BLOGSCAN - More on Senate Hearings on Industry Funded CME
There has been considerable coverage of the remarkable hearings by the US Senate Special Committee on Aging on industry funded continuing medical education (CME). See reporting by Dr Daniel Carlat on the Carlat Psychiatry Blog, and by the Prescription Project on their Postscript Blog. See also the comments by Dr Howard Brody on the Hooked: Ethics, Medicine and Pharma blog. Some key points were that the Senators failed to see why physicians cannot afford to pay for their own CME, and therefore must depend on corporate funding to support; and the Senators failed to buy the argument that medical progress vitally depends on health care corporations paying for and influencing the education physicians get.
Bloggers Can Spread the Word, Just Not About the Sponsors' Competitors
The internet, social media, web 2.0 etc have changed how important health care issues are discussed. So, it is not surprising that big health care organizations are trying to use these new media to promote their messages. New media, however, are no more immune from the effects of conflicts of interest than are old media.
An article from corporate communications company Ragan.com about how the American Heart Association (AHA) is using bloggers to get people interested in a heart-healthy diet and exercise program illustrates how even "civilian" bloggers can get caught up in the web of conflicts of interest that pervades health care. The background is:
It did seem that the AHA went to considerable effort to make sure they had recruited just the right bloggers.
I would suspect that the explicit instruction not to favor Merck's competitors would also remind the bloggers not not do say anything that might make the giant pharmaceutical company unhappy.
This is an explicit example of the adverse effects of commercial funding of not-for-profit disease advocacy groups. Corporate sponsors may not expect anything as gross as advertising in return for their money. However, they may expect something more subtle, a generally favorable attitude toward the sponsor, at least the disinclination to say anything that might put the sponsor in a negative light. After all, politeness requires that we be nice to the people who are nice to us. But being nice to sponsors may not be so nice for the people that a health care not-for-profit organization is supposed to serve.
PS - for those who like science fiction, see the preview of the new version of "V," in which Anna, the leader of the Visitors, an invasion force disguised as human-appearing, benign aliens, warns her television interviewer,
An article from corporate communications company Ragan.com about how the American Heart Association (AHA) is using bloggers to get people interested in a heart-healthy diet and exercise program illustrates how even "civilian" bloggers can get caught up in the web of conflicts of interest that pervades health care. The background is:
Keeping track of the conversations on the array of social media networks can gobble up your workday. So why not find someone else to do it for you?
The American Heart Association did just that, approaching four established bloggers with a proposal: Write about our new campaign, Go Red For Women: BetterU, and we’ll link to your blog from our site. BetterU is a 12-week online nutrition and fitness program to improve heart health among women.
The blogs appear to be working. They’ve helped drive traffic to Go Red/BetterU since the program’s June 1 launch.
It did seem that the AHA went to considerable effort to make sure they had recruited just the right bloggers.
The AHA researched potential candidates with the help of agencies Edelman PR and Edelman Digital. After a month-and-a-half, they settled on four bloggers: Joshilyn, Nyasha, Stacey, and Nadia.More interesting was the values with which the bloggers were supposed to align, particularly those relating to the program's corporate sponsors (see the logos at the bottom right of the BetterU web-site).
The criteria: The bloggers had to be female, have an enthusiastic following, be diverse in age and ethnicity, and have a high Technorati rating. Most important, their content and advertising had to align with the association’s values, says Director of Marketing Anu Gandhi.
'You’re really ultimately picking a spokesperson for Go Red for Women and the larger American Heart Association,' [senior manager for cause communications Megan] Lozito says. 'That’s a really important process for us — that it be correct and that it be the right people. So we spent a lot of time getting to know those ladies and making sure our mission would be aligned.'
From there, the association brought the bloggers to the Dallas headquarters for a full health screening at The Cooper Institute, a photo session, a preview of the BetterU program, and some message training.
Although the BetterU bloggers got some message training in Dallas, Gandhi says AHA has been hands off when it comes to what they can and can’t say about the program.
The bloggers are asked to post once a week about BetterU and follow basic guidelines—no profanity, no defamation, no writing about nor condoning any medications or treatments. She says they also ask bloggers not to talk about competitors of AHA’s two national sponsors: Macy’s and Merck Pharmaceuticals.
I would suspect that the explicit instruction not to favor Merck's competitors would also remind the bloggers not not do say anything that might make the giant pharmaceutical company unhappy.
Eight weeks into the program, they haven’t had any problems.So the bloggers recruited by the AHA may be happy, since they now have a big organization's web-site driving traffic to their blogs. The AHA may be happy, since the bloggers can spread the word about their BetterU program. I imagine the marketers at Merck may be happy too, since the bloggers have been warned about the need to keep the corporate sponsors happy. However, what may be good for all the parties in this transaction may not be so good for the general public, as another opportunity for uninhibited, honest discussion of health care issues has been lost.
'There are things we don’t want them to write, like profanity, but that’s also part of the vetting in the beginning,' Lozito says. 'We wanted to find people who believe in our mission, who speak to the same type of audience, but at the same time we want them to have their own flavor and own tone, because it’s a blog.'
This is an explicit example of the adverse effects of commercial funding of not-for-profit disease advocacy groups. Corporate sponsors may not expect anything as gross as advertising in return for their money. However, they may expect something more subtle, a generally favorable attitude toward the sponsor, at least the disinclination to say anything that might put the sponsor in a negative light. After all, politeness requires that we be nice to the people who are nice to us. But being nice to sponsors may not be so nice for the people that a health care not-for-profit organization is supposed to serve.
PS - for those who like science fiction, see the preview of the new version of "V," in which Anna, the leader of the Visitors, an invasion force disguised as human-appearing, benign aliens, warns her television interviewer,
Just be sure not to ask anything that would put us in a negative light.
BLOGSCAN - Live-Blogging Senate Hearing on Conflicts of Interest and Continuing Medical Education
Dr Daniel Carlat is live-blogging the US Senate Special Committee on Aging hearing on conflicts of interest and continuing medical education on the Carlat Psychiatry Blog, and so is Prof Margaret Soltan on the University Diaries.
Polly Want a Million (Plus)
We have frequently posted about attempts to justify financial relationships among physicians and medical academics on one hand, and pharmaceutical, biotechnology, device and other health care corporations, on the other. Some defenders of such relationships now have gone so far as to start their own society, whose meeting was covered and commented on by fellow "pharmascolds," including Dr Daniel Carlat and Dr Howard Brody. The usual justification of these relationships is that they are necessary for "innovation" and the onward progress of medical science, education, and care. I have yet to see any logic or evidence to back up these assertions, nor have I seen anyone defend these relationships who does not also have personal financial relationships of their own with health care corporations. (See examples here, here, and here.)
Meanwhile, cases of individual physicians and academics whose lucrative relationships with industry seem to generate huge conflicts of interest continue to surface. The latest example ferreted out by investigators working for US Senator Charles Grassley (R - Iowa) is that of Dr David Polly. (Recall that Dr Polly was one of the strongest defenders of Dr Thomas Kuklo, who was accused of falsifying clinical research results in a way that seemed to favor the product of his own corporate benefactor [see post here].)
The main points were reported by David Armstrong and Thomas M Burton in the Wall Street Journal,
Although there have now been many reported cases of medical academics who collected large payments from health care corporations, the services they provided in exchange for the money have not always been very clear. Defenders of financial relationships among physicians and medical academics and industry have argued that most payments were for valuable research, education, or health care activities. However, Senator Grassley's office provided the details of Dr Polly's invoices, and several of the news articles so far described what he did for the money. Per the Wall Street Journal article,
An accompanying post on the Wall Street Journal Health Blog provided more information:
So did the $1.2 million Medtronic spent on Dr Polly's services inspire any "innovation?" Did it lead to any scientific progress or improved health care? I am not sure.
It is clear, however, that a good chunk of this money went to support marketing, advocacy, and lobbying. The items in bold italics above were clearly in support of marketing, advocacy and lobbying, not science, medical education, or patient care. (To give Dr Polly the benefit of a doubt, some other items listed above could have been related to research, education, or patient care, although this is not indisputable.)
So the case of Dr Polly corroborates my deep skepticism of the financial relationships among physicians and medical academics on one hand, and corporations that sell health care goods and services on the other. We "pharmascolds," - a preferable term might be health care skeptics - suspect that many of these relationships are really about stealth marketing and advocacy. The companies often pay to market their products and services, or advocate positions to the companies' advantage, but prefer that their salespeople and advocates are cloaked in academic guises, and wreathed in the rarefied aura of respected academic institutions. (Note that some of us are just as skeptical about relationships among academic institutions and other health care not-for-profit organizations on one hand, and such corporations on the other, for analogous reasons.)
While the leadership of our formerly distinguished medical academic institutions remains infiltrated, if not dominated by people earning many thousands of dollars from health care corporations, I must remain skeptical about how much of these institutions supposedly academic output is actually stealth marketing and stealth health policy advocacy.
At the very least, medical academics, medical academic institutions, and other health care not-for-profits or NGOs should reveal in detail what payments they get from companies selling health care products or services, and how these payments could relate to the companies' marketing or lobbying efforts. In the US, some such disclosure would be mandated by the proposed "Sunshine" legislation now being considered by the US Congress. (By the way, note that this problem is hardly confined to the US, and needs global, not just American attention.)
However, physicians (at least physicians in full-time private practice, academic positions, and employed by mission-oriented not for profit organizations) should go further, and consider whether receiving industry money is worth the ongoing damage it does to our professionalism and our professional reputations. Medical schools, universities, health care foundations, disease advocacy groups, and other health care not-for-profits and NGOs should also go further, and consider whether receiving industry money is worth the ongoing damage it does to their missions, and their institutional reputations.
See also comments by Prof Margaret Soltan on the University Diaries blog.
Meanwhile, cases of individual physicians and academics whose lucrative relationships with industry seem to generate huge conflicts of interest continue to surface. The latest example ferreted out by investigators working for US Senator Charles Grassley (R - Iowa) is that of Dr David Polly. (Recall that Dr Polly was one of the strongest defenders of Dr Thomas Kuklo, who was accused of falsifying clinical research results in a way that seemed to favor the product of his own corporate benefactor [see post here].)
