Science or PR?

iVillage Member
Registered: 01-21-2010
Science or PR?
4
Sun, 03-21-2010 - 8:36pm

http://www.bmj.com/cgi/content/extract/331/7529/1412

BMJ 2005;331:1412 (10 December), doi:10.1136/bmj.331.7529.1412

Are US flu death figures more PR than science?

US data on influenza deaths are a mess. The Centers for Disease Control and Prevention (CDC) acknowledges a difference between flu death and flu associated death yet uses the terms interchangeably. Additionally, there are significant statistical incompatibilities between official estimates and national vital statistics data. Compounding these problems is a marketing of fear—a CDC communications strategy in which medical experts "predict dire outcomes" during flu seasons.

The CDC website states what has become commonly accepted and widely reported in the lay and scientific press: annually "about 36 000 die from flu" (www.cdc.gov/flu/about/disease.htm) and "influenza/pneumonia" is the seventh leading cause of death in the United States (www.cdc.gov/nchs/fastats/lcod.htm). But why are flu and pneumonia bundled together? Is the relationship so strong or unique to warrant characterising them as a single cause of death?

David Rosenthal, director of Harvard University Health Services, said, "People don't necessarily die, per se, of the virus—the viraemia. What they die of is a secondary pneumonia. So many of these pneumonias are not viral pneumonias but secondary ." But Dr Rosenthal agreed that the flu/pneumonia relationship was not unique. For instance, a recent study (JAMA 2004;292: 1955-60) found that stomach acid suppressing drugs are associated with a higher risk of community acquired pneumonia, but such drugs and pneumonia are not compiled as a single statistic.

CDC states that the historic 1968-9 "Hong Kong flu" pandemic killed 34 000 Americans. At the same time, CDC claims 36 000 Americans annually die from flu. What is going on?

Meanwhile, according to the CDC's National Center for Health Statistics (NCHS), "influenza and pneumonia" took 62 034 lives in 2001—61 777 of which were attributed to pneumonia and 257 to flu, and in only 18 cases was flu virus positively identified. Between 1979 and 2002, NCHS data show an average 1348 flu deaths per year (range 257 to 3006).

The NCHS data would be compatible with CDC mortality estimates if about half of the deaths classed by the NCHS as pneumonia were actually flu initiated secondary pneumonias. But the NCHS criteria indicate otherwise: "Cause-of-death statistics are based solely on the underlying cause of death... defined by WHO as `the disease or injury which initiated the train of events leading directly to death.'"

In a written statement, CDC media relations responded to the diverse statistics: "Typically, influenza causes death when the infection leads to severe medical complications." And as most such cases "are never tested for virus infection...CDC considers these figures to be a very substantial undercounting of the true number of deaths from influenza. Therefore, the CDC uses indirect modelling methods to estimate the number of deaths associated with influenza."

CDC's model calculated an average annual 36 155 deaths from influenza associated underlying respiratory and circulatory causes (JAMA 2003;289: 179-86). Less than a quarter of these (8097) were described as flu or flu associated underlying pneumonia deaths. Thus the much publicised figure of 36 000 is not an estimate of yearly flu deaths, as widely reported in both the lay and scientific press, but an estimate—generated by a model—of flu-associated death.

William Thompson of the CDC's National Immunization Program (NIP), and lead author of the CDC's 2003 JAMA article, explained that "influenza-associated mortality" is "a statistical association between deaths and viral data available." He said that an association does not imply an underlying cause of death: "Based on modelling, we think it's associated. I don't know that we would say that it's the underlying cause of death."

Yet this stance is incompatible with the CDC assertion that the flu kills 36 000 people a year—a misrepresentation that is yet to be publicly corrected.

Before 2003 CDC said that 20 000 influenza-associated deaths occurred each year. The new figure of 36 000 reported in the January 2003 JAMA paper is an estimate of influenza-associated mortality over the 1990s. Keiji Fukuda, a flu researcher and a co-author of the paper, has been quoted as offering two possible causes for this 80% increase: "One is that the number of people older than 65 is growing larger...The second possible reason is the type of virus that predominated in the 1990s ."

