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Are you a fan of Thomas Friedman?

Posted on February 29th, 2012 in Books,Culture by Robert Miller

A priceless book on Thomas Friedman of the New York Times by Belén Fernández

If you are a fan of columnist Thomas Friedman of the New York Times,  then you will want to read this interview with the author of a book on Friedman titled The Imperial Messenger: Thomas Friedman at Work,” by Belén Fernández, published by Verso this year (2012). An interview with the author appears in Truthout. In this book, one that surprises me simply because it should have been written long ago (but let’s be grateful to Belén Fernández for putting this together), the author masterfully documents the incomprehensible inconsistencies that are a regular feature of Friedman’s column and his life’s work. Friedman’s objective is to make you happy that you are part of a glorious American Empire and that Free Trade is the wave of our future and the golden key to our past. Agonizing as those narratives may be, the most frustrating part of Friedman’s articles are that few people check his facts. But no one has done that better than Fernández. Here I give you just one of the stories about Friedman from the book. If you have read Friedman you know that he likes to summarize the feelings of an entire nation, even though he talks to very few citizens of any country and apparently gets most of his information by talking to cab drivers.

  • [Taken from the interview with Belén Fernández in Truthout: link above]


  • People often joke that the only normal human beings Friedman converses with – outside his usual circle of CEOs and national leaders – are cab drivers. In fact Friedman has a certain insistence on speaking on behalf of the world’s inhabitants without actually speaking to them first. Readers are instructed to “just ask any Indian villager” for confirmation that U.S.-directed globalization is desirable, and are informed in 1999 that it is “stupid” to oppose globalization: “The [anti-WTO] Seattle protesters need to understand that. The people of Sri Lanka already do.” The latter insight is gleaned from Friedman’s chat with the owner of a Sri-Lanka based Victoria’s Secret underwear factory, who obviously does not qualify as “the people of Sri Lanka.””

As a corporatist newspaper, the New York Times and columnist Thomas Friedman fit each other like glove and hand and the fact that politicians, like Barack Obama consult with Friedman, gives him panache, swagger and sufficient celebrity status to keep doing and saying what he has been doing and saying all along. Whether this book by Fernández changes the conversation about Friedman remains to be seen, but it’s a good start.  Friedman is a Minnesota boy. He is very popular in this state, though at least one citizen of this community never reads him because his articles are vacuous, nonsensical and very misleading.  Perhaps his best work is achieved with the titles of his books, but then again “The World is Not Flat.”


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It is not too early to write the provisional history of the U.S. war in Afghanistan

Posted on February 28th, 2012 in Government,War by Robert Miller

Afghanistan riots over Koran Burning

Just when the war in Afghanistan threatened to become America’s silent war, one destined for the back pages or in the business section of our newspapers, violence erupted spilling the war out onto the front pages again, stimulated by new events; the news of Americans burning the Koran spread like a virulent contagion throughout the country and, at least for now, seems to pose a threat to American safety as well as the future of our war effort. It should bother everyone to see how our relationship with the Afghans can turn on a dime because there is no underlying set of mutual goals–only mutual distrust. Suddenly the horrific accounts of bombings, daring raids, roadside explosions and  effective, deadly attacks by the Taliban, have given way to massive civil demonstrations and violence from Afghans, the very people we thought were on our side. The violent eruptions over the Koran burning demonstrates that our problems in Afghanistan are not just with the Taliban. In reality, they never were just about the Taliban or, for that matter, neither were they at one time just about Al Qaeda.  Raw nerves exist throughout the country and increasingly, we hear about killings of American and NATO soldiers by Afghan soldiers and employees working inside the government. Just yesterday we learned that two American officers were killed in Kabul inside the Interior Ministry building, protected by heavy security. Many feel that it is no longer safe for Americans to be working alongside Afghans because of this danger. The recent officer killings were apparently committed by a worker employed within the Ministry (though he was not captured at the time of this writing) and reflects the growing tension between those we are attempting to bring into the government and military in hopes of entrusting them to sustain a functional civil society, even though it’s an American version of what we think they should have, as we pointedly emphasize why Afghans should raise the rent on properties owned by Al Qaeda and the Taliban. But, no matter how hard we try, how much money we put into the country, we cannot achieve a sufficient level of security such that the country can put itself back together again. In that sense it’s an eery duplication of what we achieved in Iraq. Just call Afghanistan Iraq II. The major difference between the two is the difference between oil in the ground and a pipeline above ground.

