Wednesday, October 24, 2007

Cataract surgery: The eyes have it

The Economist online, October 23rd, 2007
Replacing worn-out eye lenses has never been simpler or better

Replacing worn-out eye lenses has never been simpler or better

PAUL URSELL, an ophthalmic surgeon who works at St Helier hospital, just outside London, is one of the first people in Britain to use a new piece of equipment called the Stellaris. This is an all-in-one lens removal and replacement kit intended to treat those whose natural lenses are going cloudy and thus making them blind. It is the latest in a series of improvements to the technology of replacing damaged eye lenses with artificial substitutes. These improvements are simplifying and speeding up the surgery involved.

The ability to remove lenses darkened by cloudy imperfections, known as cataracts, and substitute them with artifical lenses, is more than half a century old. It started with the chance observation during the second world war, by Harold Ridley, a British eye doctor, that pilots whose eyes had been penetrated by perspex shrapnel from cockpit canopies did not suffer an immune reaction.

Perspex lenses have long since been replaced by silicone ones. But now the whole process of inserting those lenses is changing as well. One of the biggest innovations has been the introduction of microsurgery. Originally, inserting a new lens meant cutting a flap in the eyeball some 11mm across. Today’s microsurgery requires a cut of less than 2mm. Such small wounds heal by themselves, and do not need to be stitched. The whole process is thus less traumatic, and patients are often able to return to work the day after an operation.

Two technologies in particular have helped to reduce the size of the incisions needed. The first, phakoemulsification, uses a tiny ultrasound probe to remove the lens. An ageing lens goes yellow, cloudy and hard. Mr Ursell likens its texture to that of a gravy cube. Exposing such a lens to high-frequency sound waves breaks it up into an emulsion that can then be sucked out of the eyeball. The second innovation is injectable lenses. Progressive improvements in the design and material of artificial lenses mean it is now possible to roll them up, inject them into position in the eye through a narrow slit, and then have them unfold, naturally into place.

The tools to perform these tricks have been available for a while. The novelty of Stellaris—which is made by Bausch & Lomb, a firm based in Rochester, New York—is that all the pieces of kit are pulled together into one snazzy little box. The system can extract lenses, keep the eyeball inflated, and inject lenses in several different ways. Stellaris has options to use an older or a newer surgical technique, depending on the surgeon’s preference.

The newer form of surgery splits the instruments into two tools which enter the eye through identical tiny slits. One provides the ultrasound to break down the cataract, and also contains a vacuum to hoover out the pieces. The other tool provides fluid to keep the pressure while the lens is being extracted. That prevents the eyeball collapsing.

In short, a useful innovation. But lens replacement is not yet perfected, largely because replacement lenses themselves still have room for improvement. Standard replacement lenses have no ability to focus, so the wearer is often stuck with excellent distance vision but must use glasses for reading. That can be addressed with multifocal lenses, which have concentric rings of material that offer alternate bands of near and distant vision, but these can cause problems with a person’s night vision and his sensitivity to contrast.

What excites ophthamologists most, however, and what every lens-making company wants to achieve, is a lens that can change its focal length in the way that a natural lens does. A few such “accommodating” lenses are already on the market. The Crystalens from Eyeonics in Aliso Viejo, California, is one example. The Tetraflex by Lenstec of St Petersburg, Florida, is another. These products use the eye muscles to change the shape of the lens and move it backwards and forwards in the eye during focusing. Such products are soon likely to replace multifocal lenses. After that, light-sensitive silicone lenses may arrive. These can be customised after surgery by playing a low-intensity beam of light onto the photosensitive material. That causes the material to polymerise, and thus change shape, which means the ophthamologist can tweak the lens to alter its power. Raging against the dying of the light now has powerful technological allies.

Thursday, October 18, 2007

Evolution: Live fast, love hard, die young

The Economist: Oct 18th 2007

Chasing females can take years off life

IN THE cause of equal rights, feminists have had much to complain about. But one striking piece of inequality has been conveniently overlooked: lifespan. In this area, women have the upper hand. All round the world, they live longer than men. Why they should do so is not immediately obvious. But the same is true in many other species. From lions to antelope and from sea lions to deer, males, for some reason, simply can't go the distance.