The main points were reported by David Armstrong and Thomas M Burton in the Wall Street Journal,
In May 2006, University of Minnesota spine surgeon David Polly urged a Senate committee to fund research into the severe arm, leg and spine injuries suffered by soldiers in Iraq and elsewhere.
Dr. Polly told the committee he was testifying on behalf of the American Academy of Orthopaedic Surgeons and referenced his prior work caring for soldiers as a surgeon at the Walter Reed Army Medical Center.
What Dr. Polly didn't disclose during his testimony was that his trip to Washington was paid for by Medtronic Inc., the big medical-device maker whose bone growth product, called Infuse, has been used to treat soldiers, according to company records.Dr. Polly and colleagues in Minnesota subsequently received a $466,644 Department of Defense grant for a two-year study beginning in February 2007 to evaluate Infuse in cases where an injury is also infected, according to the university.
Dr. Polly was paid $1.14 million by Medtronic for consulting services from 2004 to 2007.
Details of Dr. Polly's consultant billing were provided by Medtronic to Sen. Charles Grassley, an Iowa Republican who has been scrutinizing the relationship between academics and industry.
Although there have now been many reported cases of medical academics who collected large payments from health care corporations, the services they provided in exchange for the money have not always been very clear. Defenders of financial relationships among physicians and medical academics and industry have argued that most payments were for valuable research, education, or health care activities. However, Senator Grassley's office provided the details of Dr Polly's invoices, and several of the news articles so far described what he did for the money. Per the Wall Street Journal article,
In total, Dr. Polly billed Medtronic for more than $50,000 in lobbying-related costs. He made trips to Washington in 2005 and 2006 and called on several members of Congress, according to the records.
According to billing records, Dr. Polly's billing rate was $4,750 for an eight-hour day in 2007, and he billed as many as 13,000 minutes a quarter -- or 216 hours over three months. In some months, he conducted at least some Medtronic business on nearly every day.
His consulting log indicates that on one occasion he spent one minute to wake up a Medtronic executive, although he listed 'no charge' for that service. He did bill Medtronic for the 30 minutes he spent in the car with that executive after waking him up.
An accompanying post on the Wall Street Journal Health Blog provided more information:
Did you ever wonder what doctors do to earn big consulting contracts from medical device companies and pharmaceutical concerns?
Records released by Medtronic to Sen. Charles Grassley, a longtime critic of the ties between academics and and health-care companies, provide a rare and detailed glimpse into the daily billings of a consultant — in this case, spine surgeon David Polly of the University of Minnesota.
Polly collected more than $1 million in four years of work for Medtronic, according to the records, which you can take a look at here.
The services he provided were many, but among them, Polly was paid to write articles for medical journals; write a chapter in a book and a book outline; recruit patients for publicity efforts; attend Medtronic national sales meetings; travel to conferences in Japan, Paris and elsewhere; lead training and educational sessions for physicians; and lobby Congress.
Polly also billed for at least two phone calls with Medtronic CEO William Hawkins as well as charging the company $2,000 when Mr. Hawkins visited an operating room. In October, 2003, he billed the company $12,000 for attending a medical meeting of the North American Spine Society, at $4,000 a day.
There are also scores of entries for work billed in five-minute increments, usually to send email or return phone calls. The bill for each five-minute charge? $49.48 a pop.
So did the $1.2 million Medtronic spent on Dr Polly's services inspire any "innovation?" Did it lead to any scientific progress or improved health care? I am not sure.
It is clear, however, that a good chunk of this money went to support marketing, advocacy, and lobbying. The items in bold italics above were clearly in support of marketing, advocacy and lobbying, not science, medical education, or patient care. (To give Dr Polly the benefit of a doubt, some other items listed above could have been related to research, education, or patient care, although this is not indisputable.)
So the case of Dr Polly corroborates my deep skepticism of the financial relationships among physicians and medical academics on one hand, and corporations that sell health care goods and services on the other. We "pharmascolds," - a preferable term might be health care skeptics - suspect that many of these relationships are really about stealth marketing and advocacy. The companies often pay to market their products and services, or advocate positions to the companies' advantage, but prefer that their salespeople and advocates are cloaked in academic guises, and wreathed in the rarefied aura of respected academic institutions. (Note that some of us are just as skeptical about relationships among academic institutions and other health care not-for-profit organizations on one hand, and such corporations on the other, for analogous reasons.)
While the leadership of our formerly distinguished medical academic institutions remains infiltrated, if not dominated by people earning many thousands of dollars from health care corporations, I must remain skeptical about how much of these institutions supposedly academic output is actually stealth marketing and stealth health policy advocacy.
At the very least, medical academics, medical academic institutions, and other health care not-for-profits or NGOs should reveal in detail what payments they get from companies selling health care products or services, and how these payments could relate to the companies' marketing or lobbying efforts. In the US, some such disclosure would be mandated by the proposed "Sunshine" legislation now being considered by the US Congress. (By the way, note that this problem is hardly confined to the US, and needs global, not just American attention.)
However, physicians (at least physicians in full-time private practice, academic positions, and employed by mission-oriented not for profit organizations) should go further, and consider whether receiving industry money is worth the ongoing damage it does to our professionalism and our professional reputations. Medical schools, universities, health care foundations, disease advocacy groups, and other health care not-for-profits and NGOs should also go further, and consider whether receiving industry money is worth the ongoing damage it does to their missions, and their institutional reputations.
See also comments by Prof Margaret Soltan on the University Diaries blog.
Wyeth: Ghostwritten Papers Fake, But Accurate
It looks like Wyeth has lost its battle to keep secret its practices regarding ghostwriting of scientific papers. The issue in question is whether ghostwriting contributed to excessive prescription of post-menopausal hormones and increased the incidence of breast cancer:
How is evidence based medicine possible if just one drug company has sponsored ghostwritten articles in 40 medical journals and other publications? What is the "total mass" of questionable articles now infecting the literature?
There are several layers of dishonesty in this activity, including foreknowledge of scientific deception through fraudulent misrepresentation of authorship by the pharma, dishonesty of the physician who "signs off" as first author, and misrepresentation by the pharma, the writing company and the physician about provenance of the article to scientific publishers.
What business does a lawyer have lecturing the public that the articles were a dishonest marketing effort masquerading as legitimate science, but were "fair and scientific?" How does he know? In addition, the "fake but accurate" excuse is getting quite shopworn. Hopefully, Sen. Grassley will approach ending this ghostwriting practice with vigor.
In fact, this raises another issue. I have written that management of pharma by those lacking biomedical bona fides is, by definition, mismanagement. This is a case in point. Wyeth's President, Board Chair and CEO Bernard Poussot lacks biomedical credentials. Harry Truman said "the buck stops here", but a in the case of scientific ghostwriting, CEO's such as Poussot cannot vouch firsthand for the accuracy and fairness of their company's science. He lacks the expertise. The buck does not stop at his desk; he is dependent on scientific underlings in such matters.
This affair is another instantiation of my belief that pharma is best led by those with relevant scientific expertise such as Merck under clinician-scientist Dr. Roy Vagelos. (It is perhaps not coincidental that Merck became a shadow of its former self under non-scientist Raymond Gilmartin.)
How appropriate, as Pfizer is led by the former top lawyer for McDonald's and Boston Chicken, bringing to life my "If you've run McDonald's, you can run anything" metaphor. If a wise investor were to take a bearish position on a stock, this merged company would be an excellent candidate.
Finally, another ghostwriter of sorts recently died, Sandford Dody (1918-2009). Dody anonymously penned best selling autobiographies of actresses Bette Davis and Helen Hayes, among many other notables. Such ghostwriting is essentially victimless, as opposed to its counterpart in the scientific domain. However, Mr. Dody had an astute observation about the practice, even when there was no trail of diseased or dead bodies.
Per the WSJ article "A Ghostwriter Who Struggled to Accept Life in the Shadows":
In the case of biomedical ghostwriting, the conspirators all "die a little" in purveying their intellectual dishonesty on a trusting public.
It's too bad some of that same public also dies, and not just a little, as wages of professorial ghostwriting sins.
Posted on Sun, Jul. 26, 2009Of course, in addition to the violation of accepted practices of authorship, such as specified by NIH and the International Committee of Medical Journal Editors, among others, such lucky authors get to "count" such papers in their academic portfolios, presumably also in violation of their own institutional policies and guidelines for fair attribution and intellectual honesty, e.g., here. Ghostwriting may also skew the tenure process, providing advantages to the unscrupulous academic over the ethical scientist or scholar. (One wonders about the true percentage of the massive number of papers claimed by some medical academics actually written by the putative first author.)
Philadelphia Inquirer
Wyeth told to release documents on ghostwriting
Associated Press
LITTLE ROCK, Ark. - A federal judge has ordered the unsealing of thousands of pages of documents pertaining to the ghostwriting practices of Wyeth Pharmaceuticals, which is being sued over hormone-replacement drugs.
U.S. District Judge Bill Wilson ordered the papers unsealed Friday at the request of a medical journal and the New York Times. Plaintiffs' attorneys presented the papers earlier at trial to show that Wyeth routinely hired medical-writing firms to ghostwrite articles that appeared in seemingly objective medical journals but included only the name of a scientific researcher as the author.
The ruling came in a case that involves about 8,000 lawsuits that have been combined before Wilson. The lawsuits focus on whether Wyeth hormone-therapy drugs Prempro and Premarin, used to treat symptoms of menopause, have caused breast cancer in some women.
The New Jersey drugmaker, which has major operations in the Philadelphia area, had already turned over the documents, which it says concern about 40 articles in medical journals and other publications, to Sen. Charles Grassley (R., Iowa).
How is evidence based medicine possible if just one drug company has sponsored ghostwritten articles in 40 medical journals and other publications? What is the "total mass" of questionable articles now infecting the literature?
Grassley sought them last year without a subpoena as part of a congressional investigation into drug-industry influence on doctors.
