Mayan Calendar Apocalypse.

To briefly recap, the Mayan Long Count calendar ends on December 21, and various people are holding forth on the fount of all wisdom, the Internet, that this will result in Something Bad ™. Whether this Something Bad ™ will be catastrophic tectonic activity, asteroid impacts or rains of frogs is left unclear (as is why a changing of the calendar will result in more catastrophes than normally associated with New Year festivities).

A recent paper in the Canadian Medical Association Journal has investigated the effects of the Mayan Doomsday (hereafter called MaD) on the conduct of clinical trials.

They conclude that all clinical trials should stop immediately as MaD is a (ahem) significant confounder.

However, this landmark paper has alerted me to the fact that there has been little investigation of the toxicological effects of MaD. This requires us to define the survivor population of MaD, and the likely mechanism of MaD.

Fortunately Wheatley-Price, Hutton and Clemons have already defined the likely survivor population. This includes zombies, other undead, the Grateful Dead, Dungeons and Dragons players and men who have read “Fifty shades of Grey”.

As a member of the expected survival cohort (Dungeons and Dragons DM, ask me about my “Gilligan’s Island meets Call of Cthulhu” adventure), I have a vested interest in understanding the toxicology of MaD.

Now we have to identify key toxicological hazards in the post MaD environment.

If MaD is due to tectonic activity, as well as devastating earthquakes we can expect a large increase in volcanic activity and widespread lava flows. This will result in large amounts of carcinogenic polyaromatic hydrocarbons (PAH’s) such as benzo-a-pyrene from the widespread combustion of organic matter. As well, large amounts of fluorine will be released into the environment.

If MaD is due to an asteroid impact, we will get PAH’s from wildfires as with tectonic activity, and the release of large amounts of the heavy metal iridium into the atmosphere with dusty particulates. If the impact is big enough then we will get earthquakes and volcanic activity as well, adding fluorine to the atmospheric contamination.

If MaD is due to a rain of frogs, then aside from the obvious ickyness of having a landscape covered in swarming squamous amphibians, there is no toxicological issue unless the frogs are poisonous.

Zombies, by not breathing or having a functional circulatory system, should be immune to the effects of the carcinogenic PAH’s, fluorine, iridium and frog poison. If anything a slight coating of PAH with added iridium should make them slightly less subject to decay.

The effects on the zombies who consume the brains of living survivors who are contaminated with PAH’s, fluorine and iridium are conjectural, but this may coat and denature their decaying intestines, rending them unable to obtain whatever it is zombies get from eating brains.

Similar considerations apply to other undead, although vampires are generally more fastidious, and may shun contaminated survivors.

The Grateful Dead (and similar septuagenarian rock bands), having survived all the carcinogens and drugs consumed during the 60’s and 70’s and beyond, will be unfazed by PAH’s, fluorine and iridium (hey, it’s heavy metal after all). They are also likely to lick the frogs in the hope of obtaining a high (the frogs are more at risk here).

The Dungeons and Dragons players are mostly techno geeks, so we will have constructed chemical warfare protection from old plastic Macintoshes, half a coke bottle, and baking soda. And zombies? Pfft! We Geeks have been preparing for the Zombie Apocalypse [*] for ages. Who created the mathematical model of surviving the zombie apocalypse? Who was behind the American Center for Disease Controls’s Zombie Apocalypse preparedness sessions?

So who bears the brunt of the volcanic and asteroidal ash giving them silicosis? Who gets lung problems from the PAH’s? Who get fluorosis swelling their joints and crippling them? Who gets febrile hallucinations from the poison frogs? Who then can’t run away from the Zombies due to their crippling health problems?

Why, the Men who read “Fifty Shades of Grey”. While the Geeks inherit the Earth.

I can’t see any downside to this, can you?

[*] We will pass lightly over the inevitable battle between the Vampires and the Zombies for the last FSOG readers, although the D&D players have large quantities of popcorn stockpiled. Why won’t the vampires go after the D&D players? I told you that vampires have good taste.

The difference between today and 2002 could have hardly been more stark. Then, a knot of us waited in the desert on a slight rise over an ancient ochre mine. The air was dry and the sun was setting over a gibber plain while the wind lashed at us.

This time, I was on a lush green hill in tropical North Queensland. The rising sun sparkled off the sea as we breathed in the humid air waiting for syzygy.

Syzygy is an alignment of planetary bodies, in this case the sun and moon, creating a solar eclipse, the first total solar eclipse in Australia since 2002. Below us, thousands of people were lined up on the beach waiting for what was, for many, a once in a lifetime event. For others – the eclipse followers – this was one more eclipse they had travelled across the world to see.

Up and down the coast, and inland, the scenes were the same, from families with eclipse glasses to serious eclipse watchers with serious telescopes and cameras with alarming telephoto lenses. But all were bound by the desire to see a rare but amazing event.

We are at an unusual point in Earth history, the moon is big enough and far enough away from Earth that when it (very occasionally), passes in front of the sun it just covers it, so we get darkness and spectacular views of the solar corona. You can see eclipses from Mars when its moon Deimos passes in front of the sun – but with only about a third of the sun covered. It’s not as spectacular as the view from Earth. But at least on Mars you don’t have to compete with thick, orgulous rain clouds.

I’d picked out my spot to view the eclipse carefully. Yorkeys Knob (in Cairns) doesn’t climb far above the sea, but it does climb a bit and had spectacular uninterrupted views to the east. Don, the sailor I was staying next to, said when he climbed Yorkeys, he pre-dialled 000 and walked up with his finger on the send button, ready for the incipient heart attack. He wasn’t joking.

When I got the feeling back in my legs, I set up my camera and binocular projection system amidst a crowd of far fitter onlookers.

The sun rose above the peak jutting out in the sea, glowing with promise. And then ran smack into a bank of cloud.

The sky, which had been fairly clear except for a band of cloud hugging the horizon, was suddenly filled with the kinds of dark pendulous clouds that promise a good soaking. So began a game of hide-and-seek, as the moon slid over the sun. We had brief glimpses of the increasingly crescent sun as gaps in the cloud came over. Finally, large chunks of the sky were clear except for one persistent cloud which was squatting, you guessed it, right over the sun.

Suddenly, the light went out as if some one had thrown a switch. There had been a pool of light underneath the recalcitrant cloud, and that too vanished. Everyone on the hill gasped or cheered. We waited, the cloud waited.

Then all of a sudden the light appeared again, a thin sliver of sunlight, like a glowing wire, broke through the cloud. We had missed totality, but we were able to see the sun appear from behind the moon clearly. After a little while, when the sun was still making crescent shadows in the leaves of the nearby trees, people started to wander off, and by the end, only a few of the diehard were left to watch the moon slide off the sun.

Each eclipse is different, and even the the same eclipse can be different from different locations. Up our end of Yorkeys and next door at Trinity beach (my other favoured location) the eclipse was hidden. Down the other end of the beach, they saw totality. Cairns was clouded out, but Palm Beach and Mareebra clear for those critical moments. Even out of those who had gone to sea to escape the cloud, some succeeded, some didn’t.

Me, while I’m sad I didn’t see the corona, I still had a marvellous experience that I am glad I didn’t miss. The next total eclipse in Australia is 2028, so I’m making plans again. But for the moment I’ll bask in the memories of this one.

There’s just two sleeps to go until the Solar Eclipse on Wednesday 14 November 2012. This is the first significant solar eclipse since 2002. If you want to make a last minute dash to north Queensland to get in the path of totality, you are probably out of luck. Flights and accommodation will be hard to get (and quite expensive), and there are no hire cars to be had for love nor money.

I’m heading up to Cairns myself, but if you are staying home, then most of Australia will see a very nice partial eclipse. There is still plenty of time to organise safe solar projection devices, but if you want to buy eclipse glasses or solar filter material then you will have to get a move on.

I have a reasonably comprehensive web page for eclipse viewing, as well I have a handy, printable PDF page that lists a whole bunch of eclipse times  which you can carry around with you. It also has a bunch of things for kids to do.

The eclipse starts shortly after sunrise. Here’s a quick table of eclipse times to whet you appetite for the upcoming event.

City	State	Time Zone	First Contact	Mid Eclipse	% Sun Covered	Last Contact
Adelaide	SA	ACDST	6.42	7.33	52%	8:22
Alice Springs	NT	ACST	5:27	6:16	73%	7:10
Brisbane	QLD	AEST	5:56	6:54	83%	7:58
Cairns	QLD	AEST	5.45	6.38	100% (total eclipse)	7.40
Canberra	ACT	AEDST	7:10	8:03	62%	9.02
Darwin	NT	ACST	5:17 (below horizon)	6:06 (just below horizon)	98%	7:00
Hobart	TAS	AEDST	6:55	7:44	45%	8:36
Melbourne	VIC	AEDST	7:15	8:05	53%	8:59
Mossman	QLD	AEST	5.44	6.38	100% (total eclipse)	7.40
Perth	WA	WADST	5:21 (below horizon)	6:00 (just below horizon)	40%	6:41
Port Douglas	QLD	AEST	5.44	6.37	100% (total eclipse)	7.39
Rockhampton	QLD	AEST	5:51	6:48	90%	7:52
Townsville	QLD	AEST	5:47	6:42	96%	7:43
Sydney	NSW	AEDST	7:06	8:01	68%	9:02

The recent announcement that Alzheimer’s disease may develop up to 20 years before we can diagnose it by conventional means comes as a coda to a year of turmoil in Alzheimer’s drug development.

The drug company AstraZenica recently announced that they were going to start pushing to develop novel anti-Alzheimer’s drugs. Coming the day after I participated in a media briefing on the recent failures in Alzheimer’s drug development (hey, according to the ABC I’m a leader in Australian Alzheimer’s research, so it must be true. Take note NH&MRC) and the massive disinvestment of drug companies in drug development for the central nervous system (AstraZenica in particular had just decimated its CNS drug development) this was quite a surprise, with a hint of irony.

However, this is an opportunity to give people an insight into how drugs are developed, And why things are rarely smooth. Drug development for Alzheimer’s disease in particular has been very frustrating with a number of high profile drugs that had been slowly moving through the drug registration process having failed, in at least one case quite spectacularly. In the face of this stream of failure, many people are thinking we need to completely rethink what we know about how Alzheimer’s disease (AD) comes about.

