Study finds volunteering decreases mortality risk among retired

Moral of the story: Start volunteering, it may save your life. This study looks at retirees and found volunteering has bidirectional affects with health. Not only is volunteering a sign of good health, it also improves health. Get yourself, your parents or your grandparents out there volunteering.

Study finds volunteering decreases mortality risk among retired The Advisory Board Company 05/19/2009

Retirees older than age 65 who volunteer have a lower mortality risk than their non-volunteering peers, according to a study presented earlier this month at the American Geriatrics Society’s annual meeting in Chicago. Although previous research identified a link between volunteering and lower mortality rates, such studies involved individuals born before 1920 and failed to adjust the results for possible confounders, such as socioeconomic status and chronic health conditions. To assess the relationship when accounting for those variables, researchers from the University of California-San Francisco and Montefiore Medical Center examined 6,360 retired men and women older than age 65 who were enrolled in the Health and Retirement Study—considered representative of all U.S. adults—in 2002. Study subjects had an average age of 78, and 60% were female. Examining participants’ volunteerism patterns, the researchers found that 12% of participants who volunteered died, compared with 26% of non-volunteers. After adjusting the data for participants’ demographics, socioeconomic status, chronic health conditions, geriatric syndromes, functional limitations, self-rated health, depression, and cognition, the researchers found that the link “wasn’t as strong, but still existed.” Commenting on the study, one researcher notes that volunteering may be associated with self-efficacy—a belief in one’s own abilities to accomplish tasks—which helps individuals remain engaged in a healthy and active lifestyle (Gordon, HealthDay, 5/8).

Moral of the story: Patents on genes are creating controversy and in the name of free speech and medical necessity need to be restricted. They are creating undue burden for patients because of the lack of market forces preventing innovating and driving up costs. As the article states, my genes can no more ethically be patented than my left arm or my brain. The laws need to change and reflect this reality. At the same time, genetically modified foods need to be revisited as the ethics of genetic patents are reviewed. It may be time to stop bowing to argibusiness and start fighting for every American.

http://www.nytimes.com/2009/05/13/health/13patent.html?em

Cancer Patients Challenge the Patenting of a Gene

By JOHN SCHWARTZ

Published: May 12, 2009

When Genae Girard received a diagnosis of breast cancer in 2006, she knew she would be facing medical challenges and high expenses. But she did not expect to run into patent problems.

Benjamin Sklar for The New York Times

Genae Girard, 39, is suing Myriad Genetics and the Patent Office over the granting of a patent on a gene. Myriad also has patented the only test that measures the risk of breast and ovarian cancer.

Ms. Girard took a genetic test to see if her genes also put her at increased risk for ovarian cancer, which might require the removal of her ovaries. The test came back positive, so she wanted a second opinion from another test. But there can be no second opinion. A decision by the government more than 10 years ago allowed a single company, Myriad Genetics, to own the patent on two genes that are closely associated with increased risk for breast cancer and ovarian cancer, and on the testing that measures that risk.

On Tuesday, Ms. Girard, 39, who lives in the Austin, Tex., area, filed a lawsuit against Myriad and the Patent Office, challenging the decision to grant a patent on a gene to Myriad and companies like it. She was joined by four other cancer patients, by professional organizations of pathologists with more than 100,000 members and by several individual pathologists and genetic researchers.

The lawsuit, believed to be the first of its kind, was organized by the American Civil Liberties Union and filed in federal court in New York. It blends patent law, medical science, breast cancer activism and an unusual civil liberties argument in ways that could make it a landmark case.

Companies like Myriad, based in Salt Lake City, have argued that the patent system promotes innovation by giving companies the temporary monopoly that rewards their substantial investment in research and development.

Richard Marsh, Myriad’s general counsel, said company officials would not be able to comment on the lawsuit until they had fully reviewed the complaint.

The coalition of plaintiffs argues that gene patents actually restrict the practice of medicine and new research.

“With a sole provider, there’s mediocrity,” said Wendy K. Chung, the director of clinical genetics at Columbia University and a plaintiff in the case.

Dr. Chung and others involved with the suit do not accuse Myriad of being a poor steward of the information concerning the two genes at issue in the suit, known as BRCA1 and BRCA2, but they argue that BRCA testing would improve if market forces were allowed to work.

Harry Ostrer, director of the human genetics program at the New York University School of Medicine and a plaintiff in the case, said that many laboratories could perform the BRCA tests faster than Myriad, and for less money than the more than $3,000 the company charged.

Laboratories like his, he said, could focus on the mysteries still unsolved in gene variants. But if he tried to offer such services today, he said, he would be risking a patent infringement lawsuit from Myriad.

Christopher A. Hansen, senior national staff counsel for the civil liberties union, said the problem was with the patent office, not the company. He recalled that when he first heard that the office had granted a patent for a gene, “I said that can’t be true.”

As the A.C.L.U. explored the restrictions on competition that companies like Myriad had put in place — blocking alternatives to the patented tests, and even the practice of interpreting or comparing gene sequences that involved those genes — the restrictions started to look like not just a question of patent law, Mr. Hansen said, but of the First Amendment’s guarantee of free speech as well.

“What they have really patented,” he said, “is knowledge.”

A patent was also granted to a single company for genetic testing on long QT syndrome, which can lead to heart arrhythmias and sudden death, and to the HFE gene, linked to hereditary hemochromatosis, a condition in which iron accumulates in the blood and can cause organ damage. Doctors and scientists have complained about both patents.

On the other hand, the company that owns the patent to the gene CFTR, which has been linked to cystic fibrosis, has licensed the testing to dozens of laboratories, drawing praise from the medical world.

The decision to allow gene patents was controversial from the start; patents are normally not granted for products of nature or laws of nature. The companies successfully argued that they had done something that made the genes more than nature’s work: they had isolated and purified the DNA, and thus had patented something they had created — even though it corresponded to the sequence of an actual gene.

The argument may have convinced patent examiners, but it has long been a sore point for many scientists. “You can’t patent my DNA, any more than you can patent my right arm, or patent my blood,” said Jan A. Nowak, president of the Association for Molecular Pathology, a plaintiff in the case.

So far, however, two panels of government experts who have looked at the issue have not found significant impediments to research or medical care caused by gene patents. A 2006 report from the National Research Council found that patented biomedical research “rarely imposes a significant burden for biomedical researchers.”

That report and others, however, warn that the patent landscape “could become considerably more complex and burdensome over time.”

In the future, genetic tests are likely to involve the analysis of many genes at once, or even of a person’s full set of genes. Some 20 percent of the human genome is already included in patent claims, amounting to thousands of individual genes, says a draft report from the National Institutes of Health. The report warns that “it may be difficult for any one developer to obtain all the needed licenses” to develop the next generations of tests.

For Lisbeth Ceriani, a single mother from Newton, Mass., and a plaintiff in the case against Myriad, the biggest obstacle that gene patents present is one of cost. She has had breast cancer and a double mastectomy, but wants to have BRCA testing to determine her risk of ovarian cancer and help her decide whether to have her ovaries removed. But Myriad has refused to work with her insurance plan, Mass Health, and paying for the test herself is beyond her means.

She is reluctant to have surgery that might prove unnecessary, she said, but she also worries about her 8-year-old daughter and the inherited risk she might face. Which is why, Ms. Ceriani said, she wants to “find out if I have the mutation, so I can take the necessary steps to stay on the planet.”

“I want to be here,” she said, “to make sure she does her screening by the time she’s 30.”

One Fish, Two Fish, Fish You Want to Buy, Fish You Never Want to Die

Moral of the story: We all know we are supposed to eat more fish. It is a diet rich is omega-3 fatty acids and low in more harmful fats. Yet at the same time we are constantly reminded of the terrible overfishing going on around the world. This website will help you select the most eco-friendly fish to help keep you healthy.

http://www.edf.org/page.cfm?tagID=1521

The website is easy to use, has recipes and health information along with lists of what fish to eat and which ones to avoid. Highly recommended.

heart-health benefits from a Mediterranean diet

Moral of the story: Time and again the Mediterranean diet is proven to be a healthy eating option. This meta-analysis (aggregates all the previous studies) finalizes the debate, if there ever was one. Time to break out the fish and olives, but remember to eat sustainably, we want everyone to be able to enjoy these health benefits many years from now.

