1610. Why the San Francisco Bay Area 350.org's Call for "Getting Out the Vote" for Democrats Is a Grave Mistake

By Kamran Nayeri, October 26, 2014

Climate justice march in Oakland, California. 

The San Francisco Bay Area 350.org has issued a call to get out the vote for the Democratic party candidates in the mid-term U.S. election, especially in the close Senate races.  

In a dramatically titled October 25 email message “Your phone calls in the next 10 days may determine the fate of the world,” (my emphasis) it declares:

“The stakes for the climate are critical in the Tuesday, Nov 4th elections.  It's best for the climate if the Democrats do well in the midterms. Terrible otherwise.  It is unusually important for grassroots people power to kick in now to Get Out The Vote (GOTV).  That's why 350 Bay Area is sending this rare call to help out in general elections.

“By signing up to call with MoveOn & Progressive Democrats of America, you will just be encouraging democratic voters to actually vote, not trying to change their mind about anything.
Please sign up for a shift -- or more than one -- now … at whatever time is convenient for you!
Sign up to make calls in these close Senate races:

• Michigan to help elect Gary Peters.

• South Dakota to help elect Rick Weiland.

• Colorado to help elect Mark Udall.

• North Carolina to help elect Kay Hagan.

• Iowa to help elect Bruce Braley.

• Kentucky to defeat Mitch McConnell.” (all emphases in the original) 

Democratic party is the graveyard of social movements
There is a long history of social movements being dragged into supporting the Democratic party, the graveyard of progressive movements in the U.S.  Witness the contemporary history of the labor movement, black liberation movement, woman liberation movement, and the environmentalist movement. Every major victory for any of these movements had come when they mobilized mass actions in the streets not when they followed a policy of getting Democrats elected.  When the latter “strategy” dominated, the mass base of these movements were demobilized expect to get them to vote for Democrats on the election day. 

As such, labor and social movements of the 1960s and early 1970s proved ill-prepared when the capitalist offensive by the corporate elite and their government began in the aftermath of the  world recession of 1973-75 that signaled the end of the post-World War II capitalist prosperity.  The leadership of these movements that have relayed on the Democratic party politicians to gain a few concession in exchange for political support for the capitalist policies of this party proved unable to resist the class war that ensued and continues to this day.   Both Republican and Democratic parties participated in this class warfare, although they employed different tactics.  Without any serious mobilization to resist these attacks, the demobilized mass base of the labor and social movements became demoralized. 

This why major environmentalist group today are reduced to Internet “campaigns” that call on their supporters to “take action” on the crisis of the day by clicking a button to send a message to this or that politician or office pleading to save this or that species, habitat, ecosystem, etc.   From a proactive movement, they have become reactive bureaucratic organizations that are not even interested in mass mobilization and street actions.   Clearly, this has been a losing game. 

The reason 350.org stands out from the main environmentalist groups is that it has resorted to focused grassroots mass actions that have successfully mobilized hundreds of thousands in the U.S. and inspired others to do the same worldwide.  The People’s Climate March is a shining example of that approach (for my brief discussion of it see here).  What we can learn from that experience is to educate, organize and mobilize more people for larger streets actions, not to ask them to elect Democrats! 

By claiming that the “next 10 days will determine the fate of the world” by electing Democrats the San Francisco Bay Area 350.org leaders make the same exact mistake that the leaders of labor and social movements, including the environmentalist movement, have committed to disastrous result.  There is no reason to make the same mistake again!

The need for an alternative to the capitalist order

Instead what is required is forging an alternative leadership to the Democratic and Republican parties that represents the interests of the 99% of the peoples of the planet and a program that ensure social and environmental justice.  We need a series of immediate and transitional demands to stop and reverse climate change and to educate, organize and mobilize in election time and beyond.  Recent reports show that in some local and state elections even Republican candidates are forced to adopt a climate friendly approach.  By resorting to get out the vote for Democrats the 350.org activists will miss an opportunity that the election time offers.  The planetary crisis, including global warming and catastrophic climate change, require radical changes to Our Way of Life mediated by the capitalist social relations of production on the global scale.  Thus, to claim that electing a few more Democratic politicians will change the “fate of the world” is ignorant at best and a disservice to the activists of the environmental movement.  

The social and planetary crisis of our day are really one and the same problem.  It is the crisis of the age of Anthropocene that began with the Agricultural Revolution to control and dominate nature on which we are but a tiny part. This alienation from nature prepared for social and individual alienation.  The global capitalist cultural and economy is the modern day manifestation of the Anthropcene.  To overcome it we need to rebuild human society from the grounds up.  To think that electing a few more Democrats to the Senate can substitute for such deep going task is to fool oneself into accepting the status quo with minor modifications. It will not address the root-cause the planetary crisis, including climate change, and social crisis.  We need a radical solution to the world problem—radical in the sense of going to the roots of the problems we face. 

Nothing less will do and humanity cannot afford committing the same errors leaderships of the labor and social movements have done for decades once again. There is precious little time for us to learn quickly, stand on our own feet and act as leaders not flowers of capitalist parties.

1609. Things Genes Cannot Do: Life Is an Orderly Collection of Uncertainties

By Kenneth Weiss and Anne Buchanan, Aeon, April 9, 2013

DNA is a metaphor for our age. It conveys the powerful idea that our identity is scientifically reducible to an unambiguous, determinative code. We hear this idea expressed all the time. The car company Bentley advertises for employees saying: ‘Hard work is in our DNA.’ The footballer David Beckham says: ‘Football is in England’s DNA.’ And a toll-collector for the Golden Gate Bridge in San Francisco says: ‘Our DNA is embedded in this bridge.’

