The EVIL of orthodontics

While most of are comfortable with the idea of cleaning our teeth or replacing them with dentures, we are troubled by the idea of mutilating our teeth with implanted braces for the purpose of “enhancing” our bite. It brings the threat of “designer smiles”, which most of rightfully find repugnant. We need to define a clear border between cleaning teeth and trying to improve upon our own teeth and those of our children.

We have crooked teeth for a reason, and should think very carefully about interfering with the natural order. John 1:3 tells us “All things were made by him; and without him was not any thing made that was made.” Teeth were made, and therefore God is made them. Further, we were made in the image of God, and for us to try to tamper or re-engineer that is hubris; for scientists and doctors to invent technology to interfere with His work is the most ultimate arrogance. Man must not play God.

This contemporary obsession with the ideal smile trivialises what makes us human. Human lives can no longer be meaningful. All of us get that great feeling when we, using hard work and dedication, overcome the limitations of our dentition and achieve something great. If our success was due to an artificially enhanced smile that we received as a child, would we get the same satisfaction? If we could just change our teeth on a whim, would we feel as good about fighting through jaw pain to finish a steak sandwich? Enough is enough – we need to stay human in this engineered age.

Furthermore, braces could lead humans to become something less than human. If the idea of Frankenstein’s monster, with metal bolts protruding from the neck, wasn’t scary enough, imagine a teenage girl with a mass of metal wires interwoven between her teeth, put there by her parents and her orthodontist who considered her natural smile to be loathsome. If the monsters of science-fiction should have taught us anything, it is that a brace-face will be monstrous to any decent human being. Repugnance is, after all, a very natural and very wise response.

But metal-mouthed monsters, a blend of human with machine, are just the thin edge of the wedge. What if we could have genetic interventions to enhance how teeth grow, and ensure that no child ever has to suffer a “bad smile”? What if we could use genetic engineering or nanotechnology to reform our teeth jaws at will, into fangs or tusks? The possibilities are so mindboggling that many think we will become post-dental being, with no jaws or teeth to speak of (those with braces, and retainers, have ‘transitional dentition’, or are transdental).

In addition, how can we justify research into enhancing our natural teeth when many in third world countries can’t even get their hands on enough food to chew with their teeth? It goes against social justice to be spending this money on enhancement, when that same money could be used to prevent the tooth decay and malnourishment that afflicts many children across the world.

The most disturbing possibility, however, of this enhancement of our pearly whites will lead to a severe form of coercion and a class divide. Those with smiles that fit our image of ‘the perfect smile’ will have a definite advantage in life over those with “crooked” teeth, and the ‘have-nots’ will essentially be forced to pay for the best dental work they can afford if they want to prevent their children from falling behind. Those who do have orthodontic enhancements will earn more money, which they will use to fund the orthodontic enhancement of their children. This will lead to the divergence of the human race into two groups: the perfect-toothed “Grin-Rich” (who will control the workplace, the media, the government) and those with natural teeth, who will be their slaves. Soon, all humans may not be created equal, and our inequality will be encoded into our teeth.

What if one day those with malocclusions are considered unfit to live, and prevented from passing on their genes for “bad” teeth? This is already starting, with many countries mandating that fluoride be added to drinking water, to ensure that all children have healthy teeth. How long before the same happens with orthodontic enhancement – when a smile unpleasant to the eye is considered so obscene that it must be eradicated.

So, if we want to stop dentistry and orthodontics leading us into a new eugenics, we need to act against dental braces. A line needs to be drawn between good and bad uses of dental technology, or we will enter a brave new world of dental injustice. A clear line, enforced across the world, needs to be in place between dental maintenance and repair, and orthodontic enhancement, or we will be forced to suffer the horrors of a post-dental future.

We’re in the game!

Australia is now in the human cloning business. Therapeutic cloning, that is. Researchers working with Sydney IVF have received this country’s first license to clone human embryos. Sure, they could go to prison if they let the embryos pass the blastocyst stage, but it’s progress nonetheless.

As a comparison, Britain allowed the first group to create human clones in 2004, and in the US private companies have always been allowed to create human clones for therapeutic purposes, and did so first in 2001. So we’re a little way behind, but one never knows where the breakthroughs will occur.

Oi oi oi, Aussie Aussie Aussie!

Human infra-red thermal vision

Infra-red (IR) vision refers to sensation AND visual integration of the wavelengths of light between 750 nm and 1mm. In contrast, the human eye can only detect light with wavelengths from 400nm (violet) to 700nm (red). It would be useful to detect infra-red light because although very hot objects emit visible light (hence the terms red hot and white hot) even modestly warm objects emit infrared light. For example, the human body emits light at a wavelength of 10 microns (or 10000nm), and if one could see these wavelengths, one would have the ability to see humans against a colder background (i.e. room temperature). Much like Predator.