Heartwire: Prevention

Meta-analysis supports heart-health benefits from a Mediterranean diet

April 16, 2009 | Marlene Busko

Hamilton, ON - Strong evidence supports the protective effect of a Mediterranean diet on risk of CHD, and overall diet pattern appears more important than individual foods [1].

These findings, from a review of close to 200 studies, are published in the April 13, 2009 issue of the Archives of Internal Medicine.

"We found strong evidence that a 'Western' diet—which is high in processed meats, red meats, butter, eggs, refined grains, and high-fat dairy products—is associated with an increased risk of CAD, so we could say [to patients]: 'You should consume less of those types of foods and gravitate more toward a "prudent" diet or a Mediterranean diet, which are both high in fruits and vegetables, legumes, whole grains, and fish,' " senior author Dr Sonia Anand (McMaster University, Hamilton, ON) told heartwire.

Although this message is not really new, what is new is the way that this review assessed the strength of the evidence, she noted.

The study also found strong evidence of increased CHD risk from consuming trans-fatty acids and foods with a high glycemic index such as white potatoes, sugar, white rice, and white bread.

Physicians should advise patients: "Lower your trans-fats, lower your saturated fats, but also watch for some of these simple carbohydrates, because they can have adverse effects as well,'' said Anand.

Diet dilemma

The relationship between diet and CHD has been studied for decades, yet there is still some confusion about which foods or diets are best, since cohort studies and randomized controlled trials have often produced discrepant results, the researchers write.

To examine the strength of the evidence supporting a causal link between diet and CHD, the researchers reviewed 146 prospective cohort studies and 43 randomized controlled trials (RCTs).

Studies were scored on how well they met four criteria of strength, consistency, temporality, and coherence. A score of 4 was considered strong evidence of a cause-and-effect relationship between dietary exposure and disease.

Dietary pattern vs single food

In the cohort studies, a Mediterranean diet—characterized by higher intake of vegetables, legumes, fruits, nuts, whole grains, cheese or yogurt, fish, and monounsaturated as opposed to saturated fatty acids—and a "prudent diet"—characterized by high intake of vegetables, fruit, legumes, whole grains, fish, and other seafood—were each associated with significantly lower risk of CHD. Similarly, strong evidence supported the benefits from monounsaturated fatty acids and foods such as vegetables and nuts and the harm from trans-fatty acids and foods with a high glycemic index.

In the RCTs, however, only the Mediterranean diet was strongly linked to risk of CHD.

"Our findings support the strategy of investigating dietary patterns in cohort studies and RCTs for common and chronic complex diseases such as CHD," the researchers write.

Study reinforces heart-healthy diet

Commenting on the results for heartwire, Dr Robert Eckel (University of Colorado, Denver) said that the study confirms previous notions about what a heart-healthy diet is all about.

It's not a matter of good foods and bad foods. It's what the overall quality of the diet is.

"I think cardiologists need to increasingly make lifestyle-related issues an important part of their practice," he added. "This is another article reinforcing that a heart-healthy diet contains certain constituents and avoids certain constituents."

Concurring with the study authors, he noted: "Overall, the dietary pattern is what needs to be emphasized. It's not a matter of good foods and bad foods. It's what the overall quality of the diet is. The Western pattern is high in saturated fat, trans-fat, and cholesterol, whereas a Mediterranean diet and 'prudent' diet include more monounsaturated or polyunsaturated fats, and there is more fish consumption."

No financial disclosures were reported.

Source

1. Mente A, de Koning L, Shannon HS, et al. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 2009; 169:659-669.

Obesity Fact or Fiction?

Moral of the story: There is a ton of information out there about obesity and being overweight. Some of it is misinformation, get the facts below. If you want links to the articles click here.

Nature: Obesity
Factor or Fiction?

FICTION: Children who are tall but heavy will eventually grow into their weight and have a healthier BMI as they age.

The Interaction of Childhood Height and Childhood BMI in the Prediction of Young Adult BMI
Steven D. Stovitz, Mark A. Pereira, Gabriela Vazquez, Leslie A. Lytle and John H. Himes
Obesity advance online publication; July 24, 2008; doi:10.1038/oby.2008.359

FACT: An estimated 17% of children and adolescents ages 2-19 years are overweight*.
*Results from 2003-2004 National Health and Nutrition Examination Survey (NHANES)

School-based Obesity Prevention Programs: An Evidence-based Review
Jonathan A. Kropski, Paul H. Keckley and Gordon L. Jensen
Obesity 16; 1009-1018; doi:10.1038/oby.2008.29

Four-year Follow-up of School-based Intervention on Overweight Children: The KOPS Study
Sandra Plachta-Danielzik, Svenja Pust, Inga Asbeck, Mareike Czerwinski-Mast, Kristina Langnäse, Carina Fischer, Anja Bosy-Westphal, Peter Kriwy and Manfred J. Müller
Obesity 15; 3159-3169; doi:10.1038/oby.2007.376

FACT: Studies have reported that up to 60% of individuals with schizophrenia and 68% of those with bipolar disorder are overweight/obese.

Impact of Obesity on Health-related Quality of Life in Schizophrenia and Bipolar Disorder
Ronette L. Kolotkin, Patricia K. Corey-Lisle, Ross D. Crosby, Jodi M. Swanson, Anne V. Tuomari, Gilbert J. L'Italien and James E. Mitchell
Obesity 16; 749-754; doi:10.1038/oby.2007.133

FICTION: Being overweight has little or no impact on calling in sick to work or school.

Relative Weight and Sickness Absence
Mikko Laaksonen, Kustaa Piha and Sirpa Sarlio-Lähteenkorva
Obesity 15; 465-472; doi:10.1038/oby.2007.55

The Relationship Between Relative Weight and School Attendance Among Elementary Schoolchildren
Andrew B. Geier, Gary D. Foster, Leslie G. Womble, Jackie McLaughlin, Kelley E. Borradaile, Joan Nachmani, Sandy Sherman, Shiriki Kumanyika, Justine Shults
Obesity 15; 2157-2161; doi:10.1038/oby.2007.256

FACT: Moving? Be careful where you settle down - unpacking your belongings in a new location may pack on extra pounds.

Neighborhood Risk Factors for Obesity
Russ P. Lopez
Obesity 15; 2111-2119; doi:10.1038/oby.2007.251

FACT: Lack of seatbelt use can be added to the list of risk factors associated with obesity.

BMI and Seatbelt Use
David G. Schlundt, Nathaniel C. Briggs, Stephania T. Miller, Carlotta M. Arthur and Irwin A. Goldzweig
Obesity 15; 2541-2545; doi:10.1038/oby.2007.303

FICTION: Women in their first year of college have a 48% chance of gaining the "freshman 15."

Freshman 15: Fact or Fiction?
Michelle L. Morrow, Kristiann C. Heesch, Mary K. Dinger, Holly R. Hull, Allen W. Kneehans, David A. Fields
Obesity 14; 1438-1443; doi:10.1038/oby.2006.163

FACT: Listen to your heart. If you're obese, you could be at risk of developing cardiovascular disease and diabetes.

Relationship of Metabolic Risk Factors and Development of Cardiovascular Disease and Diabetes
Steven M. Haffner
Obesity 14; 121S-127S; doi:10.1038/oby.2006.291

Childhood Behavioral Problems Predict Young Adults' BMI and Obesity

Moral of the story: Behavioral problems predict weight gain later in life. Simply be aware of this connection and monitor weight carefully in children with behavioral problems. Make sure they exercise and eat healthy. If you have a diagnosed behavior issue, get on that treadmill!