The documents were shown to jurors at trial but have otherwise been unavailable publicly.
Plaintiffs say ghostwriting is when a drug company conjures up the concept for an article that will counteract criticism of a drug or embellish its benefits, hires a professional writing company to draft a manuscript conveying the company's message, retains a physician to sign off as the author, and finds a publisher to unwittingly publish the work.
There are several layers of dishonesty in this activity, including foreknowledge of scientific deception through fraudulent misrepresentation of authorship by the pharma, dishonesty of the physician who "signs off" as first author, and misrepresentation by the pharma, the writing company and the physician about provenance of the article to scientific publishers.
Drug firms disseminate their ghostwritten articles to their sales representatives, who present the articles to physicians as independent proof that the companies' drugs are safe and effective.
Wyeth attorney Stephen Urbanczyk acknowledged that the articles were part of a marketing effort. But he said that they were also fair, balanced, and scientific.
What business does a lawyer have lecturing the public that the articles were a dishonest marketing effort masquerading as legitimate science, but were "fair and scientific?" How does he know? In addition, the "fake but accurate" excuse is getting quite shopworn. Hopefully, Sen. Grassley will approach ending this ghostwriting practice with vigor.
In fact, this raises another issue. I have written that management of pharma by those lacking biomedical bona fides is, by definition, mismanagement. This is a case in point. Wyeth's President, Board Chair and CEO Bernard Poussot lacks biomedical credentials. Harry Truman said "the buck stops here", but a in the case of scientific ghostwriting, CEO's such as Poussot cannot vouch firsthand for the accuracy and fairness of their company's science. He lacks the expertise. The buck does not stop at his desk; he is dependent on scientific underlings in such matters.
This affair is another instantiation of my belief that pharma is best led by those with relevant scientific expertise such as Merck under clinician-scientist Dr. Roy Vagelos. (It is perhaps not coincidental that Merck became a shadow of its former self under non-scientist Raymond Gilmartin.)
Wyeth, the world's No. 12 pharmaceutical company by sales, is being bought this fall by No. 1 drugmaker Pfizer.
How appropriate, as Pfizer is led by the former top lawyer for McDonald's and Boston Chicken, bringing to life my "If you've run McDonald's, you can run anything" metaphor. If a wise investor were to take a bearish position on a stock, this merged company would be an excellent candidate.
Finally, another ghostwriter of sorts recently died, Sandford Dody (1918-2009). Dody anonymously penned best selling autobiographies of actresses Bette Davis and Helen Hayes, among many other notables. Such ghostwriting is essentially victimless, as opposed to its counterpart in the scientific domain. However, Mr. Dody had an astute observation about the practice, even when there was no trail of diseased or dead bodies.
Per the WSJ article "A Ghostwriter Who Struggled to Accept Life in the Shadows":
... Mr. Dody, who died July 4 at the age of 90, found the work spiritually destructive. "After all," he wrote, "how does one become a ghost without dying a little?"
In the case of biomedical ghostwriting, the conspirators all "die a little" in purveying their intellectual dishonesty on a trusting public.
It's too bad some of that same public also dies, and not just a little, as wages of professorial ghostwriting sins.
The acknowledgements are where minor contributions and reviews get placed in an ethically-attributed scientific paper. Anyone who does not understand this, or rationalizes "honorary authorship" or similar workarounds to meaningful attribution does not belong in science.
The Diet-Heart Hypothesis: Subdividing Lipoproteins
Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk. It's important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor's office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids.
Lipoproteins Can be Subdivided into Several Subcategories
In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source):
Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily than large LDL. He and others subsequently showed that sdLDL are also more prone to oxidation than large LDL (1, 2).
Diet Affects LDL Subcategories
The next step in Krauss's research was to see how diet affects lipoprotein patterns. In 1994, he published a study comparing the effects of a low-fat (24%), high-carbohydrate (56%) diet to a "high-fat" (46%), "low-carbohydrate" (34%) diet on lipoprotein patterns. The high-fat diet also happened to be high in saturated fat-- 18% of calories. He found that (quote source):
Krauss then specifically explored the effect of saturated fat on LDL size (free full text). He re-analyzed the data from the study above, and found that:
Krauss also tested the effect of his dietary intervention on HDL. Several studies have found that the largest HDL particles, HDL2b, associate most strongly with HDL's protective effects (more HDL2b = fewer heart attacks). Compared to the diet high in total fat and saturated fat, the low-fat diet decreased HDL2b significantly. A separate study found that the effect persists at one year. Berglund et al. independently confirmed the finding using the low-fat American Heart Association diet in men and women of diverse racial backgrounds. Here's what they had to say about it:
Wrapping it Up
Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear, but is associated with a lower risk of heart attacks. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It's important to remember that the primary sources of carbohydrate in the modern Western diet are wheat and sugar. Are the blood lipid patterns that associate with heart attack risk in Western countries partially acting as markers of wheat and sugar intake?
* This is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins.
Lipoproteins Can be Subdivided into Several Subcategories
In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source):
The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease.Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder.
Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily than large LDL. He and others subsequently showed that sdLDL are also more prone to oxidation than large LDL (1, 2).
Diet Affects LDL Subcategories
The next step in Krauss's research was to see how diet affects lipoprotein patterns. In 1994, he published a study comparing the effects of a low-fat (24%), high-carbohydrate (56%) diet to a "high-fat" (46%), "low-carbohydrate" (34%) diet on lipoprotein patterns. The high-fat diet also happened to be high in saturated fat-- 18% of calories. He found that (quote source):
Out of the 87 men with pattern A on the high-fat diet, 36 converted to pattern B on the low-fat diet... Taken together, these results indicate that in the majority of men, the reduction in LDL cholesterol seen on a low-fat, high-carbohydrate diet is mainly because of a shift from larger, more cholesterol-enriched LDL to smaller, cholesterol-depleted LDL [sdLDL].In other words, in the majority of people, high-carbohydrate diets lower LDL cholesterol not by decreasing LDL particle count (which might be good), but by decreasing LDL size and increasing sdLDL (probably not good). This has been shown repeatedly, including with a 10% fat diet and in children. However, in people who already exhibit pattern B, reducing fat does reduce LDL particle number. Keep in mind that the majority of carbohydrate in modern America comes from wheat and sugar.
Krauss then specifically explored the effect of saturated fat on LDL size (free full text). He re-analyzed the data from the study above, and found that:
In summary, the present study showed that changes in dietary saturated fat are associated with changes in LDL subclasses in healthy men. An increase in saturated fat, and in particular, myristic acid [as well as palmitic acid], was associated with increases in larger LDL particles (and decreases in smaller LDL particles). LDL particle diameter and peak flotation rate [density] were also positively associated with saturated fat, indicating shifts in LDL-particle distribution toward larger, cholesterol-enriched LDL.Participants who ate the most saturated fat had the largest LDL, and vice versa. Kudos to Dr. Krauss for publishing these provocative data. It's not an isolated finding. He noted in 1994 that:
Cross-sectional population analyses have suggested an association between reduced LDL particle size and relatively reduced dietary animal-fat intake, and increased consumption of carbohydrates.Diet Affects HDL Subcategories
Krauss also tested the effect of his dietary intervention on HDL. Several studies have found that the largest HDL particles, HDL2b, associate most strongly with HDL's protective effects (more HDL2b = fewer heart attacks). Compared to the diet high in total fat and saturated fat, the low-fat diet decreased HDL2b significantly. A separate study found that the effect persists at one year. Berglund et al. independently confirmed the finding using the low-fat American Heart Association diet in men and women of diverse racial backgrounds. Here's what they had to say about it:
The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.Saturated and omega-3 fats selectively increase large HDL. Dr. B. G. of Animal Pharm has written about this a number of times.
Wrapping it Up
Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear, but is associated with a lower risk of heart attacks. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It's important to remember that the primary sources of carbohydrate in the modern Western diet are wheat and sugar. Are the blood lipid patterns that associate with heart attack risk in Western countries partially acting as markers of wheat and sugar intake?
* This is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins.
The Diet-Heart Hypothesis: Subdividing Lipoproteins
Two posts ago, we made the rounds of the commonly measured blood lipids (total cholesterol, LDL, HDL, triglycerides) and how they associate with cardiac risk. It's important to keep in mind that many things associate with cardiac risk, not just blood lipids. For example, men with low serum vitamin D are at a 2.4-fold greater risk of heart attack than men with higher D levels. That alone is roughly equivalent to the predictive power of the blood lipids you get measured at the doctor's office. Coronary calcium scans (a measure of blood vessel calcification) also associate with cardiac risk better than the most commonly measured blood lipids.
Lipoproteins Can be Subdivided into Several Subcategories
In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source):
Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily than large LDL. He and others subsequently showed that sdLDL are also more prone to oxidation than large LDL (1, 2).
Diet Affects LDL Subcategories
The next step in Krauss's research was to see how diet affects lipoprotein patterns. In 1994, he published a study comparing the effects of a low-fat (24%), high-carbohydrate (56%) diet to a "high-fat" (46%), "low-carbohydrate" (34%) diet on lipoprotein patterns. The high-fat diet also happened to be high in saturated fat-- 18% of calories. He found that (quote source):
Krauss then specifically explored the effect of saturated fat on LDL size (free full text). He re-analyzed the data from the study above, and found that:
Krauss also tested the effect of his dietary intervention on HDL. Several studies have found that the largest HDL particles, HDL2b, associate most strongly with HDL's protective effects (more HDL2b = fewer heart attacks). Compared to the diet high in total fat and saturated fat, the low-fat diet decreased HDL2b significantly. A separate study found that the effect persists at one year. Berglund et al. independently confirmed the finding using the low-fat American Heart Association diet in men and women of diverse racial backgrounds. Here's what they had to say about it:
Wrapping it Up
Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear, but is associated with a lower risk of heart attacks. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It's important to remember that the primary sources of carbohydrate in the modern Western diet are wheat and sugar. Are the blood lipid patterns that associate with heart attack risk in Western countries partially acting as markers of wheat and sugar intake?
* This is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins.