Everyone knows these statements aren’t literally true, but although we might understand their figurative meaning, they continue to reflect, and influence, how we think. Even biologists, being quite human, too often think metaphorically and assign properties to genes that genes don’t have. The metaphor works because our society has a deeply embedded belief in genes as clearly identifiable material things which explain our individual natures, making them inherent from the moment of our conception and thus predictable. If hydrogen and oxygen are the causal atoms of water, genes are the causal atoms of our existence.

And we’re surrounded. News stories appear every week announcing the discovery of a gene ‘for’ this trait or that. Direct-to-consumer (DTC) genetic testing and ancestry determination companies are thriving, because consumers believe their genes will tell them more about their ancestry than family stories can. They also want to know whether they are fated to suffer from particular diseases, and they believe that this too is written in their genes. Sperm banks suggest that prospective parents consider a potential donor’s hobbies, the languages he speaks, his favorite foods, or his educational attainment, as though these traits are written in his sperm.

But try or wish as we might, the idea that everything about us is reducible to genes is not supported by real-world observations. Indeed, a simplistic picture of genes as individual causal things with straightforward effects is out of date in many ways. For starters, we now know that no gene acts alone. Complex traits — such as the diseases that most of us will eventually get — result from the interactions among multiple genes and/or environmental factors. Predicting disease depends not just on identifying our genotype, the particular, unique set of DNA sequence variants we inherited, but also on predicting our future environments — what we’ll eat, drink, or breathe, the medications we’ll take, and so on — which neither DTC companies nor anyone else, no matter how ‘expert’, can do.

Because environments vary and every genome is unique, multiple studies of a given trait or disease will generally yield different results. DTC estimates of disease risk are inherently probabilistic, not fixed. The same applies to choosing a sperm donor based on behavioural traits — of which any genetic component would likely be swamped by cultural and environmental factors, such as the food the donor was exposed to when growing up, or whether he could afford to go to university.

The metaphor that corporations and nations have their own DNA, and the belief that genes have straightforwardly determinative effects, might provide a comfortable, tempting image of simple cause and effect. But it’s akin to replacing the religious concept of ‘soul’ with the modern, scientific one of ‘gene’, and that’s very misleading. It tends to assign a kind of fixed metaphysical essence, analogous to Calvinism’s predestination, and drastically simplifies what are actually complex phenomena (dogmatic beliefs are like that). And there are consequences.

Genes are certainly real, so it’s important to understand what they can tell us about ourselves. You might be told that, based on your genotype, you have a (let’s say) 15 per cent chance of heart disease. This is a risk, or probability, not a certainty, nor anything like it. Probabilities are not the same as ‘causes’, and they can be extremely difficult to grasp. For example, even in the simplest situation, such as when we flip a coin to see who pays for the drinks, we might say our thumb is the cause of the flip itself, but we tend to think of the actual result — the ‘heads’ or ‘tails’ — as down to ‘chance’.

But what do we mean by chance? It is easy to wrap our heads around ideas such as coin-flipping by assuming that every flip has a 50-50 chance of a heads or tails result. Sounds simple enough, but what if we need to predict the specific outcome of a large number of such flips, somewhat like the challenge we face in predicting, from a person’s genotype, the risk of life events such as a heart attack or diabetes? Each of us has a unique set of variants in perhaps hundreds of different genes that separately contribute to the probability of disease. What will each one do? Will they flip as ‘illness’ or ‘health’? Is that even a realistic question?

Unlike coin-flipping, disease prediction depends on knowing, assuming or guessing the underlying risk associated with each individual genetic variant, risks that differ from gene to gene, and that do not work like the simple heads and tails of a coin (which, if the coin is fair, will always carry the same risk). What kinds of ‘probabilities’ are they when it comes to understanding what can be predicted from an individual’s genes and the major life decisions that might follow? Just as a coin heavily biased towards heads can come up tails on a given flip, a person inheriting a genotype that raises the risk of diabetes might not in fact get the disease. And risks can easily be perceived as more serious than they actually are, even if we assume the risk estimate is solid. If the risk of a given disease is, say, 2 per cent in the general population, and our best guess is that your genotype raises that by a whopping 25 per cent, that still only changes your actual risk to 2.5 per cent.

So far, we’ve considered purely physical traits. What role do genes play in non-physical traits such as behavior, or even the ultimate questions of consciousness and free will? Here, the metaphoric replacement of ‘soul’ by ‘gene’ works in a different way. How much of our feelings, thoughts and behavior is actually determined from the moment we are conceived, and could in principle be read like a computer program from our genome?
The extent to which we have free will is a fundamental aspect of how we view our ‘selves’, and for many religions, relates to whether we can be held responsible for our moral behavior. The scientific view, on the other hand, goes something like this: we live in a totally material world made of matter, energy, and the forces that connect them. Since genes are the fundamental causal elements of life, it would seem inevitable that, if we knew enough, we could predict everything about all of us — our health, our behavior, and our ideas. The alternative would seem to be mysticism — invoking some sort of immaterial something-or-other that we can’t measure but that affects who and what we are. But if genetic prediction is so unreliable and complex, how did our view of ourselves get so entangled in genetic determinism in the first place, and what might all this tell us about not just physical traits, but such elusive ideas as free will?

Today’s gene metaphor is a fabric woven of two threads from the 19th century. In 1858, Alfred Russel Wallace and Charles Darwin proposed a stunning new framework for understanding life in a way that was entirely materialistic and freed from mysticism. The diversity of life, they said, is due to the historical process of evolutionary divergence from common ancestry, in which present-day traits and functions are an outcome of natural selection. Darwin and Wallace developed their theory in the Newtonian era, when the aspiration of science was to understand existence in terms of ‘laws of nature’. Darwin viewed natural selection as, like gravity, a ubiquitous, essentially deterministic causal force in a relentlessly competitive world, a view he expressed in the foundation text of evolutionary biology, On the Origin of Species (1859).