However, the 65-plus population grew just 12% between 1990 and 2000. And if flu virus was truly more virulent over the 1990s, one would expect more deaths. But flu deaths recorded by the NCHS were on average 30% lower in the 1990s than the 1980s.

If passed, the Flu Protection Act of 2005 will revamp US flu vaccine policy. The legislation will require CDC to pay makers for vaccines unsold "through routine market mechanisms." The bill will also require CDC to conduct a "public awareness campaign" emphasising "the safety and benefit of recommended vaccines for the public good."

Yet this bill obscures the fact that CDC is already working in manufacturers' interest by conducting campaigns to increase flu vaccination. At the 2004 "National Influenza Vaccine Summit," co-sponsored by CDC and the American Medical Association, Glen Nowak, associate director for communications at the NIP, spoke on using the media to boost demand for the vaccine. One step of a "Seven-Step `Recipe' for Generating Interest in, and Demand for, Flu (or any other) Vaccination" occurs when "medical experts and public health authorities publicly...state concern and alarm (and predict dire outcomes)—and urge influenza vaccination" (www.ama-assn.org/ama1/pub/upload/mm/36/2004_flu_nowak.pdf). Another step entails "continued reports...that influenza is causing severe illness and/or affecting lots of people, helping foster the perception that many people are susceptible to a bad case of influenza."

Preceding the summit, demand had been low early into the 2003 flu season. "At that point, the manufacturers were telling us that they weren't receiving a lot of orders for vaccine for use in November or even December," recalled Dr Nowak on National Public Radio. "It really did look like we needed to do something to encourage people to get a flu shot."

If flu is in fact not a major cause of death, this public relations approach is surely exaggerated. Moreover, by arbitrarily linking flu with pneumonia, current data are statistically biased. Until corrected and until unbiased statistics are developed, the chances for sound discussion and public health policy are limited.

Peter Doshi, graduate student

Harvard University pdoshi@fas.harvard.edu

iVillage Member
Registered: 01-21-2010
Sun, 03-21-2010 - 8:41pm

JAMA 2004;292: 1955-60

http://journals.lww.com/jpgn/Fulltext/2006/10000/Therapy_with_Gastric_Acidity_Inhibitors_Increases.24.aspx

Therapy with Gastric Acidity Inhibitors Increases the Risk of Acute Gastroenteritis and Community-acquired Pneumonia in Children
Rosh, Joel R. MD; Hassall, Eric MBChB, FRCPC

1Associate Professor of Pediatrics, UMD-NJ Medical School, Director, Pediatric Gastroenterology, Atlantic Health, Morristown, NJ joel.rosh@atlantichealth.org

2Professor of Pediatrics, Division of Gastroenterology, BC Children's Hospital, University of British Columbia, Vancouver BC, Canada

Therapy with Gastric Acidity Inhibitors Increases the Risk of Acute Gastroenteritis and Community-acquired Pneumonia in Children. Canani RB, Cirillo P, Roggero P, et al. Pediatrics 2006;117:e817-20.

Summary:

The authors performed a prospective, controlled trial involving 91 children, ages 4 to 36 months, who were diagnosed with gastroesophageal reflux disease (GERD) by endoscopic biopsy and pH probe. They received either high-dose ranitidine (dosage, 10 mg/kg/day) or omeprazole (dosage, 1 mg/kg/day) during a 4-month study period. The authors compiled the rates of gastroenteritis and pneumonia in these acid-suppressed patients and in a cohort of 95 healthy children matched for age, sex, growth, and number of infections in the 4 months before the treatment period. Excluded were children with conditions predisposing to recurrent infection, including diabetes, chronic lung or cardiac disease, and congenital gastrointestinal motility disorders. Data were also compiled for the 4 months before the introduction of acid-suppressive therapy. Gastroenteritis was defined as the presence of diarrhea of 2 to 7 days' duration, with or without other symptoms such as fever. Pneumonia was defined as clinical symptoms confirmed with a chest radiograph. The diagnosis of these infections was prompted by self-referral-parents were instructed to contact their primary physician or the study center if symptoms developed. The study period coincided with the time of year during which Italy experiences the highest rates of rotavirus and respiratory syncytial virus infections.