Epidemiology

Obesity (2009) 17 4, 761–766. doi:10.1038/oby.2008.594

Childhood Behavioral Problems Predict Young Adults' BMI and Obesity: Evidence From a Birth Cohort Study

Abdullah A. Mamun¹, Michael J. O'Callaghan², Susanna M. Cramb¹, Jake M. Najman¹, Gail M. Williams¹ and William Bor³

1. ¹Longitudinal Studies Unit, School of Population Health, University of Queensland, Brisbane, Queensland, Australia
2. ²Child Development and Rehabilitation Services, Mater Children's Hospital, Brisbane, Queensland, Australia
3. ³The Mater Centre for Service Research in Mental Health, Department of Psychiatry, University of Queensland, Brisbane, Queensland, Australia

Correspondence: Abdullah A. Mamun (mamun@sph.uq.edu.au)

Received 21 September 2007; Accepted 2 September 2008; Published online 15 January 2009.

Abstract

We examined whether behavioral problems in childhood and adolescence are associated with young adults' BMI and obesity, and tested whether childhood behavioral problems have a greater impact on young adults' obesity than adolescent behavioral problems. The data were from the Mater-University of Queensland Study of Pregnancy (MUSP) and Its Outcomes, a population-based birth cohort study commenced in Brisbane, Australia, in 1981. A subsample of 2,278 children for whom we had prospective information on their behavioral problems at ages 5 and 14 and measured BMI, and its categories (normal, overweight, and obese) at age 21 was chosen. Young adults who experienced behavioral problems at ages 5 or 14 had a greater average BMI and were more likely to be obese compared to young adults without behavioral problems at both ages. The childhood onset group was at greater risk of becoming obese by age 21 compared to the adolescent onset group (P = 0.04). These associations remained consistent after adjusting for a variety of potential covariates including maternal characteristics (i.e., demographics and life style), child dietary patterns, family meals, television (TV) watching, and participation in sports and exercise at 14 years. Childhood as well as persistent behavioral problems during childhood and adolescence predicts young adults' BMI and obesity. Although further studies are needed to confirm this association, there is a need for close monitoring of children presenting with behavioral problems.

Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates

Moral of the story: Eat less, exercise more. Do not try a new fad diet because it supposedly is the best for losing weight. Pick a diet that will make you eat healthier, less food and you will actually like and adhere to. The type of diet doesn't actually matter for losing weight.

Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates

Frank M. Sacks, M.D., George A. Bray, M.D., Vincent J. Carey, Ph.D., Steven R. Smith, M.D., Donna H. Ryan, M.D., Stephen D. Anton, Ph.D., Katherine McManus, M.S., R.D., Catherine M. Champagne, Ph.D., Louise M. Bishop, M.S., R.D., Nancy Laranjo, B.A., Meryl S. Leboff, M.D., Jennifer C. Rood, Ph.D., Lilian de Jonge, Ph.D., Frank L. Greenway, M.D., Catherine M. Loria, Ph.D., Eva Obarzanek, Ph.D., and Donald A. Williamson, Ph.D.

ABSTRACT

Background The possible advantage for weight loss of a diet that emphasizes protein, fat, or carbohydrates has not been established, and there are few studies that extend beyond 1 year.

Methods We randomly assigned 811 overweight adults to one of four diets; the targeted percentages of energy derived from fat, protein, and carbohydrates in the four diets were 20, 15, and 65%; 20, 25, and 55%; 40, 15, and 45%; and 40, 25, and 35%. The diets consisted of similar foods and met guidelines for cardiovascular health. The participants were offered group and individual instructional sessions for 2 years. The primary outcome was the change in body weight after 2 years in two-by-two factorial comparisons of low fat versus high fat and average protein versus high protein and in the comparison of highest and lowest carbohydrate content.

Results At 6 months, participants assigned to each diet had lost an average of 6 kg, which represented 7% of their initial weight; they began to regain weight after 12 months. By 2 years, weight loss remained similar in those who were assigned to a diet with 15% protein and those assigned to a diet with 25% protein (3.0 and 3.6 kg, respectively); in those assigned to a diet with 20% fat and those assigned to a diet with 40% fat (3.3 kg for both groups); and in those assigned to a diet with 65% carbohydrates and those assigned to a diet with 35% carbohydrates (2.9 and 3.4 kg, respectively) (P>0.20 for all comparisons). Among the 80% of participants who completed the trial, the average weight loss was 4 kg; 14 to 15% of the participants had a reduction of at least 10% of their initial body weight. Satiety, hunger, satisfaction with the diet, and attendance at group sessions were similar for all diets; attendance was strongly associated with weight loss (0.2 kg per session attended). The diets improved lipid-related risk factors and fasting insulin levels.

Conclusions Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize. (ClinicalTrials.gov number, NCT00072995 [ClinicalTrials.gov] .)

NEJM february 26, 2009 vol. 360 no. 9

Depression and antidepressant use linked to sudden cardiac death

Moral of the story: You may want to stay on the antidepressants, but knowing your risks can help you to manage them. Being aware that you are at an increased risk for coronary heart disease means that you can better manage your other risk factors, and should try even harder to manage them. So get to work!

HeartWire - Arrhythmia/EP

Depression and antidepressant use linked to sudden cardiac death

March 9, 2009 | Lisa Nainggolan

New York, NY - A new analysis has found that major depression predicted cardiovascular morbidity and mortality in women participating in the Nurses' Health Study [1]. The hazard ratios were strongest for fatal events and were driven by the association of depression—in particular, antidepressant use—with sudden cardiac death (SCD). Dr William Whang (Columbia University, New York, NY) and colleagues report their findings in the March 17, 2009 issue of the Journal of the American College of Cardiology.

But the authors and accompanying editorialists conclude that, at the present time, the benefits of appropriately prescribed antidepressant use likely outweigh the risk of SCD.

"The absence of proof that antidepressants might cause cardiac events is more relevant than conclusive proof that this effect is absent. Nevertheless, these findings are sufficiently sobering to warrant heightened clinical surveillance and to initiate studies to definitively address this relationship," say Drs Sanjiv M Narayan and Murray B Stein (University of California, San Diego [UCSD]) in an accompanying editorial comment [2].

Whang told heartwire that he believes the biggest clinical implication of this new study "is that management of coronary heart disease risk factors may be especially important among women with depressive symptoms."

Those using antidepressants three times more likely to suffer SCD

Whang et al prospectively studied 63 469 women in the Nurses' Health Study without baseline coronary disease, stroke, or malignancy. They studied depressive symptoms and a proxy variable for clinical depression consisting of severe symptoms and/or antidepressant use and their relationship to cardiovascular events.

Questionnaires in 1992, 1996, and 2000 assessed depressive symptoms, with major depression defined by a validated five-point mental-health-index score (MHI-5) of <53,>

Of the women, 7.9% had MHI-5 scores of <53,>

From 1996 onward, the proxy variable of severe symptoms and/or antidepressant use was most associated with SCD in multivariable models (HR 2.33), and the risk was primarily due to a specific relationship between antidepressant use and SCD (HR 3.34).

Narayan and Stein say the work of Whang et al stands out from previous research of this kind: "[This research] is particularly exciting. The authors should be congratulated for these important data on the etiologic role of depression and its treatment on cardiovascular outcomes in a very large cohort of healthy individuals."

Arrhythmia a possible mechanism, but further study needed

"This surprising results merits scrutiny," the editorialists say. Numerous pharmaceutical agents might contribute to arrhythmic mortality, and in the present study, 61% of subjects were using selective serotonin-reuptake inhibitors (SSRIs), while 39% used other, nonspecified antidepressants.

"Our study raises questions about the mechanism by which depression is associated with sudden cardiac death," Whang told heartwire. "This is not the first study to link risk of SCD to depression. Our study is consistent with prior analyses that have found an association between depressive symptoms and a higher mortality in patients with CHD, and it points to arrhythmia as a possible mechanism for this worse prognosis."

Narayan and Stein say: "It is unclear whether SSRI agents might cause [sudden cardiac arrest]. While cardiac events are well documented with . . . tricyclic antidepressants, evidence for a link with SSRIs is mixed."

"Moreover, it is quite possible that antidepressant use merely indicates that depression is of sufficient severity to merit treatment." It is well established that patients with depression after acute coronary syndrome, for example, are less likely to adhere to their cardiac medication regimens, note the UCSD doctors, although treating the depression improves adherence.