The tension between American/NATO forces and Afghans has sharply escalated as a result of the Koran burnings, and the recent image of American soldiers urinating on the dead body of a resistance fighter has added to the outrage demonstrated in the streets.  To Muslims, these acts fit the image they have of Americans and their presence in Afghanistan. Most Americans do not understand how much we are hated in that part of the world and when Bush/Cheney/Rumsfeld formulated the word “islamofacism” to describe radicals in the region, it was very clear to Afghans that they were referring to all Muslims, not just a few radicals. We ignore the polls that tell us that we are viewed more as a threat to Afghan society, rather than an ally. Even President Karzi, the leader we installed,  can’t make up his mind about us and we are desperately seeking a solution to this war that involves a negotiated settlement with the Taliban.

In Eric Margolis’ book “American Raj: Liberation or Domination?: Resolving the Conflict Between the West and the Muslim World,” published in 2008,  he attempts to provide the American public with a view of what people in the Middle East think of Americans and why we find conflicts in that region so difficult to resolve. We don’t have a problem starting a war in this region, usually associated with quick military victories and what seems like a triumphant victory. But then the problems begin. Margolis’ message is especially relevant as he has traveled all over the region, reporting and following in the footsteps of his mother who also was a journalist in the Middle East. Afghans understand that they will be there long after we leave and they also clearly understand that our motives are never pure, but always involve a financial benefit that serves our own interests. Our intrusion into Afghanistan and the problems that we are having in that region reflect the poorest public relations effort ever perpetrated from one country onto another. Before Muslims understood what we were really like, at the close of WWII, we were viewed as honest, hard-working Americans who lived up to the demands of their noble constitution. At one time, Muslims viewed us as a model for their own future. It did not take long however for them to understand that what we offered was merely a different form of hegemonic control. Afghans believe for example that the American motivation for invading their country was so that we could be dealing with a more compliant partner than the Taliban to allow the construction of a major pipeline through the region to distribute natural gas from the Caspian Sea and avoid the distribution system of the Russians. This deal was set to go through, but, in 1998 American embassies in Nairobi and Dar es Salaam were bombed by Al Qaeda, operating within Afghanistan, as Osama bin Laden had moved there from Sudan in 1996. The course of history changed that day.