Lipoproteins Can be Subdivided into Several Subcategories
In the continual search for better measures of cardiac risk, researchers in the 1980s decided to break down lipoprotein particles into sub-categories. One of these researchers is Dr. Ronald M. Krauss. Krauss published extensively on the association between lipoprotein size and cardiac risk, eventually concluding (source):
The plasma lipoprotein profile accompanying a preponderance of small, dense LDL particles (specifically LDL-III) is associated with up to a threefold increase in the susceptibility of developing [coronary artery disease]. This has been demonstrated in case-control studies of myocardial infarction and angiographically documented coronary disease.Krauss found that small, dense LDL (sdLDL) doesn't travel alone: it typically comes along with low HDL and high triglycerides*. He called this combination of factors "lipoprotein pattern B"; its opposite is "lipoprotein pattern A": large, buoyant LDL, high HDL and low triglycerides. Incidentally, low HDL and high triglycerides are hallmarks of the metabolic syndrome, the quintessential modern metabolic disorder.
Krauss and his colleagues went on to hypothesize that sdLDL promotes atherosclerosis because of its ability to penetrate the artery wall more easily than large LDL. He and others subsequently showed that sdLDL are also more prone to oxidation than large LDL (1, 2).
Diet Affects LDL Subcategories
The next step in Krauss's research was to see how diet affects lipoprotein patterns. In 1994, he published a study comparing the effects of a low-fat (24%), high-carbohydrate (56%) diet to a "high-fat" (46%), "low-carbohydrate" (34%) diet on lipoprotein patterns. The high-fat diet also happened to be high in saturated fat-- 18% of calories. He found that (quote source):
Out of the 87 men with pattern A on the high-fat diet, 36 converted to pattern B on the low-fat diet... Taken together, these results indicate that in the majority of men, the reduction in LDL cholesterol seen on a low-fat, high-carbohydrate diet is mainly because of a shift from larger, more cholesterol-enriched LDL to smaller, cholesterol-depleted LDL [sdLDL].In other words, in the majority of people, high-carbohydrate diets lower LDL cholesterol not by decreasing LDL particle count (which might be good), but by decreasing LDL size and increasing sdLDL (probably not good). This has been shown repeatedly, including with a 10% fat diet and in children. However, in people who already exhibit pattern B, reducing fat does reduce LDL particle number. Keep in mind that the majority of carbohydrate in modern America comes from wheat and sugar.
Krauss then specifically explored the effect of saturated fat on LDL size (free full text). He re-analyzed the data from the study above, and found that:
In summary, the present study showed that changes in dietary saturated fat are associated with changes in LDL subclasses in healthy men. An increase in saturated fat, and in particular, myristic acid [as well as palmitic acid], was associated with increases in larger LDL particles (and decreases in smaller LDL particles). LDL particle diameter and peak flotation rate [density] were also positively associated with saturated fat, indicating shifts in LDL-particle distribution toward larger, cholesterol-enriched LDL.Participants who ate the most saturated fat had the largest LDL, and vice versa. Kudos to Dr. Krauss for publishing these provocative data. It's not an isolated finding. He noted in 1994 that:
Cross-sectional population analyses have suggested an association between reduced LDL particle size and relatively reduced dietary animal-fat intake, and increased consumption of carbohydrates.Diet Affects HDL Subcategories
Krauss also tested the effect of his dietary intervention on HDL. Several studies have found that the largest HDL particles, HDL2b, associate most strongly with HDL's protective effects (more HDL2b = fewer heart attacks). Compared to the diet high in total fat and saturated fat, the low-fat diet decreased HDL2b significantly. A separate study found that the effect persists at one year. Berglund et al. independently confirmed the finding using the low-fat American Heart Association diet in men and women of diverse racial backgrounds. Here's what they had to say about it:
The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.Saturated and omega-3 fats selectively increase large HDL. Dr. B. G. of Animal Pharm has written about this a number of times.
Wrapping it Up
Contrary to the simplistic idea that saturated fat increases LDL and thus cardiac risk, total fat and saturated fat have a complex influence on blood lipids, the net effect of which is unclear, but is associated with a lower risk of heart attacks. These blood lipid changes persist for at least one year, so they may represent a long-term effect. It's important to remember that the primary sources of carbohydrate in the modern Western diet are wheat and sugar. Are the blood lipid patterns that associate with heart attack risk in Western countries partially acting as markers of wheat and sugar intake?
* This is why you may read that small, dense LDL is not an "independent predictor" of heart attack risk. Since it travels along with a particular pattern of HDL and triglycerides, in most studies it does not give information on cardiac risk beyond what you can get by measuring other lipoproteins.
Are the Health Plans of the Very Rich Different from Yours and Mine?
Yesterday, the New York Times published an intriguing story about "Cadillac" (that is, expensive) health insurance plans,
It was not clear from this article how many top corporate executives have such plans, and whether leaders of other kinds of organizations, like large not-for-profits, also have them.
My main concern about such plans is not how much they contribute to top corporate leaders' compensation packages. Such packages are generally already so outrageously huge that providing $40,000 rather than $13,000 worth of health insurance is a trivial increase. My concern is not that plan recipients' demands for health care will collectively increase health care costs, because they include only a tiny portion of the population.
My main concern, instead, is how much these plans further insulate already cocooned top executives from the vicissitudes of daily life, particularly related to coping with our current dysfunctional health care system. What benefits executive health care plans provide is not clear, but presumably they insulate executives from having to deal with the managed care/ health insurance bureaucracy which frustrates patients seeking particular services, but not necessarily the most expensive, or least beneficial services. Such executives might thus not have gut level appreciation of how dysfunctional the health care system has become for even insured patients. Since top executives often are disproportionately influential members of the "superclass," their disconnection from the realities of dysfunctional health care is likely to translate into little real support by the powers that be for meaningful health care reform. There support may be further retarded by the influence of their fellow superclass members whose personal fortunes depend on the status quo in health care.
Real improvement of health care may depend on finding leaders who have better understanding of the plight of real people.
Goldman Sachs is one of the nation’s richest banks, and hundreds of top Goldman employees have a health care package to match — one of the 'gold-plated Cadillac' plans cited by those involved in the health care debate in Washington.
Goldman’s 400 or so managing directors and its top executive officers participate in the bank’s executive medical and dental program as part of their benefits, according to documents filed with the Securities and Exchange Commission. The program generally costs the bank $40,543 in premiums annually for each participant’s family.
Those taking part in the plan include the company’s chief executive, Lloyd C. Blankfein, and four other top officers, as well as managing directors, whose base salary is $600,000.
Goldman’s medical coverage entered the health care discussion on Sunday when David Axelrod, senior adviser to President Obama, cited the Goldman program as an example of the expensive benefits the administration might consider taxing to help pay for its health care program.
'The president actually was asked this the other day by Jim Lehrer, and what he said was that this was an intriguing idea to put an excise tax on high-end health care policies like the ones that the executives at Goldman Sachs have, the $40,000 policies,' Mr. Axelrod said.
A proposal by Senator John F. Kerry, Democrat of Massachusetts, would impose an excise tax on the insurers that issue policies like Goldman’s, with the expectation that the insurers would pass along most, if not all, of the cost to employers who buy the plans.
Leaders of the Senate Finance Committee, which is working on bipartisan version of the health care legislation in Congress, had long expressed interest in taxing some employer-provided benefits — a move many budget experts say would help slow the steep rise in health costs.
Negotiators have not yet determined the value of the plans that would set off a tax on the insurance companies; the numbers under discussion range from $20,000 to $40,000 annually, a senior administration official said.
The lower end of that range would increase the amount of money the tax would raise but would also hit some middle-class workers, whose unions in some cases negotiated robust health benefits in lieu of pay increases. Typical employer-provided plans cost $13,000 to $20,000 per family, depending on the location and the age of the plan participants.
A health care package costing $40,000 or more a year would generally have no co-payments or deductibles, according to Paul Fronstin, an analyst at the Employee Benefit Research Institute, a Washington nonprofit that studies benefits. It would also have no limits on doctors or procedures, no restrictions on pre-existing conditions and no requirements for referrals.
Few people have such policies, Mr. Fronstin said. 'It would only be top executives who run big businesses, mainly people in the C suite,' said Mr. Fronstin, referring to companies’ chief officers.
It was not clear from this article how many top corporate executives have such plans, and whether leaders of other kinds of organizations, like large not-for-profits, also have them.
My main concern about such plans is not how much they contribute to top corporate leaders' compensation packages. Such packages are generally already so outrageously huge that providing $40,000 rather than $13,000 worth of health insurance is a trivial increase. My concern is not that plan recipients' demands for health care will collectively increase health care costs, because they include only a tiny portion of the population.
My main concern, instead, is how much these plans further insulate already cocooned top executives from the vicissitudes of daily life, particularly related to coping with our current dysfunctional health care system. What benefits executive health care plans provide is not clear, but presumably they insulate executives from having to deal with the managed care/ health insurance bureaucracy which frustrates patients seeking particular services, but not necessarily the most expensive, or least beneficial services. Such executives might thus not have gut level appreciation of how dysfunctional the health care system has become for even insured patients. Since top executives often are disproportionately influential members of the "superclass," their disconnection from the realities of dysfunctional health care is likely to translate into little real support by the powers that be for meaningful health care reform. There support may be further retarded by the influence of their fellow superclass members whose personal fortunes depend on the status quo in health care.
Real improvement of health care may depend on finding leaders who have better understanding of the plight of real people.
BLOGSCAN - Reports from the ACRE Meeting
The proceedings at the first meeting of the benignly titled Association of Clinical Researchers and Educators (ACRE) was chronicled on the Carlat Psychiatry Blog here, and on Postscript, the Prescription Project blog here. ACRE, founded by Dr Thomas Stossel (see relevant post here on the sorts of arguments Dr Stossel has made), was founded to defend academics who are paid on the side by drug, biotechnology, and device companies from the complaints of the "pharmascolds." What I found most troubling was that the conference was officially opened by Dr Jeffrey Flier, the Dean of the Harvard medical school, implying a medical school endorsement of this group, and featured presentations by the presidents of the American Association of Clinical Endocrinologists, and the American Society of Hypertension, implying endorsement by these medical societies. But also see the comments by Dr Howard Brody on the Hooked: Ethics, Medicine and Pharma blog that there may be a silver lining to this cloud.