One theory is that males must compete for female attention. That means evolution is busy selecting for antlers, aggression and alloy wheels in males, at the expense of longevity. Females are not subject to such pressures. If this theory is correct, the effect will be especially noticeable in those species where males compete for the attention of lots of females. Conversely, it will be reduced or absent where they do not.

To test that idea, Tim Clutton-Brock of Cambridge University and Kavita Isvaran of the Indian Institute of Science in Bengalooru decided to compare monogamous and polygynous species (in the latter, a male monopolises a number of females). They wanted to find out whether polygynous males had lower survival rates and aged faster than those of monogamous species. To do so, they collected the relevant data for 35 species of long-lived birds and mammals.

As they report this week in the Proceedings of the Royal Society, the pattern was much as they expected. In 16 of the 19 polygynous species in their sample, males of all ages were much more likely to die during any given period than were females. Furthermore, the older they got, the bigger the mortality gap became. In other words, they aged faster. Males from monogamous species did not show these patterns.

The point about polygyny, according to Dr Clutton-Brock, is that if one male has exclusive access to, say, ten females, another nine males will be waiting to topple the harem master as soon as he shows the first sign of weakness. The intense competitive pressure means that individuals who succeed put all their efforts into one or two breeding seasons.

That obviously takes its toll directly. But a more subtle effect may also be at work. Most students of ageing agree that an animal's maximum lifespan is set by how long it can reasonably expect to escape predation, disease, accident and damaging aggression by others of its kind. If it will be killed quickly anyway, there is not much reason for evolution to divert scarce resources into keeping the machine in tip-top condition. Those resources should, instead, be devoted to reproduction. And the more threatening the outside world is, the shorter the maximum lifespan should be.

There is no reason why that logic should not work between the sexes as well as between species. And this is what Dr Clutton-Brock and Dr Isvaran seem to have found. The test is to identify a species that has made its environment so safe that most of its members die of old age, and see if the difference continues to exist. Fortunately, there is such a species: man.

Dr Clutton-Brock reckons that the sex difference in both human rates of ageing and in the usual age of death is an indicator that polygyny was the rule in humanity's evolutionary past—as it still is, in some places. That may not please some feminists, but it could be the price women have paid for outliving their menfolk.

Thursday, October 11, 2007

Medicine: Blood Simple

The Economist: Oct 11th 2007

Because they lack an essential component, blood transfusions may be killing some of the people they are intended to save

IF THERE were any sure bets in medicine, you might think that “blood transfusions save lives” would be one of them. But there aren't. Even though deaths caused in the 1980s by accidental HIV infection mean that donated blood is now screened meticulously to keep it free of infectious agents, there is still a nagging feeling that something is wrong.

In 2004, for instance, Sunil Rao of Duke University Medical Centre, in North Carolina, carried out a study of people suffering from acute coronary syndrome (a specific type of heart attack). One conclusion that could be drawn from his research was that unnecessary blood transfusions might be causing tens of thousands of deaths in America alone. Dr Rao found that patients who had had a transfusion because of a low red blood-cell count had an 8% chance of dying within 30 days. Without a transfusion, only 3% died. Those numbers need to be treated with caution. As Dr Rao points out, the patients who underwent transfusion were, on average, sicker and older than those who did not. Nevertheless, his study is not the only indication of something amiss.

In recent years, research has suggested that transfusion is not necessarily a good thing for patients suffering from serious injuries, for those who have undergone surgery and even for those who are anaemic. And a study carried out earlier this year found that critically ill children whose red blood-cell counts had dropped by half fared no better after a transfusion than those who did not receive one.

As a result of all this, questions are being asked about whether something happens to blood when it is banked that causes it to stop working properly. What that might be has remained a mystery. But it may be one no longer. A group of Dr Rao's colleagues, led by Jonathan Stamler, think the answer is a gas called nitric oxide—or, rather, a lack of it.

Out of gas

The main reason for giving a patient blood is that it carries oxygen. It carries lots of other things, too, such as glucose. But it is a lack of oxygen that will kill you quickest. However, as Dr Stamler points out, what determines whether transfused blood works as a treatment is not merely how much oxygen it is carrying, but whether that oxygen can reach the tissues that need it. This is where nitric oxide comes in.

