Medical Journalism in the War on Alzheimer’s

They say that truth is the first casualty of war. So how is the truth doing in news coverage of medical research on dementia now that we have finally declared War on Alzheimer’s?

ImageThe question is prompted by the recent major article on the genetics of early onset Alzheimer’s disease by New York Times science reporter Gina Kolata in last week’s NYT Magazine. The article immediately generated a lot of positive buzz in the Alzheimer’s research and caregiver communities. It’s the kind of piece that usually garners awards, not opprobrium. So let me begin by saying what Kolata does right before making the case that she gets the most important things very, very wrong.

Kolata’s writing is a beautiful, and she tells a compelling story of the members of a family struggling to live with the burden of knowing that they may have a gene for early onset Alzheimer’s, and their sometimes enthusiastic and sometimes ambivalent involvement in medical research that can tell them for sure. She also describes some complicated genetic science with commendable clarity.

The problem is that Kolata uncritically accepts the perspective of Alzheimer’s researchers in a way that violates the fundamental value of systematic skeptical inquiry that ought to be at the heart of both journalism and science. There is nothing new or exceptional in this, of course. Frankly, Kolata’s many articles in the Times hyping the latest Alzheimer’s research, like so much of medical reporting in general, reminds me of the sort of journalistic failure, most egregiously by Judith Miller of the Times, that led so many to accept the Bush administration’s claims about weapons of mass destruction in Iraq. Just as uncritical reporting of the Bush administration’s false claims about the presence of WMDs, and its rosy assessment of how American troops would be received by the Iraqi people after dislodging Saddam, influenced the public and congress to support a war in Iraq, uncritical reporting of the sorts of claims made in the article about the imminence of therapeutic breakthroughs will influence the public and congress to continue supporting the war on Alzheimer’s and the growth of the biomedical industrial complex behind it.

Now I am not saying that the motivations of medical researchers in Alzheimer’s or other fields are the same as warmongers in the Bush administration On the whole, I am a fan of Alzheimer’s and other medical researchers and the work they do. But good journalists, whether they are covering the war on terrorism or the war on disease, should be skeptical of sources that have an obvious self-interest. And medical researchers have an obvious self-interest in presenting their research in the most favorable light possible. Thus it should be no surprise, even to people familiar with the daunting complexities of understanding, treating and preventing dementia, that the researchers profiled in the article “say that within a decade there could be a drug that staves off brain destruction and death.” But Kolata should have raised questions about this claim, and talked to experts not directly involved in the research who are far less optimistic about its potential to so quickly lead to effective treatments.

Kolata’s article uncritically reiterates two other important aspects of the perspective of many Alzheimer’s researchers: a warped view of history, and an oversimplification of the disease.

Fairytale History

Regarding history, Kolata spends about 800 words connecting German psychiatrist Alois Alzheimer’s first encounter in 1901 with a patient with what we would today call early-onset Alzheimer’s to contemporary research. Alzheimer brilliantly described the pathological features of the disease, but lacked the scientific tools needed to understand what caused it let alone how to do anything to stop it. “There matters stood until the latter part of the 20th century,” when contemporary researchers heroically enter the stage with powerful new technologies to penetrate the mysteries of the brain and will soon, we are assured, be able to set things right.

Image

Alois Alzheimer (1864-1915)

While it is attractively simple and flattering for researchers to think of themselves as part of a unified, continuous research enterprise stretching back more than a century in which they finally are able make progress on the medical mystery Alois Alzheimer unearthed in the brain of his patient more than a century ago, the truth is a good deal more complicated than that. Scientific and clinical research on dementia has never been a unified enterprise. The goals and approaches of researchers and clinicians are strongly shaped by the historical contexts in which they practice, and given the dramatically different context in which Alzheimer practiced, it is highly unlikely that he shared our concerns about age-associated cognitive decline. Though no one has done a serious historical study focusing on Alzheimer and his lab, I have looked at the available evidence enough to conclude that Alzheimer and his contemporaries simply did not view the disease that was named for him as terribly interesting or important. When he died in 1915, none of the admiring colleagues who eulogized him – not even Emil Kraepelin who named the disease for him in 1910 – listed the discovery of Alzheimer’s disease as one of his major accomplishments.

