Cataract: Biochemistry, Epidemiology and Pharmacology by John Harding,
Chapman & Hall, pp 333, £60
More than 25 million people around the world are blind because of cataracts,
opacity of the lens of the eye. It is most common in developing countries
but is, however, increasing in incidence in the developed nations whose
populations now contain a higher proportion of elderly people and where
it is going to be a substantial health and economic burden. Canny eye researchers
in the US spotted this rise years ago. They successfully lobbied Ronald
Reagan to slash funding for cancer research and give it to lens research.
They used a particularly sharp argument: cancer kills people whereas cataracts
makes them a cost to the nation. Reagan bought it.
There is no cure for cataracts although many folk remedies have been
flogged from antiquity to the present day. Surgical removal of the opaque
lens is relatively simple and is arguably the most ancient surgical technique;
popping the diseased lens through a small nick in the side of the eye takes
seconds and might account for the miraculous ability of Jesus to restore
sight. Gustave Flaubert writes that the operation was performed by the village
blacksmith in the 19th century. But modern cataract surgery is expensive
and the waiting lists are longer than ever. Blindness after the operation
is a common complication of a surgical procedure designed to improve sight.
In any case, new cases of cataracts far outstrip – at least in developing
countries – the ability of eye surgeons to remove the diseased lens. Prevention,
as with all disease, is clearly better than cure.
Harding’s book is a nicely judged and readable living history that begins
by taking us on a whistle-stop tour through the basic biology of the lens.
The author casually and succinctly describes its detailed metabolism, protein
structure, cytoskeletal organisation, genetics, biophysical arrangement,
multifunctional proteins and growth. He reminds us that a wealth of biological
knowledge first came from the lens. Harding then discusses the worldwide
problem of cataracts, its increasing importance, the risk factors that have
been identified and the various approaches used to control it. He ruthlessly
savages various theories of cataractogenesis and happily snipes away at
views he can’t quite kill, but doesn’t like. Harding clearly cares deeply
about the problem of cataracts and gives short, entertaining shrift to some
of the sillier notions that might impede progress, be they biochemical or
epidemiological.
Advertisement
For instance, Harding asks why cataracts are far more prevalent in developing
than developed countries. He takes us through the epidemiological evidence
purporting to show a role for sunlight in the development of cataracts and
finds it wanting. He pours scorn on proposals to attach lightmeters to the
foreheads of individuals – for a decade or so – and refers us to studies
showing that sunlight-related diseases do not correlate with the occurrence
of cataracts. He then develops the biochemical reasoning which makes it
unlikely that changes in lenses with cataracts are related to ultraviolet
light.
But if not sunlight, then what? The sunniest countries in the developing
world are also the poorest: malnutrition is rife and they tend to have poor
sanitation. In particular, life-threatening and severe diarrhoea are endemic.
So Harding proposed and showed that diarrhoea is a major risk factor for
cataracts in India. As an encore he reveals that bouts of diarrhoea are
a risk factor for cataracts even in that bastion of civilisation, Oxfordshire.
Since cataracts are an important predictor of mortality and share risk
factors with heart, nerve and kidney disease, it is likely that diarrhoea
will receive far closer attention in future. Other researchers have suggested
that cataracts could be caused by nutritional factors. Limiting the diet,
for example, slows down cataracts in experimental animals. But Harding notes
drily: ‘Malnutrition does not seem to have lowered the prevalence of cataract
in the Third World.’
The author also takes a look at the development of drugs to combat cataracts.
He identifies the flawed thinking that led to the abject failure of a multimillion
pound drug development programme aimed at the prevention of cataracts in
people with diabetes. He documents the simple (and cheap) observations which
helped to show that aspirin, and similar analgesics, are powerful protective
agents against cataracts. The lens and the heart (both protected by aspirin)
have a lot in common.
It is also an object lesson to observe that Harding is justifiably sceptical
about a ‘genetic causation’ of this disease. He notes there is only one
documented family with inherited cataracts out of a total of 150 000 sufferers
in Britain. This familial frequency is as great as in other common disorders.
So my advice to Harding is that he should apply for a million-pound grant
to study that one family. He’d no doubt be given it in our silly ‘blame
the genes’ scientific climate and could use the loot for something useful
such as following up the ideas presented in this well-written book.
Simon P. Wolff is lecturer in toxicology at Univesity College and Middlesex
School of Medicine.
![Astronomers have long known that understanding how star clusters come to be is key to unlocking other secrets of galactic evolution. Stars form in clusters, created when clouds of gas collapse under gravity. As more and more stars are born in a collapsing cloud, strong stellar winds, harsh ultraviolet radiation and the supernova explosions of massive stars eventually disperse the cloud, and their light can bear down on other star-forming regions in the galaxy. This process is called stellar feedback, and it means that most of the gas in a galaxy never gets used for star formation. Researching how star clusters develop can answer questions about star formation at a galactic scale. Now, the state of the art has been further developed with both Hubble and Webb working together to provide a broad-spectrum view of thousands of young star clusters. An international team of astronomers has pored over images of four nearby galaxies from the FEAST observing programme (#1783), trying to solve this mystery. Their results show that it is the most massive star clusters that clear away their gaseous shroud the fastest, and begin lighting their galaxy the earliest. The team identified nearly 9000 star clusters in the four galaxies in different evolutionary stages: young clusters just starting to emerge from their natal clouds of gas, clusters that had partially dispersed the gas (both from Webb images), and fully unobstructed clusters visible in optical light (found in Hubble images). With Webb???s ability to peer inside the gas clouds, they were able to then estimate the mass and age of each cluster from its light spectrum. This image shows a section of one of the spiral arms of Messier 51 (M51), one of the four galaxies studied in this work, as seen by Webb???s Near-Infrared Camera (NIRCam). The thick clumps of star-forming gas are shown here in red and orange, representing infrared light emitted by ionised gas, dust grains, and complex molecules such as polycyclic aromatic hydrocarbons (PAHs). Within these gas complexes, each tens or hundreds of light years across, Webb reveals the dense, extremely bright clusters of massive stars that have just recently formed. The countless stars strewn across the arm of the galaxy, many of which would be invisible to our eyes behind layers of dust, are also laid bare in infrared light. [Image description: A large, long portion of one of the spiral arms in galaxy M51. Red-orange, clumpy filaments of gas and dust that stretch in a chain from left to right comprise the arm. Shining cyan bubbles light up parts of the gas clouds from within, and gaps expose bright star clusters in these bubbles as glowing white dots. The whole image is dotted with small stars. A faint blue glow around the arm colours the otherwise dark background.]](https://images.newscientist.com/wp-content/uploads/2026/05/13114322/SEI_296271016.jpg)