Nitric oxide increases the flow of blood to tissues by dilating the arteries that penetrate those tissues. The best known example is the erectile tissue of the penis (Viagra works by sustaining the signal that the gas gives). However, it is not just penile blood vessels that nitric oxide relaxes. When a red blood cell reaches any tissue in need of oxygen it releases nitric oxide in order to dilate the capillaries. Only then can it deliver its cargo. And that is doubly true of the cells in stored blood since red blood cells become less flexible with age, and thus less able to squish into capillaries. Dr Stamler thus wondered if a lack of nitric oxide was causing the problems associated with transfusions.

What he and his colleagues discovered, and published this week in the Proceedings of the National Academy of Sciences, was that the amount of nitric oxide in stored blood does indeed decrease—and does so rapidly. Within a day of storage, blood loses 70% of its nitric oxide. After a few days, up to 90% has been lost.

A second paper in the same journal, by Dr Stamler's colleague Timothy McMahon, confirmed this result (in fact, it showed that the initial drop of around 70% happens within three hours of collection) and showed that it was not caused by the way blood is processed, but merely by the passage of time. Dr McMahon also established that stored blood does indeed lose its ability to dilate blood vessels.

Dr Stamler is in little doubt about the significance of these findings. Furthermore, he warns that putting blood lacking nitric oxide into the body does not merely dilute what gas is already present in the bloodstream. Blood that is poor in nitric oxide will scavenge the gas from other tissues, causing the vessels in those tissues to constrict. If the tissue in question is heart muscle, the result will be a heart attack.

These papers, therefore, make a strong case that a lack of nitric oxide is creating the problems with transfusions—though as Michael Strong, the president of the American Association of Blood Banks, points out, they do not settle the issue once and for all. That would require a proper, randomised clinical trial.

And therein lies the rub. Because blood transfusion is such an old practice (it dates back to 1818) it has never been subjected to modern clinical standards. Nobody is questioning whether car-crash victims, say, should have transfusions after massive blood loss. Without it they would undoubtedly die. But for those not threatened with exsanguination it is far less clear whether a transfusion is a good idea. There are no rules about when to transfuse and who to do it to. These are matters of judgment, and knowledge is typically passed from doctor to doctor.

The good news from this study is that the problem should be easy to correct. If nitric oxide is what is needed, it can be added to banked blood just before transfusion. As part of the project, Dr Stamler tried this with dogs. He found that old blood replenished with nitric oxide is as good as fresh blood at relaxing blood vessels. And that, he thinks, points to a bigger possibility than merely returning blood to normal. Blood boosted with nitric oxide might be used as a therapy for people who have had heart attacks by providing extra oxygen in the crucial minutes after an attack, before the affected heart muscle has died. At that point, blood transfusions would no longer be part of the problem: they would be part of the cure.

Wednesday, October 10, 2007

Some hard talk about towns

Cities and natural disasters
Some hard talk about towns

Oct 4th 2007

IT ISN'T just an urban myth: life in a city really is getting more dangerous, and the sources of peril are not just human ones like muggers and reckless motorists. A report by UN-Habitat, an agency responsible for human settlements, says the number of natural disasters affecting urban populations has risen four-fold since 1975.

Some of the reasons are obvious, others less so. As the world's population grows, people are crowding into mega-metropolises, where life's risks are horribly concentrated. The after-effects of a natural disaster can be especially dire in a vast, densely-packed area where sewers fail and disease spreads.

At a pace that no urban planner can control, slums spring up in disaster-prone areas—such as steep slopes, which are prone to floods, mudslides or particularly severe damage in an earthquake. Many of the world's cities are located on coasts or rivers where the effects of climate change and extreme weather events, from cyclones to heatwaves to droughts, are brutally and increasingly felt. Economic dislocation and human pain are also caused by events (like recent floods in the Indian city of Kolkata, see above) that are too small to grab global headlines.

But there is no reason for the sort of fatalism that regards disasters, and their disproportionate effects on the urban poor, as something that has “always been with us” and will inexorably get worse. (more...)