Show Hide image

Game of Thrones season four begins with no end in sight for book series

Are you tired of waiting for the rest of George R R Martin's A Song of Ice and Fire?

HBO’s Game of Thrones is the Jägerbomb to Tolkien’s ginger beer. How else to describe a fantasy series in which a moment of interrupted incest leads to civil war and the threat of human extinction at the hands of spectral frost monsters? It’s bloody, political and raunchy, populated by a well-drawn cast of sociopaths and misfits. And whilst it pales against the character-driven dramas like Breaking Bad and House of Cards to which we’ve recently been treated, Walter White’s shenanigans never involved dragons and full-frontal nudity.

Season four of the show premieres today. That’s exciting news for aficionados. But another sad milestone for fans of the cycle of novels from which Game of Thrones is adapted – A Song of Ice and Fire by George R R Martin – which remains incomplete after eighteen years of prevarication and delay.

Frank Underwood never ate a raw horse heart. Image: HBO

Here’s the timeline. Game of Thrones (the book) was released in 1996. A Clash of Kings followed in 1999, as did A Storm of Swords a year later. Then things started to go wrong, probably when Martin’s editors stopped speaking truth to power – the man is known to hold a grudge against their tribe. Fans waited five years for A Feast for Crows. Then six years for A Dance with Dragons. Three years on and The Winds of Winter still lacks a publication date. Fragments of the manuscript are occasionally leaked to Martin’s website, but like Chinese water torture this irregular trickle has driven readers to despair. They are desperate to know whether Martin is capable of redeeming himself after Crows and Dragons, which were by most accounts poorly paced and occasionally dull. Don't ask about A Dream of Spring, which will complete the heptalogy in some ineffably distant future.

The more impatient members of Martin’s entourage call themselves “GRRuMblers”. They are an entitled and obnoxious lot, given to venting their frustrations in whinging blog pieces and message board posts. But Martin also has defenders amongst those who argue that buying a book does not create an implicit contract for the delivery of future services. In the words of Neil Gaiman, “George R R Martin is not your bitch”.

Peter Dinklage as Tyrion Lannister. Image: HBO

One assumes that Martin has good reason to avoid a J K Rowling-paced publication schedule. The pressure to satisfy a fan base Vulture calls the most devoted in pop culture must be nerve-shattering. He certainly does not seem hurried by a fear of looming mortality, unlike those readers who like comparing Martin’s age (65) to that of fellow fantasy novelist Robert Jordan (58), who died in 2007 midway through concluding his epic Wheel of Time series. (Why must we be so fearful of Martin shuffling off anyway? Many unfinished works are considerably better than hurriedly completed ones. Compare Kafka’s The Trial to the autobiography of Jade Goody etc.)

Martin's great error was appending a note to the back of A Feast For Crows which assured readers that a sequel would be along the next year. That surely created some kind of obligation. As it happened, A Dance with Dragons took Martin longer to complete than the ministry of Jesus, Magellan’s circumnavigation, Paradise Lost and the Manhattan Project.

Giants and dragons and direwolves, oh my! Image: HBO

Game of Thrones season four will be thrilling. But it will also remind fans of the books they are missing. HBO executives will no doubt push hard for A Song of Ice and Fire to be completed now their series has caught up with Martin’s pen (here's speculation as to what might happen if they fail to crack the whip). For readers who have inhabited the world of Westeros since the first Clinton administration, a long wait for resolution may soon be approaching the beginning of the end. 

Getty
Show Hide image

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