MRFIT Mortality
The Multiple Risk Factor Intervention trial was a very large controlled diet trial conducted in the 1980s. It involved an initial phase in which investigators screened over 350,000 men age 35-57 for cardiovascular risk factors including total blood cholesterol. 12,866 participants with major cardiovascular risk factors were selected for the diet intervention trial, while the rest were followed for six years. I discussed the intervention trial here.
During the six years of the observational arm of MRFIT, investigators kept track of deaths in the patients they had screened. They compared the occurrence of deaths from multiple causes to the blood cholesterol values they had measured at the beginning of the study. Here's a graph of the results (source):
Click on the graph for a larger image. Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality.
Possible explanations from other studies include higher cancer rates and higher rates of accidents and suicide. But the study didn't provide those statistics so I'm only guessing.
The MRFIT study cannot be replicated, because it was conducted at a time when fewer people were taking cholesterol-lowering drugs. In 2009, a 50-year old whose doctor discovers he has high cholesterol will likely be prescribed a statin, after which he will probably no longer have high cholesterol. This will confound studies examining the association between blood cholesterol and disease outcomes.
Thanks to The Great Cholesterol Con by Anthony Colpo for the MRFIT reference.
During the six years of the observational arm of MRFIT, investigators kept track of deaths in the patients they had screened. They compared the occurrence of deaths from multiple causes to the blood cholesterol values they had measured at the beginning of the study. Here's a graph of the results (source):
Click on the graph for a larger image. Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality.
Possible explanations from other studies include higher cancer rates and higher rates of accidents and suicide. But the study didn't provide those statistics so I'm only guessing.
The MRFIT study cannot be replicated, because it was conducted at a time when fewer people were taking cholesterol-lowering drugs. In 2009, a 50-year old whose doctor discovers he has high cholesterol will likely be prescribed a statin, after which he will probably no longer have high cholesterol. This will confound studies examining the association between blood cholesterol and disease outcomes.
Thanks to The Great Cholesterol Con by Anthony Colpo for the MRFIT reference.
MRFIT Mortality
The Multiple Risk Factor Intervention trial was a very large controlled diet trial conducted in the 1980s. It involved an initial phase in which investigators screened over 350,000 men age 35-57 for cardiovascular risk factors including total blood cholesterol. 12,866 participants with major cardiovascular risk factors were selected for the diet intervention trial, while the rest were followed for six years. I discussed the intervention trial here.
During the six years of the observational arm of MRFIT, investigators kept track of deaths in the patients they had screened. They compared the occurrence of deaths from multiple causes to the blood cholesterol values they had measured at the beginning of the study. Here's a graph of the results (source):
Click on the graph for a larger image. Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality.
Possible explanations from other studies include higher cancer rates and higher rates of accidents and suicide. But the study didn't provide those statistics so I'm only guessing.
The MRFIT study cannot be replicated, because it was conducted at a time when fewer people were taking cholesterol-lowering drugs. In 2009, a 50-year old whose doctor discovers he has high cholesterol will likely be prescribed a statin, after which he will probably no longer have high cholesterol. This will confound studies examining the association between blood cholesterol and disease outcomes.
Thanks to The Great Cholesterol Con by Anthony Colpo for the MRFIT reference.
During the six years of the observational arm of MRFIT, investigators kept track of deaths in the patients they had screened. They compared the occurrence of deaths from multiple causes to the blood cholesterol values they had measured at the beginning of the study. Here's a graph of the results (source):
Click on the graph for a larger image. Coronary heart disease does indeed rise with increasing total cholesterol in American men of this age group. But total mortality is nearly as high at low cholesterol levels as at high cholesterol levels. What accounts for the increase in mortality at low cholesterol levels, if not coronary heart disease? Stroke is part of the explanation. It was twice as prevalent in the lowest-cholesterol group as it was in other participants. But that hardly explains the large increase in mortality.
Possible explanations from other studies include higher cancer rates and higher rates of accidents and suicide. But the study didn't provide those statistics so I'm only guessing.
The MRFIT study cannot be replicated, because it was conducted at a time when fewer people were taking cholesterol-lowering drugs. In 2009, a 50-year old whose doctor discovers he has high cholesterol will likely be prescribed a statin, after which he will probably no longer have high cholesterol. This will confound studies examining the association between blood cholesterol and disease outcomes.
Thanks to The Great Cholesterol Con by Anthony Colpo for the MRFIT reference.
How "Independent" a Source of Health Care Reform Data?
This week, a Washington Post article discussed who provides the data being cited in the ongoing US debate about health care reform.
But how independent is the Lewin group?
Is it only an appearance of conflict, and how objective is the Lewin Group's work?
So, in summary, a group providing ostensibly "independent" data and opinions about an important health care policy debate is actually a subsidiary of a commercial managed care organization/ health care insurance company which clearly has vested interests in certain policy options. While the consulting group apparently struggles to be objective, its top leader reported that is fashions its reports at the behest of its clients, and that clients can "bury" reports that offend them, possibly because they do not serve their vested interests.
It is not surprising that participants in the current, noisy debate about health care reform, like many other health policy debates, have vested interests, and that their positions are likely to promote these interests. However, what should at least be disturbing is how often those with vested interests try to appear to be disinterested and independent. Should we trust "independent" voices that actually are conflicted, or those who cite "independent" views that actually come from interested parties?
By the way, we first posted about the Lewin Group's actual status as an Ingenix, and hence UnitedHealth subsidiary here in January, 2009, and first posted about how its contribution to the current health care reform debate was being touted as independent here in April, 2009. That a news organization with the status of the Washington Post is now picking up this story suggests a little optimism that the anechoic effect might be weakening.
The political battle over health-care reform is waged largely with numbers, and few number-crunchers have shaped the debate as much as the Lewin Group, a consulting firm whose research has been widely cited by opponents of a public insurance option.
To Rep. Eric Cantor (Va.), the House Republican whip, it is 'the nonpartisan Lewin Group.' To Republicans on the House Ways and Means Committee, it is an 'independent research firm.' To Sen. Orrin G. Hatch (Utah), the second-ranking Republican on the pivotal Finance Committee, it is 'well known as one of the most nonpartisan groups in the country.'
But how independent is the Lewin group?
Generally left unsaid amid all the citations is that the Lewin Group is wholly owned by UnitedHealth Group, one of the nation's largest insurers.
More specifically, the Lewin Group is part of Ingenix, a UnitedHealth subsidiary that was accused by the New York attorney general and the American Medical Association of helping insurers shift medical expenses to consumers by distributing skewed data. Ingenix supplied UnitedHealth and other insurers with data that allegedly understated the 'reasonable and customary' doctor fees that insurers use to determine how much they will reimburse consumers for out-of-network care.
In January, UnitedHealth agreed to a $50 million settlement with the New York attorney general and a $350 million settlement with the AMA, covering conduct going back as far as 1994.
Ingenix's chief executive, Andrew Slavitt, said the company's data was never biased, but Ingenix nonetheless agreed to exit that particular line of business. 'The data didn't have the appearance of independence that's necessary for it to be useful,' Slavitt said.
Lewin Group Vice President John Sheils said his firm had nothing to do with the Ingenix reimbursement data. Lewin has gone through 'a terribly difficult adjustment' since it was bought by UnitedHealth in 2007, he said, because the corporate ownership 'does create the appearance of a conflict of interest.'
'It hasn't affected . . . the work we do, and I think people who know me know that I am not a good liar,' Sheils said.
Is it only an appearance of conflict, and how objective is the Lewin Group's work?
Lewin's clients include the government and groups with a variety of perspectives, including the Commonwealth Fund and the Heritage Foundation. A February report by the firm contained information that could be used to argue for a national system known as single-payer, the approach most threatening to insurers, Sheils noted.
But not all of Lewin's reports see the light of day. 'Let's just say, sometimes studies come out that don't show exactly what the client wants to see. And in those instances, they have [the] option to bury the study,' Sheils said.
So, in summary, a group providing ostensibly "independent" data and opinions about an important health care policy debate is actually a subsidiary of a commercial managed care organization/ health care insurance company which clearly has vested interests in certain policy options. While the consulting group apparently struggles to be objective, its top leader reported that is fashions its reports at the behest of its clients, and that clients can "bury" reports that offend them, possibly because they do not serve their vested interests.
It is not surprising that participants in the current, noisy debate about health care reform, like many other health policy debates, have vested interests, and that their positions are likely to promote these interests. However, what should at least be disturbing is how often those with vested interests try to appear to be disinterested and independent. Should we trust "independent" voices that actually are conflicted, or those who cite "independent" views that actually come from interested parties?
By the way, we first posted about the Lewin Group's actual status as an Ingenix, and hence UnitedHealth subsidiary here in January, 2009, and first posted about how its contribution to the current health care reform debate was being touted as independent here in April, 2009. That a news organization with the status of the Washington Post is now picking up this story suggests a little optimism that the anechoic effect might be weakening.
Physicians Down Under Get Direct About Danger of Bad HIT
Too often, physicians acquiese to demands by hospital executives that they adjust to and use health IT, even if that health IT is flawed. This is despite the fact that liability for patient care resides with the physicians, not the HIT vendor or executives.
Several physicians Down Under have had enough:
Such discrepancies between one hospital and the next regarding HIT require critical evaluation - erring on the side of patient safety, not IT vendor convenience. Considering the aforementioned UK House of Commons report and the "near miss disasters" mentioned by the Australian physicians, such due diligence is mandatory in my opinion.
Further, American physicians can probably learn from these Australian counterparts in being vocal about HIT problems.
-- SS
Several physicians Down Under have had enough:
Doctors issue deadly warning
Daily Examiner, Grafton, Australia
David Bancroft | 23rd July 2009
It seems incredible that a patient record system that aims to improve treatment could kill people [not so incredible to the informed - e.g., see "Bad Informatics Can Kill" - ed.], but that is a claim being made about a new system that is almost certainly going to be introduced into the Grafton Base Hospital next week.