The control group had 19 cases of gastroenteritis compared with 43 in the treated group (P = 0.001; OR = 3.58), and 2 control pneumonias compared with 11 in the treated group (P = 0.03; OR = 6.39). The baseline infection rates in the treatment and control cohorts during the 4 months before the start of the study were the same. The increased infection rate in the treated group lasted beyond the 4 months of the study.

Comment:

There are some methodological vulnerabilities in this study. Most important, the primary outcomes were self-reported and the trial was open label. In this setting, knowing that their children were receiving a newly prescribed medication, the parents may have been more vigilant and more likely to report new symptoms compared with the parents of healthy, untreated children. In addition, the children in the treated group were diagnosed with GERD after their parents sought medical care for symptoms suggestive of GERD. Again, such parents may have had a lower threshold for seeking medical attention than those of healthy controls. These selection biases could have confounded the results.

The working definition of gastroenteritis in this study was quite liberal and could have captured cases of changes in stool pattern due to dietary changes or even introduction of the study medication itself. In addition, the groups were not controlled for daycare attendance as a risk factor for acquisition of infections-this is important, given the age of the study population.

Aside from these factors, Dr Canani and his colleagues deserve high commendation for performing a prospective, controlled study of this important topic in children. The odds ratios of risk are impressive, even when given the potential for inflation by the biases already mentioned. On the other hand, the dose of proton pump inhibitor administered was relatively low, and this may have reduced the magnitude of the findings.

This study adds to a growing literature on risks of infection in acid-suppressed individuals. For example, acid suppression has been linked to an increase in community-acquired pneumonias in adults 1, an increased pneumonia incidence in mechanically ventilated patients 2,3, an increased risk of Clostridium difficile infection 4, and an increase in necrotizing enterocolitis in very low birth weight infants 5.

Although much more data are required, these emerging data should serve as reminder to all of us that although the use of acid suppressives has benefited patients enormously, the use of any treatment is a risk-benefit equation. Recent trends toward the widespread empirical use of acid suppressives are of concern, especially in young children 6. It is also important for the prescribing physician to remember that even when acid suppression is indicated, it is not necessary to make patients achlorhydric to achieve symptom response or healing.

Joel R. Rosh, MD

Associate Professor of Pediatrics, UMD-NJ Medical School

Director, Pediatric Gastroenterology

Atlantic Health, Morristown, NJ

joel.rosh@atlantichealth.org

Eric Hassall, MBChB, FRCPC

Professor of Pediatrics Division of Gastroenterology

BC Childrens Hospital/University of British

Columbia Vancouver BC, Canada

REFERENCES
1. O'Keefe GE,Gentiello LM,Maier RV. Incidence of infectious complications associated with the use of histamine-2-receptor antagonists in critically ill trauma patients. Ann Surg 1998;227:120-5.
Cited Here...

2. Messori A, Trippoli S, Vaiani M, et al. Bleeding and pneumonia in intensive care patients given ranitidine and sucralfate for prevention of stress ulcer: meta-analysis of randomised controlled trials. BMJ 2000;321:1-7.
Cited Here...

3. Laheij RJF, Sturkenboom MC, Hassing RJ, et al. Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs. JAMA 2004;292:1955-60.
Cited Here... | PubMed | CrossRef

4. Dial S, Alrasadi K, Manoukian C, et al. Risk of Clostridium difficile diarrhea among hospital inpatients prescribed proton pump inhibitors: cohort and case-control studies. CMAJ 2004;171:33-8.
Cited Here... | PubMed | CrossRef

5. Guillet R, Stoll BJ, Cotten CM, et al. Association of H2-blocker therapy and higher incidence of necrotizing enterocolitis in very low birth weight infants. Pediatrics 2006;117:137-42.
Cited Here...