"Clearly, the burden of proof rests on confirming this association. There are abundant data attesting to the safety and efficacy of SSRIs in particular, and a relative paucity showing adverse cardiac effects," they conclude.

Whang et al agree: "Although antidepressant medication use might be a marker of worse depression, its specific association with elevated risk of SCD merits further study."

Twin study shows depression itself independently associated with heart disease Chicago, IL - Separately, new research suggests that depression itself remains a significant contributor to incident heart disease after genetics and environmental, mental, and physical factors are controlled for [3]. The study, performed in 1200 male twins who served in the US military during the Vietnam War, was reported by Dr Jeffrey F Scherrer (Washington University School of Medicine and St Louis Veterans Affairs Medical Center) at the American Psychosomatic Society meeting last week "In this study, we have demonstrated that exposure to depression is contributing to heart disease only in twins who have high genetic risk and who actually develop clinical depression," says Scherrer in a Washington University School of Medicine statement. "In twins with high genetic risk common to depression and heart disease but who never develop depression itself, there was no increased risk for heart disease. The findings strongly suggest that depression itself independently contributes to risk for heart disease," he notes.

Narayan reports receiving speaking honoraria or serving as a consultant for St Jude Medical, Boston Scientific, Medtronic, Biosense-Webster, and Cambridge Heart. Stein receives or has received in the past three years research support from Eli Lilly and GlaxoSmithKline and is currently or in the past three years has been a consultant for BrainCells, Bristol-Myers Squibb, Eli Lilly, EPI-Q, Forest Laboratories, Hoffman La-Roche Pharmaceuticals, Integral Health Decisions, Jazz Pharmaceuticals, Johnson & Johnson, Mindsite, Pfizer, Sanofi-Aventis, Sepracor, Transcept Pharmaceuticals, and Virtual Reality Medical Center.

Sources

1. Whang W, Kubzansky LD, Kawachi I, et al. Depression and risk of sudden cardiac death and coronary heart disease in women. Results from the Nurses' Health Study. J Am Coll Cardiol 2009; 53:950-958
2. Narayan SM and Stein MB. Do depression or antidepressants increase cardiovascular mortality? The absence of proof might be more important than the proof of absence. J Am Coll Cardiol 2009; 53:959-961
3. Dryden J. Depression increases risk for heart disease more than genetics or environment [press release]. March 3, 2009. Available at: http://mednews.wustl.edu/news/page/normal/13643.html?emailID=23300.

Moral of the story: The financial crisis may in fact be an overall positive factor in health care reform. Between the stimulus bill and the need for new funds at a state level there may be some movement here. This article talks about taxing food that are unhealthy while subsidizing healthy foods. This blog wholeheartedly supports such a measure, as long as it is applied towards food groups such as soda and candy and not unhealthy subsitance foods that would unfairly target poor populations that rely on such foods. A soda tax would go a long way towards keeping milk money for milk and budgets in the black.

“Fat taxes” and the financial crisis

The Lancet, Volume 373, Issue 9666, Pages 797 - 798, 7 March 2009

Original Text

Karen McColl

Introducing taxes on junk foods and subsidies for healthy foods has been hotly debated in several countries. Could such moves build healthier populations and economies? Karen McColl reports.

The Governor of New York has proposed a new “soda tax” as part of measures to balance the state's budget following the shortfall caused by the financial crisis. The potential for so-called “fat taxes” on unhealthy foods—or subsidies on healthier foods—to improve public health has been the subject of much debate. Could these economic measures help respond to the financial crisis? There has been much talk about “green solutions” to the economic downturn. Could there be a role for public health solutions too?

In December, 2008, New York's Governor, David Paterson, proposed a new 18% tax on non-diet soft drinks as part of plans to tackle the state's largest ever budget deficit. State policy makers predict that the new tax—which, if approved, would come into force on June 1—would lead to a 5% drop in soft drink consumption and would also raise US$404 million for health-care spending in the first year.

The soft drinks tax is part of a package of proposals to tackle obesity in the state's children. But officials confirm that the projected $14 billion budget shortfall this year—caused by the meltdown in New York's financial services sector—presented a new opening for this type of tax.

The argument that using taxes or subsidies to influence food prices could be a valuable tool in preventing obesity and other diet-related disease in industrialised countries is not new. There has been debate in several countries—including Denmark, France, New Zealand, and the UK—about the possibilities for using taxes or subsidies in this way.

In economic terms, so-called “fat taxes” or “junk food taxes”—like taxes on tobacco or alcohol—make sense. The costs to society resulting from obesity and other diet-related diseases are immense—in terms of health-care costs, sickness absence, welfare payments, and lost tax revenue—and these are not reflected in food pricing. In New York state alone, for example, treatment for obesity-related health problems costs $6·1 billion each year.

Research suggests that, hypothetically, taxes do have considerable potential to influence food choices, change diets, and improve health. In the UK, for example, Oliver Mytton and colleagues modelled three different tax scenarios and concluded that a carefully designed tax could avert up to 3200 deaths from cardiovascular disease each year. A report published in 2007 by the Danish Academy of Technical Sciences concluded that a tax exemption for “healthy” products (including fruit, vegetables, rice, pasta, potatoes, and fish products) combined with a 30% tax increase on “unhealthy” products would bring the Danish population's diet in line with national dietary guidelines. The Academy's report ignited widespread debate and the Danish Government established a new Commission on Disease Prevention, which is due to report on this issue later this month.

But research also highlights that poorly designed measures could have unintended—and even counter-productive—effects. This is because changes in the price of one food product can affect the consumption of other products that are either eaten with or instead of that food. Many foods are related to other food products in this way and it can be difficult to predict these effects. In one of the scenarios tested by Mytton and colleagues, beneficial reductions in saturated fat intakes were partly offset by an increase in salt consumption and decreases in polyunsaturated and monounsaturated fat intakes. They concluded that the taxes proposed under that particular scenario would do more harm than good and called for new taxes to be carefully targeted.

The most controversial aspect of the “fat tax” debate is that any new tax on unhealthy foods is likely to hit poorest groups hardest. A “fat tax” would be regressive—in other words, low-income households would spend a higher proportion of their income on the tax than higher income households. The potential effect of New York's proposed “soda tax” on the state's poorest citizens, for example, has been heavily criticised. “The Governor of New York announced a few weeks ago that he was not going to impose any taxes on the rich. Yet the same governor seems to have no qualms imposing regressive taxes on the African American poor”, said Adam Drewnowski, director of the University of Washington's Center for Obesity Research. “If you look at the map of soft drinks consumption in NYC and the map of poverty you will see that they are—in fact—one and the same.”

AIM: End-of-life discussions drive down treatment costs, improve quality of life

Moral of the story: If you have a terminal illness discuss end-of-life decisions with your physician. You will be thankful in many ways as you will be on the same page as your doctor and painful, intensive treatments may be forgone for more comfortable arrangements.

AIM: End-of-life discussions drive down treatment costs Daily Briefing - The Advisory Board Company 03/11/2009

Terminally ill patients who discussed end-of-life (EOL) care with their physicians had significantly lower health care costs and were more likely to have a better quality of life (QOL) in their final week of life compared with patients who did not have these conversations, according to a study published this week in the Archives of Internal Medicine (AIM). For the study, researchers from the Boston-based Dana-Farber Cancer Institute and colleagues followed a cohort of 627 patients with advanced cancer who were recruited for the longitudinal, multi-institutional Coping With Cancer Study between September 2002 and December 2007. At baseline—on average, six months before death—188 of 603 participants reported they had EOL discussions with their physicians. According to the findings, patients who had these discussions were more likely than their counterparts to acknowledge that they were terminally ill and report a desire to avoid dying in an ICU; patients who had EOL discussions were also less likely to prefer that their physicians take aggressive measures to extend life for a few days. As a result, the cost of care in the final week of life for patients who had discussed EOL goals with physicians averaged 35.7% lower (at an average of $1,876) than the cost of care for patients who did not have an EOL dialogue with their physicians, whose care during their final weeks of life averaged $2,917, according to aggregate costs of care determined using data from the 2004 Nationwide Inpatient Sample. Additionally, higher costs of treatment in the final week of life were not associated with better outcomes; rather, high-cost patients experienced a worse quality of death, as reported by their caregivers. Noting that 30% of annual Medicare expenditures are attributed to the 5% of beneficiaries who die, and that about one-third of the expenditures in the last year of life are spent in the last month—mostly on life-sustaining care—the study’s authors suggest that EOL discussions between patients and providers may be an effective approach to curtailing medical care expenditures while improving patients’ quality of life and death. Specifically, the authors assert that if the “national proportion of individuals reporting EOL discussions” with health care providers increased to 50%, the cost difference between EOL and non-EOL patients could top $76 million nationally, based on the total number of U.S. cancer deaths annually. To that end, the authors support the adoption of strategies to “promote increased communication,” including direct reimbursement for EOL discussions, improved physician education regarding EOL communication, and expansion of hospital palliative care programs. Additionally, the authors suggest that oncologists and palliative care physicians co-manage care of patients with late-stage cancer.