Earlier this month, leading health officials from the Lismore Base Hospital wrote to the North Coast Area Health Service (NCAHS) claiming a new Surginet electronic medical record system that had been operating in the hospital for several months would 'inevitably' lead to the death of patients.
But the health service said changes had been made to the Surginet electronic medical record (EMR) system since the concerns were raised by the four senior clinicians on July 2, and the system had been operating 'satisfactorily' in Sydney without patient concerns being raised. ["Without concerns raised" does not mean they do not exist - ed.]
In their letter to NCAHS chief executive officer Chris Crawford, which was copied to the Minister for Health John Della Bosca, the four medical specialists said there had been recurring problems over several months and 'these have not improved'.
“This has resulted in unnecessary compromise of patient safety,” they wrote.
“There have been repeated well demonstrated cases of near miss disasters due to these problems. [Will patients be as lucky the next time? - ed.]
“We believe that negative patient outcomes, including death, will inevitably result from the continuing use of this system.
“Surginet is fundamentally flawed.
“New technology should: improve the quality of our work; help us to be more efficient, and; make routine tasks easier.
“EMR Surginet does none of these; in fact it has had the opposite effect.
“We believe that the Surginet EMR system is unsafe and will result in patient morbidity and mortality.”
Surginet was to be implemented at the Grafton Base Hospital yesterday, but after concerns were raised with the area health service, implementation was delayed until next Wednesday.
A health service spokesman said the implementation had been delayed so the software producers, Cerner [an American company behind the HIT products that caused difficulty in the UK - see the UK House of Commons report here, esp. points 5 and 6 - ed.], could speak with Grafton surgeons and anaesthetists prior to the implementation about any concerns they may have.
“NCAHS takes any concerns raised about patient safety seriously and is addressing these,” the spokesman said.
“It should be emphasised that Surginet is operating satisfactorily in Sydney hospitals without patient safety concerns being raised. [Again, that does not mean they do not exist; clinicians may be afraid to speak out and working furiously to establish workarounds to problems - ed.]
“It is a system used worldwide that can be adapted to accommodate local work practices in NSW hospitals. ["Can be adapted" - anything "can be adapted". But has this application actually been adapted to the culture in NSW hospitals? - ed.]
“Arrangements are being made for discussions to be held with the department heads by representatives of the EMR project team and Cerner.”
The spokesman said Surginet had recently been introduced at the Maclean Hospital and there had been no complaints and the NCAHS had actually received a letter of thanks from the hospital. [A letter of thanks from whom at the hospital, exactly, and based on what substantive claims? - ed.]
Such discrepancies between one hospital and the next regarding HIT require critical evaluation - erring on the side of patient safety, not IT vendor convenience. Considering the aforementioned UK House of Commons report and the "near miss disasters" mentioned by the Australian physicians, such due diligence is mandatory in my opinion.
Further, American physicians can probably learn from these Australian counterparts in being vocal about HIT problems.
-- SS
Inquiry to Joint Commission on points I raised in my July 22, 2009 JAMA letter on HIT
As I posted here, my letter "Health Care Information Technology, Hospital Responsibilities, and Joint Commission Standards" was published in JAMA on July 22, 2009. A preview of the letter can be seen here, or a full version here if you subscribe to JAMA.
This JAMA letter covered some of the same points I addressed extensively at my Drexel HIT website essay "Hold Harmless and Keep Defects Secret Clauses", including the major point that hospital executives signing HIT "Hold Harmless" and "Defects Nondisclosure" contracts are in violation of Joint Commission standards for conduct related to safety, and in violation of their fiduciary responsibilities towards patient and employee safety and freedom from undue liability.
I've sent the following inquiry to Paul M. Schyve, M.D., Senior Vice President, The Joint Commission:
-- SS
This JAMA letter covered some of the same points I addressed extensively at my Drexel HIT website essay "Hold Harmless and Keep Defects Secret Clauses", including the major point that hospital executives signing HIT "Hold Harmless" and "Defects Nondisclosure" contracts are in violation of Joint Commission standards for conduct related to safety, and in violation of their fiduciary responsibilities towards patient and employee safety and freedom from undue liability.
I've sent the following inquiry to Paul M. Schyve, M.D., Senior Vice President, The Joint Commission:
July 24, 2009I await a response.
Paul M. Schyve, M.D.
Senior Vice President
The Joint Commission
schyve@jointcommission.org
Cc: MChassin@jointcommission.org, otrippi@jointcommission.org
Dear Dr. Schyve,
In testimony to the House Committee on Veterans' Affairs on July 22, 2009 at this link , you state:... The Joint Commission has established standards that require the hospital to:
- Create a culture in which adverse events are reported and evaluated for underlying ("root") causes, and preventative actions are taken.
- Identify high-risk processes and prospectively determine their possible modes of failure, the effects of those failures, and the actions that will prevent the failures or mitigate their effects.
- Establish a culture of safety throughout the hospital. This accreditation standard became effective January 1, 2009, although its purpose and expectations were publicized for over a year in advance.
In my JAMA letter to the editor of July 22, 2009 entitled " Health Care Information Technology, Hospital Responsibilities, and Joint Commission Standards" ( link ), I point out that the Hold Harmless and Defects Nondisclosure clauses signed by hospital executives in contracting for healthcare information technology (such as CPOE and EHR systems) are in violation of Joint Commission safety standards, as well as hospital executive fiduciary responsibilities to patients and clinicians. These clinical IT systems can and do cause medical errors and patient harm.
My letter was in response to Koppel and Kreda's March 25, 2009 article " Health Care Information Technology Vendors' "Hold Harmless" Clause: Implications for Patients and Clinicians ", JAMA. 2009;301(12):1276-1278.
I am interested in the Joint Commission's response to the issues I raise.
-- SS
The Diet-Heart Hypothesis: A Little Perspective
Now that we've seen that the first half of the diet-heart hypothesis-- that dietary saturated fat and cholesterol elevate serum cholesterol and low-density lipoprotein (LDL)-- is false, let's take a look at the second half. This is the idea that elevated serum cholesterol causes cardiovascular disease, also called the "lipid hypothesis".
Heart Attack Mortality vs. Total Mortality
We've been sternly warned that high serum cholesterol leads to heart attacks and that it should be reduced by any means necessary, including powerful cholesterol-lowering drugs. We've been assailed by scientific articles and media reports showing associations between cholesterol and heart disease. What I'm going to show you is a single graph that puts this whole issue into perspective.
The following is drawn from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.), which is one of the longest-running observational studies ever conducted. The study subjects are fairly representative of the general population, although less racially diverse (largely Caucasian). The graph is of total mortality (vertical axis) by total cholesterol level (horizontal axis), for different age groups:
If you're 80 or older, and you have low cholesterol, it's time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there's no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group.
Here's more data from the Framingham study, this time heart attack deaths rather than total mortality (from the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.):
Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn't a great predictor of heart attacks in the general population.
These findings are consistent with other studies that looked at the relationship between total cholesterol and heart attacks in Western populations. For example, the observational arm of the massive MRFIT study found that higher cholesterol predicted a higher risk of heart attack in men age 35-57, but total mortality was highest both at low and high cholesterol levels. The "ideal" cholesterol range for total mortality was between 140 and 260 mg/dL (reference). Quite a range. That encompasses the large majority of the American public.
The Association Between Blood Cholesterol and Heart Attacks is Not Universal
The association between total cholesterol and heart attacks has generally not been observed in Japanese studies that did not pre-select for participants with cardiovascular risk factors (Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.). They also aren't observed on Kitava, where no one seems to have heart attacks or stroke regardless of cholesterol. This suggests that total blood cholesterol as a marker of heart attack risk is not universal. I suspect it would not necessarily apply to someone eating an atypical diet.
Subdividing Cholesterol into Different Lipoprotein Particles Improves its Predictive Value
So far, this probably hasn't shocked anyone. Even entrenched proponents of the lipid hypothesis admit that total cholesterol isn't a great marker. Researchers long ago sliced up total cholesterol into several more specific categories, the most discussed being low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These are tiny fatty droplets containing fats, cholesterol and proteins. They transport cholesterol, fats, and fat-soluble vitamins between tissues via the blood.
The LDL and HDL numbers you get back from the doctor's office typically refer to the amount of cholesterol contained in LDL or HDL per unit blood serum, but you can get the actual particle number measured as well. One can also measure the level of triglyceride (a type of fat) in the blood. Triglycerides are absorbed from the digestive tract and manufactured by the liver in response to carbohydrate, then sent to other organs via lipoproteins.
The level of LDL in the blood gives a better approximation of heart attack risk than total cholesterol. If you're living the average Western lifestyle and you have high LDL, your risk of heart attack is up to twice the risk of someone who has low LDL. LDL particle number has more predictive value than LDL cholesterol concentration. The latter is what's typically measured at the doctor's office. For example, in the EPIC-Norfolk study (free full text), patients with high LDL cholesterol concentration had a 73% higher risk of heart attack than patients with low LDL. Participants with high LDL particle number had exactly twice the risk of those with low LDL number. We'll get back to this phenomenon in a future post.
In the same study, participants with low HDL had twice the heart attack risk of participants with high HDL. That's why HDL is called "good cholesterol". This finding is fairly consistent throughout the medical literature. HDL is probably the main reason why total cholesterol doesn't associate very tightly with heart attack risk. High total cholesterol doesn't tell you if you have high LDL, high HDL or both (LDL and HDL are the predominant cholesterol-carrying lipoproteins). Also from the EPIC-Norfolk study, participants with high triglycerides had twice the risk of heart attack as participants with low triglycerides. Triglycerides and HDL are inversely related to one another, that is, if a person has high HDL, they're likely to have low triglycerides, and vice versa. This has also been consistent between studies.
Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is high LDL (particularly LDL particle number), low HDL and high triglycerides.