Evolutionary determinism was the first thread of the gene metaphor. Natural selection preserves only what is inherited from the successful organisms in the past. The second thread comes from Darwin’s contemporary, Gregor Mendel, who conducted his studies of peas in order to understand the nature of inheritance. His findings also fit the Newtonian worldview perfectly. If natural selection was a law of nature, like gravity, then Mendel’s laws of inheritance promised to identify the fundamental building blocks of biological causation. By choosing specific traits that he knew bred true, Mendel identified a pattern of inheritance that provided perhaps the most powerful tool for research design in the history of science. The genetic research that followed eventually led to the identification of the nature of DNA, the locations and structure of genes in DNA, and the understanding of how they code for proteins. But that same Mendelian thinking made us conceptual prisoners of the deterministic, law-like interpretation of genetic function that leads us to think of traits themselves, not just genes, as discretely packaged units, produced by discretely packaged genes. That suggests that a pea seed already contains mini-green peas, or that a fertilised human egg contains a tiny human: a kind of genetic superstition.

Mendel showed that inheritance was probabilistic in the same sense as coin-flipping. Each parent carries two copies of every gene, and they each transmit, at random, one of those copies to each of their offspring. But once the particular randomly transmitted copies are inherited, their effects in the offspring follow causally deterministic principles: the resulting peas were either green or yellow, wrinkled or smooth.

There are plenty of instances in which genes do seem to be determinative, and work as they did for Mendel’s peas. Hundreds of known diseases, for example, appear to be caused by one or just a few genetic changes that disrupt or destroy a gene in some major way. Examples include cystic fibrosis, muscular dystrophy, and diseases of the nervous system such as Rett syndrome or Tay-Sachs disease. But as a rule, these ‘Mendelian’ diseases are a minority of rare traits that appear early in life, regardless of lifestyle exposures. The success for medical genetics in picking this easy-to-find ‘low-hanging fruit’ hasn’t given us a way to harvest the rest.

This isn’t for want of trying. Billions of dollars have been spent on searching for ‘the’ genes ‘for’ such common diseases as obesity, heart disease, type 2 diabetes, stroke, hypertension, cancers, asthma, and countless other afflictions. There have been few notable successes. The frustration is great because for most traits, including most diseases, members of an affected person’s family tend to have increased risk of the same trait or disease, in ways that can’t entirely be blamed on shared environment. This strongly reinforces the DNA metaphor by suggesting that genes must be contributing to risk in important ways. But if so, how can they be as slippery as eels when we try to find them? The reason is that the fabric of genetic causation is probabilistic both in terms of the inheritance of genes, and their effects.

The standard ‘scientific method’ we were all taught in school was based on stating, and then testing, a specific hypothesis about what causes some outcome; for example, that mutations in the LDL receptor gene (which affects cholesterol levels) can cause heart disease. However, most studies of such specific hypotheses have come up empty. The growing availability of wholesale DNA sequencing technology, largely initiated by the completion of the human genome project in 2003, led to the widespread abandonment of standard hypothesis-based genetics, to be replaced by what is called ‘hypothesis-free’ genomics.

In keeping with the DNA metaphor, the idea of the genomic approach is to assume that genes simply must be causing a trait of interest, and to look across the entire genome to find variants that are more common in individuals with the trait than in those without it. The hope was that we would soon eliminate the debilitating or fatal diseases to which most of us now fall victim, once we had exhaustive knowledge of genome-wide variation.
Genomic studies searching for causal genes have grown ever larger and more expensive, but commensurately important results have yet to roll in. Most of the estimated overall genetic influence on the traits or diseases of interest is still unidentified. What we’re finding instead is ‘polygenic’ causation, that is, that many different parts of the genome contribute mainly trivial individual effects.

A typical well-studied example is Crohn’s disease, an inflammatory bowel disease that runs in families, and thus would seem to have a major genetic component. However, the most recent study, by Heather Elding and colleagues at University College London, published in The American Journal of Human Genetics, estimates that the number of genes associated with the disease is around 200, most with very small effects, which explains only a small amount of the genetic background of this disease. To liken this again to coin-flipping, variants at each ‘causal’ gene affect risk in some probabilistic way, usually very small — far from 50-50 — and with no guarantee whatever that the same variant provides the same risk in different people who carry it, or in different populations, or in men or women, or at different ages. It’s as though each coin keeps changing its probability of coming up heads. Thus, the predictive power of this type of ‘personalised genomic medicine’ is generally very weak, like trying to predict the outcome of hundreds of individual-specific coin-flips. That’s why, with some fortunate exceptions, the clinical or therapeutic value of all these genetic studies has so far been slight.

It’s a similar story for normal traits as it is for disease. Height is an easily measured trait that clearly runs in families, and many studies have been done looking for genes for this trait. More than 400 contributing genetic regions, from an estimated 700 or so, have been found but, again, none with very large effects. In fact, to date, only 10 per cent or so of the variation in height has been explained, as a study from Exeter University published in Nature in October 2010 demonstrated. Many more genes will be found to contribute, but environmental factors such as diet or illness will as well.

