<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_446"
                     title="Proteins Linked to Stress-Induced ACS (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/tb/18373?impressionId=1265786391074"
                     
      The heart-pounding excitement of Sunday&apos;s Super Bowl football game might have sent some fans to hospital with acute coronary syndrome.&lt;br&gt;
&lt;br&gt;But researchers in Germany say it may be possible to distinguish these cases from people whose coronary syndrome wasn&apos;t stress-related.&lt;br&gt;
&lt;br&gt;Two proteins known as endothelin-1 (ET-1) and &lt;span&gt;monocyte&lt;/span&gt; chemoattractant protein-1 (MCP-1) appear to be highly sensitive and specific markers of excitement-induced acute coronary syndromes, according to Ute Wilbert-Lampen, MD, and colleagues at Ludwig-Maximilians-Universit&amp;#228;t in Munich.&lt;/p&gt;
&lt;p&gt;In a cohort study, the two compounds were markedly elevated in people whose coronary syndromes were associated with excitement and stress over World Cup soccer games, the researchers reported in the Feb. 16 issue of the &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;And the protein levels were significantly higher than in either healthy controls or a group of matched patients whose coronary syndrome was not associated with the soccer matches, the researchers said.&lt;/p&gt;
&lt;p&gt;Wilbert-Lampen and colleagues reported in 2008 that they had found 2.7-fold spike in the incidence of acute cardiovascular events in association with the 2006 World Cup soccer matches. (See &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Atherosclerosis/8171&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Atherosclerosis/8171&quot; target=&quot;_blank&quot;&gt;Cardiovascular Events Spike During Critical World Cup Soccer Matches&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;Although excitement and stress caused the events, exactly how remained unclear, they reported in the journal.&lt;/p&gt;
&lt;p&gt;To help clarify the issue, they looked at 58 representative patients from the earlier analysis for whom blood samples were available. They were compared with the same number of healthy controls and 58 reference patients with acute coronary syndromes&lt;strong&gt; &lt;/strong&gt;who reported no emotional involvement with the World Cup.&lt;/p&gt;
&lt;p&gt;In addition to ET-1 and MCP-1, blood samples were tested for a range of substances, including soluble CD40L (sCD40L), soluble vascular cell adhesion molecule-1 (sVCAM-1), tumor necrosis factor-&amp;#945; (TNF-&amp;#945;), high-sensitivity C-reactive protein (hsCRP), and regulated on activation, normal T-cell expressed and secreted (RANTES).&lt;/p&gt;
&lt;p&gt;The researchers found: &lt;ul&gt; &lt;li&gt;The study group had average ET-1 levels of 4.0 picograms per milliliter, compared with 2.0 for the reference patients and 1.1 for the health controls. Both between-group differences were significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001.&lt;/li&gt; &lt;li&gt;A similar pattern was seen for MCP1 and TNF-&amp;#945;.&lt;/li&gt; &lt;li&gt;The other markers  --  sVCAM-1, hsCRP, and RANTES -- yielded less clear results.&lt;/li&gt; &lt;li&gt;In both groups of patients, ET-1 was significantly correlated (at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) with sCD40L and with MCP-1, but other markers were correlated with one or the other or neither.&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;In a receiver operating curve analysis, ET-1 and MCP-1 were found to have diagnostic potential, the researchers said, with the areas under the curve being 0.99 and 0.98, respectively.&lt;/p&gt;
&lt;p&gt;In such an analysis, an area under the curve of 1.0 would mean the proposed diagnostic tool would be completely accurate, without either false positives or false negatives.&lt;/p&gt;
&lt;p&gt;Using a cutoff of 3.1 picograms per milliliter, ET-1 had a sensitivity of 100% and a specificity of 96.6%, the researchers said, while a cutoff of 396 picograms per milliliter for MCP-1 resulted in 93.1% sensitivity and 93.1% specificity.&lt;/p&gt;
&lt;p&gt;One implication of the findings, the researchers said, is that it may be valuable to begin developing prophylactic and therapeutic drugs targeting ET-1.&lt;/p&gt;
&lt;p&gt;They noted that because of the design of the original study, a range of information was not available, including data on troponin or stress-hormone levels, cardiovascular risk factors, infarct size, or clinical outcome.&lt;/p&gt;