STUDY FINDS END-OF-LIFE COSTS HIGHER AMONG BLACK, HISPANIC PATIENTS

In another study published in AIM, researchers from the Boston University School of Medicine and colleagues analyzed records of of more than 158,000 Medicare beneficiaries who died in 2001, finding that black and Hispanic patients have substantially higher EOL costs than white patients. Specifically, the mean cost of care for white patients averaged $20,166 across the last six months of life, compared with $26,704 for black patients and $31,702 for Hispanic patients. Although the study did not examine the direct cause of treatment cost disparities, the researchers attributed nearly 85% of the higher costs for non-white patients to greater use of ICU care and intensive procedures. According to the CMO of the American Cancer Society, higher utilization of life-extending procedures among minority patients may stem in part from the fact that minority populations are less likely to receive preventive care and establish long-term relationships with physicians (Zhang et al., AIM, 3/9 [subscription required]; Hanchate et al., AIM, 3/9 [subscription required]; Tanner, Associated Press/Los Angeles Times, 3/9; Stern, Reuters, 3/9; Smith, MedPage Today, 3/9).

Large meta-analysis links anger, hostility with CHD risk, particularly in men

Moral of the story: Take 10 deep breaths before you get angry, your heart will thank you later.

Heartwire - Prevention

Large meta-analysis links anger, hostility with CHD risk, particularly in men

March 10, 2009 | Deborah Wormser

London, UK - Anger and hostility were associated with a 19% increase in coronary heart disease (CHD) events in healthy individuals and a 24% increase in risk among those with preexisting CHD, researchers report in the first large, systematic meta-analysis to show significant links between those two mind states and CHD [1].

"The harmful effect of anger and hostility has been widely asserted, but previous reviews have been inconclusive," Dr Yoichi Chida and Dr Andrew Steptoe (both from University College London, UK) write in their review published in the March 17, 2009 issue of the Journal of the American College of Cardiology.

"Intriguingly, the harmful effect of anger and hostility on CHD events in the healthy populations was greater in men than women," the researchers write. In the healthy-population studies, the researchers found a strong association between anger and hostility and CHD in men (HR 1.22, p<0.001),>

"Previous meta-analyses failed to show significant associations of anger and hostility with CHD," Chida told heartwire. Chida added that this report includes several studies published since the last major meta-analytical review.

Chida's review included 21 articles (71 606 individuals) on CHD outcomes in healthy populations and 18 articles (n=8120) of people with preexisting CHD, from studies conducted in Australasia, Europe, and America. Anger and hostility were associated with increased CHD events in the healthy-population studies, with a combined HR of 1.19 (p=0.008), and those emotions were associated with poor prognosis in the population with existing CHD (HR 1.24, p=0.002). In the studies of individuals with baseline CHD, the poor prognosis associated with anger and hostility persisted after researchers fully controlled for basal disease status and treatment, the article states.

Although the body of research investigating the association between anger and hostility and CHD has grown during the past 25 years, several reviews of the literature have produced different findings, possibly because some looked at individual facets of the overall construct, such as hostility alone. Another possible confounder could be the inclusion of cross-sectional, retrospective, and prospective studies in previous reviews, the researchers write in their analysis, which was limited to prospective cohort investigations.

The analysis found that CHD risk appeared to be mediated through high-risk behaviors, with the association between anger/hostility and CHD becoming no longer significant after full adjustment for behavioral factors such as smoking, physical activity, body-mass index, or socioeconomic status.

Small but notable risk

In an accompanying editorial [2], Dr Johan Denollet and Dr Susanne S Pedersen (both from Tilburg University, the Netherlands) point out that while the overall size of the associations between anger and hostility and subsequent CHD reported by Chida et al might seem small, it appears notable when compared with the 11% increased risk associated with von Willebrand factor in the Reykjavik Study [3].

"This meta-analytic review is of high scientific quality and provides us with a reliable estimate of the risk associated with anger/hostility," Denollet told heartwire. "This review has important clinical implications, because it supports the notion that adverse psychological factors do matter in the development and progression of CHD. Moreover, these findings indicate that psychological factors, in this case anger/hostility, start to show their adverse effect after a couple of years, suggesting that these factors are especially of importance in the long run and that more long-term follow-up studies are needed."

Symptoms of anger/hostility should be taken seriously. "Clinicians may consider referring their coronary patients with high levels of anger for behavioral intervention," he said in the interview with heartwire.

Regarding the findings that the association between anger/hostility and CHD appears mediated by lifestyle behaviors and socioeconomic status, Denollet told heartwire, "I think that a number of these unhealthy lifestyles—smoking, overeating—may reflect attempts to downregulate feelings of tension associated with anger/hostility. Socioeconomic status may reflect a vulnerability factor for increased levels of anger/hostility."

One important direction for future research would be the role of emotion-regulation strategies that might moderate the effects of anger and hostility.

"There is some evidence that suppression of anger increases the risk of hypertension and coronary disease and that inhibition of emotion and behavior in general may further increase the risk of stress-related CHD. Future research should more often focus on the interplay between negative emotions and emotion-regulation strategies as a determinant of major coronary events," Denollet said.

"I think we need to be careful to not simply conclude that 'anger is bad for the heart.' After all, anger is a natural emotion that can be very adaptive (eg, as a warning signal), provided that this negative emotion is regulated and used in a socially meaningful and adaptive way," he added.

Chida receives support from the Kanae Foundation for the Promotion of Medical Science and the Medical Research Council. Steptoe receives support from the British Heart Foundation. Denollet and Pedersen report no disclosures.

Sources

1. Chida Y, Steptoe A. The association of anger and hostility with future Coronary Heart Disease. J Am Coll Cardiol 2009; 53:936-946. DOI:10.1016/j.jacc.2008.11.044.
2. Denollet J, Pedersen SS. Anger, depression, and anxiety in cardiac patients. J Am Coll Cardiol 2009; 53:947-9.
3. Danesh J, Wheeler JG, Hirschfield GM, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. New Engl J Med 2004; 350:1387-97.

Very low LDL and normal BP result in slowest progression of atherosclerosis

Moral of the story: 2 thing - Blood Pressure, LDL. Worry about those two things. Get them back to normal and you will go a long way towards preventing heart disease.

Heartwire - Clinical cardiology

Very low LDL and normal BP result in slowest progression of atherosclerosis

March 23, 2009 | Michael O'Riordan

Cleveland, OH - Patients with coronary artery disease (CAD) who reduce LDL cholesterol to very low levels and achieve a normal systolic blood pressure have the slowest progression of coronary atherosclerosis as assessed by intravascular ultrasound (IVUS), a new study has shown [1]. The findings, according to investigators, support the need for intensive management of global risk in patients with CAD.

"What's happened in recent years with the advent of more potent statins and all the education done around that is that getting people to LDL goal is achieved fairly well," senior investigator Dr Steven Nissen (Cleveland Clinic, OH) told heartwire. "But getting people to dual goals is not done well around the country. We wanted to tell people that there really is some pretty good evidence here that if you get your blood pressure down to normal and your LDL down below 70, this is a disease that can not only be halted, but potentially can even regress."