Height and Crohn’s disease are just two of many instances of this same basic pattern. Behavioral and psychiatric traits are proving to be just as intractable, and the story is similar with the same kinds of studies in other species, as varied as yeast, insects, and plants. What is being documented is the blunt reality of the state of nature. No matter how unwelcome it might be for those who still hope for simple deterministic-like genetic causation, complex traits are affected (one should perhaps no longer say ‘caused’) by multiple genes with individually small and typically fickle effects. In addition, nobody disputes that there is usually a hefty, indeed often predominant, environmental component to the risk of disease, although it’s typically not very seriously considered by geneticists. These environmental factors are themselves quite complex and elusive to assess, or even identify.

Perhaps the most important single fact lurking in all of this is that when numerous genes contribute to a trait, the specific set of contributing variants is different for every individual. This is a many-to-many causal relationship: there are many genetic paths to a single height, blood pressure, triglyceride, or cholesterol level. Equally, a given genotype is consistent with many different trait values. Each genetic variant is a very weak ‘coin flip’ with unstable probabilities, and everyone is flipping a different set of coins. So, even if we identify the genotype of an individual, we can’t as a rule accurately predict its effects, even though this is just what ‘personalised genomic medicine’ has promised to do.

This makes another aspect of the DNA metaphor problematic. Instead of the widespread view of life as raw, relentless Darwinian competition leading to a single ‘fittest’ way to be, a far better way to see it is in terms of cooperation. By cooperation we do not necessarily mean the social, emotional variety. Cooperation describes the way in which a trait is produced by many factors, the countless genes and lifestyle aspects that contribute to the trait. If these factors do not work adequately together, the trait will not successfully be built into an embryo in the first place. Extensive webs of cooperation within us — genes with genes, organelles with organelles, cells with cells, tissues with tissues, and so on — mean that except for the rare disastrous instances, individual contributing genes neither spell doom nor success on their own. If there are many ways to fail — as the rare, serious genetic mutations show — there are a great many more ways to succeed.

Another way to view cooperation among genes is that evolution has provided a kind of redundancy that protects individuals from harmful mutations and overly harsh screening by natural selection. If each gene is, in itself, not a deterministic cause of some useful trait, then the organism can often do just fine with modification of or even loss of that gene, because other contributing genes cover for it, or any one modification has only a trivial effect. We know, for example, that many well-known variants that are clearly associated with very serious human disease are the normal state in other species. Indeed, whole-genome sequence studies have consistently shown that all of us carry a significant number of defunct or seriously disrupted genes, and this can include genes whose mutations are clearly implicated in some disease contexts, even if we ourselves are healthy.

All this might seem confusing: genes are molecules and hence fundamental causal agents of life, yet their effects are highly probabilistic and very hard to pin down or predict. As we have tried to explain, although genetics and evolutionary research are often very technical, the issues are actually reasonably simple. That’s fortunate, because an understanding of how life and evolution work as an orderly collection of uncertainties can lead us to a better sense of what is ‘inherent’ in our nature, and why.
In this light, we can return to the intriguing topic of behavior and, particularly, of free will. What we know about life undermines the explanatory power of molecular reductionism: that is, the attempt to use genetic variants to predict not only physical traits but also higher-level phenomena – such as the ability to do calculus, or write poetry – which seem to ‘emerge’ magically out of nowhere. For scientists attempting to understand life’s complexity, this might be the winter of our discontent, but Richard III’s soliloquy was written in Shakespeare’s hand — not his genome.

Complex organisation arises from webs of interaction among causal factors. Even if individual factors cannot be held responsible for particular developments, complex phenomena such as people, skills, skulls, languages, and even football teams clearly do exist, and have a material rather than any mystical or immaterial basis. In fact, emergent complexity takes essentially the same form, and presents the same challenge, in the very different contexts of biology, ecology, anthropology, sport — and free will.

But here’s the conundrum we mentioned earlier: if science says that the world is an entirely material phenomenon following universal laws of causation, then even the idea that we are responsible for our thoughts and actions comes under siege. Personality? Intelligence? Criminality? Political preference? You name it — even our moral decisions must, in principle, be predictable from our inherent, inherited genome. Yet, our thoughts and actions seem to be even farther beyond the reach of gene-based prediction than physical traits such as diabetes or height, which we’ve seen to be extremely complex in their causation. Is this just a temporary limit in scientific knowledge, or is something more profound going on here?

The question is more than incidental, because it raises the rigid idea of a mind/body dualism. Dualism asserts that mind and consciousness, whatever they are, are free from the usual material constraints. In other words, we have free will, just since we feel that we do. Free will is at the heart of assumptions that we are morally responsible for our actions, which in turn affects social and legal policy as well as religious notions of earned salvation. Clearly, if individuals are just the product of their genes, then they can’t be held responsible. Yet, how can they not be the product of their genes?

An answer might lie in the understanding of complex causation that we have presented here. We aren’t qualified to deal with religious issues about moral responsibility, but from a scientific point of view there is no mind/body dualism. Mind, wondrous though it might be, is in fact the product of molecular forces, including genes. Yet the mind seems fundamentally unpredictable from genes. The reason is that the brain and its activities are the result of countless billions, if not trillions (or more) of ordinary molecular and cellular interactions of all sorts, each of them probabilistic, from gene usage to the formation of neural connections, beginning before birth and extending over our lifetime’s experiences. During development, our brains are programmed to ‘wire’ up in a very general way, but the details in each individual are the result of experience, and our individual behaviours are the result of our brains responding to our unique set of experiences.

We should not be at all surprised that, just like most other traits, behaviour is not specifically predictable from genes. The massive web of probabilism makes such prediction weak at best, just as we’ve seen for physical traits. Our mental activities feel as if they are free, and their unpredictability supports that feeling. But the reason is that the causation involved is so complex and deeply probabilistic that it is, in effect, unpredictable even if we were to try to enumerate all the contributing factors. In that sense, for all practical purposes, we are indeed free.

