Dylan Thomas reads TS Eliot NS parody

“As we get older, we do not get any younger”

After the competition page was hijacked from The Week-End Review, “absorbed” by the New Statesman in 1933, parodies have a formed a regular feature of the magazine’s back pages. In 1946, Faber and Faber published an anthology of the best entries, edited by NS literary editor GW Stonier, with illustrations by Nicolas Bentley. In his introduction, Stonier wrote:

It will never do, in this atomic age, to be a wit. Let the witty journalist beware, he is in danger of insulting his readers; the witty politician is a self-confessed enemy of the people; the witty parson – but he vanished long, long ago. To be dull – hugely, incontestably dull – has become a hall-mark of sincerity, and woe to him who tries to improve the occasion. Insect! Anti-democratic! But there are crannies where the nimble-witted lurk, signalling distractedly and indulging a frivolity they daren’t display. Given an excuse, finding the signal returned, they will even publish a little.

A competition page, with its aura of party games, provides such an excuse. The demands are light: an epigram, an anecdote, a letter, a limerick, a parody, verse or prose for an occasion. Light but not necessarily easy, as the would-be competitior discovers…

Perhaps the most notable addition to the anthology is “Chard Whitlow”, written by the poet, translator and dramatist Henry Reed. The poem is sur-titled Mr Eliot’s Sunday Evening Postscript, and will be republished in full next year as part of the New Statesman’s centenary proceedings. However, to tide you over until then, here, reading with all the stolid grace of Mr Eliot himself, is Dylan Thomas, who will celebrate an anniversary of his own next year – having laid in a cemetary in Laugharne, Carmarthenshire, since 1953.

Dylan Thomas, doing what he loved best. Photo: Getty Images.

Philip Maughan is a freelance writer in Berlin and a former Assistant Editor at the New Statesman.

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The best defence against Alzheimer’s

Spoiler: the best way to avoid Alzheimer's is to stay young.

At the recent meeting of the European Academy of Neurology in Copenhagen, doctors were signing up to attend a workshop teaching non-specialists to test for cognitive decline in their patients. How do you tell the difference between a scatterbrain and a case of early dementia?

It’s a question that is increasingly urgent. Last year, 47.5 million people were living with dementia. That will have risen to 75.6 million by 2030 and will reach 140 million in 2050. The World Health Organisation has declared that dementia should be regarded as a global public health priority. But what can we do about it?

The primary cause of dementia, accounting for roughly 70 per cent of cases, is Alzheimer’s disease. It’s all very well to put a name to it, but we don’t have a clear understanding of the mechanisms that cause it – or medicines to battle it. Alzheimer’s drugs have a high rate of failure. In the decade to 2012, 99.6 per cent of newly developed drugs failed to make it past clinical trials. There is no cure for Alzheimer’s and none on the horizon, either.

There was, however, a small breakthrough last month. A study published in the journal Science Translational Medicine suggests that Alzheimer’s could be a result of fighting infections from other diseases that would, if left unchecked, ravage the brain. The hard lumps of sticky plaque in the brain that characterise the onset of Alzheimer’s seem to be the result of the immune system attempting to isolate and neutralise microbes and other pathogens that have made their way into the brain. The plaques catch pathogens, preventing infection from taking hold. Unfortunately, it’s a case of damned if you do, damned if you don’t: the plaques also trigger inflammation that leads to the death of brain cells.

This observation mirrors another catch-22 with Alzheimer’s. Some researchers have suggested that the drug failures might be averted by getting candidate treatments to the disease earlier, before symptoms appear. Put simply, the drugs may stand a better chance of success when trying to counter the first stages of damage to the brain. The problem is: how do you get that early diagnosis?

There are various genetic indicators for a heightened predisposition to developing Alzheimer’s. A gene called apolipoprotein E, for instance, comes in three variants: one kind seems to reduce the risk of Alzheimer’s while another increases it. Other genes – variously associated with the body’s uptake of cholesterol, its propensity to engender inflammation and the efficiency of communication between neurons – also have a role to play in raising or lowering the chances of onset.

However, the interplay between genetic factors, environmental factors and what appears to be pure luck makes foreknowledge of whether Alzheimer’s will strike any individual impossible. It’s no wonder that the US National Institutes of Health does not generally recommend genetic testing as a worthwhile route for anyone wanting to know their future. After all, a result that indicates you are more likely than the average person to develop dementia is, in many ways, little more than a heavy psychological burden, to be borne until the symptoms start to appear – a scenario that keeps you stressed (a grave health risk) even if onset never happens. If the drugs don’t work yet, why would anyone sign up to be tested?

In the absence of a reliable test or cure, the best advice seems to be to delay ageing as much as possible, particularly where cardiovascular health is concerned. It’s an observation that fits with last month’s breakthrough. The plaque-provoking pathogens reach the brain through the weakening of the blood-brain barrier, a wall of cells that wraps around blood vessels and prevents foreign bodies from passing into the brain’s circulatory system. This weakening happens with age, suggesting that action to delay the degradation of the cardiovascular system will also delay the onset of Alzheimer’s disease.

Here, at least, we have some good news: the rate of appearance of dementia cases seems to be in decline. This may be a spin-off of our attempts to cut deaths from heart disease. It seems that as we take control of blood pressure and cholesterol levels, making significant improvements to our heart and circulatory function, we are unwittingly improving our cerebral health, too – almost certainly because the brain requires good blood flow to operate well.

The surest way to avoid Alzheimer’s, then, is simple to state and impossible to achieve. All you have to do is stay young. 

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is At the Edge of Uncertainty: 11 Discoveries Taking Science by Surprise.

This article first appeared in the 23 June 2016 issue of the New Statesman, Divided Britain