Günter Grass and the free speech moment

A travel ban is still censorship.

Over the past few days, a "free speech moment" has been unfolding. These are the controversies where we get to discuss the first principles of free expression, and they usually begin when someone does something extremely offensive. Think of the public trolling of Anjem Choudry, or the English Defence League.  Think of Liam Stacey, charged with a criminal offence for tweeting. Think of every controversial columnist, paid by the newspapers to be politically incorrect. These moments are frustrating, but at least campaigners like me are asked to make the case for free expression afresh, on sites such as this one.

This week, the "free speech moment" has had both an historical and international flavour. Günter Grass, the Nobel Prize Winning German author, angered the Israeli government after he wrote a poem about their militarism.  Israel, incensed that a former conscript in the Waffen-SS should write such a criticism, responded by placing a travel ban on the author.  In the most recent twist, Grass has escalated the controversy by likening the Israeli government’s actions to those of the East German Stasi.

There are two unresolved issues here.  The first is whether a travel ban (declaring Grass a persona non grata, unwelcome should he wish to visit Israel again) is censorship.  Clearly, such a move is less severe than the formal banning of Grass’s books; and many authors around the world (for example, in Iran, which was cited in the poem) suffer imprisonment for their transgressions. Nevertheless, placing this restriction on a person, purely because of what they have written, is a form of censorship.

It prevents any Israeli citizens who happen to agree with Grass’s poem (and I am sure there are many, from every religion) from inviting him to speak. It precludes the possibility that those in Israel who enjoy Günter Grass’s oeuvre would ever have the chance to meet him at a literary event.  A voice is suppressed. Until recently, the UK Border Agency were in the habit of denying authors and artists entry to the UK because a gallery opening or a book tour was considered a form of "work". English PEN campaigned for reform of the system on the basis that freedom of expression also includes freedom of information, the right to hear dissenting voices. A travel restriction on an author denies this freedom, which makes it undemocratic.

Such bans also have a "chilling effect" on other writers – will authors who regularly visit Israel now self-censor, if they hold opinions that the Israeli government doesn’t want to hear?

The second issue is over Günter Grass’s actual words, including his latest ‘Stasi’ interjection? These "free speech moments" are frustrating because defending someone’s right to say something is usually equated with defending the content of what they say. Those whom the speaker has offended are always ready to conflate the two issues. We should remember that the oft-cited Tallenter quip on free speech (“I hate what you say, but defend to the death your right to say it”) also works perfectly well in reverse: I defend Günter Grass’s right to say things . . . but I hate what he says. The writer Kenan Malik goes further, and makes the point that if one vigorously defends free expression, one also has a moral duty to retort when people say unpleasant things.

I don’t think that Günter Grass is saying abhorrent things, though in my opinion he has been deeply insensitive. His last comment is clearly a doubling-down, and the result is polarising. His poem, despite taking on the form of introspection, has not persuaded anyone that was not already of his point-of-view. For such an accomplished writer, celebrated for his turn of phrase, this is a shame. The great power of poetry and prose is their ability to help the reader empathise with someone of a different culture or history. Personally, I think Grass is capable of this, and should have written a different poem.  But to say this is an act of literary criticism, not a statement of the principles of free speech.

Robert Sharp is head of campaigns & communications at English PEN

Silenced? Günter Grass Photo: Getty Images
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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