It is sobering to point out that none of these issues about determinism, probability, complex causation — and even their implications for free will — are new. They can be traced back to the classical philosophers, and were vigorously debated along with the development of probability and statistics in the 18th through to the 19th centuries, and then reinforced by discoveries in sub-atomic physics in the 20th century. The significance and challenge of probabilistic multifactorial causation have been recognised. What is new is that we have a much better documentation of this problem from a genetic point of view. But, conceptually, we have not advanced very much in our understanding of what are deeply puzzling aspects of the way the cosmos — including life — works.

Human beings don’t like things that are unexplained. We want the comfort and sense of safety that comes from predictability. Perhaps as we are evolved biological organisms, uncertainty is unsettling to us. And, in the scientific era, we assume a material understanding of causation. That’s what the idea of determinism represents in a simple, easy-to-grasp way. We want to be in control, to be able to manipulate nature to alleviate the problems that we face in a finite life in a finite world. We want our causes to be simple, real causes, and that is perhaps why the metaphor of the gene as the atom of causation in life is so easy to absorb, and its subtleties so easy to overlook. We are made very uneasy by things that are only probabilistic unless, as in coin-flipping, we can sense what’s going on. When we can’t see it, and causation is many-to-many, that is far too much for our minds to deal with easily. Yet that seems to be the reality of the world.

1608. MI5 Spied on Leading British Historians for Decades, Secret Files Reveal

By Richard Norton-Taylor, The Guardian, October 23, 2014

Eric Hobsbawm in his study.  Photo: Anne Katrin Purkiss/Rex Features

MI5 amassed hundreds of records on Eric Hobsbawm and Christopher Hill, two of Britain’s leading historians who were both once members of the Communist party, secret files have revealed.

The scholars were subjected to persistent surveillance for decades as MI5 and police special branch officers tapped and recorded their telephone calls, intercepted their private correspondence and monitored their contacts, the files show. Some of the surveillance gave MI5 more details about their targets’ personal lives than any threat to national security.

The files, released at the National Archives on Friday, reveal the extent to which MI5, including its most senior officers, secretly kept tabs on the personal and professional activities of communists and suspected communists, a task it began before the cold war. The papers also show that MI5 opened personal files on the popular Oxford historian AJP Taylor, the writer Iris Murdoch, and the moral philosopher Mary Warnock after they and Hill signed a letter supporting a march against the nuclear bomb in 1959.

Lady Warnock told the Guardian on Thursday night: “I’d love to see the file, or anybody’s file come to that, to see what was/is regarded as suspicious … I am completely taken aback and even faintly flattered.”

Hobsbawm, who was refused access to his files when he asked to see them five years ago, died in 2012, and Hill died in 2009. Many passages, sometimes whole pages, of their files remain redacted and an entire file on Hobsbawm has been “temporarily retained”. The files include long lists of names and addresses of letters written by Hobsbawm and Hill.

They make clear that MI5 frequently read – or was sent – copies of as many as 10 letters a day. At the same time, its officers, or special branch officers, or their informants – one of whom was given the codename Ratcatcher – were secretly taking notes of their phone calls and meetings.

The files show that Hobsbawm, who became one of Britain’s most respected historians and was made a Companion of Honour by Tony Blair, first came to the notice of MI5 in 1942 when he and 38 colleagues were described as being “obvious members of the CPGB [the Communist party of Great Britain] on Merseyside”. He became number 211,764 on MI5’s index of personal files. Although he was cleared of “suspicion of engaging in subversive activities or propaganda in the army”, MI5 noted it was doubtful that he would be suitable for the Intelligence Corps. Roger Hollis, later head of MI5, and Valentine Vivian, the deputy chief of MI6, prevented him from joining the Foreign Office’s political intelligence department.

At the end of the war, in July 1945, an MI5 officer noted: “As he is known to be in contact with communists I should be interested to see all his personal correspondence”.
MI5 said the object of keeping checks on Hobsbawm was “to establish the identities of his contacts and to unearth overt or covert intellectual Communists who may be unknown to us”. Similarly, Hill was kept under surveillance, the files note, to establish “the identity of his contacts at the University [of Oxford] and in the cultural field generally, and to obtain the names of intellectuals sympathetic to the [Communist] party who may not already be known to us”.

Telephone intercepts disclosed that Hobsbawm and his family were friendly with Alan Nunn May – a British physicist who had confessed to spying for Russia and was released from jail in 1952 – and on one occasion put him up for the night. There is no evidence in the files of any attempt by either Hobsbawm or Hill to spy for Moscow or that the Russians were interested in them for any such purpose.

One early file on Hobsbawm describes his uncle Harry, with whom he sometimes stayed, as “sneering, half Jew in appearance, having a long nose”.

The surveillance intruded into the targets’ relationships. Hobsbawm is recorded in 1952 as having “difficulties with his [first] wife, who,” an MI5 officer noted, “does not consider him to be a fervent enough Communist”.

Christopher Hill

A report in 1950 revealed how Hill’s first wife, Inez, was becoming “sick to death” of his Communist party affiliation, which she had previously shared. “There seems to be some reason to believe that she is not only fed up with her husband’s politics but also with her husband’s political activities, especially as his political sympathies lead him, according to her, to give a considerable amount of his money to the party,” the report stated. A subsequent report revealed she was having an affair with another Communist party official.
Hobsbawm never left the Communist party but the MI5 files show he argued with the party leadership so strongly that it considered dismissing him, according to transcripts of MI5’s bugged conversations.