AD is just one of many dementias that affect people as they age, but it is the most common one in Australia and most of the developed world. AD incidence increases sharply with age, around 1 in 4 people over 85 years old will be affected by the disease. While most people are aware that AD is associated with increasing memory loss, which is distressing enough in itself, fewer are aware that AD is now the third biggest killer of people over 65. The handful of drugs that we have for AD simply slow the progression of the disease and don’t treat its causes.

In someone with AD, the brain shrivels, however this is the end stage of a much longer process. Until recently, the only way to really determine if someone is suffering from AD or one of the other dementias was to scoop their brain out, slice it up and look for some key pathological hallmarks (not surprisingly most elderly people object to this).

Aside from brain shrinkage there are tell-tale accumulations of protein, dead and dying nerve cells and inflammatory cells called amyloid plaques. With special stains we can also see abnormal tangles of protein inside the nerves.

The protein that forms the plaques, beta amyloid (Aß), is thought to be a key player in AD. Your body makes Aß as a normal part of your brain function. However, normally this protein remains soluble and is cleared from the body. For reasons that are not clear, in AD the Aß folds into a different shape which makes it start to link up with other Aß proteins to make huge insoluble aggregates.

These aggregates (or the clumps of protein leading to the aggregates) are directly toxic to nerve cells (a large part of my research involves squirting aggregated Aß onto pretend nerve cells then trying to stop them dying). They also stimulate the special inflammatory cells in the brain to secrete a range of substances as if they were responding to invading bacteria. But with no bacteria about nerve cells are collateral damage.

We know that in people who have mutations in the Aß protein, or the enzymes which make it, are more likely to develop Alzheimer’s, we know that people who have more copies of the Ab genes are more likely to develop Alzheimer’s. We know that people who have a variant lipoprotein that is not as efficient at clearing Aß are more likely to develop AD. Dogs, who have a similar Aß protein to us, develop an Alzheimer’s like disease while rats and mice whose Aß is different from ours don’t.

When we put the mutant human genes for Aß and its processing enzymes that are associated with high risk for Alzheimer’s into mice, they develop plaques and a number of features (but not all), of the human disease. All this is consistent with Aß being a key player, and a potential drug target.

So drug development has focused on inhibiting the enzymes that make Aß and finding ways to clear Aß from the body, the lead compound for clearing Aß being antibodies.

And they have all been abject failures. More than failure, one of the drugs that inhibited the formation of Aß made people worse. Some people picking over the smoking remains of one of the antibody trials think that there are faint indications that something good might be happening, but scepticism abounds.

How could this have gone so wrong? Biology is complicated, especially the central nervous system, with a huge number of cell types and hormones and neurotransmitters all with multiple and subtle interactions, and the potential for things to pear-shaped is quite high. Even in (comparatively) simpler systems things we think we understand can do as they dashed well please (as a cancer researcher about angiogenesis inhibitors some time).

With such a series of high profile failures, people are suggesting that we need to completely revamp our understanding of the causes of AD and dump Aß as a central player. Even being a dedicated Aß researcher, I’m sympathetic to this idea, but the fact is everything we have tried in AD has failed miserably.

Since 1998 there have been 101 drug trials for AD which have attacked every conceivable mechanism we think is at work in AD. This has resulted in only 3 new drugs, which are variants of the existing disease slowing drugs and don’t attack the underlying cause at all.

Since you won’t get much change from a billion dollars for each drug that makes it into large scale clinical trials, these failures represents a massive hemorrhage of funds from the companies trying to develop anti-AD drugs.

Even when we target other processes we know are involved in AD, such as inflammation and oxidative stress, we have had no success. That goes for Ginkgo and fish oils as well. Given this all pervasive failure of everything, something else must be going on.

And that thing may be time.

This is where the new research comes in. Using a range of sensitive tests for brain function, and detecting the rogue Aß protein in blood and cerebrospinal fluid in people who have a mutation in the Aß gene that makes them more susceptible to AD, the researchers were able to find increases in Aß, changes in brain structure and subtle reduction in brain function up to 20 years before most of these people were due to develop detectable disease.

If the same finding holds true for the vast majority of AD sufferers who do not have this mutation, damage may begin as early as 20 years before we see the frank disease. Our current attempts to treat AD may be far too late to help. By the time we get to diagnosing AD or even the milder forms of memory loss that precede AD, there will have been substantial but subtle damage to the nerve cells.

Right now there is a big trial about to start using a variety of preventative drugs in people with the mutation when they are young, to see if AD can be stopped this way. We will have to wait several years for the results, but we may finally be making inroads into this distressing disease.

Every year consumer advocate Choice magazine hands out its “Shonky" awards for products that, to put it mildly, do not live up to the manufacturers claims of effectiveness or quality. Being on the shonky list is no badge of honour. This year we have a fine crop of shonkies, but what caught my eye was number 8 on the list, Natures Way homoeopathic medicine for kids. This citation joins other such distinguished award winners as Sensa Slim and the Power Balance bracelet.

You can read the citation in full over at the choice website, so I won’t simply reiterate the points made in that article. Well, okay,I will. Unlike many homeopathic medicines, these ones actually have some (although minute) amounts of substance in them. One of these is Nux Vomica, otherwise known as the poison strychnine.

To be fair, the strychnine is only present in a one in a trillion dilution. As we have no idea what the starting concentration of strychnine was before they started diluting it, all we can say is the concentration is slightly higher in these remedies than if you waved a strychnine plant vaguely in the general direction of a bottle of this “medicine”.

Am I the only one who finds it ironic that with the current anxiety about “toxins”, and the popularity of “detox diets” and “detox remedies”, that people are willing to give a solution containing a real, bonafide toxin to their kids (albeit insanely diluted).

It is even more ironic that people are worried about giving their kids vaccines with minute, non-harmful levels of formaldehyde in them (levels lower that the kids own bodies produce naturally or are found in fruit), when there is strong evidence of the health benefits of vaccination.

There is absolutely no evidence that these products have any effect whatsoever, yet the worries that arise with vaccines don’t seem to surface with these strychnine containing products.

This is a well deserved Shonky, but sadly, I doubt it will change people’s habits.

You can vote for your favorite Shonky from the current crop here.

Image Credit: Ian Musgrave Australians can never look at the sky the same way again. When you go out tonight to look at the southern sky, you will know that alpha Centauri, the red star in the iconic pointers, the pair of stars that point to the Southern Cross, has an Earth-sized world orbiting it.

A hellish, red hot world, true. One that screams around it’s sun (alpha Centauri B, alpha Centauri is a triple star system) in just over 3 days. It snuggles closer to its sun than Mercury does to ours and its surface is most likely covered in a magma ocean. Not the place that bright eyed pioneers would fly to in gleaming silver spaceships.

But its a world around one of the southern hemisphere’s iconic and brightest stars. Sure we have something like 800+ confirmed planets around other stars, a fair few solar systems, and even one or two have planets in the hypothetical habitable zones of their suns.

But the vast majority are too dim to see with the unaided eye, or barely visible, and rejoice in names like GJ 1214b, Gleise 581 e, Upsilon Andromedae A and 55 Cancerii e.

Image Credit: Ian MusgraveAlpha Centauri Bb, simulated in Celestia with two of its three suns visible. 

In contrast alpha Centauri is bright, and part of an easily recognisable asterism. It looms large not only in the skies of the southern hemisphere, but also our fiction and imaginations.

In terms of our stepping stones into space, The Moon, Mars* and then alpha Centauri, the triple star system on our doorstep a little over 4 light years away, has loomed large. Alpha Centauri has featured heavily in science fiction too, and Pandora, the world of the Na'vi, orbits Alpha Centauri A. The new world orbits alpha Centauri B as mentioned above.

Could there be other planets in the alpha Centauri system, ones that are more like our familiar planets?

Certainly, although they may be hard to find. This new world (we have to think of a name for it, Mustafar is already taken, how about magmamare) was discovered by the slight doppler shift in its stars light as the planet tugged on its sun as it orbited.

This means in these kinds of searches its easier to find big things close to their suns (which explains why until recently most of the extrasolar planets we found were massive things bigger than Jupiter as close or closer than Mercury). To find a Jupiter- like world in a Jupiter like orbit, we would have to watch the system for 36 years (as we need to watch 3 orbits to make sure the signal is real).

So there’s a real chance that there are other, more familiar worlds circling the alpha Centauri system, and you can bet people will be looking for them now.

Next time you go outside and look south at the pointers, you will now know that there is a world, out there, not of our solar system, that is tantalisingly just beyond our reach.

You can find the original paper describing the discovery here. A good discussion at Nature, and another good article at Centauri Dreams.

*Venus, despite looking like Earth’s twin, never seems to garner quite the same attention, perhaps because Mars is in the direction of out.

Perfluorooctanoic Acid (PFOA) is in the news this week with two recently released studies. As you may remember from one of my previous articles, PFOA is persistent organic pollutant which can accumulate in the environment (including food, although most people are exposed to PFOA from drinking water). As well, it is quite long lived, and has the potential to reach levels which can affect our health.

The first paper (Perfluorooctanoic Acid and Cardiovascular Disease in US Adults) adds further information about the potential effects POFA on the heart and blood vessels. Previous animal and indirect studies have suggested that PFOA exposure may harm the heart and blood vessels.

The results of this cross sectional study suggest that adults with the highest levels of PFOA in their blood are more likely to have cardiovascular disease than those with the lowest levels.

However, there are a number of limitations which make interpretation of these results difficult. A cross-sectional study looks at the relationship between a disease and other variables (such as PFOA concentration in the blood) in a defined population at a single point (or short period) in time.

In this case the measurement of blood PFOA levels were done once either in 1999-2000 or 2003-2004 and the actual long term exposure to PFOA may be very different from that suggested by a single measurement. We know for example that blood levels for PFOA were falling during the study due to regulation of this chemical.

Also, the incidence of cardiovascular disease was self reported, which is subject to bias. The objective measure of blood vessel function had a much weaker association with PFOA. Unusually, the association disappeared in smokers and people with Body Mass Index’s less than 30.

As well, there were significant differences in lifestyle, education and background between the people with the lowest levels of PFOA and those with the highest. PFOA may simply be a marker for low socioeconomic status, which itself is known to be correlated with risk of cardiovascular disease.

Finally, studies of people who have been chronically exposed to significant levels of PFOA have not show statistically significant increases in cardiovascular disease for those exposed to PFOA.