The results of the study are published in the March 24, 2009 issue of the Journal of the American College of Cardiology.

Seven studies rolled into one

To clarify the relationship between LDL cholesterol and systolic blood pressure and their effects on coronary plaque progression, the researchers, led by Dr Adnan Chhatriwalla (Cleveland Clinic) studied 3437 patients with established CAD enrolled in seven clinical trials. The studies included REVERSAL, CAMELOT, ACTIVATE, ASTEROID, ILLUSTRATE, PERISCOPE, and STRADIVARIUS, a group of trials that investigated statins, acyl coenzyme A:cholesterol acyltransferase (ACAT) and cholesteryl ester transfer protein (CETP) inhibitors, rimonabant, ACE inhibitors, and calcium-channel blockers, among others.

Patients were stratified into four groups based on their average on-treatment LDL-cholesterol levels and systolic blood pressure:

• LDL cholesterol <70 mg/dL and systolic blood pressure <120 mm Hg.
• LDL cholesterol <70 mg/dL and systolic blood pressure >120 mm Hg.
• LDL cholesterol >70 mg/dL and systolic blood pressure <120 mm Hg.
• LDL cholesterol >70 mg/dL and systolic blood pressure >120 mmHg.

Changes in atheroma burden were monitored by IVUS, which was measured at baseline and at 18 to 24 months.

Patients with very low LDL-cholesterol levels and normal systolic blood pressure, group 1, had the least progression in percent atheroma volume (PAV) and total atheroma volume (TAV). In addition, these patients also had less frequent atheroma progression and more frequent regression. In patients with systolic blood pressure >120 mm Hg who still had very low LDL cholesterol levels, group 2, less progression of PAV and TAV was also observed.

"It really makes a big difference if you can get both down," said Nissen. "It's a big payoff for patients if physicians are diligent about getting LDL and blood pressure under control."

Among patients with LDL-cholesterol levels >70 mg/dL, normal systolic blood pressure was associated with no greater reduction in PAV or TAV, suggesting that lipid lowering has a larger impact than blood-pressure control on plaque progression, findings supported by recent clinical trials.

The findings challenge current treatment recommendations for hypertension, noted Nissen, and he recommends treating prehypertensive patients with coronary disease, those with pressures of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic. In the CAMELOT study, he points out, the calcium-channel blocker amlodipine decreased the risk of cardiovascular events in patients with CAD and normal blood pressure, as did the ACE inhibitor enalapril, but to a lesser extent.

"Remember that these are all people who have coronary artery disease," said Nissen. "These are not your typical primary-prevention patients with hypertension. They already have atherosclerotic disease in their coronaries. We think the evidence is pretty strong that if you already have plaques in your coronaries, you really to have a lower blood-pressure target. . . . Our IVUS data suggest that there is opportunity here to help patients."

Nissen admitted that the issue needs to be studied further and that the ongoing AQUARIUS study will assess changes in atherosclerotic disease progression with aliskiren (Tekturna, Novartis) when given in addition to standard therapy in CAD patients with prehypertension.

More data still needed

In an editorial accompanying the published study, Drs Jonathan Tobis and Alice Perlowski (University of California, Los Angeles) write that human and animal data make clear that a combination of aggressive lipid and blood-pressure control are necessary for a maximum attenuation of plaque progression, improved endothelial function, and reduced inflammation caused by oxidative stress [2].

Regarding the treatment of prehypertensive patients, Tobis and Perlowski write that a lack of data has contributed to a delayed acceptance of the need for drug therapy. In addition to AQUARIUS, the ongoing SPRINT, which is comparing intensive blood-pressure control (<120>130 mm Hg who have one additional risk factor, will help answer those questions.

The editorialists note that plaque progression/regression on IVUS is helpful in determining whether or not clinicians are helping their patients, but hard clinical end points are still needed, especially as they are shown to correspond with predictions based on the IVUS surrogates. Until then, "conclusions derived from these trials should be considered inferential, to be used as guides for future trials focused on clinical-outcomes measures," they write.

Asked about the polypill, Nissen told heartwire that he was not an initial fan, but with these and other data, he is starting to warm up to it. "The idea of having something that you go and get for $10 for three months that would control your blood pressure and your lipids, this study makes the case that it might make some sense."

New results about a polypill approach for primary prevention, combining a BP-lowering drug, a statin, and aspirin in a single pill, will be presented at the American College of Cardiology 2009 meeting next week.

Nissen reports receiving research support from AstraZeneca, Eli Lilly, Pfizer, Takeda, Sankyo, and Sanofi-Aventis and that he donates honoraria, consulting fees, and other payments directly to charity. Chhattriwalla reports no conflicts.

Sources

1. Chhatriwalla AK, Nicholls SJ, Wang TH, et al. Low levels of low-density lipoprotein cholesterol and blood pressure and progression of coronary atherosclerosis. J Am Coll Cardiol 2009; 53: 1110-1115.
2. Tobis JM, Perlowski A. Atheroma volume by intravascular ultrasound as a surrogate for clinical endpoints. J Am Coll Cardiol 2009; 53: 1116-1118.

Meat Intake and Mortality

Moral of the story: Reducing meat consumption may not be a bad idea. You do not necessarily have to eliminate it from your diet, but maybe you shouldn't have filet mignon 7 days a week. The study shows that those people eating the most red and processed meat were more likely to die than those eating the least amount of red and processed meat. Causes of mortality were cancer and cardiovascular related. This is a gigantic study so trust the results.

Meat Intake and Mortality

A Prospective Study of Over Half a Million People

Rashmi Sinha, PhD; Amanda J. Cross, PhD; Barry I. Graubard, PhD; Michael F. Leitzmann, MD, DrPH; Arthur Schatzkin, MD, DrPH

Arch Intern Med. 2009;169(6):562-571.

Background High intakes of red or processed meat may increase the risk of mortality. Our objective was to determine the relations of red, white, and processed meat intakes to risk for total and cause-specific mortality.

Methods The study population included the National Institutes of Health–AARP (formerly known as the American Association of Retired Persons) Diet and Health Study cohort of half a million people aged 50 to 71 years at baseline. Meat intake was estimated from a food frequency questionnaire administered at baseline. Cox proportional hazards regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) within quintiles of meat intake. The covariates included in the models were age, education, marital status, family history of cancer (yes/no) (cancer mortality only), race, body mass index, 31-level smoking history, physical activity, energy intake, alcohol intake, vitamin supplement use, fruit consumption, vegetable consumption, and menopausal hormone therapy among women. Main outcome measures included total mortality and deaths due to cancer, cardiovascular disease, injuries and sudden deaths, and all other causes.

Results There were 47 976 male deaths and 23 276 female deaths during 10 years of follow-up. Men and women in the highest vs lowest quintile of red (HR, 1.31 [95% CI, 1.27-1.35], and HR, 1.36 [95% CI, 1.30-1.43], respectively) and processed meat (HR, 1.16 [95% CI, 1.12-1.20], and HR, 1.25 [95% CI, 1.20-1.31], respectively) intakes had elevated risks for overall mortality. Regarding cause-specific mortality, men and women had elevated risks for cancer mortality for red (HR, 1.22 [95% CI, 1.16-1.29], and HR, 1.20 [95% CI, 1.12-1.30], respectively) and processed meat (HR, 1.12 [95% CI, 1.06-1.19], and HR, 1.11 [95% CI 1.04-1.19], respectively) intakes. Furthermore, cardiovascular disease risk was elevated for men and women in the highest quintile of red (HR, 1.27 [95% CI, 1.20-1.35], and HR, 1.50 [95% CI, 1.37-1.65], respectively) and processed meat (HR, 1.09 [95% CI, 1.03-1.15], and HR, 1.38 [95% CI, 1.26-1.51], respectively) intakes. When comparing the highest with the lowest quintile of white meat intake, there was an inverse association for total mortality and cancer mortality, as well as all other deaths for both men and women.

Conclusion Red and processed meat intakes were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality.