Biological IR vision has many problems, the least of which is that n o visual pigment exists that can pick up infra-red light. There are many pigments that can detect ultraviolet (UV) light, with many birds, reptiles, fish and even some mammals (and insects, but their eye is sufficiently different to be irrelevant here) having visual pigments that absorb maximally at around 350-360nm (but can still detect light with a wavelength of 280nm, well into the near UV spectrum). It appears to be relatively easy to evolve UV vision, but IR vision is much harder. As far as I know, the deep-sea dragonfish, a fish that lives deep underwater where almost no light exists, has a porphyropsin that can detect into the near-infrared (these fish also produce their own deep red light, allowing them to see while no other fish can – not unlike a man-made night vision goggles) but even that has can barely detect photons of wavelengths of 750nm. Just barely into infra-red and certainly far short of the 10000nm required for heat-vision.

The animals most famous for their infra-red ‘heat vision’ are the pit vipers (Crotalinae), though Boas and pythons (Boidae) have also independently evolved a more primitive version. They detect thermal radiation with wavelengths from 400nm (i.e. violet) all the way to 10600nm, but they do so not with their eyes, but with loreal pits (in Crotalinae) or labial pits/scales (in Boidae). These are small indentation just around the mouth – which in the Crotalinae are shaped very much like a pinhole camera – and detect heat not infra-red photons. In that sense, they are really just specialised structures that sense heat in the same way we humans can if we hold our hands over an open fire, and so probably utilise a heat-gated ion channel like the vannilloid receptor channel activated in human nerves by heat, pain, rubbing alcohol and chilli peppers. That said, the sensory information from these thermoreceptive pits (or scales) do integrate into the optic tectum, so it is very likely that the snakes are able to see the heat map of their world visually. But is it likely to have low spatial and temporal resolution and would be very short-sighted (a few metres at the most).

So, what is the issue with infrared photoreceptions? Why don’t they exist in nature already? Well, I’ve actually come up with four issues, only one of which may be easily solved (or may not be a problem in the first place).

First, immediately in front of the photoreceptors in the eye of all vertebrates is a few centimetres of water-based vitreous and aqueous fluid. Infra-red radiation is much lower in energy than visual light (remember the energy of a photon is inversely proportional to its wavelength), and water is very good at absorbing infra-red light. Therefore the eye would not actually be transparent for infra-red light, so may absorb a substantial fraction of the photons (van der Berg, 1997) before it hits the retina. It’s might not be so bad, though, because at the low energy of 10000nm, the light may even be too weak to be absorbed by water.

Second, neither of the two photo-active molecules in vertebrates photoreceptors, 11-cis-retinal (A1) or 11-cis-3,4-dehydroretinal (A2), would not stable if it was absorbing at this wavelength. In order to activate these pigments, energy must be supplied from either the light or from the thermal energy (Ala-Laurila et al, 2004). The lower the wavelength of light, the less energy the photons have, so the greater the thermal energy must contribute to the activation energy. The thermal energy, however, can activate the photoreceptor by itself – one of the reasons why cold-blooded creatures are theoretically more sensitive to single photons (because a single photon even is indistinguishable from random thermal activation, and cold creatures will have less thermal activity) (Aho et al, 1988). If we were trying to set up a molecule that would activate from an infra-red photon, even one with a much shorter wavelength than 10 microns, we’d have a molecule that would activate very easily due to thermal noise. In other words, we’d have a lot of ‘static’ in a thermal visual system – so much so, that I doubt we’d be able to even see anything.

The third problem is the neural circuitry that would be required to process another colour. The retina has colour opponent ganglion cells, which feed into the colour-sensitive parvocellular layers of the lateral geniculate nucleus, which in turn stimulate sets of neurons called blob cells in the the visual cortex (Dacey, D.M., 1996). These systems are responsible for processing colour differences (for example, the difference between green and blue). There is a rare syndrome known as cerebral achromatopsia, where a person has a loss of colour vision (see the world in shades of gray) despite fully function cone photoreception, because of lesions to the parts of the brain responsible for this colour discrimination (Barbur et al, 1994). That said, it may be an undamaged brain will be able to adapt to accommodate any changes to colour-related inputs, even during adulthood (Neitz et al, 2002).

The last problem and perhaps the greatest problem with allowing humans to visualise thermal emissions, is that the eye itself it an emission source. The eye is covered in warm blood vessels, each emitting at the same wavelength as the other humans who we would like to detect with our thermal vision. Thermal signals from behind the photoreceptors could perhaps be shielded, allowing the photoreceptor cells to only detect signals from directly in front of it, but even the aqueous and vitreous humours and corneal cells are emitting thermal signals. The internal signal would still likely be greater than that reaching the photoreceptors from external emissions sources (like another person) . Pythons and pit vipers are cold-blooded, so they don’t have this problem. But to a warm-blooded human, it would be like trying to look out into the night from inside a brightly-lit room.

Therefore, I can only see two options for thermal vision in humans. One, we could have separate eyes mounted on a cold antennae, or use thermal-vision goggles. Considering that the latter option is already used, I say that method is the easiest to follow – one day, we may even integrate the output from such goggles into our visual cortex. Until then, despite its popularity as a possible enhancement, biological ly integrated infra-red thermal vision in humans will have to wait.