The current study is suggestive, but is a long way from showing that exposure to the background levels of PFOA in our environment harms our heart and blood vessels. It requires follow up with studies that track exposure to PFOA to better understand the possible role of PFOA in cardiovascular disease.

The next paper is Maternal Concentrations of Polyfluoroalkyl Compounds during Pregnancy and Fetal and Postnatal Growth in British Girls. Here girls with higher prenatal exposure to polyfluroinated chemicals were smaller at birth than those with lower exposure.

However, it suffers from the same limitations as the previous study (a single measurement of the chemicals may not reflect the real exposure, and it is difficult to full correct for other environmental factors that may have a role).

As well, there were only 17 low birth weight girls in the sample, the result could well be by chance alone.

We should keep an eye on levels of pefluorinated compounds, and try to minimise our exposure to them as a matter of course, but there is currently no good evidence that the levels mots of us are exposed to are harmful.

Certainly more research is needed, but the current guidelines on minimising risk for cardiovascular disease and increasing baby health (including increasing consumption of fresh fruit and vegetables) are those that minimise exposure to these chemicals in the first place.

In many ways the history of the Olympics is the history of athletes trying to kill themselves with increasingly sophisticated drugs. In the original Olympics the athletes used various herbal stimulants and psychotropic mushrooms to give themselves an edge. In the modern Olympics and competitive sport generally, almost as soon as a drug has come on the market, it has been (Ab)used in competitive sport. From cocaine to nitrous oxide, from amphetamines to beta agonists to erythropoietin, drugs have been taken up with verve despite limited evidence they actually improve performance and the occasional death.

Possibly the strangest performance enhancing drug was (is) Strychnine.

Strychnine?

Aficionados of murder mysteries will immediately recognise Strychnine as a poison. Agatha Christie preferred arsenic to Strychnine it is true (and even arsenic has been used as a performance enhancing drug), but Strychnine is one of the top poisons in our consciousness.

Strychnine is an alkaloid found in many species of Strychnos plants, but in the west we mostly get it from Strychnos nux-vomica. Extracts of this plant are widely used as poison arrow/dart toxins. Strychnine is a tetanising poison. It causes convulsive muscle contractions that can tear muscle and snap tendons, and which ultimately stop breathing.

Strychnine does this by interfering with the inhibitory neurotransmitter system, which puts a brake on the stimulatory nerves. Without this moderating influence the excitatory signals to muscles can almost literally tear the body apart.

This would make Strychnine an unlikely performance enhancing drug but for Paracelsus’s dictum. Several traditional African medicines use Strychnos extracts that have been treated to lower the toxin content. Some of these are increase blood pressure. Low doses of Strychnine give people a subjective feeling of stimulation, although it’s not clear that Strychnine actually does increase performance.

While low doses of of Strychnine do increase swimming activity in lampreys and tadpoles, it’s hard to say if this will translate to sustained increases in performance needed to give elite athletes the edge.

Certainly strychnine consumption has been associated with adverse events, the first recorded sporting death in the modern era (Arthur Linton in 1896) was possibly due to Strychnine consumption. But then again, athletes of that time consumed cocktails of many drugs. These could contain combinations of caffeine, cocaine, alcohol, ether and strychnine.

Thus when Thomas Hill collapsed after completing the Olympic marathon in 1904, it is impossible to tell if it was the 2 milligrams of Strychnine his manager gave him during the race, or the copious amounts of brandy that he consumed that was responsible. Strychnine use was so common that athletes became habituated to the drug, and could tolerate doses that would kill ordinary people. Strychnine is one of the few illegal drugs with a minimum performance level (200 ng/mL).

Times change, endurance event organisers no-longer provide athletes with free drugs. Strychnine is now banned, although every so often people are caught using it. You might think that athletes would balk at consuming a poison, but in the drive for glory, commonsense often gets left in the dust.

The Therapeutic Goods Administration (TGA) has considered a proposal to list 1,3-dimethylamylamine (DMAA) as a schedule 9 compound. Schedule 9 compounds are prohibited substances which have no therapeutic potential, for example Heroin (although there is the possibility of therapeutic use for this drug).

The TGA has now made a ruling, announced today, and placed DMAA in appendix C of the scheduled drug list.

Well, that’s all very nice, but what is DMAA and why on Earth should I care

Well, it’s obvious you are not a body builder.

DMAA is an aliphatic amine which looks a bit like amphetamine. Although it is a stimulant, it is not clear if DMAA actually works like amphetamine. DMAA was introduced as a nasal decongestant by Eli Lilly in 1948, but was withdrawn in the 1970’s.

DMAA was reintroduced as a natural supplement, based on it’s alleged presence in Geranium extracts. However, it turns out Geraniums have no DMAA in them, and all DMAA in supplements and pills would appear to be synthetic.

The sports and dietary supplement industry put it in various preparations for weight loss and performance enhancement. DMAA seems to be used most in pre-workout supplements, although recently DMAA has been in use as a party drug. The party drug use was a significant concern in the TGA’s deliberation.

The supplement users reacted with some incredulity (and a lot of stockpiling) to the impending ban on DMAA. DMAA is banned by most sporting bodies for use by athletes, but that is because it is a stimulant, and stimulants in general are banned by sporting bodies. Is DMAA really as bad as Heroin?

With the recent ruling, it appears the TGA thinks DMAA is as bad as Borage.

What, Borage, the herb?

Yes, borage (suspected hepatotoxicity).

Oh come on, it looks like amphetamine, it’s got to be bad surely

Merely looking like another compound is no guarantee that something will have the same properties as that compound, as drug companies have learnt to their cost, even small changes in structure can have big effects on how fast a substance breaks down, or activates biochemical pathways.

Data on the potency and mechanism of action of DMAA is hard to come by. You have to go wayback in time to find some of this data. For example The Dispensatory of the United States of America 1950 Edition, reports that DMAA’s systemic toxic effects in animals were “greater than that of ephedrine and less than that of amphetamine,” .

Experimental administration of DMAA to humans at levels consistent with supplement use, alone, or together with caffeine (which is in a lot of DMAA containing supplements), shows DMAA can cause a modest increase in blood pressure taken as a one off dose. If you take it for 10 days or more blood pressure appears to return to normal (doi: 10.4137/NMI.S8568, doi: 10.4137/NMI.S8885).

Outside of these controlled experiments DMAA has been associated with a number of adverse events, such as panic attacks, seizures, stress-induced cardiomyopathy, and is suspected to be involved in two deaths. While these reports are consistent with the known pharmacological effects of DMAA, causation has not been established in these cases, especially as DMAA is often consumed with high doses of caffeine, which has also been associated with similar adverse effects.

However, in New Zealand, consumption of DMAA as a party drug has been associated with a case of cerebral hemorrhage. It is almost certainly the use of DMAA as a party drug that has the TGA most worried.

What we also don’t know is how frequent these adverse events are (again, this assumes that DMAA is the only culprit in theses events, the caffeine may also contribute in the events associated with supplements).

Given the relatively few reported events and the widespread use of these supplements, we might suspect the frequency is low. But we also know that adverse events are under-reported, and the exact number (or even ball-park number) of users is unclear.

So the extent of physical harm caused by DMAA is uncertain, although probably less than for amphetamine if we go by emergency admissions. The addictive potential of DMAA is not known, but is also probably less than that of amphetamine.

Sounds like we should treat it like amphetamine

Well, if we are to consider it to be exactly the same as amphetamine, then the appropriate schedule would be schedule 8, not 9. However, it is extremely unlikely that DMAA is equivalent to amphetamine. This was the approach taken in today’s TGA ruling.

So what would be appropriate? Caffeine is used in a similar way in supplements, and in energy drinks is associated with a similar spectrum of harms to DMAA with at least one reported death, should the TGA have treated DMAA like caffeine?

Classification of any drug must balance benefits and harms. Making body-builders feel as if they have more energy is not much of a benefit when compared to even a small possibility of cardiomyopathy and other cardiovascular harms.

Ironically, it seems DMAA may not be much of a performance booster, at least, it doesn’t improve running performance. We have no empirical evidence other than testimonials that DMAA improves anything else, it may just be a placebo.

And the use of DMAA as a party drug, where very large amounts may be taken increasing the likely hood of serious cardiovascular harm or death, is the real worry. On the other hand, treating a mild stimulant as if it were as harmful as heroin was an overreaction.

So what is this appendix C classification?

It’s for drugs and chemicals that can be harmful but not so harmful as to warrant listing as schedule 9. This listing is acknowledges that DMAA is not as harmful as heroin, but still harmful enough to remove it from use.

I used the example of Borage before. Borage is a herb that was used as a herbal medicine, but it caused liver damage. Now it is illegal to make herbal medicines that contain Borage. On the other hand no none has ever been busted for having Borage growing in their backyard, whereas growing opium poppies would get you in trouble quick smart.

Body builders will be annoyed, but it is very hard to argue that making body builders feel like they have more energy outweighs preventing harmful DMAA use, cerebral hemorrhage is a terrible price to pay for a party drug buzz.

So what will bodybuilders do for stimulants now?

They already take bucket-loads of caffeine, it’s doubtful they need more.

Speaking of Caffeine, shall I fire up the espresso machine?

Certainly!

It is a truth universally acknowledged that a person in want of coolness is in want of a tan. And increasingly, that tan is coming out of a bottle. To get the kind of deep-all over tan that Aussie legend is made of takes hours out in the sun that could be better spent playing the latest sporting game on your computer console du Jour. And let’s not forget Australia’s world record skin cancer rates, as the SunSmart message gets through our tans now follow the shape of the rashies we wear.

So, if we are off to a special event and don’t want to look like pallid addicts of daytime reality shows/computer games, more and more Australians put on a fake tan. A recent American expose may have people thinking twice or even thrice before slapping on that tan. As it turns out, there are some things to be concerned about, but they are not really what you might think.

At the heart of the worry is a chemical with the unprepossessing name of dihydroxyacetone (DHA, not to be confused with another DHA, Docosahexaenoic acid, which is used as a food supplement). This is the active ingredient of most fake sprayon tans. Sounds toxic doesn’t it? Well, it’s actually a simple sugar you body makes as part of normal metabolism. Your cells will happily slurp it up and burn it for fuel.

But your body makes formaldehyde too, and you wouldn’t want to slather that on your skin. What it comes down to is the dose, and, as readers of this column know by now (say it after me), it’s the dose that makes the poison.