6. Hassall E. Mistaking 'life' (as we know it) for 'disease'. Am J Gastroenterol 2006. In press.
Cited Here...

iVillage Member
Registered: 01-21-2010
Sun, 03-21-2010 - 10:17pm

My facebook reply -

All those lies and there is plenty of proof that the vaccine doesn't even work~

Policy VS Evidence:

"Three problems are immediately apparent. The first is heavy reliance on non-randomised studies (chiefly cohort studies), especially in the elderly. This makes assessment of methodological quality an important part of data interpretation."... See More

http://www.bmj.com/cgi/content/full/333/7574/912

Straight from a package insert:
" FLULAVAL is an influenza virus vaccine indicated for active immunization of adults 18 years of age and older against influenza disease caused by influenza virus subtypes A and type B contained in the vaccine. This indication is based on immune response elicited by FLULAVAL, and there have been no controlled trials demonstrating a decrease in influenza disease after vaccination with FLULAVAL.”

http://us.gsk.com/products/assets/us_flulaval.pdf

There is no proof it works in the elderly:

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2808%2961160-5/fulltext

http://www.fiercevaccines.com/story/study-no-hard-evidence-flu-vaccine-protects-elderly/2010-02-18

There is no proof that caregivers for the elderly are protected by vaccination:

http://www.nationalpost.com/news/story.html?id=2668629&p=1

There is no proof of efficacy in children:

http://www.usnews.com/health/managing-your-healthcare/research/articles/2008/10/06/kids-flu-shot-largely-ineffective-over-past-few.html

Actually, just the opposite is true:

http://www.sciencedaily.com/releases/2009/05/090519172045.htm

I have to wonder how many deaths were actually caused by the TREATMENT of the flu. My friend is a nurse and she told me that they immediately dose the elderly with antivirals and NSAIDS/Tylenol whenever they suspect flu. They do this before they even test for flu...

http://www.naturalnews.com/027548_swine_flu_vaccines_death_risk.html

And then lets go back a little further and realize how the H1N1 got its roots:

http://www.cnn.com/2009/US/04/22/missing.virus.sample/

http://www.fas.org/biosecurity/education/dualuse/FAS_Basler/2_A.html

http://www.bloomberg.com/apps/news?pid=20601087&sid=afrdATVXPEAk&refer=home

http://www.bloomberg.com/apps/news?pid=20601124&sid=ajw2AS.d1wK8

iVillage Member
Registered: 06-16-2009
Tue, 03-23-2010 - 4:05am
For example, acid suppression has been linked to an increase in community-acquired pneumonias in adults 1, an increased pneumonia incidence in mechanically ventilated patients 2,3, an increased risk of Clostridium difficile infection 4, and an increase in necrotizing enterocolitis in very low birth weight infants 5.

Although much more data are required, these emerging data should serve as reminder to all of us that although the use of acid suppressives has benefited patients enormously, the use of any treatment is a risk-benefit equation. Recent trends toward the widespread empirical use of acid suppressives are of concern, especially in young children 6. It is also important for the prescribing physician to remember that even when acid suppression is indicated, it is not necessary to make patients achlorhydric to achieve symptom response or healing.


This is interesting.

Photobucket

iVillage Member
Registered: 01-21-2010
Tue, 03-23-2010 - 3:37pm
I know, the number of babies on these drugs is unreal. Why not figure out what causes the acid to begin with??? I took Prilosec (spelling?) when I was pregnant 5 years ago. After reading about it and the others, I was devastated that I took the stuff! Growing up my Dad took Rolaids every single day and I remember eating them, just because they were there. I probably took a bottle a day when I was pregnant both times, but again - after reading about them I won't take anything now. Why? Because after learning what CAUSES the acid, I no longer have the need...why can't we do that with babies? Oh it makes me so mad!