Health News Review

After four years and after publishing more than 1,100 stories on HealthNewsReview.org, we’ve probably only received a handful (fewer than 10) messages from people who felt we were too soft in our review of a story. But our review of a New York Times story on Alzheimer’s Disease was way too soft in the eyes of Dr. Jerome Hoffman, a UCLA emergency medicine specialist, who wrote to me. (This despite the fact that our review stated that the story “was inaccurate…encourages confusion…likely to mislead readers…fails to mention costs…does not alert readers to the possible financial consequences of a test indicating that a person is likely to develop Alzheimer’s Disease…perhaps the NYT will pursue this as a next-day folo….discussion of potential harms seems imbalanced….caveats are overshadowed by the strong wording of the headline and lead sentence….fails to note the industry connections of key researchers and the industry funding of the study.”)

He gave me permission to quote directly from his email:

Dear Gary,

Let me start off by saying that I love your work — it is routinely outstanding. So I’m a little embarrassed that I’m only writing now, when I believe you could (and should) have done a better job re: the latest NYT puff piece by Gina Kolata. (I suspect you’ve seen Vera Sharav’s review of same, which I think does a better job of addressing head-on some of the most critical aspects of this.)

I understand that it is best to bend over backward to avoid any remote appearance of stridor, and also acknowledge that you are typically not afraid to be direct and pointedly critical; still, given the real harm surely caused by Ms Kolata’s endless hucksterism (backed by the clout of the NYT), I think you missed an opportunity to address not only the outrageous distortions in this particular piece (“100% accurate” — which is not only on the face of it inaccurate, as you point out, but is surely much worse than she and the researchers claim, given huge methodologic issues re: the “gold” standard, and their confusing how often it’s present once disease is clinically evident with how well it predicts later disease, at earlier and earlier pre-clinical times), but larger issues, like failure to mention conflicts of interest or give real credence to contrary views (in an instance where these should be stressed at least as much as usual), conflation of association with cause, creation of disease (hyper-amyloidemia) whose purpose is surely to allow some drug company to develop a blockbuster drug that will be “proven” in some study to “decrease amyloid burden” (even if it has zero effect on any patient-oriented end-point), and a half-dozen other important ones.

You do regularly make big-picture points, but I believe it’s particularly important to hold the NYT’s foot to the fire. One only has to read the posts about her article to see how effective she (and the companies pushing these, and so many other, tests) are with their use of the combination of fear-mongering and “hope-mongering” (evidence and conflicts of interest be damned). Of course there are also a bunch of thoughtful and critical comments, but there are lots on the order of “it doesn’t matter if it’s really true, we must try to do something about this terrible disease!”

One other point I feel obliged to make – I believe your comment that “the story is newsworthy” is actually a huge stretch. As one of the more astute readers posted at the NYT website, one could surely find dozens of “promising developments” hailed by the Times each year that we’ll never hear of again. Worse, almost all the ones we do later hear about are great successes only in terms of profit (but not health). It’s ironic that Kolata compared this test with cholesterol — since the “best” that’s likely to come of it is that it will label zillions of people, and get them to take drugs for years and years … even if “the amyloid hypothesis” proves as misleading as the cholesterol hypothesis. This story will actually become newsworthy if and only when the years of testing you mention are done, and prove productive, and there is (separately) an actual useful intervention that aborts Alzheimer’s Disease progression; even if both of these unlikely events actually happen, it surely won’t be for ages and ages — so running a top of the front-page story in the NYT, now, is vastly counterproductive … unless the goal is to create desperate expectations, so that when the inevitable anti-amylase drug comes along, it will be impossible for FDA, or Medicare, to say no.

I hope you’ll understand that these comments come from someone who greatly admires the excellent work that you routinely do. (I have written you before, simply to praise your work; but it remains unfortunate that people mostly write to complain … so for that I do apologize.)

Best,

Jerry Hoffman

Reflecting on what we DID say in our review, I believe Dr. Hoffman missed some key points. However, I am very pleased that he wrote and I’m very pleased to post his comments.

One reason we maintain this site – and especially this blog – is to encourage more intelligent discussion of the quality (or lack thereof) in health care news and information disseminated to news consumers and health care consumers.

For now I won’t debate any of what Dr. Hoffman wrote. I open this up to other readers.

Please weigh in on this – or on any of our reviews or blog posts – any time.


ADDENDUM ON AUGUST 18:

See the Harvard Health Blog post,
“Alzheimer’s study on biomarkers generates debate.”

Comments

Marilyn Mann posted on August 16, 2010 at 12:08 pm

I share Dr. Hoffman’s discomfort with the idea of approving Alzheimer’s drugs based on surrogate endpoints. However, I was under the impression, based on a July NYT article, that the FDA had stated that it did not intend to approve Alzheimer’s drugs on that basis. The article linked below states:
“The Food and Drug Administration says it needs to know not just that plaque was reduced or even that it disappeared, but that those who took a drug ended up with better memory and better ability to think and reason as compared with those who did not take the drug.”
http://www.nytimes.com/2010/07/17/health/research/17drug.html
If anyone knows otherwise, please chime in.

Merrill posted on August 17, 2010 at 8:54 am

Did Jerry really mean to say that the cholesterol hypothesis was misleading? Statins are overprescribed, but they have been proven via randomized controlled clinical trials to lower the risk of heart attack, stroke and death in well-defined groups at risk.
IF a company developed a drug that inhibits the formation of beta-amyloid plaques, and IF in RCTs it is shown that inhibition leads to slower progression to full-blown Alzheimer’s in people with mild cognitive impairment, wouldn’t that be a good thing?
The beta-amyloid thesis hasn’t been proved (like Jerry, I’m skeptical; clearing away plaque may be like clearing away the rubble of a slowly collapsing building – it does nothing to maintain the rooms of memory held within). The test touted by Kolata was clearly flawed. But that doesn’t mean all surrogate markers are garbage or overprescription based on their use is inevitable.

Julian Lieb,M.D posted on August 28, 2010 at 8:43 pm

Access Pubmed, and enter “prostaglandins.” You will find that excessive synthesis of prostaglandin E2 stimulates the production of amyloid. Venture capital triggered the suppression of prostaglandins in preference to genomics and biotechnology, thus corrupting any hope of medical progress.