You know the wonderful brown of a crusty loaf of bread? Well the same chemical reaction between sugars and proteins in the bread dough that makes the crust brown is how DHA makes your skin brown. Because DHA is more reactive than sugars like glucose though, you don’t have to sit in an oven for half an hour or so.

Glucose, although much slower at reacting than DHA, can also do these reactions at body temperature. One of the problems that diabetics can have is that after many years of high blood glucose levels, the slow reaction of glucose with the proteins in their blood vessels damages them and leads to circulation problems, kidney problems and eye problems.

So, even though DHA is an important metabolic fuel, you might suspect that high levels would cause problems. And if we incubate bacteria or mammalian cells with high concentrations of DHA, we find that the cause the sorts of damage that we suspect will lead to cancer and other problems. Of course, marinating a thin layer of cells in a petri dish with high concentrations of DHA doesn’t exactly mimic what happens when you slather it on your skin.

After all, the brown colouring you crave is due to the DHA reacting with the outer layers of keratin in your skin. Only a minute fraction of what you apply to your skin gets anywhere near living cells, which will promptly slurp it up to use as fuel. When we give very large doses of DHA to animals, for a very long time, very little happens to them.

In toxicological terms, the difference between what you get exposed to through your skin, and the lowest levels that are seen to cause effects in animals, is the Margin of Safety. The Margin of Safety for DHA applied to the skin is around a thousand fold for the worst case exposures we can think of.

But, and you knew there would be a but didn’t you, this is for DHA applied to skin, which is okay if you are rubbing on a lotion or cream. But what has happened in the last few years, and the focus of the American ABC report, is the rise of the spray tan.

While DHA wending it’s way through layers of keratin is vastly reduced in concentration before it reaches any living cells, what happens if we breath in droplets of spray?

Droplets of spray with relatively high concentrations could come in direct contact with the living cells lining the nose and lungs. This will be still be a relatively small dose, as only a fraction of the fine spray will get in, but still the effects of low, persistent exposure of these tissues to DHA is unclear.

In theory, people getting spray tans (at least in the US and Denmark), should be instructed to keep their mouths closed and be wearing nose filters (there are a number of different spray methods, and the exact details of the filter systems will be different for each method). But the issue found by the American ABC was that these instructions were not being followed. In Australia, my very, very small informal survey suggests that nose filers are not used here either.

Even then, the customers are at relatively low risk, even if they come back once a week, every week of the year. The ones at higher risk are the attendants running the booths. They are further away from the mists produced, but they are there every day of the week. Unless the salon has adequate air flow and exhaust fans, the possibility of chronic exposure the DHA is quite real, and we have no idea what the consequences of this exposure is.

There is no need to panic, but if you do indulge in spray on tans, it would be a good idea to be moderate in your use, and go to salons that use best practise safety. If you run one of these salons, please check the is adequate ventilation and air exhaust to lower your exposure.

Memo to CAM enthusiasts, try not to shoot yourself in the foot publicly next time.

I am, of course, referring to the recent article in the Medical Journal of Australia “The Legitimacy of Academic Complementary Medicine” (conversation article here). This is a supposed reply to the article “Tertiary education institutions should not offer pseudoscientific medical courses” (see the Conversation piece here).

The “Legitimacy” article pretty comprehensively misses the point of MacLennan and Morrison’s original. However, my article “What CAM courses at universities should look like” covers most of those misconceptions, so I won’t revisit them here. Instead I want to focus on the following statement, because it effectively destroys the credibility of the entire article.

"Complementary medicine, like conventional medicine, is riddled with poor scientific methodology and lacks a comprehensive evidence base. The BMJ compiles and updates the evidence for medical interventions (3000 to date) and currently considers that 51% of medical treatment is of unknown effectiveness and that only 11% is definitively beneficial, with another 23% probably beneficial.7"^[1]

Wow, that looks pretty bad doesn’t it, 51% of all treatments are of unknown effectiveness. Well, it does until you actually go to the referenced site (indicated by the 7). Why don’t you go there now? Scroll down to to the diagram the “Legitimacy” article authors got their figures from.

Now read the caption.

The “Legitimacy” article strongly implies that 51% of all current therapies have no evidence of effectiveness. But the diagram doesn’t mean what the “Legitimacy” authors think it means. As the caption makes clear, the scary figures do not relate to all, or even most, current therapies.

The site with the scary diagram is part of the journal Clinical Evidence, which publishes reviews of clinical trials that are performed to determine if therapies work (or are better than existing therapies, or don’t interact with existing therapies and so on). Not surprisingly, a lot of new therapies have not yet accumulated enough evidence to show they work (or fail to work) and more research is needed.

There is also the situation in which a given therapy works perfectly well for disease A, but the patient subsequently develops disease B. It is currently unclear if the drug for disease A will interfere with the therapy for disease B. However disease A is sufficiently serious you don’t want to stop the drug.

Not surprisingly, these sorts of situations are also under research. Importantly, most of these therapies (not all are drugs) have not progressed to general clinical use.

As a reality check, I looked at the Clinical Evidence summaries for heart failure (you’ll have to trust me on this unless you have a subscription to Clinical Evidence). Anti-platelet agents are listed as “unknown effectiveness”, the 51% category the “Legitimacy” authors imply are being used without good evidence.

Now, let’s go to the Australian Heart Foundation’s guidelines for treating heart failure. Are anti- platelet drugs being used as treatment for heart failure?

No.

This is just one example, but I checked quite a few to be sure. The “unknown effectiveness” treatments (not just drugs ^[2]) are mostly treatments that are not used in therapy, unlike what the “Legitimacy” authors try to imply.

This is the whole point of doing clinical trials, to find out if new treatments work, or are better than existing treatments, or can be combined with other treatments. Most complimentary and alternative medicine has nowhere near this level of evidence. In the cases where CAM has been extensively tested, most of it doesn’t work (see here, here, here and here).

To present a site which reports results of treatments being tested to ensure they work before they are used as a sign of the failure of modern medicine is to so profoundly misunderstand how medicine is conducted as to invalidate the rest of the argument in the “Legitimacy” article. At least next time read the caption to the diagram before you use the figures.

[1] Leaving aside, of course, the question of how the argument “some medicine is rubbish, so lets teach more rubbish” even makes sense.

[2] Exercise is only “likely to be beneficial” for heart failure. But you would want to include exercise for a range of other reasons (depending on how severe the heart failure as). This again illustrates how the “Legitimacy” authors fail to understand what the Clinical Evidence figures represent.

Here’s another interesting link of some relevance.

There is a persistent belief that drinking coffee is bad for you. Some alternative medicine systems eschew all coffee drinking (but are enthusiastic about coffee enemas). Certainly if you overindulge the sleeplessness and tremors will remind you of the perils of too much of a good thing. But there is a longstanding belief that long term consumption of coffee is in some nebulous way “bad”. This is despite coffee being packed with the sorts of antioxidants you would pay good money for at the health food store.

Now a new study suggests that people who drink coffee are less likely to die.

Wow! Great! I’ll just fire up the espresso machine then.

Hold on, firstly, the effect is modest, you are around 10% less likely to die if you are drinking 6 or more cups of coffee a day. Secondly, it’s an association. We don’t know if it’s the coffee drinking leading to less death, or something else which coffee drinkers are more likely to do.

Oh, so I should pack the espresso machine away.

No, there is now a fair bit of evidence that modest coffee consumption can give you some degree of protection against things like Parkinson’s Disease and Alzheimer’s disease (again though, we don’t know if it’s coffee per se that gives protection, or something else that coffee drinkers do). And coffee tastes good too.

But the apparent health benefits of any food or beverage should not be an excuse to overindulge, like the people who use the reported benefits of drinking modest amounts of red wine as an excuse to drink bottles of the stuff in one go.

So while I get the espresso going, what is the latest evidence?

A research team followed a group of nearly 400,000 people for 14 years, or until they died ( whichever came first). They gave the people extensive questionnaires about coffee drinking, food consumption, lifestyle and measured a range of health parameters at the start of of the study. Then after the 14 years they looked at the death rates in coffee drinkers and non-coffee drinkers.

They found that more coffee drinkers died.

Wait! What!

That’s the problem with looking at these sorts of studies simplistically. There are a whole other bunch of factors that influence death rates. In epidemiology speak these are called “confounders” (because They confound interpretation). It turns out that most coffee drinkers also smoke, so the increased death rate was due too smoking differences between coffee and non-coffee drinkers.

If the researchers had not measured smoking rates in the people, they would have been fooled into thinking that coffee was bad for you. This is also why we say that the coffee drinking – less death is just an association, the increased life-span could be due to something that wasn’t measured, even though lots of things were measured.

So how did they work out coffee drinking was good for you?

In epidemiology speak they “ controlled for the confounders”. If you compare just smokers who don’t drink coffee with those that do, coffee drinking smokers livers longer than non-coffee drinking smokers. Of course, it’s not quite as simple as that. When you have a lot of measurements you have to do some clever mathematics to sort it all out.

So is it a good study?

Yes, they had a big group of people they followed for a sufficiently long time, they only looked at people who were reasonably healthy when they started following them (so disease progress patterns couldn’t mess things up) and they measured a heck of a lot of lifestyle factors.

One problem is, as the researchers point out themselves, that they only asked people about their coffee consumption at the beginning of the study. So they had no way of knowing if people decreased or increased their consumption, or switched to or from decaf.

Another thing they didn’t measure was the type of coffee, apart from crudely separating caffeinated from non-caffeinated. So we have no way of knowing if most people were drinking Floor-Sweepings brand instant coffee or Heart Burtser double espressos.

The latter information is important if we want to generalise to other populations. US coffee as generally consumed is somewhat different in strength to how the Europeans take it. I vividly remember visiting a friend of mine in Seattle. At the time I was working as a postdoctoral student in Berlin. There was an industrial strength filter coffee machine outside my lab door, pumping out vicious black heart starters almost 24/7. My mate proudly took me to the street in Seattle where he claimed the best coffee in the US was served.

It tasted like pinkelwasser. That is not a compliment.

Sounds uninspiring, so how is coffee making people live longer?

We know how it’s not doing it. It’s not caffeine, as decaffeinated and caffeinated coffee had pretty much the same effect (except for injuries and accident, where caffeinated coffee was a clear winner).

Coffee is chock full of antioxidant chemicals such as polyphenols and Chlorogenic acid. We know that people who consume foods rich in antioxidants have better health outcomes and live longer than people who don’t. We also know that feeding people pure antioxidant vitamins is a waste of time. The antioxidant status of food may be unrelated to health, but may be a marker for something else in these foods.