&lt;p&gt;Despite those gaps, the study has &quot;some exciting features,&quot; according to Karina Davidson, PhD, of Columbia University College of Physicians and Surgeons in New York City.&lt;/p&gt;
&lt;p&gt;Among other things, she wrote in an accompanying editorial, the study provides &quot;evidence for the importance&quot; of ET-1 in stress-induced ischemic syndromes.&lt;/p&gt;
&lt;p&gt;It may now be possible, she argued, to identify what other factors come into play and eventually to determine who is at risk for such events.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by Else Kr&amp;#246;ner-Fresenius Stiftung. The researchers did not report potential conflicts.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_411"
                     title="Older Women with Gout at Risk of MI (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Cardiology/MyocardialInfarction/tb/18319?impressionId=1265786391074"
                     
      &lt;p&gt;Elderly women with gout are at increased risk of acute myocardial infarction (MI), even more so than men with this painful arthritis, a population-based study found.&lt;/p&gt;
&lt;p&gt;After adjusting for age, comorbidities such as hypertension and diabetes, and prescription drug use, the relative risk of MI among women ages 65 and older was 1.39 (95% CI 1.20 to 1.61), according to Mary A. De Vera of the Arthritis Research Centre of Canada in Vancouver, and colleagues.&lt;/p&gt;
&lt;p&gt;In comparison, the multivariate relative risk among men was 1.11 (95% CI 0.99 to 1.23, &lt;em&gt;P&lt;/em&gt;=0.003 for interaction), the researchers reported online in the &lt;em&gt;Annals of the Rheumatic Diseases&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Men with gout are known to be at higher risk for coronary heart disease and acute MI, but corresponding data for women were sparse.&lt;/p&gt;
&lt;p&gt;So De Vera and colleagues conducted a cohort study using the British Columbia Linked Health Database, comparing the incidence rates of MI between 9,642 patients with gout and 48,210 matched controls with no history of ischemic heart disease.&lt;/p&gt;
&lt;p&gt;A total of 3,890 of the cases were women, as were 19,450 of the controls.&lt;/p&gt;
&lt;p&gt;The gout incidence rate in women ages 65 to 85 years was 2.5 per 1,000 person-years, and 2.9 per 1,000 person-years in those ages 85 and higher.&lt;/p&gt;
&lt;p&gt;The rates in men of the corresponding ages were 5.7 and 6.5 per 1,000 person-years.&lt;/p&gt;
&lt;p&gt;Hospital records indicated that the incidence rates of acute MI among women and men were 6.7 and 10.7 per 1,000 person-years, respectively.&lt;/p&gt;
&lt;p&gt;During a median of seven years&apos; follow-up there were 3,268 incident cases of MI, including 996 in women.&lt;/p&gt;
&lt;p&gt;In unadjusted analysis, the relative risk of acute MI among women with gout was 1.67 (95% CI 1.45 to 1.93), while that for men with gout was 1.19 (95% CI 1.07 to 1.32).&lt;/p&gt;
&lt;p&gt;Multivariate analysis determined that the relative risk for nonfatal MI in women was 1.41 (95% CI 1.19 to 1.67), while that in men was 1.11 (95% CI 0.98 to 1.25, &lt;em&gt;P&lt;/em&gt;=0.005 for interaction).&lt;/p&gt;
&lt;p&gt;The gender difference did not show up in fatal events, however. The relative risk for fatal MI was 1.33 in women (95% CI 0.99 to 1.78) and 1.10 in men (95% CI 0.88 to 1.38, &lt;em&gt;P&lt;/em&gt;=0.30 for interaction).&lt;/p&gt;
&lt;p&gt;Overall, there was a 39% increased risk for MI among women with gout, an association that was independent of age, comorbidities, and use of prescription drugs including nonsteroidal anti-inflammatories, diuretics, statins, anticoagulants, and aspirin.&lt;/p&gt;
&lt;p&gt;The association was significantly stronger than for men, according to the researchers.&lt;/p&gt;
&lt;p&gt;These gender differences may relate to serum uric acid levels and metabolism. Levels in men are about 1 mg/dL higher, although levels do rise in women at menopause.&lt;/p&gt;
&lt;p&gt;&quot;Thus, the relative physiological impact of having gout or a certain level of hyperuricemia may be stronger among women than men,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;Possible mechanisms for the contribution of hyperuricemia to cardiovascular disease include vascular smooth muscle cell proliferation and inflammation, as well as platelet adhesiveness and aggregation.&lt;/p&gt;
&lt;p&gt;&quot;Inflammation associated with gout may also have a role in potential mechanisms, including promotion of atherogenesis and thrombogenesis, similar to other inflammatory arthritides associated with cardiovascular disease,&quot; the investigators noted.&lt;/p&gt;