Moreover, the claim that nothing of significance happened regarding the medical understanding of Alzheimer’s disease and senile dementia between Alzheimer’ and the latter twentieth century ignores a major historical development. In the middle decades of the twentieth century, a group of American psychiatrists developed a psychodynamic framework for understanding and managing dementia and made sweeping claims about how it finally removed some of the mystery shrouding the condition and would soon lead to efficacious means of preventing cognitive deterioration in old age. It is perhaps understandable that contemporary researchers, trained in biological psychiatry and neuroscience and focused on pathology in the brain, have forgotten this chapter in the history of Alzheimer’s research. It is unfortunate though, if only because considering the now largely forgotten work of researchers who thought themselves on the cusp of being able to prevent dementia just might lead today’s researchers to consider the virtues of humility and circumspection in making claims about imminent progress.

While it might be presumptuous of me to suggest that Kolata should have known all this by making herself familiar with my work, she need not perpetuate a history of the field that is so obviously driven by the biases of contemporary researchers. It should not take a historian to recognize a self-serving fairy tale.

Simplifying Alzheimer’s

Regarding the oversimplification of the disease, there are a couple of points to make. First, the many scholars, clinical professionals and caregivers who have been working to lessen the stigma and despair associated with dementia – whom I am proud to count myself among – might take issue with the unremitting grimness with which Kolata represents having dementia. Without denying or diminishing the very real losses and challenges imposed by dementia, we have been working in different ways to show that a life cannot be reduced to a disease, even a disease that brings profound cognitive deterioration. Possibilities for human flourishing remain. Kolata’s story, like so much reporting on Alzheimer’s, represents people with dementia as pure victims – unable to comprehend or resist in any way a disorder that takes everything from them.

But I am willing to cut Kolata some slack here. While we need more stories about living well with dementia, that is not the story Kolata set out to write, and the one she did is important. Her story is about the dread associated with early-onset, familial Alzheimer’s disease, the very rare form of dementia that is associated with several autosomal-dominant gene mutations. Frankly, early-onset familial Alzheimer’s does seem more dreadful to me than the much more common variant that occurs at much older ages. Some may regard this as ageism, but developing a profound cognitive disability in your fifties or even forties does seem much worse than developing it in your seventies, eighties or nineties. And living with the sharp either/or risk of a Mendelian gene for dementia in one’s family seems much more dreadful to me than the gradually increasing risk for dementia associated with the normal vicissitudes growing older.

The problem is that Kolata’s story tends to conflate this very rare form of early-onset dementia, which is estimated to account for only one to five percent of all cases of Alzheimer’s, with the category as a whole. The story acknowledges this explicitly at only one point, nearly 700 words into a 5,400 word story, when it describes the rationale of the Dominantly Inherited Alzheimer Network (DIAN) project:

Though as much as 99 percent of all Alzheimer’s cases are not a result of a known genetic mutation, researchers have determined that the best place to find a treatment or cure for the disease is to study those who possess a mutation that causes it. It’s a method that has worked for other diseases. Statins, the drugs that are broadly prescribed to block the body’s cholesterol synthesis, were first found effective in studies of people who inherited a rare gene that led to severe and early heart disease.

Alzheimer’s is the sixth leading cause of death in this country, and is the only disease among the 10 deadliest that cannot be prevented, slowed or cured. But DIAN investigators say that within a decade there could be a drug that staves off brain destruction and death.”