Three years later, when 9/11 hit us, Al Qaeda probably had about 300 members and Afghans did not believe that the United States would declare war on so few people–but there were many Afghans who understood that the U.S. declared war on Afghanistan (an unofficial war of the type we have conducted ever since the close of WW II) to control the country and its future destiny with a pipeline.  If this is a war that’s winding down, it’s winding down for us, not for the Taliban. They’re not going anyplace. If the “Long war” characterizes any side, it is that of the Taliban, not the Americans. We are war-wary and exhausted and no longer certain of our objectives in Afghanistan. Nation building? Counterinsurgency? Pacification? At one time or another these names have all appeared within our lexicon for the Afghan war, but like any buzz word they have all run their course, including the generalmania period of Patraeus and McChrystal. We no longer have a moniker for the war in Afghanistan, but it doesn’t mean our efforts are any less deadly to Afghanistans. The Taliban just have to wait until we leave, after which they know that the puppet government we have established will not offer significant resistance in our absence and Karzi himself would like to conclude a peace treaty with the Taliban before we leave. In the meantime, it’s the Taliban consider it their responsibility to extract as much pain and suffering from the U.S. Army troops as they have suffered underneath the boot of those same soldiers. As for accurate reporting about the war, you cannot trust the mild or even rosy reports of embedded journalists, which includes just about everyone,  because their vision of the situation is that which the military insists they see. As an embedded journalist you see what the military wants you to see, their eyes are your eyes and, at least in Iraq, there were far too many examples of Congressman giving a televised tour of their visit to illustrate how safe it was, dressed in a full body armor suit, surrounded by sharp shooters lined up along the roofs of the aligning buildings. John McCain went to Iraq under such circumstances to announce that it looked like we were finally winning the war because of the “surge.” The far more dangerous non-embedded journalists are the ones we should seek out and, as I have noted previously, reports that come back from journalists like Jeremy Scahill (see below) do not suggest we are making significant progress in the war–quite the opposite. In the meantime we put lots of our efforts into destabilizing Pakistan, a much larger country than Afghanistan and one that comes with its own supply of nukes. In two more years, Obama has promised to end the war in Afghanistan. When General Patraeus was in charge, he promised, like GW Bush, to give us a new version of the “Long War.” Under his leadership, we went from the “shock and awe” policies of the Bush administration, courtesy of Donald Rumsfeld, with a heavy emphasis on technology, to the counter insurgency strategy and the “surge injections” of more troops. It is doubtful that this worked in Iraq when Patraeus tried it in 2006, but there is little question that the Afghanistan surge did not work and Patraeus is no longer running that war, but instead came home to run the CIA. No one is defending the surge in Afghanistan and our own estimate of the war is that it’s a “stalemate.”

In case you haven’t heard, the “Long War” is over–it died of natural causes and shear exhaustion. The Afghan war we are fighting now uses Special Forces and missile firing drones to take out suspected terrorists in an ever-increasing arch of countries in Africa. The new model for conducting the war in Afghanistan is based on the way in which we killed bin Laden last year. Should the Republicans mention the Middle East in this year’s Presidential election, they will mention Iran and avoid talking about Afghanistan, because Obama already killed bin Laden. The Republicans will be far more comfortable blaming the rising cost of gasoline on Obama (despite the fact that during Obama’s three years America’s production of oil has increased, not decreased), numb to the fact that their own rhetoric against Iran may have already contributed to the rising cost of oil.

If you want to read reports on the Afghan war from a non-embedded reporter, you need to seek out journalists such as Jeremy Scahill and Rick Rowley. These two reporters went to Afghanistan last year, arranged their own schedule and visits without military escort or a travel guide. Very few reporters take such risks.  They reported last year that our military actions in Afghanistan were destroying our objective because we were killing too many Afghans and the opposition to our presence was building. We don’t hear about these events because they are carried out by Special Forces that conduct night-time raids and often kill whole families indiscriminately in retaliation for a nearby roadside bomb that went off in the neighborhood.  In the Vietnam war we were outraged by the disaster of My Lai, but the way operations are carried out by Special Forces in Afghanistan, we just don’t hear about them, primarily because they are not written up. You cannot claim access through the Freedom of Information Act if nothing about the raid was written down. And, we don’t hear too much about drone strikes which are also becoming a new component of the way we conduct our wars. Despite our poor history in fighting and winning wars in the Middle East in the last decade, we will hear this year about how the Obama administration should be bombing Iran to prevent them from getting a nuclear capability, despite the fact that there’s no evidence they have one.  This year the Republicans running for the Presidency have added incompetency to the list of their afflictions including the absence of any world view of politics or diplomacy.