&lt;p&gt;A strength of the study was its population-based design, which makes its findings generalizable. Limitations include the potential for misclassification of diagnosis because of the use of diagnostic codes, and the inability to adjust for lifestyle factors such as smoking.&lt;/p&gt;
&lt;p&gt;Nonetheless, according to the investigators, &quot;These findings provide support for the aggressive management of cardiovascular risk factors for male and female patients with gout.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was partly funded by the National Institute of Health.&lt;/p&gt;&lt;p&gt;The authors have received support from the Canadian Arthritis Network/The Arthritis Society, and one disclosed receiving research funding and honoraria from TAP Pharmaceuticals and Savient.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_348"
                     title="No Rebound Seen After Antiplatelet Withdrawal (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Cardiology/PCI/tb/18226?impressionId=1265786391074"
                     
      &lt;p&gt;No evidence of a platelet aggregation rebound occurs with abrupt discontinuation of clopidogrel (Plavix) in patients undergoing percutaneous coronary intervention (PCI), investigators in a randomized clinical trial concluded.&lt;/p&gt;
&lt;p&gt;Values for adenosine diphosphate (ADP)-induced platelet aggregation did not differ significantly between patients whose clopidogrel therapy was withdrawn abruptly and those in whom clopidogrel was tapered before discontinuation, they wrote in an article in the Feb. 9 issue of the &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The findings also showed that tapering of clopidogrel does not lead to lower platelet aggregation values after clopidogrel withdrawal, according to Dirk Sibbing, MD, of Technical University Munich in Germany, and colleagues&lt;em&gt;&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;The time course of platelet aggregation values  --  regardless of the device, the agonist, or the agonist concentration used  --  after clopidogrel cessation provides no evidence for the existence of a rebound phenomenon of platelets after discontinuing clopidogrel,&quot; they wrote in conclusion.&lt;/p&gt;
&lt;p&gt;For patients undergoing PCI, dual antiplatelet therapy with aspirin and clopidogrel has become the mainstay for prevention of thrombotic events. Lifelong aspirin therapy is recommended for patients after PCI, but clinical guidelines recommend discontinuation of clopidogrel after six or 12 months. The standard practice is to withdraw clopidogrel abruptly, the authors noted.&lt;/p&gt;
&lt;p&gt;Recent studies have shown a clustering of thrombotic events in the first few weeks after discontinuation of long-term clopidogrel therapy. The observations have led to the hypothesis of a rebound phenomenon of platelet aggregation. However, the hypothesis had not been examined specifically within the context of clopidogrel withdrawal.&lt;/p&gt;
&lt;p&gt;&quot;Because different studies have demonstrated that insufficient suppression of platelet reactivity to ADP is associated with an increased risk of thrombotic events after coronary stent placement, the observed clustering of adverse events reported in clinical studies might be related to an intermittent status of platelet hyperreactivity or so-called platelet rebound with very high ADP-induced platelet aggregation levels,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;A tapering of clopidogrel treatment over a certain period of time before stopping the intake of the drug completely might provide a beneficial treatment strategy to attenuate this supposed rebound phenomenon of platelets.&quot;&lt;/p&gt;
&lt;p&gt;Sibbing and colleagues designed a randomized clinical trial to determine whether a rebound phenomenon exists after discontinuation of clopidogrel and whether the rebound can be attenuated by a clopidogrel-tapering regimen.&lt;/p&gt;
&lt;p&gt;The investigators enrolled 69 patients receiving clopidogrel in association with PCI procedures. In all cases, discontinuation of clopidogrel was planned.&lt;/p&gt;
&lt;p&gt;The patients were randomized to two strategies of discontinuation: tapering of the clopidogrel dose over four weeks, followed by discontinuation; or treatment for four weeks, as planned, followed by abrupt discontinuation.&lt;/p&gt;
&lt;p&gt;Investigators assessed platelet aggregation at enrollment and during weeks two through eight after randomization. Aggregation was assessed simultaneously by light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA).&lt;/p&gt;