Author Affiliations: Nutritional Epidemiology Branch (Drs Sinha, Cross, Leitzmann, and Schatzkin) and Biostatistics Branch (Dr Graubard), Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland.

Task force revises aspirin guidelines for heart attack, stroke

Moral of the story: Men between 45 and 79 should likely be taking asprin while women between 55 and 79 should likely be taking apsrin to prevent stroke. Talk to your physician about risk of GI bleeding. Thousands of lives could be saved by following these guidelines.

Task force revises aspirin guidelines for heart attack, stroke

Cardiovascular Business
Wednesday March 18, 2009

The U.S. Preventive Services Task Force has recommended aspirin use for primary prevention of heart attack and stroke in the March 17 issue of the Annals of Internal Medicine, citing its improved specificity over previous guidelines.

The task force found that men between the ages of 45 and 79 should use aspirin to reduce their risk for heart attacks when the benefits outweigh the harms for potential gastrointestinal bleeding. Women between the ages of 55 and 79 should use aspirin to reduce their risk for ischemic stroke when the benefits outweigh the harms for potential gastrointestinal bleeding.

However, the task force was against the use of aspirin for stroke prevention in women younger than 55 years and for MI prevention in men younger than 45 years.

"The task force has taken positive steps to lend clarity to patients and physicians about the value of aspirin for prevention of cardiovascular events," said American College of Preventive Medicine (ACPM) President Mark B. Johnson, MD. "The new guidelines make it clear that physicians, as a matter of routine practice, should be discussing the pros and cons of daily aspirin use with patients in the target groups."

An ACPM-sponsored survey published in the May 2007 edition of the American Journal of Preventive Medicine found a conversation between the patient and physician to be the strongest predictor of appropriate aspirin use, and that only about one in three patients who are at high risk are actually taking daily aspirin. A separate study by the Partnership for Prevention found that 45,000 lives could be saved each year if 90 percent of the target population took a low-dose aspirin every day. The studies led the American Medical Association (AMA) to adopt a policy to increase education among physicians on the importance of appropriate aspirin counseling.

With the release, the UPSTF updates its aspirin recommendations from 2002, which called on clinicians to discuss aspirin use for primary prevention with adults who are at increased risk for cardiovascular disease. The new USPSTF findings actually recommend aspirin use where benefits outweigh the harms, and further define the appropriate age and gender groupings for which aspirin is indicated.

"We think the new guidelines provide another tool in the armamentarium of the physician and the patient for assuring that a discussion about cardiovascular risk and potential aspirin use routinely takes place in the clinical setting," said David Shih, MD, senior director of medical affairs at ACPM.
Last Updated ( Thursday, March 19 2009 )

Moral of the story: Religious individuals live a little longer but incur a greater cost, both in terms of quality of life in the final days and the number of greenbacks the use trying to get those last extra few days. Should taxpayers be spending so much money on such aggressive care?

Religious Belief Linked to Desire for Aggressive Treatment in Terminal Patients

By RONI CARYN RABIN

Published: March 17, 2009 - NYTimes

Terminally ill cancer patients who drew comfort from religion were far more likely to seek aggressive, life-prolonging care in the week before they died than were less religious patients and far more likely to want doctors to do everything possible to keep them alive, a study has found.

The patients who were devout were three times as likely as less religious ones to be put on a mechanical ventilator to maintain breathing during the last week of life, and they were less likely to do any advance care planning, like signing a do-not-resuscitate order, preparing a living will or creating a health care proxy, the analysis found.

The study is to be published Wednesday in The Journal of the American Medical Association.

“People think that spiritual patients are more likely to say their lives are in God’s hands — ’Let what happens happen’ — but in fact we know they want more aggressive care,” said Holly G. Prigerson, the study’s senior author and director of the Center for Psychosocial Oncology and Palliative Care Research at the Dana-Farber Cancer Institute in Boston.

“To religious people, life is sacred and sanctified,” Dr. Prigerson said, “and there’s a sense they feel it’s their duty and obligation to stay alive as long as possible.”

Aggressive life-prolonging care comes at a cost, however, in terms of both dollars and human suffering. Medicare, the government’s health plan for the elderly, spends about one-third of its budget on people who are in the last year of life, and much of that on patients at the very end of life.

Aggressive end-of-life care can lead to a more painful process of dying, researchers have found, and greater shock and grief for the family members left behind.

The new study used both a questionnaire and interviews to assess the level of reliance on religious faith for comfort among 345 patients with advanced cancer. The patients, most of them belonging to Christian denominations, were followed until they died, about four months on average.

A vast majority of patients, religious or not, did not want heroic measures taken. Still, 11.3 percent of the most religious patients received mechanical ventilation during the last week of life, compared with only 3.6 percent of the least religious.

The most religious patients were also more likely than less religious ones to be resuscitated in the last week of life and to be treated in an intensive-care unit as they died, although those differences may have been due to chance.

“Doctors don’t always acknowledge, and I’m pretty sure patients are telling us, that God is really important in their lives,” said Dr. Gerard Silvestri, a cancer specialist at the Medical University of South Carolina in Charleston, S.C., who has studied end-of-life decision making.

A study by Dr. Silvestri in 2003 found that while cancer patients listed their oncologist’s recommendation as the most influential factor affecting their decisions about medical care, their faith in God was the second-most-influential factor, ranking higher than the recommendations of their family doctors, their spouses and children, and even information about whether treatment would cure the disease.

Moral of the story: Finally there is data to back up the uselessness of the PSA test. Do not bother with this! They haven't used it for years in Europe.

Prostate Cancer Test Found to Save Few Lives

By GINA KOLATA

Published: March 18, 2009- NYTimes

The PSA blood test — the screening test for prostate cancer — saves few if any lives and exposes large numbers of men to risky and unnecessary treatment, two large and rigorous studies have found.

The findings raise new questions about the rapid and widespread adoption of the test, which measures a protein released by prostate cells. It was introduced in 1987 and quickly became a routine part of preventive health care. Experts debated its value, basing their views on data that often involved statistical modeling and inferences.

Now, with the new data, cancer experts said men should carefully consider the test’s risks and benefits before deciding to be screened. Some may decide not to be screened at all.

The studies, said Dr. Otis Brawley, the chief medical officer at the American Cancer Society, are “some of the most important studies in the history of men’s health.”

For years, the cancer society has urged men to be informed before deciding to have a PSA test. “Now we actually have something to inform them with,” he said. “We’ve got numbers.”

Dr. H. Gilbert Welch, a professor of medicine at Dartmouth who studies cancer screening, also welcomed the new data. “We’ve been waiting years for this,” he said. “It’s a shame we didn’t have it 20 years ago.”

Both reports were published online on Wednesday by The New England Journal of Medicine. One involved 182,000 men in seven European countries; the other, by the National Cancer Institute, involved nearly 77,000 men at 10 medical centers in the United States.

In both, participants were randomly assigned to be screened — or not — with the PSA test, whose initials stand for prostate-specific antigen. In each study, the two groups were followed for more than a decade while researchers counted deaths from prostate cancer, asking whether screening made a difference.

The European data involved a consortium of studies with different designs. Taken together, the studies found that screening was associated with a 20 percent relative reduction in the prostate cancer death rate. But the number of lives saved was small — seven fewer prostate cancer deaths for every 10,000 men screened and followed for nine years.

The American study, which had a single design, found no reduction in deaths from prostate cancer after most of the men had been followed for 10 years. Every man has been followed for at least seven years, said Dr. Barnett Kramer, a study co-author at the National Institutes of Health. By seven years, the death rate was 13 percent lower for the unscreened group.

The European study saw no benefit of screening in the first seven years of follow-up.

The reason screening saved so few lives, cancer experts say, is that prostate cancers often grow very slowly, if at all, and most never endanger a man if left alone. But when doctors find an early-stage prostate tumor, they cannot tell with confidence whether it will be dangerous so they usually treat all early cancers as if they were life-threatening.

As a result, the majority of men, whose early-stage cancers would not harm them, suffer serious effects of cancer therapy but get no benefit. Others, with very aggressive tumors, may not be helped by screening because their cancer has spread by the time it is detected.