Writer Doris Lessing in 1957. Photograph: Hulton-Deutsch Collection/Corbis
At a fraught meeting at the party’s headquarters at King Street in London’s Covent Garden, at the end of 1956, Hobsbawm, Hill and the writer Doris Lessing agreed to write a letter attacking the party leadership’s “uncritical support … to Soviet action in Hungary”, a reference to the crushing of the uprising there. That support, the letter explained, was “the undesirable culmination of years of distortion of facts”. Hill, who left the party a year later, used the phrase “the crimes of Stalin” at the meeting, according to the MI5 report. The party’s paper, the Daily Worker, refused to publish the letter which was later run by Tribune, the leftwing weekly.

Unlike the very public manifestation of McCarthyism in the US, the discreet British version had its victims. Although political activities did not affect Hill’s academic career, Hobsbawm was prevented from getting the Cambridge lectureship he wanted. He was later appointed professor at Birkbeck College, London.

The documents show that years later MI5 was furious with the BBC for allowing Hobsbawm to broadcast. In October 1962, an MI5 officer noted: “My BBC contact tells me that Hobsbawm is still an occasional contributor to the Third Programme … Some recent talks were entitled ‘Sicilian Peasant Risings’ and ‘Robin Hood’.” What is described as “slightly unexpected” was a series of talks on “Jazz”.

Earlier that year, MI6 asked MI5 if they had any objection to telling the CIA that Hobsbawm was going on a tour of South America funded, to its surprise, by the Rockefeller Foundation (Hobsbawm had already visited Cuba). In a document marked Top Secret, dated 13 May 1963, MI5 told MI6: “A reliable and very delicate source has reported that Hobsbawm visited a number of countries.”

The files also reveal that the FBI feared that the atom bomb pioneer Robert Oppenheimer would use a visit to Britain to defect to Russia. He had come under investigation in America for his leftwing sympathies and in 1954 the FBI urged MI5 to put him under surveillance if he entered the UK. In a cable from the US embassy, legal attache JA Cimperman wrote: “Information has been received that Oppenheimer may defect from France in September 1954. According to the source, Oppenheimer will first come to England and then go to France, where he will vanish into Soviet hands. No further details are available.”

MI5 was anxious to assist. One officer noted: “Undoubtedly, if Oppenheimer came here under the shadow of reliable reports that he was possibly going to defect to the Russians, we should treat the matter as of major importance and in that light do what we could to help.” The warning proved to be a false alarm and no such attempt occurred.

Hill, who became a celebrated historian of the English civil war and was later elected Master of Balliol College, Oxford, first came to MI5’s notice when he visited Russia as an undergraduate in 1935. On his return a year later, MI5 noted that Hill “has the appearance of a Communist; but his baggage which was searched by HM Customs, did not contain any subversive literature”.

The files show he was turned down after applying for a post in military intelligence. He “should not be employed as a lecturer to the Forces”, MI5 insisted in 1946.

In 1953, MI5 described Hill as a “popular history don at Balliol … a Marxist and Communist party member”. It added, apparently with relief: “He does not, however, engage in Soviet studies. His period is the seventeenth century.”

One file contains a copy of a letter to Tribune supporting an anti-nuclear bomb march organised for 27 November 1959. It was signed by Murdoch, Taylor and Warnock, as well as Hill. MI5 had opened personal files on all of them.

Three years later, in October 1961, MI5 noted that Hill had become “a strong supporter of the Campaign for Nuclear Disarmament”. It added: “This fact, however, does not shed any light on his political sympathies, since very many shades of left wing opinion are opposed to nuclear weapons.”

Lord Lipsey, who had been asked by Hobsbawm to inquire about the possibility of MI5 keeping files on him, said on Thursday: “As a supporter of increased openness I am at least delighted that these files have finally been released.”

Eric Hobsbawm
Born: Alexandria, June 1917
Died: September 2012 
Main Works:
The Age of Revolution (1962)
Industry and Empire (1968)
The Age of Capital (1975)
The Age of Empire (1987)
The Age of Extremes (1994) 
Interesting Times (2002)
Globalisation, Democracy and Terrorism (2007)
How to Change the World (2011) 
(Hobsbawm also wrote The Jazz Scene (1959), originally under the pseudonym, Francis Newton)

Christopher Hill
Born: York, 1912
Died: February 2003
Main works:
Economic Problems Of The Church (1955)
Puritanism And Revolution (1958)
Society And Puritanism In Pre-Revolutionary England (1964)
Intellectual Origins Of The English Revolution (1965)
God’s Englishman (1970)
The Century Of Revolution (1961)
Reformation To Industrial Revolution (1967).
The World Turned Upside Down (1972)
Milton And The English Revolution (1977)
Some Intellectual Consequences Of The English Revolution (1980)
The World Of The Muggletonians (1983)
The Experience Of Defeat (1984)
John Bunyan and His Church (1988)
The English Bible In 17th-century England (1993)
Liberty Against The Law (1996)

1607. Climate Change: E.U. Greenhouse Gas Deal Falls Short of Expectations

By James Kanter, The New York Times, October 24, 2014

European Union meeting decides on policies that fall short to curb climate change

BRUSSELS — The deal reached early Friday by the European Union to cap its greenhouse gas emissions was meant to increase pressure on the rest of the world to achieve a landmark accord on climate protection next year, the bloc’s leaders said.

The approval of a target to slash emissions by 2030 by at least 40 percent, compared with 1990 levels, makes the European Union the first major global emitter to put its position on the table ahead of an important United Nations climate meeting in Paris at the end of 2015.

That target will send “a strong signal to other big economies and all other countries,” said Connie Hedegaard, the European Union commissioner for climate action. “We have done our homework; now we urge you to follow Europe’s example,” she said.