Throughout the rest of the story, Kolata drops the qualifiers “early onset,” “familial” and most importantly, “rare” and simply uses the term “Alzheimer’s disease.” In the online version of the story, the first reference to Alzheimer’s disease is even linked to the NYT Health Guides general entry for Alzheimer’s disease. The elision of this important distinction has undoubtedly fueled the needless fear many people often have of being at greatly increased risk for dementia because a relative developed cognitive problems in their seventies or eighties, which can be seen in some of the many comments from readers to the online version of the article  It also reinforces the central dogma of the contemporary Alzheimer’s field – that it is a single disease, distinct from aging, caused by some unified patho-physiological mechanism that can be isolated and addressed with a linear therapeutic intervention.

As Kolata must surely be aware, many if not most researchers in the Alzheimer’s field will acknowledge privately though not so often in public that this central dogma is shaky.  In this case, some closer attention to the real history of Alzheimer’s research would be helpful. The term Alzheimer’s disease was originally created to describe cases of dementia – such as the 51-year-old woman Alzheimer encountered in 1901 – where the clinical and pathological features of senility appeared at a relatively early age. Though Alzheimer and his contemporaries had no inkling of the genetic basis, they thought that early onset was sufficient grounds for a separate disease category. In the late 1970s, a group of American researchers, government officials within NIH and activist caregivers lobbied successfully to drop the distinction. Their goal was to generate awareness and funding for biomedical research into dementia, and they were very savvy about the political ramifications of disease categorization. Since there was no meaningful clinical or pathological distinction between Alzheimer’s and senile dementia, they argued that the two should be considered a single entity – and that entity, crucially, should be called Alzheimer’s. By combining the two categories, they could claim that the condition was a major health problem afflicting millions of people; by calling it Alzheimer’s rather than senile dementia, they could claim it was not aging, but a dread disease worthy of a massive, publicly funded research initiative to understand its cause and discover a means of effective treatment or prevention.

Ironically, among the most important research findings generated by the torrent of funding that was unleashed by the political power of the re-conceptualization of Alzheimer’s was the discovery of the genes associated exclusively with the early onset form – which would logically seem to support a return to the original distinction made by Alzheimer and his contemporaries. But the concept of Alzheimer’s as a single, unified disease distinct from aging remains too powerful to abandon. So at the level of policy advocacy and popular news accounts at least, most researchers continue to talk as though Alzheimer’s disease were quite a clear-cut thing, when the reality is much more complicated.

Researchers in the DIAN project and others described in the article are exploring the distinction between presenile and senile dementia, and hoping that the ability to identify and follow subjects from families with early onset genes to test the use of drugs at much earlier stages in the development of Alzheimer’s will be quick route to a drug that can effectively prevent the disease.

I hope this strategy pays off, and that in a few years we will see more big stories of successful drug trials from the DIAN project – though even then I hope they will be stories that more accurately represent the complexities of medical research on Alzheimer’s. But given the complexity of dementia and the difficulty of identifying efficacious patho-physiological targets for drugs in a disorder with multiple, inter-related causal mechanisms, I think it much more likely that the drugs tested in these trials will be of limited value. In that case, if we read about it in publications like the NYT at all, it will likely be a much smaller item buried in the back pages. Meanwhile reporters like Kolata will be on to writing splashy front page articles about the next imminent breakthrough.

That’s how we roll in the War on Alzheimer’s.

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About Jess

Jesse F. Ballenger is author of Self, Senility and Alzheimer's Disease in Modern America: A History" (Johns Hopkins Press, 2006), and co-editor of two interdisciplinary volumes on Alzheimer’s disease: Concepts of Alzheimer Disease: Biological, Clinical and Cultural Perspectives (Johns Hopkins, 2000), and Treating Dementia: Do We Have a Pill for It? (Johns Hopkins, 2000). He teaches in the Bioethics program at Penn State University.

Posted on June 15, 2012, in Media coverage and tagged , , . Bookmark the permalink. 6 Comments.

  1. “Statins, the drugs that are broadly prescribed to block the body’s cholesterol synthesis, were first found effective in studies of people who inherited a rare gene that led to severe and early heart disease.”