Prostate cancer is not the only one that is hard to stop with screening. If the European study is correct, mammography has about the same benefit as the PSA test, said Dr. Michael B. Barry, a prostate cancer researcher at Massachusetts General Hospital who wrote an editorial accompanying the papers. But prostate cancers often are less dangerous than breast cancers, so screening and subsequent therapy can result in more harm.

In the European study, 48 men were told they had prostate cancer, and needlessly treated for it, for every man whose death was prevented. With mammography, about 10 women receive a diagnosis and needless treatment for breast cancer to prevent one death.

Dr. Peter B. Bach, a physician and epidemiologist at Memorial Sloan-Kettering Cancer Center, says one way to think of the data is to suppose he has a PSA test today. It leads to a biopsy that reveals he has prostate cancer, and he is treated for it. There is a one in 50 chance that, in 2019 or later, he will be spared death from a cancer that would otherwise have killed him. And there is a 49 in 50 chance that he will have been treated unnecessarily for a cancer that was never a threat to his life or health.

Prostate cancer treatment can result in impotence and incontinence when surgery is used to destroy the prostate, and painful defecation or chronic diarrhea when the treatment is radiation.

When the American and European studies began, in the early 1990s, PSA testing was well under way in the United States, and many expected that the screening test would make the prostate cancer death rate plummet by 50 percent or more. Dr. Brawley was at the cancer institute then, though not directly involved with its prostate cancer screening study. But he saw the reactions.

Some urologists said the study was unethical, because some people would not be screened, and demanded it be shut down, he said. One group of black urologists encouraged black men not to participate because blacks have a greater risk of prostate cancer and it seemed obvious they should be screened.

Some thought that they would see fewer cancer deaths among the screened men as quickly as five years. But as the studies continued, it became clear that screening would not have a large, immediate effect — if it did, the studies would have been stopped and victory declared. Cancer researchers began turning to less rigorous sources of data, with some arguing that screening was preventing prostate cancer deaths and others arguing it was not.

In the United States, many men and their doctors have made up their minds — most men over age 50 have already been screened, and each year more than 180,000 receive a diagnosis of prostate cancer. In Europe, said Dr. Fritz H. Schröder of Erasmus University, the lead author of the European study, most men are not screened. “The mentality of Europeans is different,” he said, and screening is not so highly promoted.

The publication, of data from the two studies should change the discussion, said Dr. David Ransohoff, an internist and cancer epidemiologist at the University of North Carolina.

“This is not relying on modeling anymore,” Dr. Ransohoff said. “This is not some abstract, pointy-headed exercise. This is the real world and this is real data.”

Both studies will continue to follow the men. It remains possible that the United States study will eventually find that screening can reduce the prostate cancer death rate, researchers say, or that both studies will conclude that there is no real reduction.

In the meantime, Dr. Brawley said, “I certainly think there’s information here that’s food for thought.”

The benefits of prostate cancer screening, he said, are “modest at best and with a greater downside than any other cancer we screen for.”

Web Link

Mortality Results from a Randomized Prostate-Cancer Screening Trial (The New England Journal of Medicine)

Screening and Prostate-Cancer Mortality in a Randomized European Study (The New England Journal of Medicine)

Metabolic disorders linked to cognitive decline

Moral of the story: Manage your chronic diseases! Stay on top of treatment, exercise and see your doctor. The last thing you want on top of diabetes is Alzheimer's disease.

Metabolic disorders linked to cognitive decline
March 17, 2009 Allison Gandey
Edited from Medscape Medical News—a professional news service of WebMD

New York, NY and Seattle, WA - Evidence is mounting that metabolic and neurological diseases share common risk factors, according to two studies in the March 2009 issue of the Archives of Neurology.
"Preventing heart disease, stroke, and diabetes—or making sure these conditions are well managed in patients diagnosed with them—can potentially slow the disease progression of Alzheimer's," senior author on one of the studies, Dr Yaakov Stern (Columbia University, New York), said in a news release. Stern et al, led by Dr Elizabeth Helzner (Columbia University) hypothesized that vascular factors such as heart disease, stroke, diabetes, hypertension, smoking, and blood lipid levels may predict the progression of Alzheimer's disease [1]. The group studied 156 patients followed for a mean of 3.5 years. Participants were from the Washington Heights and Inwood Columbia Aging Project, a multiethnic, community-based, prospective study of aging in northern Manhattan.
Researchers found that patients with a history of diabetes and elevated levels of cholesterol, especially LDL cholesterol, had faster cognitive decline. In fact, each 10-U increase in cholesterol and LDL cholesterol was associated with a 0.10-standard-deviation decrease in cognitive score per year of follow-up (p<0.001 for total cholesterol; p=0.001 for LDL cholesterol).
Investigators found that a history of heart disease and stroke were associated with cognitive decline only in carriers of the APOE e4 allele.
"These findings indicate that controlling vascular conditions may be one way to delay the course of Alzheimer's, which would be a major development in the treatment of this devastating disease," Stern said.Fluctuations in weight may boost dementia risk
In the second study published in the same issue of the Archives of Neurology, investigators show that obese middle-aged adults and underweight elderly people have an increased dementia risk [2].
Using data from the Cardiovascular Health Study, researchers studied the body-mass index (BMI) of participants at mid- and late life. Patients were from a community-dwelling sample at four US sites.
Investigators included 2798 people. Of these, 480 had incident dementia, 245 had Alzheimer's disease, and 213 had vascular dementia.
They found that middle-aged patients who were obese had an increased risk for dementia (BMI >30 vs normal-weight BMI 20 to 25), adjusted for demographics (hazard ratio 1.39; 95% CI 1.03-1.87), although this observation was weakened after adjustment for cardiovascular risk factors (hazard ratio 1.36; 95% CI 0.94-1.95).
These results help explain the 'obesity paradox.'
But the risk estimates were reversed in assessments of late-life BMI. Underweight people, those with a BMI of less than 20, had an increased risk for dementia (hazard ratio 1.62; 95% CI 1.02-2.64). Surprisingly, being overweight later in life was not associated with an increased risk (hazard ratio 0.92; 95% CI 0.72-1.18), and being obese reduced the risk for dementia (hazard ratio 0.63; 95% CI 0.44-0.91).
"These results help explain the 'obesity paradox,' " the researchers, led by Dr Annette Fitzpatrick (University of Washington, Seattle), write. "Differences in dementia risk across time are consistent with physical changes in the trajectory toward disability."
These findings suggest that the predictive ability of BMI changes across time, they note
"Weight loss occurs with comorbidities at older ages and is often reflective of poor health," write Fitzpatrick and her team. "Weight loss, along with psychological, behavioral, and mobility problems, is one of the principal manifestations of Alzheimer's disease. Weight loss may predate dementia onset by as much as 10 years."
The researchers conclude: "These results reinforce the necessity of monitoring weight loss closely in older adults."
The complete contents of Medscape Medical News, a professional news service of WebMD, can be found at www.medscape.com, a website for medical professionals.
Sources
Helzner EP, Luchsinger JA, Scarmeas N, et al. Contribution of vascular risk factors to the progression in Alzheimer disease. Arch Neurol 2009; 66:343-348.
Fitzpatrick AL, Kuller LH, Lopez OL, Midlife and late-life obesity and the risk of dementia: cardiovascular health study. Arch Neurol 2009; 66:336-342.
Related links
Adherence to Mediterranean diet reduces risk of major chronic diseases [Prevention > Prevention; Sep 12, 2008]
Heart disease linked to poor cognitive function in middle age [Brain/Kidney/Peripheral > Brain/Kidney/Peripheral; Jul 23, 2008]
Low HDL-C associated with poor memory [HeartWire > Brain/Kidney/Peripheral; Jun 30, 2008]
High cholesterol linked to increased AD risk [HeartWire > Medscape Medical News; Nov 06, 2006]
Low cholesterol linked to reduced cognitive function [HeartWire > News; Mar 23, 2005]
Lipid metabolism abnormalities observed in brain aging and Alzheimer's disease [HeartWire > News; Feb 15, 2004]