But environmentalists said the agreement, approved at a summit meeting here after late-night marathon negotiations, amounted to a weak compromise reflecting the complexity of managing a bloc of 28 member nations with widely varying energy systems. Elements of the deal were watered down to account for countries like Poland that rely on carbon-heavy coal, and for countries like Britain that were unwilling to accept binding targets on such other measures as the percentage of energy that comes from renewable sources and energy efficiency.

“The E.U. deal was probably the best compromise that progressive countries could hope for, given concerns of various nations about coal-burning and competitiveness,” said Richard Black, the director of the Energy and Climate Intelligence Unit, a nonprofit organization in Britain. “However, it is also a compromise with the climate system and with the needs of future generations.”

The European Union had come to the 2030 target after determining that it was the only way the union could keep its 2009 pledge to cut greenhouse gas emissions by up to 95 percent of 1990 levels by midcentury.

Mr. Black said even so, he doubted that the new target would “allow the E.U. to meet its long-term target of virtually eliminating carbon emissions.”

The deal also included a clause — demanded by nations like Hungary that are concerned about their global competitiveness — to reconsider the carbon reduction target if an ambitious international treaty is not reached next year.

But Angela Merkel, the German chancellor, and François Hollande, the French president, both suggested that the target would not be adjusted downward no matter the outcome of the United Nations talks next year.

The United Nations has been pressing for a climate deal that will require significant action by major economies like the United States and the European Union, as well as China, India and Brazil.

The global effort poses significant problems for President Obama: While he has pushed for domestic carbon pollution cuts and for a global climate deal, there is almost no chance that the current Senate will vote to ratify a climate change treaty, and there may be even less chance after the midterm elections, should Republicans gain the Senate majority. Instead, Mr. Obama’s climate change negotiators are working with their international counterparts to forge a hybrid deal blending a mix of binding and nonbinding provisions — what the negotiators are calling “politically binding.”

The major polluting nations will most likely set their targets in the first half of next year. It remains unclear what they will look like.

But even as the European Union has tried to pave the way by setting its climate targets early, experts said they may not be as ambitious as they first appear.

The deal requires a 40 percent cut in emissions from levels in 1990, a period when carbon pollution from European coal plants was at high levels. In the United States, President Obama is pushing policies to cut carbon pollution by 17 percent from levels in 2005, a year in which carbon pollution was much lower, according to Robert N. Stavins of the Harvard Project on Climate Agreements. The European Union deal could still top that, but probably by only a few percentage points using the 2005 benchmark.

“It puts them once again in first place if there is a race to be out first — but the race between first and second place might be quite small, depending on baseline years,” said Robert Stavins, director of Harvard University’s environmental economics program.

Curbing emissions that contribute to a changing climate has long been a popular cause in Europe. Policy makers here frequently highlight how their industries and citizens emit lower levels of greenhouse gases like carbon dioxide than those of the United States and other industrialized countries.

But recently there has been less enthusiasm among Europeans for a green agenda. The reasons include the stagnant economy that has depressed manufacturing, jobs and wages, and an unwillingness to adopt new regulations that could worsen Europe’s declining international competitiveness.

There have also been reductions in funding for green projects, and concerns about nuclear energy as an alternative since the disaster at Fukushima, Japan.

In addition, there has been diminished interest in identifying renewable alternatives, given the advent of technologies to extract cheap shale gas despite its uncertain prospects in Europe.

European leaders have also been a bit more reluctant to take steps against climate change since a climate conference in Copenhagen ended in failure five years ago.

The talks were “not easy, not at all,” said Herman Van Rompuy, the president of the European Council, the body that represents European Union leaders.

The result was an overall package that was significantly weaker than what countries like Germany and Sweden had been seeking.

A target of generating at least 27 percent of its energy from renewable sources will be binding at the European Union level, but not at the national level. That raised questions among climate experts about how the target would be enforced.

A separate target for improving energy efficiency by at least 27 percent was “indicative” only, meaning it would not be binding even at the bloc level. The target also was lower than the 30 percent proposed by the European Commission.

But the outcome suited David Cameron, the British prime minister, who had been concerned that binding targets on renewable sources and energy efficiency would give ammunition to his political opponents who contend that he has surrendered too much sovereignty to Brussels. Climate goals could now be accomplished at “the least cost to our industries, at the least cost to our consumers, and the least cost to families up and down Britain who don’t want to pay any more on their energy bill than they otherwise should have to,” Mr. Cameron said.

1606. Ebola Vaccine, Ready for Test, Sat on the Shelf Because Africans Could Not Pay

By Denise Grady, The New York Times, October 23, 2014

GALVESTON, Tex. — Almost a decade ago, scientists from Canada and the United States reported that they had created a vaccine that was 100 percent effective in protecting monkeys against the Ebola virus. The results were published in a respected journal, and health officials called them exciting. The researchers said tests in people might start within two years, and a product could potentially be ready for licensing by 2010 or 2011.

It never happened. The vaccine sat on a shelf. Only now is it undergoing the most basic safety tests in humans — with nearly 5,000 people dead from Ebola and an epidemic raging out of control in West Africa.

Its development stalled in part because Ebola is rare, and until now, outbreaks had infected only a few hundred people at a time. But experts also acknowledge that the absence of follow-up on such a promising candidate reflects a broader failure to produce medicines and vaccines for diseases that afflict poor countries. Most drug companies have resisted spending the enormous sums needed to develop products useful mostly to countries with little ability to pay.