    The disease Kolata is presumably referring to is familial hypercholesterolemia (FH). FH is an autosomal dominant disease that exists in two forms, heterozygous FH and homozygous FH. Heterozygous FH, which some members of my family suffer from, is the form that occurs when a person inherits one copy of the mutation. This occurs in approximately 1/500 people worldwide. Homozygous FH is the form in which the person has two copies of the FH mutation and occurs in 1 out of 1 million people.

    The statement that statins were first found effective in studies of people with FH is somewhat misleading, if by “effective” one means the prevention of heart attacks and other cardiovascular events. When statins were developed in the late 1980s, FH patients were excluded from the clinical trials that were conducted to show than statins not only lowered LDL but also prevented heart attacks, strokes and death. It was considered unethical to give an FH patient a placebo. To this day, no randomized controlled trial of statins with clinical endpoints has been done in FH patients and it is unlikely that one will ever be done.

    The ASAP trial compared a high dose statin with a moderate dose statin in heterozygous FH patients, but the endpoint was carotid intima media thickness, “IMT” (i.e., thickness of the carotid artery measured by ultrasound. There was also a trial of statin vs. placebo in teenage FH patients using IMT as an endpoint.

    There are two observational studies based on the registry of British FH patients and the registry of Dutch FH patients showing the benefits of statins in FH.

  2. Thanks for that very informative comment. I presume I can find out more about this part of the statins story, which I knew nothing about, on your blog, which I will be sure to check out.

  3. “Without denying or diminishing the very real losses and challenges imposed by dementia, we have been working in different ways to show that a life cannot be reduced to a disease, even a disease that brings profound cognitive deterioration”

    Thank you for exploring the complexities. Another informative post. I shall be recommending your blog to a few of my colleagues.

  4. Correction, I should have said “when statins came on the market in the late 1980s,” since they were developed before that. I have not discussed the history of statins on my blog. There is a book, The Cholesterol Wars, by Daniel Steinberg, that goes into the history of statins.

  5. You are quite correct that Alzheimer’s Dementia is a complex collection of different diseases. There are now at least two genetic forms of early onset that together account for a small percentage. Debate goes on as to how many cases of senile dementia are “Alzheimer’s type”, multi-infarct (multiple mini-strokes), or other forms. As with most neurodegenerative diseases, the overt symptoms occur when the reserve capacity of the brain has been exhausted. This creates two very large problems. First, is to develop a diagnostic test with high stringency for sensitivity (marked by the rate of false negatives) and specificity (marked by the rate of false positives) that can pick up the disease long before overt symptoms occur. Second, the development of a drug to prevent the progression of someone so diagnosed would require large numbers of patients to be treated for many years. Currently, memantine (Namenda) is designed to stop the progression of the disease and is about as least noxious of a drug that you can find. But, ask physicians if they had a patient test positive for early signs of the progression of Alzheimer’s would they put that patient on a daily dose of Namenda for the remainder of their life. Most will say “No.” Then what will happen to an experimental or newly marketed drug?

    BTW: My mother-in-law was diagnosed with moderate Alzheimer’s five years ago, I talked the neurologist into starting her on Namenda, which he did and later added donepezil (Aricept). Her deterioration since has been minimal, but is that due to the Namenda or just her natural course? She lives in the moment. She came over on the Queen Mary I as a war bride in 1946, so my wife last year took her back on the QM II and she had a blast. Ask her about it, and there is no memory of the trip. So, what?

    The other issue in Kolata’s article is the question in her title. How does one live knowing that they have a gene that predicts early onset dementia? Well Gina, how does one live knowing that they have the gene for Huntington’s chorea, a mid-life onset horrible fatal disease? She should read the blogs in the Huntington patient sites and follow the debate as to whether or not to get tested. Very interesting to read back-and-forth over this issue.

  1. Pingback: Alzheimer’s disease, familial hypercholesterolemia, and clinical trials « Marilyn Mann's Blog

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