So whether it’s the antioxidants in coffee is unclear. This hasn’t stopped companies from adding extra antioxidants to instant coffee though (although they were doing this well before this study came out). Maybe it’s something completely unrelated, like coffee drinkers are more likely to walk to their local coffee shop, getting a bit more exercise.

So if I want to live longer?

Choose you parents carefully, eat plenty of fresh fruit and vegetables, get more exercise, develop or participate in social networks. Why not walk down to your local coffee shop and share a cappuccino with your friends?

Coffee’s ready

Milk and two sugars please.

I’ve written before about the toxins secreted by the Cane Toad. The toad’s venom is a complex mix of chemicals. The most important is related to digoxin, the toxin found in the Foxglove plant, and works the same way. It changes the excitability of the heart muscle, causing the heart to contract wildly and ineffectually, or stop completely.

This brew of poisons is what makes an animal that would normally be a crunchy treat into a last meal for native lizards, local marsupial carnivores and dogs. The surviving predators tend to give the toxic toads a wide berth.

Yet, ironically, this very toxin that protects the toad may be its undoing, according to some clever research reported in The Conversation today.

Because it’s not just the adults that are poisonous. The toads eggs also produce some of the toxins that adults produce, and secrete them into the water.

Lots of animals use chemical signals to find food (think sharks following traces of blood) or mates (pheromones secreted by moths and other insects that drift on the wind) where mere visual identification would not be effective. These chemical signals can also be used as a warning (don’t eat me, I’m poisonous).

The wafts of toad egg toxin drifting through the water deter predators from eating the eggs (water beetles for example, rather than the dogs and lizards the adults face). This generally works well, except for one problem.

The cane toad tadpoles are cannibals.

Any pond where toads lay their eggs will have a finite amount of food. If all the Cane Toad eggs in a pond hatched, the tadpoles would rapidly run out of food. So it pays the early hatching tadpoles to hunt down and eat the Cane Toad eggs that have not yet hatched.

But if Cane Toad eggs are hidden in murky waters in the breeding ponds, how does a Cane Toad tadpole efficiently hunt down the eggs? By following chemical cues. And what chemical cue is unique to the Cane Toad eggs? The very toxin that protects them from other predators! No other animal in Australia produces these toxins.

Of course, Cane Toad tadpoles are resistant to the toxins that the Cane Toad eggs secrete, so the toxin is not a deterrent to them snacking down on the eggs.

We know this because of the research by Rick Shines' team, reported in the Proceedings of the Royal Society B (full free article here).

Now here’s the clever bit: the researchers used this information to devise a way to clear out Cane Toads from their breeding areas.

By smearing a small amount of Cane Toad toxin in a trap, and letting the toxin leak out into the water of a pond, the hungry Cane Toad tadpoles seeking to consume their as yet unhatched brethren sniff out the poison, swarm up into the traps and are caught.

It’s like the pheromone traps we use to catch insect pests, but instead of attracting them with a potential mate, we attract the tadpoles with a potential meal.

Excitingly, it looks like the traps were able to virtually clear out the ponds of Cane Toad tadpoles with minimal effects on other fauna. Probably because the toxin that attracts the Cane Toad tadpoles repels native fish and native frogs.

Currently our methods of control are backbreakingly laborious, either hand collecting adults (like in of Toad Day Out, when North Queenslanders compete to gather as many of the warty creatures as possible for mass extermination), or traps for adults, which require frequent emptying.

We can see how well that has worked, by the relentless spread of the pest across northern Australia. You only need a few pregnant females to escape and your work is undone.

The toxin traps have the potential to clear breeding ponds efficiently, and to be easily transportable to wild terrain.

Of course, the Cane Toad is spread over such a wide area and has penetrated into such difficult to reach landscapes that any control method will be facing heroic challenges.

Still, it would be gently ironic if the very toxin that makes Cane Toads such a devastator of native wildlife were to contribute to their removal or control.

The iTelescope SSO webcam is going well with some dropouts, http://www.ustream.tv/channel/itelescope

The Universe Today webcam is going strong. http://www.universetoday.com/95630/watch-the-transit-of-venus-live/

Can’t currently connect to the RiAus livestream or the transit.org livestream, and astronomers without borders website has disappeared. http://home.mira.net/~reynella/skywatch/transven12.htm#webcams

UPDATE: The Sun is toying with me!

The transit seen from the Solar Dynamic Orbiter http://ow.ly/i/FYep/original

UPDATE: the RiAus Adelaide livestream is overwhelmed, but the Perth one should come online soon. http://livestreaming.riaus.org.au/

UPDATE 9:57 am: My first (out of focus) mobile phone image http://astroblogger.blogspot.com.au/2012/06/mobile-phone-transit.html

SDO transit movie: http://www.youtube.com/watch?v=N-4iipHgUbo

UPDATE June 8: Other Peoples Transit of Venus Images and Videos http://astroblogger.blogspot.com.au/2012/06/other-peoples-transit-of-venus-images.html

The historic transit of Venus is tomorrow (6 June), starting early in the morning. While some of you will have taken time off work (or made simple observing devices to take to work), not everybody can do this. Also, your locality may be clouded out. Webcams to the rescue!

My transit website has a list of live web-feeds, and links to sites with even more web-feeds. I’d like to draw attention to two:

The iconic Siding Spring Observatory will have a live feed courtesy of iTelescope.Net, the Research School of Astronomy and Astrophysics and the Australian Astronomical Observatory. The web-cast will start on June 6, 2012 at 8am local time at Siding Spring (June 5, 2012 at 22:00 UTC). http://www.ustream.tv/channel/itelescope

The Royal Institute Australia will also have a live stream: http://riaus.org.au/events/livestreaming-of-the-transit-of-venus/

I blog for iTelescope and I’m associated with RiAus through the Australian Science Communicators SA.

As well there are a number of public viewings.

If you still want to make some projection systems, then there is a step by step guide for making a cheap binocular projection system here http://astroblogger.blogspot.com.au/2012/05/step-by-step-guide-to-making-binocular.html
and how to know where to point your telescope when you can’t look through the viewfinder. http://astroblogger.blogspot.com.au/2012/05/okay-so-how-do-i-point-my-telescope-at.html

And don’t forget the excellent Venus Transit Series here at the conversation.

Venus nears its moment in the sun, but what’s a transit anyway? – Joni Horner

Transit of Venus: a tale of two expeditions – David Coward

Transit of Venus: a must-see for everyone … no seriously – Duncan Steel

An upcoming transit – Helen Maynard-Casely

Who amongst us hasn’t wished, in the wee small hours when we are staring at the bedroom ceiling wide awake, heart pumping, bitterly regretting that last, late night espresso, that there was an anti-caffeine pill. Well ThinkGeek, that repository of all things cool for us thinking geeks*, is selling pills that are claimed to rapidly remove caffeine from our coffee saturated bodies. Theoretically they should work, but practically they probably don’t.

Which is a good thing.

So how are they supposed to work?

Our livers come equipped with a range of enzymes that break down chemicals foreign to the body. Plants, bacteria and fungi all produce chemicals that are harmful to us, and our bodies have evolved a range of enzymes to deal with them. Some of these foreign chemicals stimulate the body to make more of these enzymes, presumably to deal with an increased toxic threat.

The body can’t differentiate between potentially harmful chemicals and potentially helpful medicinal chemicals. So several herbal medicines increase the amount of breakdown enzymes. The herbal anti-depressant St. John’s Wort is a powerful enzyme inducer for example.

Caffeine, the heart pumping, sleep banishing component of coffee is broken down by the enzyme CYP1A2. Several drugs and chemicals can stimulate the body to make more CYP1A2. So theoretically, if we gave a drug to increase the enzyme levels, caffeine would be broken down faster and we would get to snooze compatible blood levels of caffeine much sooner.

One such drug is the alkaloid rutaecarpine, from Evodia rutaecarpa, used in herbal medicines. If you give this drug to rats, it will cause them to break down caffeine screamingly fast. Rutaecarpine forms the basis of the anti-caffeine pills sold through ThinkGeek.

But wait, you just said it was unlikely to work.

Yes, I did. For two reasons. Firstly, in all the animal studies I’ve seen, they gave the drug for 3 days before testing the rats ability to break down caffeine. In order to work, the drug must get the body to make more enzyme. This is typically a leisurely affair, with between 24 to 72 hours before you see a substantial increase in enzyme levels in an animal or human. It’s a lot faster if you squirt the drug on cells growing in a dish, but even then I’ve only seen papers that found increased enzyme levels at 18 hours.

Obviously, if you want to get a good nights rest following the double espresso you had at 10 o'clock, you don’t want to wait 18 or more hours to see an effect. The instructions for these tablets say to take them 2-4 hours before going to bed, that’s nowhere near enough time to for the enzyme levels to increase appreciably.

Even if somehow the enzymes levels shot up in 4 hours to double the speed caffeine removal, a normal person takes 6 hours to drop their blood concentration by half. Doubling the rate of removal decreases the time to 3 hours, so it’s still going to be a while before you drift off to the land of nod.

The second reason is if the dose makes the poison, it also makes the drug. The smallest dose I’ve seen used (again over a 3 day period), was 50 milligram per kilogram. The tablets are being sold as 100 milligram per dose. Which, if you are a 70 kilogram person, works out to 1.4 milligrams per kilogram. 20 times less than the rats were getting.

Even if we allow for the fact that dosages don’t scale up up linearly**, you would need to take something like 6 tablets to get the smallest doses used in the rat.

Okay, so the dose is likely too low and the time frame too short. Why is a good thing this drug won’t work as advertised?

As well as taking a while to increase the levels of CYP1A2, once the levels are up, it takes a while for them to come down. Again, this is typically around 24 honours, but can be up to a week.

So you take your anti-caffeine pill, get your caffeine levels down and enjoy some snooze for a blissful 8 hours. Then you leap out of bed, put on your morning coffee, slam back the cup of brew and …. Nothing, because your CYP1A2 is still at high levels chomping away at your caffeine, and will be doing so into late into the afternoon.

Possibly not what you wanted.

Also, if you are on theophylline for your asthma, it’s an analog of caffeine and will be broken down as well, so your asthma control is out the window for around 24 hours. If you are on antidepressants, some anti-cancer drugs, paracetamol, some blood pressure drugs and the anti-clotting drug warfarin (amongst others) these will also be broken down so fast that they will not work properly.