It appears that Americans want to forget our war in Afghanistan and we are still in search of what or how a victory in that region of the world will be defined, no matter how it ends for the United States. At the moment, the war in Afghanistan seems like it will end like the war in Iraq: we will find some delusional way to declare a victory and leave the  country in shambles, but perhaps we will have added a pipeline to the landscape of Afghanistan and recruited enough people to guard it. And of course we never mention how we have devastated the culture of Iraq and put some of its archeological sites under asphalt to make room for our war machine. Andrew Bacevich, writing in TomDispatch has recently characterized the history of our wars in Afghanistan and Iraq, as we prepare to engage terrorists on an expanded map, with new bases for drones without every asking why or what it is we plan to get out of it and whether it can be done that way under our constitution. The new war plan under the Obama administration is one in which the war will become a silent war, made by executive decisions over life and death of not just terrorists, but anyone the President feels is a threat to the United States. If America should suddenly lose her status as a superpower, I am convinced that the American public will be the last to find out about it. Since GW Bush, we have heightened the authority of our President to make life and death decisions over people we refer to as terrorists, including U.S. Citizens. This is too much authority to put into the hands of a single President. Now more than ever, we need to have Congress take back their abandoned authority, the one spelled out in the constitution–that only congress has the right to declare war and congress should review the military budget periodically–we have far to many black budget items in the military budget and far too little authority over defense spending.

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A victory for molecular medicine in the fight against cystic fibrosis

Posted on February 18th, 2012 in General by Robert Miller

Cystic Fibrosis Channel (CFTR) in the cell membrane; ivacaftor works on the outside of the cell to increase the ease with which chloride ions can move through the channel formed by CFTR protein that spans the cell membrane many times

It seemed like a major medical miracle at the time: the defective gene which causes cystic fibrosis (CFTR gene which stands for Cystic Fibrosis Transmembrane Conductance Regulator) was identified and the world was waiting for the next step, perhaps a quick cure for the disease which many hoped would be realized shortly after discovery of the offending gene. After all, knowledge of the gene and the amino acid sequence of CFTR seemed like overcoming the major hurdle and the rest would be easy–a drug designer game–no problem. The CFTR gene identification however, was in 1989 and, although improvements in palliative therapeutic methods over the past forty years have dramatically prolonged the survival rate of those  afflicted with the disease (from an average age of 11 years to 37), no magical cure had emerged more than twenty years since the gene was first discovered. Now, very recently, the drug VX-770 (ivacaftor) was introduced that seems to offer a breakthrough for at least one subclass of patients with Cystic Fibrosis. As it turns out, Cystic Fibrosis is a disease that contains many different mutations of the CFTR gene, and only the mutation known as G551D, which has defective CFTR proteins that reach the surface of the cell are responsive to the drug (ivacaftor works by enhancing the transport of chloride through the CFTR channels, which improves the ability of the channel to participate in normal fluid regulation, reducing the sticky mucous secretions that, in the respiratory system, create a high risk of infection and restriction to normal air flow and oxygen exchange).  The G551D  mutation only accounts for 4 to 5% of the Cystic Fibrosis population. But the hope is that this drug will also help other mutations of the gene if they have at least some CFTR channels that make it to the surface of the cell.

Most of the cystic fibrosis patients have defects in the protein such that they never get placed in the cell membrane, because they are not folded properly and not recognized by the cell “as suitable for service.” Once the CFTR protein is properly placed in the cell membrane, it works by allowing chloride ions to more readily traverse the ion channel that they form, typically moving from the inside to the outside of the cell (with sodium and water coming through other channels) to provide a less viscous secretion into the respiratory tracts (other organs besides the lungs are similarly affected). Thus, while no single drug is likely to  relieve the entire panoply of cystic fibrosis mutations, this first step using ivacaftor has proven very promising in clinical trials. It is a novel drug that was created by twenty years of intensive research and new discoveries along the way that verified how complex a problem we face in generating a suitable cure, even if the structure of the disease-causing protein has been deciphered. VX-770 (ivacaftor) was developed by a method known as High Throuput Screening (HTS) in which 228,000 chemically diverse drug-like compounds were screened using a cellular assay for identifying CFTR potentiators. A multiple author paper was published in PNAS in 2009 and the results of a successful clinical trial were reported in the November 3, 2011 issue of the New England Journal of Medicine.