EPO is a nootropic

Erythropoietin (EPO), a hormone that increases red blood cells and is used as a performance enhancer for athletic performance, has now been shown to enhance memory in normal, healthy mice. Mice that received EPO injections had enhanced memory for 3-4 weeks afterwards, which is longer than the elevation in red blood cell count lasts.

This effect isn’t actually novel, as other researchers had noticed that EPO improved brain function over 18 years ago (Grimm et al, 1990), and research into mental illness has also suggested that EPO has an effect on brain function (Ehrenreich et al, 2004). But it was always thought to be dependent on the change in red blood cells, but more recent evidence has suggested it works independently of effects on blood cells (Miskowiak et al, 2007). This mouse model confirms this.

Of course, the researchers have been focusing on this as a treatment, but anyone can see that this is a promising enhancement too. This mouse research showed that EPO enhanced memory and athletic function in healthy mice. It enhances both athletic and mental performance – how good is that?

Then again, if EPO becomes a common cognitive enhancer, it will mean that few of us normal people would ever be able to compete in the Olympics. It was only in 2004 that caffeine was allowed in professional competition, but pretty soon college students will be doping themselves with EPO as a biochemical study aid. It will be interesting when almost all normal people would not be able to pass an Olympic-level drug test.

The possibility exists, however, that we may want the cognitive boost without increasing our red blood cells too much. And now that we know the cognitive effects of EPO are independent of red blood cell production, this may be possible too. Make a drug that stimulates the brain like EPO does, but doesn’t effect an increase in red blood cells. And this study has gone a long way to unraveling the relevant effects of EPO on neuronal plasticity that underly the enhancement to memory circuitry in the brain, which means that we may be able to find drugs that do so more effectively than EPO or act on other brain functions.

FOXO3A is old news

According to The Australian, researchers have found a longevity gene. Researchers from Hawaii and Japan have found that men with the homozygous GG genotype of the gene FOXO3A live longer, have less cancer and cardiovascular disease, and maintain higher physical and mental abilities into old age.

If we read the actual study, we note that the researchers had a hypothesis that genes like this would be correlated to living longer. It’s involve in insulin signalling, which relates to caloric restriction and also the known life-extending modification in animals. So already, it was pretty obvious this gene would be involved in humans. All (all!) the researchers did was show it.

I might just point out that on my list of eight genetic modifications for dramatically increasing your chances of living forever, I said this (this was back in April):

4. Increase your expression of AMPK

And the introduction of this study mentions the AMP kinase (controlled by the AMPK gene):

A number of factors appear to extend lifespan in C. elegans in a DAF-16 dependent manner, such as AMP kinase, 14–3-3 proteins, the lin-4 microRNA, and heat shock factor.

The human homologue of DAF-16 includes four FOXOs: FOXO1, FOXO3, FOXO4 and FOXO6.

So really, what this study has found is that FOXO3A is a master regulator of the many little genes that have been implicated in ageing. Which was already expected based on homology, but it turns out this is really true in humans. And with a very strong correlation too – now we just have to investigate this further. Does it have this effect in women? Can we extend the lifespan of mice by genetic interventions, perhaps changing the alleles of this gene? And will this allow us to extend human lifespan past 100-120 years?

It’s a good discovery, but it’s not ‘the longevity gene’ – it’s a regulator of a set of longevity genes. And there will be many others too, probably with overlapping effects.

Fidelity enhancements

Surprisingly little has been said about the claim that a ‘monogamy gene’ has been found in people. This is probably because the RS3 334 repeat is in a gene, avpr1a, that is a vasopressin receptor element (Walum et al, 2008). Both oxytocin/vasopressin (pretty much the same peptide, differing at only two residues) have been well known to play a role in pair bonding in all mammals, with oxytocin more relevant in females and vasopressin more relevant in males (Neumann, 2008). I was expecting a bit more of an upset, but I guess the anti-enhancement people aren’t any more shocked than I am about this discovery. But seeing as I haven’t blogged about this, it may be an interesting time to do so now.

First, this research has a real potential to increase our control over our own relationships. If we become worried that we will succumb to temptation and cheat on our partners, we can simply reaffirm our relationship by stimulating the vasopressin receptors. Oxytocin and vasopressin in the brain correlate to acting more trustworthy (Zaket al, 2005). Think of it as biological marriage counselling – it would probably be far more effective too.

One the other hand, if we do not want to be tied down to a single partner, we may be able to alleviate the jealousy felt by loved ones by adjusting the vasopressin/oxytocin system back the other way. It would probably be more complicated in this case, especially if we wanted to ensure that people were just as happy in a non-monogamous group, because these peptides are linked to sex drive and anxiety.

There may be some interesting dilemmas here though. Oxytocin increases the degree to which people trust others (Kosfield, Heinreichs et al, 2005), which creates an environment where cheaters can better prosper (as game theory would indicate). And if a polygamist and a monogamist fall in love, who is expected to change their view with the vasopressin modification?

Of course, these two peptides are not the only things involved in pair bonding behaviour, especially in the complicated brains of human beings. Nonetheless, I think this will be a very useful tool for future relationships. Essentially, this will allow for human relationships to be far less random. Love is blind, but with this knowledge of biology we can take love by the hand and guide it to where we want it to be.