While the drug site does advise you that you should consult your doctor about medication before consuming the pills, most people taking over the counter medications like paracetamol are unlikely to check with their doctor first.

So inducing CYP1A2 is not such a great idea.

No, it takes too long to work, it’s not specific to caffeine, and lasts too long afterwards. We Geeks would do much better to forgo the double espressos late at night.

*My favorite Dr. Who mug comes from thinkGeek.

** typically, you have to multiply the rat dose by 0.16 to get the equivalent human dose for many medications. So the human equivalent of 50 mg/kilogram is 8 mg/kilogram. This means a 70 kilogram human would need 560 mg a day for 3 days to have the same effect, not a single 100 mg tablet.

Hat tip to David Kroll of TerraSigillata.

In the aftermath of the announcement that the government will remove the 30% private insurance rebate for alternative medicines found to be ineffective, last Saturdays Adelaide Advertiser carried a double page spread on the issue. The first comment was from a naturopath:

"the primary aim is that the patients stay well, and that's more and more the province of the natural therapist rather than the GP or the orthodox medical system"

This got me reflecting, while staring at a “sometimes foods” poster stuck on the side of a sweets vending machine in the Women’s and Children’s Hospital, “more and more”? I’d like to see some evidence of that. Orthodox preventative medicine incorporates a broad swathe of interventions, many of which don’t look like medicine, and so aren’t immediately apparent.

What Preventative Medicine Looks Like

The provision of clean, potable water is a massive governmental enterprise, which most of us don’t see working, but has saved literally millions of lives. Growing up in Queensland, prevention of mosquito borne disease involved a range of governmental Mosquito control schemes from releasing mosquito fish in waterways to control mosquito larvae to public education so that people could eliminate mosquito breeding areas in their homes and gardens.

Consider smoking, the fall in smoking (and heart disease and lung cancer as a result) was due to a coordinated decades long campaign that involved health providers, community support schemes, advertising (both the awareness of health effects and where you could go to help quit) and legislative instruments controlling cigarette advertising and packaging. The role of Naturopaths in this massive public preventative health campaign was rather small.

Consider good nutrition and exercise, these are central elements in Naturopathy. But despite Naturopaths enthusiasm for good nutrition and exercise, promoting this is a massive effort involving all health care providers and and governmental instrumentalities.

From the various public health campaigns (remember Life be In It and Norm? Now we have the balloon people exhorting us to eat well and exercise more on TV and the sides of buses, the “Walk to School” campaign to get kids exercising more) to various legislative instruments (from the changes to tuckshop rules in schools to promote healthy choices, the “sometimes foods” labelling campaign, nutritional labelling on foods). Promotion of healthy eating and exercise is a large scale program.

Despite the importance of nutrition and exercise to Naturopaths, and their enthusiastic promotion of the same, to claim an increasing role for Naturopaths compared to the orthodox system is, well, sheer day dreaming. But there is more.

A Preventative Health Strategy without Vaccination?

If Naturopaths want to be considered as a serious partner in promoting preventative medicine they need to confront vaccination. Vaccination is one of our greatest preventative tools against infectious disease. Deaths from diphtheria, tetanus and Haemophillus Influenza B have plummeted following vaccination, the great killer smallpox is extinct, the crippling disease polio is almost extinct. Yet historically, Naturopathy was firmly opposed to vaccination.

These days the situation is more ambiguous, there are several Naturopathy organizations in Australia. Some don’t mention vaccination at all, some “balance” authoritative vaccination information sites with vaccine disinformation sites and still others present only misinformation (see also here). Preventative medicine is more than eating well and getting exercise. If Naturopathy wants to play an important role in preventative medicine, they need to come to terms with vaccination.

I leave you with this link to an alleged “infographic”, I am mildly amused that the Large Hadron Collider is seen as one of the top threats to humanity, and “weaponised” vaccines?

The site hosting the infographic isn’t one guy and his dog ranting though, this is one of the major natural therapies websites and referred to by the Australian Natural Therapists Association for vaccine information. I’d like to see the naturopathy community speak out against such nonsense. Wouldn’t you?

In the aftermath of the budget, one set of cuts may have been missed. The government is looking to remove the 30 per cent private health insurance rebate for some “alternative” medicines and therapies that have no evidential support.

In the list are ear candling, Reiki, homoeopathy and aromatherapy. The government has appointed Chief Medical Officer, Professor Chris Baggoley to review the evidence for these therapies. He’s not going to find much, what evidence there is all suggest these therapies are ineffective.

Interestingly, this announcement seems to preempt the National Health and Medical Research Councils review of homoeopathic therapy.

The announcement coincided with an editorial in the Journal of the American Medical Association by internationally renowned vaccine expert Dr. Paul Offit on the US National Center for Complementary and Alternative Medicine (the full article is here and requires a subscription, but there is a free interview and podcast available). Specifically set up by CAM enthusiasts to test CAM, it has singularly failed to find effective CAM therapies. As Dr. Offit says:

“NCCAM officials have spent $374 000 to find that inhaling lemon and lavender scents does not promote wound healing; $750 000 to find that prayer does not cure AIDS or hasten recovery from breast-reconstruction surgery; $390 000 to find that ancient Indian remedies do not control type 2 diabetes; $700 000 to find that magnets do not treat arthritis, carpal tunnel syndrome, or migraine headaches; and $406 000 to find that coffee enemas do not cure pancreatic cancer”.

If even an institute specifically set up to find effective CAM therapies can’t find them, the Australian Governments' review will be relentlessly negative.

Unfortunately, other CAM therapies such as acupuncture are exempted from the review.

For aficionados of ear candling, none of these therapies will be banned, you just have to pay for them yourself without getting an insurance rebate from the government.

I have been reading an attempted defense of homoeopathy that was published recently. There is a lot that is wrong in this alleged defense of homoeopathy (see here for some background), but one thing that caught my eye was a list of drugs that supposedly work at homoeopathic dilution levels.

The list surprised me, as I work with some of the drugs involved. It contains at least one inaccuracy, one logical fallacy and one conceptual misunderstanding.

However, this is an opportunity to give some insight into how drugs work.

But first let me explain the supposed purpose of the table. Homoeopathy as you know operates on two priciples, the alchemical principle that “like cures like” and the use of ultradilute substances.

In principle, homoeopathy is like adding one molecule of sulfuric acid to to 10,000,000,000,000,000,000,000,000,000 molecules of hydrochloride (battery) acid and expecting to get limpid, non acidic water.

Actually, many common homoeopathic dilutions are so extreme that not one molecule of the original material will be present in the remedy.

But not all homoeopathic dilutions are that extreme, in some there is a chance that some molecules may be present.

Let’s set aside the peculiarity of an argument that says “sure most of our remedies have no molecules of the original substance left in it, but some of our weaker remedies (or accessories to the main remedy in which the main ingredient actually isn’t there) do have something in them”, let’s have a look at the table.

That concentration, it doesn’t mean what you think it means.

The table (you have to scroll down a bit) purports to show the concentrations at which several biological substances have a “threshold” effect and their equivalent homoeopathic dilutions.

The first thing that caught my eye was the entry for acetylcholine, the chemical that makes your muscles contract in response to nerve activity (like the restless tapping of your fingers as you think “where is he going with this”).

Acetylcholine is purported in this table to have a threshold effect at 0.0001 picograms per millilitre, equivalent to a homoepathic 16X dilution. Now I use acetylcholine a lot in my research and teaching. The threshold for acetylcholine is quite well known, and it is nowhere near 0.0001 pg per ml. In some sensitive preparations the sensitivity may be as low as 0.1 nanogram per ml, around a million times more concentrated than claimed, mostly it’s higher than that.

However, my overall point is not that the author got something wrong, although it reduces our confidence in his other statements. There are two important conceptual errors underlying the entire table.

One threshold does not rule them all

One is that just because some very potent hormones can have threshold effects in the realm of some of the least extreme homoeopathic dilutions it doesn’t mean that any random substance in homoeopathy will have a physiological effect.

Especially substances like silica, which has no physiological effect, or acetic acid which requires a high concentration to have a physiological effect.

For example, caffeine is present in some homoeopathic sleeping remedies at both 4C and 30C (how do they do that?). A 4C dilution is 0.00000001 gram per millilitre (using the terminology of the table) but the threshold for the action of caffeine is over a hundred times higher: 0.000002 gram per ml. So a 4C dilution of caffeine is not going to do anything, even though there will be some actual caffeine molecules in the remedy.

In some cases we should be glad that the concentrations are very low. Aconite, a potent poison, is present some homoeopathic stress remedies at 9X, which is fortunately too low to poison you. It may be even lower. It’s likely aconite is made from plant material containing aconite rather than pure aconite. So the concentration will be more on the order of 14X or 0.0000000000001 g per millilitre.

Again, the fact that some homoeopathic remedies have small amounts of material in them is no answer to the fact that the majority of remedies at 30X or 30C or greater dilutions are unlikely to have even one molecule of substance in them.

The dose is not enough.

There is another conceptual issue here as well. Remember that the concentrations listed for these hormones are “threshold” effects, the point where we can just detect an effect. These effects are important in understanding the dynamic range of a hormone system, but useless in medication, as they will not cause a therapeutically meaningful response. A “threshold” concentration of insulin which just marginally activates the insulin receptor will not control a diabetics' glucose levels.

Furthermore, the threshold effects for hormones occur when the cell or tissue is immersed in a solution of the hormone at that concentration (or it’s the concentration in body fluids). But the concentrations of hormones are being compared to the concentrations of homoeopathic solutions in a bottle or in a pill.

Even if you were to take a millilitre of homoeopathic remedy (a very high dose), and if it were perfectly absorbed (very unlikely), and the substance only entered the blood, rather than tissue fluid generally, the concentration of substance will be around 5,000 times smaller in your body. Well below any threshold effects.

As I mentioned earlier, there is a lot wrong with this attempted defense of homoeopathy, but in this one table alone demonstrates fundamental misunderstandings of the action of hormones and the action, absorption and distribution of drugs. Which is not surprising for a system that hasn’t got out of the 19th century.

Various groups (eg here) have been citing an article currently in press, “Glyphosate induced cell death through apoptotic and autophagic mechanisms” by Gui et al., as evidence that the herbicide glyphosate is linked to Parkinson’s disease. It’s not, not by a long shot, and you know what I’m going to say next: “it’s the dose that makes the poison”.