In the next post, I'll slice up the lipoproteins even further and comment on their association with cardiovascular disease. I'll also begin to delve into how diet affects the lipoproteins.
Heart Attack Mortality vs. Total Mortality
We've been sternly warned that high serum cholesterol leads to heart attacks and that it should be reduced by any means necessary, including powerful cholesterol-lowering drugs. We've been assailed by scientific articles and media reports showing associations between cholesterol and heart disease. What I'm going to show you is a single graph that puts this whole issue into perspective.
The following is drawn from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.), which is one of the longest-running observational studies ever conducted. The study subjects are fairly representative of the general population, although less racially diverse (largely Caucasian). The graph is of total mortality (vertical axis) by total cholesterol level (horizontal axis), for different age groups:
If you're 80 or older, and you have low cholesterol, it's time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there's no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group. Here's more data from the Framingham study, this time heart attack deaths rather than total mortality (from the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.):
Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn't a great predictor of heart attacks in the general population. These findings are consistent with other studies that looked at the relationship between total cholesterol and heart attacks in Western populations. For example, the observational arm of the massive MRFIT study found that higher cholesterol predicted a higher risk of heart attack in men age 35-57, but total mortality was highest both at low and high cholesterol levels. The "ideal" cholesterol range for total mortality was between 140 and 260 mg/dL (reference). Quite a range. That encompasses the large majority of the American public.
The Association Between Blood Cholesterol and Heart Attacks is Not Universal
The association between total cholesterol and heart attacks has generally not been observed in Japanese studies that did not pre-select for participants with cardiovascular risk factors (Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.). They also aren't observed on Kitava, where no one seems to have heart attacks or stroke regardless of cholesterol. This suggests that total blood cholesterol as a marker of heart attack risk is not universal. I suspect it would not necessarily apply to someone eating an atypical diet.
Subdividing Cholesterol into Different Lipoprotein Particles Improves its Predictive Value
So far, this probably hasn't shocked anyone. Even entrenched proponents of the lipid hypothesis admit that total cholesterol isn't a great marker. Researchers long ago sliced up total cholesterol into several more specific categories, the most discussed being low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These are tiny fatty droplets containing fats, cholesterol and proteins. They transport cholesterol, fats, and fat-soluble vitamins between tissues via the blood.
The LDL and HDL numbers you get back from the doctor's office typically refer to the amount of cholesterol contained in LDL or HDL per unit blood serum, but you can get the actual particle number measured as well. One can also measure the level of triglyceride (a type of fat) in the blood. Triglycerides are absorbed from the digestive tract and manufactured by the liver in response to carbohydrate, then sent to other organs via lipoproteins.
The level of LDL in the blood gives a better approximation of heart attack risk than total cholesterol. If you're living the average Western lifestyle and you have high LDL, your risk of heart attack is up to twice the risk of someone who has low LDL. LDL particle number has more predictive value than LDL cholesterol concentration. The latter is what's typically measured at the doctor's office. For example, in the EPIC-Norfolk study (free full text), patients with high LDL cholesterol concentration had a 73% higher risk of heart attack than patients with low LDL. Participants with high LDL particle number had exactly twice the risk of those with low LDL number. We'll get back to this phenomenon in a future post.
In the same study, participants with low HDL had twice the heart attack risk of participants with high HDL. That's why HDL is called "good cholesterol". This finding is fairly consistent throughout the medical literature. HDL is probably the main reason why total cholesterol doesn't associate very tightly with heart attack risk. High total cholesterol doesn't tell you if you have high LDL, high HDL or both (LDL and HDL are the predominant cholesterol-carrying lipoproteins). Also from the EPIC-Norfolk study, participants with high triglycerides had twice the risk of heart attack as participants with low triglycerides. Triglycerides and HDL are inversely related to one another, that is, if a person has high HDL, they're likely to have low triglycerides, and vice versa. This has also been consistent between studies.
Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is high LDL (particularly LDL particle number), low HDL and high triglycerides.
In the next post, I'll slice up the lipoproteins even further and comment on their association with cardiovascular disease. I'll also begin to delve into how diet affects the lipoproteins.
The Diet-Heart Hypothesis: A Little Perspective
Now that we've seen that the first half of the diet-heart hypothesis-- that dietary saturated fat and cholesterol elevate serum cholesterol and low-density lipoprotein (LDL)-- is false, let's take a look at the second half. This is the idea that elevated serum cholesterol causes cardiovascular disease, also called the "lipid hypothesis".
Heart Attack Mortality vs. Total Mortality
We've been sternly warned that high serum cholesterol leads to heart attacks and that it should be reduced by any means necessary, including powerful cholesterol-lowering drugs. We've been assailed by scientific articles and media reports showing associations between cholesterol and heart disease. What I'm going to show you is a single graph that puts this whole issue into perspective.
The following is drawn from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.), which is one of the longest-running observational studies ever conducted. The study subjects are fairly representative of the general population, although less racially diverse (largely Caucasian). The graph is of total mortality (vertical axis) by total cholesterol level (horizontal axis), for different age groups:If you're 80 or older, and you have low cholesterol, it's time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there's no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group.
Here's more data from the Framingham study, this time heart attack deaths rather than total mortality (from the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.):Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn't a great predictor of heart attacks in the general population.
These findings are consistent with other studies that looked at the relationship between total cholesterol and heart attacks in Western populations. For example, the observational arm of the massive MRFIT study found that higher cholesterol predicted a higher risk of heart attack in men age 35-57, but total mortality was highest both at low and high cholesterol levels. The "ideal" cholesterol range for total mortality was between 140 and 260 mg/dL (reference). Quite a range. That encompasses the large majority of the American public.
The Association Between Blood Cholesterol and Heart Attacks is Not Universal
The association between total cholesterol and heart attacks has generally not been observed in Japanese studies that did not pre-select for participants with cardiovascular risk factors (Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.). They also aren't observed on Kitava, where no one seems to have heart attacks or stroke regardless of cholesterol. This suggests that total blood cholesterol as a marker of heart attack risk is not universal. I suspect it would not necessarily apply to someone eating an atypical diet.
Subdividing Cholesterol into Different Lipoprotein Particles Improves its Predictive Value
So far, this probably hasn't shocked anyone. Even entrenched proponents of the lipid hypothesis admit that total cholesterol isn't a great marker. Researchers long ago sliced up total cholesterol into several more specific categories, the most discussed being low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These are tiny fatty droplets containing fats, cholesterol and proteins. They transport cholesterol, fats, and fat-soluble vitamins between tissues via the blood.
The LDL and HDL numbers you get back from the doctor's office typically refer to the amount of cholesterol contained in LDL or HDL per unit blood serum, but you can get the actual particle number measured as well. One can also measure the level of triglyceride (a type of fat) in the blood. Triglycerides are absorbed from the digestive tract and manufactured by the liver in response to carbohydrate, then sent to other organs via lipoproteins.
The level of LDL in the blood gives a better approximation of heart attack risk than total cholesterol. If you're living the average Western lifestyle and you have high LDL, your risk of heart attack is up to twice the risk of someone who has low LDL. LDL particle number has more predictive value than LDL cholesterol concentration. The latter is what's typically measured at the doctor's office. For example, in the EPIC-Norfolk study (free full text), patients with high LDL cholesterol concentration had a 73% higher risk of heart attack than patients with low LDL. Participants with high LDL particle number had exactly twice the risk of those with low LDL number. We'll get back to this phenomenon in a future post.
In the same study, participants with low HDL had twice the heart attack risk of participants with high HDL. That's why HDL is called "good cholesterol". This finding is fairly consistent throughout the medical literature. HDL is probably the main reason why total cholesterol doesn't associate very tightly with heart attack risk. High total cholesterol doesn't tell you if you have high LDL, high HDL or both (LDL and HDL are the predominant cholesterol-carrying lipoproteins). Also from the EPIC-Norfolk study, participants with high triglycerides had twice the risk of heart attack as participants with low triglycerides. Triglycerides and HDL are inversely related to one another, that is, if a person has high HDL, they're likely to have low triglycerides, and vice versa. This has also been consistent between studies.
Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is high LDL (particularly LDL particle number), low HDL and high triglycerides.
In the next post, I'll slice up the lipoproteins even further and comment on their association with cardiovascular disease. I'll also begin to delve into how diet affects the lipoproteins.
Heart Attack Mortality vs. Total Mortality
We've been sternly warned that high serum cholesterol leads to heart attacks and that it should be reduced by any means necessary, including powerful cholesterol-lowering drugs. We've been assailed by scientific articles and media reports showing associations between cholesterol and heart disease. What I'm going to show you is a single graph that puts this whole issue into perspective.
The following is drawn from the Framingham Heart study (via the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.), which is one of the longest-running observational studies ever conducted. The study subjects are fairly representative of the general population, although less racially diverse (largely Caucasian). The graph is of total mortality (vertical axis) by total cholesterol level (horizontal axis), for different age groups:
If you're 80 or older, and you have low cholesterol, it's time to get your affairs in order. Between the age of 50 and 80, when most heart attacks occur, there's no association between cholesterol level and total mortality. At age 50 and below, men with higher cholesterol die more often. In the youngest age group, the percent increase in mortality between low and high cholesterol is fairly large, but the absolute risk of death at that age is still low. There is no positive association between total cholesterol and mortality in women at any age, only a negative association in the oldest age group. Here's more data from the Framingham study, this time heart attack deaths rather than total mortality (from the book Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.):
Up to age 47, men with higher cholesterol have more heart attacks. At ages above 47, cholesterol does not associate with heart attacks or total mortality. Since the frequency of heart attacks and total mortality are low before the age of 47, it follows that total cholesterol isn't a great predictor of heart attacks in the general population. These findings are consistent with other studies that looked at the relationship between total cholesterol and heart attacks in Western populations. For example, the observational arm of the massive MRFIT study found that higher cholesterol predicted a higher risk of heart attack in men age 35-57, but total mortality was highest both at low and high cholesterol levels. The "ideal" cholesterol range for total mortality was between 140 and 260 mg/dL (reference). Quite a range. That encompasses the large majority of the American public.