Now, as the growing epidemic devastates West Africa and is seen as a potential threat to other regions as well, governments and aid groups have begun to open their wallets. A flurry of research to test drugs and vaccines is underway, with studies starting for several candidates, including the vaccine produced nearly a decade ago.

A federal official said in an interview on Thursday that two large studies involving thousands of patients were planned to begin soon in West Africa, and were expected to be described in detail on Friday by the World Health Organization.

With no vaccines or proven drugs available, the stepped-up efforts are a desperate measure to stop a disease that has defied traditional means of containing it.

“There’s never been a big market for Ebola vaccines,” said Thomas W. Geisbert, an Ebola expert here at the University of Texas Medical Branch in Galveston, and one of the developers of the vaccine that worked so well in monkeys. “So big pharma, who are they going to sell it to?” Dr. Geisbert added: “It takes a crisis sometimes to get people talking. ‘O.K. We’ve got to do something here.’ ”

Dr. James E. Crowe Jr., the director of a vaccine research center at Vanderbilt University, said that academic researchers who developed a prototype drug or vaccine that worked in animals often encountered a “biotech valley of death” in which no drug company would help them cross the finish line.
To that point, the research may have cost a few million dollars, but tests in humans and scaling up production can cost hundreds of millions, and bringing a new vaccine all the way to market typically costs $1 billion to $1.5 billion, Dr. Crowe said. “Who’s going to pay for that?” he asked. “People invest in order to get money back.”

The Ebola vaccine on which Dr. Geisbert collaborated is made from another virus, V.S.V., for vesicular stomatitis virus, which causes a mouth disease in cattle but rarely infects people. It had been used successfully in making other vaccines.
Continue reading the main story
The researchers altered V.S.V. by removing one of its genes — rendering the virus harmless — and inserting a gene from Ebola. The transplanted gene forces V.S.V. to sprout Ebola proteins on its surface. The proteins cannot cause illness, but they provoke an immune response that in monkeys, considered a good surrogate for humans, fought off the disease.

The vaccine was actually produced in Winnipeg, Manitoba, by the Public Health Agency of Canada. The Canadian government patented it, and 800 to 1,000 vials of the vaccine were produced. In 2010, it licensed the vaccine, known as VSV-EBOV, to NewLink Genetics in Ames, Iowa.

The Canadian government donated the existing vials to the World Health Organization, and safety tests of the vaccine in healthy volunteers have begun.

NewLink’s product is one of two leading vaccines being tested. The other, which uses a cold virus that infects chimpanzees, was developed by researchers at the National Institutes of Health and GlaxoSmithKline. The first tests of an earlier version of it, employing a different cold virus, began in 2003.

Several other vaccine candidates, not as far along, are also in the pipeline and may be ready for safety testing next year. Once any drugs or treatments pass the safety tests, they will be available for use in larger numbers of people, and health officials are grappling with whether they should be tested for efficacy in the traditional way, in which some people at risk are given placebos instead of the active drug.

Governments and the military became interested in making vaccines against Ebola and a related virus, Marburg, during the 1990s after a Soviet defector said the Russians had found a way to weaponize Marburg and load it into warheads. Concerns intensified in 2001 after the Sept. 11 terrorist attacks and anthrax mailings.

“The National Institutes of Health came up with a program called Partnerships in Biodefense that partnered researchers like me with companies, usually small companies,” Dr. Geisbert said.
The government money led to major advances in the laboratory, Dr. Geisbert said, but was insufficient to cover the huge costs of human trials. Nor could the small companies that were involved in the early studies in animals afford to pay for human trials. No finished product came to market.

Dr. Geisbert moved on, working on treatments for Ebola and another version of the V.S.V. vaccine. For the vaccine work, his main collaborator has been Dr. Heinz Feldmann, the chief of virology at the Rocky Mountain Laboratories in Hamilton, Mont., part of the National Institute of Allergy and Infectious Diseases.

The newer version of the vaccine uses a slightly different form of V.S.V., one that Dr. Geisbert said he thought might be less likely to cause side effects, and more likely to gain quick approval because it has been used as the basis for an H.I.V. vaccine and is known to the Food and Drug Administration. But the new version, VesiculoVax, made by Profectus Biosciences in Baltimore, has not yet been tested in humans.

The V.S.V. products are live vaccines, with replicating viruses that may cause a reaction. It is not clear what level of side effects will be considered acceptable.

Chills and nausea are possible, Dr. Geisbert said, but he added, “Who cares, if you survive Ebola?”

Most vaccines are given to prevent disease before people are exposed to it, and the plan is to use Ebola vaccines that way. But the V.S.V. vaccines have also been shown to protect monkeys even after the animals have been exposed to a heavy dose of Ebola — if given soon after exposure.

Researchers hope that they will work that way for people, too. If they do, health workers and family members who have been in contact with a patient might be protected, instead of having to spend 21 days of dread, waiting to see if they get sick.

Dr. Geisbert spends much of his time working with Ebola and other deadly viruses in a Biosafety Level 4 laboratory at the Galveston National Laboratory, where the researchers wear spacesuits that each come with an independent air supply, and visiting journalists are required not to report which floor the labs are on.

This month, one of his tasks is to test the Profectus vaccine and an experimental treatment against the Ebola strain that is causing the current epidemic. The virus is from a species called Ebola Zaire, against which the products have already been shown to work. But different strains within a species can vary genetically by 2 percent to 7 percent, Dr. Geisbert said.

Most of the time, those small variations do not matter, and a drug or treatment that works against one strain will work against all. But once in a while, the difference matters.

“We don’t know for 100 percent certainty until we prove it in animals,” Dr. Geisbert said. “The companies I work with are smart. They want that answer sooner rather than later, before they go investing millions of dollars to put this into humans.”