The findings centre around what happens when you incubate a cancer cell line, PC-12 cells, with glyphosate. Now, I’m quite familiar with these cells, I use them (or rather, I cause my research students to use them), in my research into anti-Alzheimer’s drugs, and although a great fan of these cells as models I am painfully aware of their limitations.

Nerve cells are really hard to grow in tissue culture, but PC-12 cells, despite being cancer cells, are tolerably close to real nerve cells for doing things like screening drugs or basic toxicology, like the studies of Gui et al. One of the problems is that we can put concentrations of drugs on our cells in dishes that we could not hope to achieve in real people.

And thus it is in this study, the concentration at which they just achieved a toxic effect on PC-12 cells after 3 days exposure was 5 milli Molar (mM). That’s high, you would have to drink two cups of raw glyphosate* to achieve that sort of concentration in your blood plasma, and that will have you in hospital quick smart (5mM is the threshold of lethal plasma concentrations). You are certainly not going to be drinking raw glyphosate for 3 days.

The threshold concentration for lethality in PC-12 cells is around a million times higher than what people who actually spray glyphosate on crops are exposed to in their blood, let alone the sorts of concentrations consumers would be exposed to. Especially since glyphosate is rapidly broken down in the environment, and very poorly absorbed from the gut or skin.

Now, I know that chronic exposure to sub-lethal concentrations of substances may have long term risks, but this study does not point in that direction. Long term animal studies have shown no signs of Parkinson’s disease, and epidemiological studies show no significant association of glyphosate with Parkinson’s in humans.

So the results of this study which use toxic concentrations of glyphosate in PC-12 cells throw absolutely no light on any putative link between Parkinson’s and glyphosate. Yet through the wonders of the Internet the Gui et al. paper will be cited as “evidence” that glyphosate causes Parkinsonism for years to come.

• this is assuming you are using the most popular concentrate (360 g/Litre), you weight 80 Kg, using a low estimate for volume of distribution of 2.3 Litres/Kg and you are using 250 ml cups.

Today’s article by Caleb Ferguson and Patricia Davidson on the dangers of energy drinks highlights one of the key themes of this blog “Sola dosis facit venenum”. Energy drinks owe their stimulating property mostly to caffeine and caffeine-like compounds. Caffeine and its relatives theophylline (tea) and theobromine (chocolate) heighten our alertness. This caffeine boost is part of the pleasurable effect of a good cup of coffee

Coffee has even been used as a medicine, due to its caffeine content. In the 1890’s two strong demitasse cups of coffee were recommended for asthma sufferers. The caffeine in coffee relaxed the muscles in the bronchial tubes of the lungs, making breathing easier. These days we still use caffeine’s relative, theophylline, to treat asthma.

Caffeine may be medicine, but, and you know I’m going to say this, “the dose makes the poison". Caffeine also makes the heart beat faster and stronger, and high concentrations of caffeine can cause severe heart problems (amongst other things) and death. One of the problems with energy drinks is that, especially in combination with alcohol, you can more easily get an overdose of caffeine than, for example, slugging back double espressos.

So how much caffeine will kill you? Luckily there is a handy website where you can find out how many cans of energy drink, cups of coffee or bars of chocolate you will need to consume before expiring. Death by Caffeine.

While some of the figures are reassuringly high, people vary with their sensitivity to caffeine, and their ability to break it down. Worryingly, research recently reported in the Medical Journal of Australia showed that people drinking no more than the recommended amount of energy drinks showed significant signs of toxicity (like palpitations and even parts of their heart muscle dying).

In fact the average consumption of people presenting to the emergency department was between 3-8 cans (although one heroic individual consumed 80 cans). These figures show that some people are far more at risk than the simple calculator suggests.

Also, while Death by Caffeine suggests that chugging back 30 cups of espresso one after the other won’t kill the average person (you need more like 156 for an 80 kg person), you certainly won’t feel bright and shiny at the end (indeed with the gastrointestinal effects, your end will be anything but shiny).

So consume your caffeine wisely folks!

A common refrain in any discussion of herbal medicines is “it’s been used for hundreds/thousands of years, it must be safe”. Unfortunately this is not necessarily true. If the herbal ingredients cause chronic disease, or rare but serious side effects, these adverse events can be easily missed.

After all, comfery tea was used for centuries without people realising it caused liver disease. The once popular Sassafrass tea turned out to be carcinogenic.

Two recent publications highlight the issues around safety of herbal medicines. The first, reported here at The Conversation by the authors of the study, shows that many herbal Traditional Chinese Medicines are adulterated with a range of other plant and animal material.

While I won’t be losing any sleep over endangered Saiga antelope horn being contaminated with goat and sheep horn, it’s the range of other undeclared plant materials that are the worry.

Finding that there is undeclared Ephedra in herbal Traditional Chinese Medicines is a serious issue, as Ephedra can kill, and Ephedra containing herbal medicines are banned in Australia.

Even more worrying is the finding of Aristolochic acid in things such as laryngitis medicine. Aristolochic acid is a nephrotoxin, and more insidiously, a carcinogen.

While in these cases, the content of things such as Aristolochic acid is undeclared, Aristolochic acid containing plants are part of traditional Chinese herbal medicines. The second study I mentioned looked at the link between Traditional Chinese medicines and the high rates of a rare kidney cancer in Taiwan.

In Taiwan there is a high usage of Traditional Chinese Medicine, at least one third of the population is exposed to medicines containing Aristolochic acid. At the same time the Taiwanese have the worlds highest rates of a rare kidney cancer, urothelial carcinoma of the upper urinary tract.

The study found a “smoking gun” between the known carcinogen Aristolochic acid and the cancer, by finding the chemical signature produced when Aristolochic acid mutates DNA.

Once again I’ll remind you that Aristolochic acid containing herbs are a part of standard Traditional Chinese Medicine, not a contaminant. Despite their use for hundreds, if not thousands of years, the harm due to Aristolochic acid containing herbs has only recently come to light due to systematic research through conventional medicine.

These studies are a timely reminder that “natural” is not synonymous with “safe”, and herbals can be used for hundreds of years with serious toxicity being noticed by traditional practitioners.

I was intrigued by an all-too-short, short news item reporting that a Queensland research group has won funding to study the use of spider venoms as treatments for cancer. Venoms for cancer? This might surprise people, as the point of venoms is to kill or injure things. How can they be used as medicine?

The reason is of course the dictum of my blog patron “it is the dose that makes the poison”. To kill or harm you the venom has to interfere with the body’s processes, often in interesting ways that humans hadn’t discovered until we studied the venom. By using a controlled dose we can use that effect to treat disease.

One of our most successful treatments for high blood pressure is a modified version of a South American Pit Viper venom. A large dose of the venom causes your blood pressure to plummet, a small dose lowers it. Hundred of thousands of people are living better lives by taking a little bit of (highly) modified venom each day.

I’m sure the Queensland team will find something in spider venom to kill cancer cells (like this study here), but that’s the easy part. Killing cancer cells is quite easy, cyanide will effectively do the trick. But killing cancer cells without killing the rest of you is hard. After all, cancer cells are your cells, driven to grow uncontrollably by mutations in the cells growth machinery.

So far, with a few exceptions, most of our treatments exploit the fact that cancer cells grow much faster than ordinary cells, so are directed at the mechanisms of growth. Unfortunately, bone marrow cells, the cells that line your gut and the cells in your hair follicles also grow rather fast, and tend to be hit by our treatments. Which is why many cancer therapies cause horrible gastrointestinal problems and cause your hair to fall out.

Most likely, a spider venom would work in this way, hitting fast growing cells. If we are really lucky, a venom component might target something unique to the cancer. All cancers are caused by mutations in the cells growth pathways, our newest anti-cancer drugs target these mutant pathways. In some cancers like chronic myeloid leukaemia, there is a key mutation present in most of these cancers. Drugs targeting this mutated enzyme produce an 80-90% remission rate with none of the horrible side effects of drugs based on growth alone.

Sadly, because of the diversity and complexity of the cells growth mechanisms, in general not all cancer cells have the same suite of mutations. Thus most cancer drugs aimed at the mutant pathways have much more modest effects. But even these modest effects can be very worthwhile, especially in cancers that have currently few treatments, like Glioma.

A scorpion venom is currently under trial for Glioma. It doesn’t attack growth pathways per se, but accessory pathways. A peptide derived from a different scorpion venom binds almost exclusively to tumour tissue, and is being trialed to deliver anti-cancer treatments direct to the tumour.

So discovering a spider venom for cancer is quite realistic. Even if it’s a more general “kill all rapidly dividing cells” type, it’s possible to make delivery systems that will take the venom directly to the cancer. Cancers have very few features that distinguish them from normal cells, and making this kind of delivery system is not easy, but it remains a possibility. I will follow the Queensland groups work with great interest.

So next time you see a spider, give it some respect, its venoms could one day help cancer victims.

If, like me, you intend to spend part of the Easter celebration nibbling the ears of chocolate Bilbies, you might be surprised to learn that you are consuming medicine.

Xoxalatl was a product of meso and southern America, the Mayans and other cultures of the region regarded it as sacred, and it was prized for its medicinal and aphrodisiacal qualities. Chocolate was reserved for men of high rank such as priests, and, somewhat uncomfortably, sacrificial victims.

Chocolate was used by the Maya as a drink, although their milk free version, often with added chillies, would be almost unrecognisable to modern chocolate drinkers used to the milk infused sweetened concoction we have today. The European conquerors of South America rapidly adopted the medicinal use of chocolate.

In the 16th century Western medicine closely resembled that of the Maya and Asian systems, in the sense that ailments were divided into pairs of opposing qualities, such as hot/cold dry/moist. Chocolate as a drink was seen to be a hot/dry medicine, to be used for cold/damp ailments. Curiously, chocolate as a paste was seen as a cold medicine.

Chocolate was used for a multitude of conditions, and its use as a medicine evolved over the centuries. Chocolate could be used by itself, in mixtures with other herbs, or as a simple carrier to mask the taste of other medicines. One of the more sphincter tightening uses was a mixture of oil of chocolate, crushed millipedes, “sugar of lead” and opium for treating haemorrhoids.

Aside from its consistent use as an aphrodisiac, the general uses of chocolate as a medicine fell into three broad categories, as a source of nutrition to the feeble or emaciated, as a stimulant for the moribund and at lower doses, a relaxant and a “soother” of digestion.