While this promising new drug gives us all reason to celebrate and enhance our hopes for future developments in this dreaded disease, we must also sober up for the struggle ahead, because this new drug (ivacaftor) does not address the central problem faced by the majority of patients with cystic fibrosis. About 90% of cystic fibrosis patients suffer from a form of the disease in which they do not produce a CFTR protein that partitions across  the cell membrane and would thus not be amenable to ivacaftor treatment. In a way, the drug works like hooking up your hose to a power washer, which increases the pressure and flow of water, but would not work without a source of water and the plumbing necessary to bring it to the device. The task ahead for the majority of cystic fibrosis patients is more sobering when compared to the achievement with ivacaftor and the subset of patients with G551D. Indeed a more complete cure, covering the entire spectrum of the cystic fibrosis patient population will very likely have to come from a gene replacement  strategy. But we have good news on that front as well: we have already had success with therapeutic gene-replacement approach in treating diseases such as Leber’s Congenital Amaurosis, through the injection of a single dose of adenovirus into the eye which had a copy of a healthy gene that replaced the defective RPE65 gene. RPE65 is required to regenerate the visual pigment (rhodopsin) that is necessary for the first step in capturing photic stimuli. Thus the patients with this deficiency were blind from an early age. Now the treated subjects can see and this mode of therapy will spread to eventually include many different forms of blindness, including retinitis pigmentosa, one of the major causes of human blindness.

It was once the case that drug therapy development was by fortuitous accident. The delay between the discovery of the gene and the first drug to target and improve CFTR action points out the difficulty that modern medicine faces: the transition from the era of chemical medicine (where you use the shotgun approach to try a lot of things and if one works you often don’t know why–such as the accidental discovery that antihistamines (chlorpromazine) dramatically improved some symptoms of schizophrenia and led to the elimination of several hundred thousand hospital beds in the 1950s that had been devoted to their care–even though the drug does not cure the disease) to molecular medicine (where the drug is designed to interact with targeted features of the offending molecule, or you replace the gene or prevent its expression)–can be a long, arduous and very painful process, filled with moments of hope and despair much like the medical quest for an AIDS vaccine; it is now more than thirty years since the AIDS virus was first discovered. We keep thinking that we will shorten the delay between discovery and cure, that each new breakthrough towards adopting molecular approaches will allow us to reach a threshold where a new pathway is illuminated to light the way for quickly curing all genetically-based diseases through a magical form of gene replacement therapy, while non-inherited chronic diseases will be cured with greater precision in drug development, like the results with ivacaftor. Each breakthrough like ivacaftor  treatment for cystic fibrosis gives us hope that we are approaching such a threshold and that we are getting closer to a  much broader and wiser view of the disease landscape.  But to get there, we still have to get a lot smarter about biology before any kind of medical avalanche for cures will flood the broad human pathology terrain.

When I was a medical student, during my rotation in medicine as a clinical clerk in my junior year, we admitted a young girl to the hospital with a raging pneumonia caused by her cystic fibrosis condition. It was a life-threatening situation, but she was finally discharged after a long period of antibiotic and pulmonary therapy. She was about 12 and was full of energy with high expectations for her future, though by then she had been admitted many times to the hospital with similar infections and she had obviously been afflicted with the disease from the time of her birth. The disease had also retarded her growth. It seemed like everyone in the hospital went out of their way to greet this young patient, as she was cheerful, charming and expressed with optimism the idea that she might have passed the most dangerous period of her disease and could now look forward to a future with more certainty and plan accordingly. Yet, a year later, I learned that she had been admitted again with another bout of pneumonia and died in the hospital. I never forgot that young patient and I think that experience accounts for my long-standing interest in cystic fibrosis and the CFTR ion channel.


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