The Association Between Blood Cholesterol and Heart Attacks is Not Universal
The association between total cholesterol and heart attacks has generally not been observed in Japanese studies that did not pre-select for participants with cardiovascular risk factors (Prevention of Coronary Heart Disease, by Dr. Harumi Okuyama et al.). They also aren't observed on Kitava, where no one seems to have heart attacks or stroke regardless of cholesterol. This suggests that total blood cholesterol as a marker of heart attack risk is not universal. I suspect it would not necessarily apply to someone eating an atypical diet.
Subdividing Cholesterol into Different Lipoprotein Particles Improves its Predictive Value
So far, this probably hasn't shocked anyone. Even entrenched proponents of the lipid hypothesis admit that total cholesterol isn't a great marker. Researchers long ago sliced up total cholesterol into several more specific categories, the most discussed being low-density lipoprotein (LDL) and high-density lipoprotein (HDL). These are tiny fatty droplets containing fats, cholesterol and proteins. They transport cholesterol, fats, and fat-soluble vitamins between tissues via the blood.
The LDL and HDL numbers you get back from the doctor's office typically refer to the amount of cholesterol contained in LDL or HDL per unit blood serum, but you can get the actual particle number measured as well. One can also measure the level of triglyceride (a type of fat) in the blood. Triglycerides are absorbed from the digestive tract and manufactured by the liver in response to carbohydrate, then sent to other organs via lipoproteins.
The level of LDL in the blood gives a better approximation of heart attack risk than total cholesterol. If you're living the average Western lifestyle and you have high LDL, your risk of heart attack is up to twice the risk of someone who has low LDL. LDL particle number has more predictive value than LDL cholesterol concentration. The latter is what's typically measured at the doctor's office. For example, in the EPIC-Norfolk study (free full text), patients with high LDL cholesterol concentration had a 73% higher risk of heart attack than patients with low LDL. Participants with high LDL particle number had exactly twice the risk of those with low LDL number. We'll get back to this phenomenon in a future post.
In the same study, participants with low HDL had twice the heart attack risk of participants with high HDL. That's why HDL is called "good cholesterol". This finding is fairly consistent throughout the medical literature. HDL is probably the main reason why total cholesterol doesn't associate very tightly with heart attack risk. High total cholesterol doesn't tell you if you have high LDL, high HDL or both (LDL and HDL are the predominant cholesterol-carrying lipoproteins). Also from the EPIC-Norfolk study, participants with high triglycerides had twice the risk of heart attack as participants with low triglycerides. Triglycerides and HDL are inversely related to one another, that is, if a person has high HDL, they're likely to have low triglycerides, and vice versa. This has also been consistent between studies.
Together, this suggests that the commonly measured lipoprotein pattern that associates most tightly with heart attack risk in typical Western populations is high LDL (particularly LDL particle number), low HDL and high triglycerides.
In the next post, I'll slice up the lipoproteins even further and comment on their association with cardiovascular disease. I'll also begin to delve into how diet affects the lipoproteins.
Pseudo-Evidence Based Medicine Threatens Health Care Reform Based on "What Works"
As I posted yesterday, the increasingly noisy debate about health care reform in the US has not dealt much with the issues we often discuss on Health Care Renewal. These include problems in how health care organizations are led which threaten physicians' and other health care professionals' core values using tactics including perverse incentives, deception, and intimidation.
Last night, however, President Obama held a news conference mostly devoted to health care issues, in which he stressed the importance of changing not just how health insurance works, but how health care decisions are made. As Newsweek's "The Gaggle" blog reported,
So what the President seems to be advocating is making health care more evidence-based, perhaps in the formal sense of evidence-based medicine.
As a card-carrying evidence-based medicine advocate, I certainly agree, but let me reiterate that evidence-based medicine is not just medicine based on some sort of evidence. As Dr David Sackett, and colleagues wrote [Sackett DL, Rosenberg WM, Muir Gray JA, Haynes RB, Richardson WS. Evidence-based medicine; what it is and what it isn't. BMJ 1996; 312: 71-72. Link here. ]
Furthermore,
One can find other definitions of EBM, but nearly all emphasize that the approach is designed to appropriately apply results from the best clinical research, critically reviewed, to the individual patient, taking into account that patient's clinical characteristics and personal values.
So far, so good. I believe the proper application of "real" (as described above) evidence-based medicine has the potential to improve patient outcomes while moderating health care costs. However, we have pointed out how problems arising from concentration and abuse of power in health care threaten the evidence-based medical ideal.
First, there are major problems with the development of the sort of clinical research evidence required by the EBM process. We have discussed how clinical research is frequently manipulated by those with vested interests in producing results that favor the products or services that they sell. The critical review process inherent in EBM is meant to cope with less than optimally designed and implemented research. However, the process was designed to cope with honest mistakes and inevitable trade-offs, not deliberate manipulation by vested interests.
Worse, we have discussed how vested interests may engineer the suppression of research when manipulation fails to produce the desired results. The EBM process assumes that the research on which decisions should be based is an unbiased sample of research that was done (and done to advance science, not commercial or ideological interests). When research whose results are unwanted by vested interests is suppressed, the resulting distortion of the evidence base may irretrievably bias the EBM process.
Finally, we have posted about how vested interests have distorted the discussion, dissemination, and teaching of the results of clinical research. They may develop systematic stealth marketing campaigns, often employing supposed "key opinion leaders," who are paid on the side by marketers, and using "medical education and communication companies"as marketing fronts whose publication strategies include deceptive tactics such as "ghost-writing."
Thus, a rising tide of "pseudo-evidence based medicine" threatens to overwhelm even the most conscientious physicians trying to practice evidence-based medicine.
So, while I applaud President Obama's advocacy of reforming health care to emphasize what the best evidence suggests really works, I do not think this effort will get far unless we deal with the rising tide of pseudo-evidence based medicine. As a minimum, we need full and detailed disclosure of all the relationships among vested interests and medical research and education, and a much greater role for research and education that is not subsidized by corporations bent on using research and education to market their products and services.
Last night, however, President Obama held a news conference mostly devoted to health care issues, in which he stressed the importance of changing not just how health insurance works, but how health care decisions are made. As Newsweek's "The Gaggle" blog reported,
Can I guarantee that there are going to be no changes in the health care delivery system? No. The whole point of this is to try to encourage changes that work for the American people and make them healthier. The government already is making some of these decisions. More importantly, insurance companies right now are making those decisions. And part of what we want to do is to make sure that those decisions are being made by doctors and medical experts based on evidence, based on what works, because that's not how it's working right now.
So what the President seems to be advocating is making health care more evidence-based, perhaps in the formal sense of evidence-based medicine.
As a card-carrying evidence-based medicine advocate, I certainly agree, but let me reiterate that evidence-based medicine is not just medicine based on some sort of evidence. As Dr David Sackett, and colleagues wrote [Sackett DL, Rosenberg WM, Muir Gray JA, Haynes RB, Richardson WS. Evidence-based medicine; what it is and what it isn't. BMJ 1996; 312: 71-72. Link here. ]
Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence based medicine means integrating individual clinical expertise with the best available external clinical evidence from systematic research. By individual clinical expertise we mean the proficiency and judgment that individual clinicians acquire through clinical experience and clinical practice. Increased expertise is reflected in many ways, but especially in more effective and efficient diagnosis and in the more thoughtful identification and compassionate use of individual patients' predicaments, rights, and preferences in making clinical decisions about their care. By best available external clinical evidence we mean clinically relevant research, often from the basic sciences of medicine, but especially from patient centred clinical research into the accuracy and precision of diagnostic tests (including the clinical examination), the power of prognostic markers, and the efficacy and safety of therapeutic, rehabilitative, and preventive regimens.
Furthermore,
Evidence based medicine is not 'cookbook' medicine. Because it requires a bottom up approach that integrates the best external evidence with individual clinical expertise and patients' choice, it cannot result in slavish, cookbook approaches to individual patient care. External clinical evidence can inform, but can never replace, individual clinical expertise, and it is this expertise that decides whether the external evidence applies to the individual patient at all and, if so, how it should be integrated into a clinical decision.
One can find other definitions of EBM, but nearly all emphasize that the approach is designed to appropriately apply results from the best clinical research, critically reviewed, to the individual patient, taking into account that patient's clinical characteristics and personal values.
So far, so good. I believe the proper application of "real" (as described above) evidence-based medicine has the potential to improve patient outcomes while moderating health care costs. However, we have pointed out how problems arising from concentration and abuse of power in health care threaten the evidence-based medical ideal.
First, there are major problems with the development of the sort of clinical research evidence required by the EBM process. We have discussed how clinical research is frequently manipulated by those with vested interests in producing results that favor the products or services that they sell. The critical review process inherent in EBM is meant to cope with less than optimally designed and implemented research. However, the process was designed to cope with honest mistakes and inevitable trade-offs, not deliberate manipulation by vested interests.
Worse, we have discussed how vested interests may engineer the suppression of research when manipulation fails to produce the desired results. The EBM process assumes that the research on which decisions should be based is an unbiased sample of research that was done (and done to advance science, not commercial or ideological interests). When research whose results are unwanted by vested interests is suppressed, the resulting distortion of the evidence base may irretrievably bias the EBM process.
Finally, we have posted about how vested interests have distorted the discussion, dissemination, and teaching of the results of clinical research. They may develop systematic stealth marketing campaigns, often employing supposed "key opinion leaders," who are paid on the side by marketers, and using "medical education and communication companies"as marketing fronts whose publication strategies include deceptive tactics such as "ghost-writing."
Thus, a rising tide of "pseudo-evidence based medicine" threatens to overwhelm even the most conscientious physicians trying to practice evidence-based medicine.
So, while I applaud President Obama's advocacy of reforming health care to emphasize what the best evidence suggests really works, I do not think this effort will get far unless we deal with the rising tide of pseudo-evidence based medicine. As a minimum, we need full and detailed disclosure of all the relationships among vested interests and medical research and education, and a much greater role for research and education that is not subsidized by corporations bent on using research and education to market their products and services.
Subscribe to:
Posts (Atom)