How did chocolate do all this? Chocolate, as either a drink or paste, has a high concentration of oils which provide energy and nutrition, later versions with added milk and sugar also added to the food value of drinking chocolate, which allowed people with difficulty eating to gain nutrition. Chocolates use in cholera in the 19th century owes its properties to providing fluids for rehydration as well as energy while the disease ran its course.

Chocolate also has a number of pharmacologically active substances. The main one is Theobromine. The name comes from the scientific name of the cocoa plant, Theobroma caco, Theobroma meaning “food of the gods”. Theobromine is similar to caffeine, and has similar effects on the body; producing increased alertness (and agitation at higher concentrations) as well as relaxing the muscles in the lungs, making breathing easier.

Chocolate also has anandamide, a substance related to the active component of cannabis. Eating the several kilograms or so of chocolate needed to get enough anandamide into you to have an effect would tax even the most serious chocoholic. There are also some substances that slow the breakdown of anandamide. But whether there is enough to significantly increase anandamide levels to have an effect is very doubtful.

But that’s not all. Chocolate also contains the psychoactive substance phenylethyamine. While there is a reasonable level of this chemical in chocolate, most people’s bodies break it down rapidly. However, if you get headaches (not hangover headaches) from drinking red wine or eating blue cheese, your body doesn’t breakdown chemicals like phenylethyamine effectively, and you might get a buzz from chocolate.

And of course chocolate, particularly dark chocolate, is chock full of antioxidants. While antioxidants are relentlessly touted on TV and in magazines as a wonderful source of health, they don’t actually do much in real life.

Chocolate was primarily used as medicine until the 19th century, when it began to be replaced by more specific treatments. However as its use as medicine waned chocolates use confectionery waxed. The first use of chocolate for Easter eggs was in the early 19th century. With modern chocolate compounding methods chocolate confectionery became more accessible, becoming incorporated into human mating rituals. And the use of chocolate in Easter eggs (and rabbits and Bilbies) exploded.

Interest in chocolate and health has been revived recently, as the oils (and maybe the anti-oxidants) in chocolate (particularly dark chocolate) appear to reduce heart disease. But as one review puts it, “Further experimental studies are required to confirm a potentially beneficial effect of chocolate consumption.” So don’t rush out and stock up on dark chocolate Easter Bilbies to ward off heart disease.

Even the ancient Mayans knew that “the dose makes the poison”, and cautioned that too much chocolate was bad for you, but moderate consumption was good, so enjoy your Easter chocolate in sensible doses.

In an interesting conjunction of events, I brought home the DVD “Cane Toads; the Conquest” to show our Japanese exchange students something uniquely, if weirdly, Australian, on the weekend of Toad Day Out, when North Queenslanders compete to gather as many of the warty creatures as possible for mass extermination.

Growing up in Queensland, I understand the impulses that drive ordinary, kindly people into orgies of mass toadicide. It’s not just the sheer numbers of the things, making a walk to the outside loo somewhat perilous and coating kilometres of roads with lethal-skid inducing amphibians, it’s that they are toxic massacrers of wildlife.

Originally brought into North Queensland to control the cane beetle, they completely ignored their designated target, and promptly began eating great swaths of local insects and reproducing like mad. Predators of all things squamous and hoppy, including native lizards, the local marsupial carnivores and dogs soon found that the cane toad was not just another crunchy treat, but deadly poison.

Many frogs and toads secrete poisonous substances to discourage predators. After a mouthful of poison frog it’s a terminally stupid predator that will try eating them again. This may not do the chewed on frog or toad much good, but its relatives will prosper. Cane toads secrete a venom from the backs of their necks, it is so potent that dogs who drink from water bowls the toads have been sitting in can be poisoned. With the toad-induced carnage of native wildlife and pets you can see why people are infuriated by them.

The toads venom is a complex mix of chemicals. The most important is related to digoxin, the toxin found in the Foxglove plant, and works the same way. It changes the excitability of the heart muscle, causing the heart to contract wildly and ineffectually, or stop completely. In the spirit of my blogs namesake, we have harnessed these properties of digitalis in small doses to treat heart failure, where the heart does not beat strongly enough.

Toad venom has found its way into Traditional Chinese Medicine. Chan Su, amongst other things, is used as both a topical anaesthetic and an aphrodisiac. It is basically dried toad venom. Unsurprisingly, given the potency of toad venom and the variability of toxin levels in these preparations, there have been reports of severe toxicity and even death from using Chan Su.

Of course, lethality never stopped people in search of intoxication, In my youth, there were a fair few people who tried licking the toads, or smoking their dried skins, as a way of getting high. I’m surprised that more people weren’t killed this way.

With no effective predators in Australia the cane toads have marched relentlessly West and South, they are already in Kakadu, crossing supposedly impenetrable geographic barriers, and some scientists predict we will eventually see them in Adelaide. The parasitic lung worm that was a possible biological control agent doesn’t have seemed to paned out.

However, there might be one hope, paradoxically lizards that feed on the introduced toxic plant “mother of millions” are resistant to the toad toxins. So perhaps a crash breeding program of toxin resistant super lizards may stop the advance of the cane toad. That couldn’t possibly go wrong, could it?

Global Astronomy Month starts today, April the 1st. An initiative of Astronomers without Borders to raise awarness of our night skies, there will be star parties, image competitions and more. See the Global Astronomy Month homepage for more information, follow the Australian GAM facebook page, or visit the IceInSpace GAM page.

To start off, there’s an online Messier Marathon at 18:00 hours UT on April 1, (that’s 4 am April 2, AEST) UPDATE: Due to bad weather the Messier marathion will be held on April 10.

The extraordinary standoff between the Therapeutic Goods Administration (TGA) and the website Homeopathy Plus! has escalated. Well, a bit.

As a bit of background you should know that to be sold in Australia, all health products must be on the Australian Register of Theraputic Goods. For a product to make treatment claims other than an anodyne “may assist with …”, the TGA must see evidence that those claims are supported. Typically this involves boxes and boxes of the original data from animal experiments and clinical trials, which are pored over by independent experts to evaluate the claims. Seriously, the boxes of data from the preclinical work alone can fill an entire wall to chest height.

Making treatment claims without evidence is considered rather naughty, after all the consequences of a product making a claim that it will reduce blood sugar levels in diabetics, when it doesn’t are somewhat more serious that a product claiming to leave dishes sparking clean when it doesn’t.

Back in 2009 a complaint was made to the TGA about advertisements for, amongst other things, “homoeopathic vaccines”, including “vaccines” for meningococcal disease. The meningococcal vaccine was a 10^-60 dilution, and therefor has a negligible probability of having any molecule of the starting material in it.

Given that the homoeopaths freely admit this lack of material, and claim that an undefined “energy” is somehow producing this effect, and the seriousness of meningococcal infection, you would expect the TGA would require a bucket load of evidence, along the lines of the masses required for conventional medicines, to allow these vaccines to be licensed to be advertised and sold. A couple of papers in homoeopathic publications so obscure I can’t even find their abstracts will not cut it.

Unsurprisingly, if somewhat slowly, the TGA had determined in August 2011 that Homeopathy Plus! was making claims for homeopathic, homeoprophylaxis and homeoprophylactic products that were misleading and unsupported by evidence (see here for some examples), and told them to alter their advertising and website.

Homeopathy Plus! promptly ignored them.

The next step could have been legal action to force Homeopathy Plus! to make the changes or fine them. Instead the TGA have done the equivalent of looking stern and wagging their finger harder and issued another order for them to alter the advertising and web site and issue a retraction (see the full text in legalese here).

As of this evening (March 29) Homeopathy Plus! has not altered its website. Anyone willing to take a bet on the chances of Homeopathy Plus! complying this time?

Someone named Philippus Theophrastus Aureolus Bombastus Von Hohenheim would hardly be expected to be a shy, retiring type. Even his self-appointed nick name, Paracelsus, which means “beyond Celsus”, was hardly self effacing. Paracelsus was claiming to surpass the famed Roman doctor Celsus. No wilting violet, Paracelsus was a larger-than-life opinionated iconoclast. Like his much quieter contemporary, Copernicus, he lit a fuse that would lead to a revolution after his death.

Paracelsus is considered the father of modern medicinal chemistry and toxicology. It was Paracelsus who coined the term “it is the dose that makes the poison” (although he probably said it in Latin – Sola dosis facit venenum is much cooler).

He was also an Alchemist. Today we associate Alchemy with mystical quests to turn lead into gold (or Harry Potter). But medicine then was very different to today. After all, one of Galileo’s duties was to teach celestial dynamics to medical students, so that as doctors they could cast their patients' horoscopes. There was also a strong practical Alchemical tradition which dealt with everything from making perfumes to medicines.

In a world where the ancients ruled, and diseases were thought of in terms of opposing humours, Paracelsus tried to base medicine on observation and experiment. He rejected the standard complex medications, which were mixtures of sometimes up to 50 ingredients, in favour of simpler medications based on pure substances.

Paracelsus' “poisons” included salts of zinc, tin and mercury. Theses medications may seem somewhat heroic to us today, but faced with insanity and death from tertiary syphilis, taking mercury until your teeth started wobbling in their sockets was seen as a reasonable trade off (sexual abstinence didn’t seem to occur to them, a salutary lesson to anyone trying to teach sexual hygiene today).

Paracelsus' poisons are still with us, we no longer use mercury to treat syphilis, and the mercury-containing Mercurochrome antiseptic that stained my generations knees red has been replaced with iodine, but pure medicines containing gold, silver, platinum and other metals are used to treat everything from arthritis to cancer.

But his poisons are still with us in a broader sense, since Paracelsus' poisons are, well, everything. True, it does take a bit of effort to kill yourself by drinking carrot juice or water, but it can and has been done. Much has changed since Paracelsus' day, due to the culture of observation and experiment that he helped start, but his central idea that the dose makes the poison underlies our decisions on safe limits of chemicals in the environment and whether the risks associated with drugs outweigh their benefits.

If people were more familiar with Paracelsus' maxim, they would panic less about exposure to traces of formaldehyde smaller than what their body makes though normal metabolism, and be less likely to slam back energy drinks until they get toxic effects.

Thus this column is titled Paracelsus' poisons, where I will keep an eye on drugs, toxins, venoms, environmental chemicals and what they mean for us.