&lt;p&gt;The primary endpoint was the highest rate of ADP-induced platelet aggregation by LTA in weeks five through eight after clopidogrel withdrawal.&lt;/p&gt;
&lt;p&gt;Platelet aggregation by LTA peaked at 73% in the group that had clopidogrel abruptly withdrawn and at 69.3% in the tapering group, resulting in a nonsignificant difference (&lt;em&gt;P&lt;/em&gt;=0.21). The between-group values did not differ across the range of ADP concentrations used (1.25 to 20 &amp;#181;mol/L).&lt;/p&gt;
&lt;p&gt;Results by MEA were similar: The peak aggregation value associated with abrupt withdrawal was 925 AU x min compared with 890 AU x min with clopidogrel tapering (&lt;em&gt;P&lt;/em&gt;=0.55).&lt;/p&gt;
&lt;p&gt;Studies with different agonists of platelet aggregation also yielded similar results in the two patient groups.&lt;/p&gt;
&lt;p&gt;Despite finding no difference between the two strategies for clopidogrel withdrawal, the authors did not rule out the possibility of a beneficial effect of tapering clopidogrel.&lt;/p&gt;
&lt;p&gt;&quot;It could be hypothesized that, apart from the maximal values of platelet aggregation observed, a more gradual increase of platelet aggregation values achieved by a clopidogrel-tapering regimen is beneficial for the reduction of thrombotic events,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;In fact, we observed a relatively rapid increase of platelet aggregation values in the [abrupt withdrawal] group of patients in our study. Whether this rapid increase might be disadvantageous in case of stopping clopidogrel treatment remains uncertain.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by Cordis, Medtronic, and Dynabyte.&lt;/p&gt;&lt;p&gt;Sibbing disclosed relationships with Dynabyte and Eli Lilly.&lt;/p&gt;&lt;p&gt;Co-author Adnan Kastrati disclosed relationships with Eli Lilly, sanofi-aventis, and Bristol-Myers Squibb.&lt;/p&gt;&lt;p&gt;Co-author Nicolas von Beckerath disclosed relationships with Eli Lilly and sanofi-aventis.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_361"
                     title="Hidden Dangers of Herbal Meds Reviewed"
                     score="0.009"
                     href="http://www.medpagetoday.com/PrimaryCare/AlternativeMedicine/tb/18244?impressionId=1265786391074"
                     
      Herbal medicines are not always the harmless nostrums that many patients and even some physicians think, but may actually contribute to cardiovascular morbidity and mortality, researchers warned in a review covering 44 years of research into the subject.&lt;br&gt;
&lt;br&gt;Many such products, including aloe vera, ginkgo biloba, ginseng, and green tea, can interact with conventional cardiovascular drugs and lead to serious adverse reactions, according to Arshad Jahangir, MD, of the Mayo Clinic in Scottsdale, Ariz., and two other Mayo physicians.&lt;br&gt;
&lt;br&gt;&quot;There is a clear need for better public and physician understanding of herbal products through health education, early detection and management of herbal toxicities, scientific scrutiny of their use, and research on their safety and effectiveness,&quot; they wrote in the Feb. 9 &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Jahangir and colleagues also called for increased regulation of such products, at least requiring manufacturers of herbal medicines to register with the FDA and provide evidence of good manufacturing practices.&lt;/p&gt;
&lt;p&gt;&quot;Some of these adverse drug reactions are preventable,&quot; Jahangir told &lt;em&gt;MedPage Today&lt;/em&gt; in a telephone interview. &quot;Simple things like taking a good history or giving that history and discussing these issues, probably we can avoid [such reactions].&quot;&lt;/p&gt;
&lt;p&gt;Other physicians contacted by &lt;em&gt;MedPage Today&lt;/em&gt; and ABC News agreed that the growth in popularity of herbal medicines poses problems for physicians and patients.&lt;/p&gt;
&lt;p&gt;&quot;Because these remedies are &apos;natural,&apos; their potential dangers are not considered the same way they would be if they were medication,&quot; commented Suzanne Steinbaum, MD, a cardiologist at Lenox Hill Hospital in New York City, in an e-mail.&lt;/p&gt;
&lt;p&gt;&quot;For many reasons, patients tend not to disclose to their doctors if they are taking herbal remedies, including fear that their doctors won&apos;t approve or they will be told to stop them,&quot; Steinbaum added. &quot;This lack of knowledge and full-disclosure, for some, might be a fatal omission.&quot;&lt;/p&gt;
&lt;p&gt;Jahangir and colleagues reviewed nearly 90 publications that have addressed herbal or complementary therapies and cardiovascular effects since 1966.&lt;/p&gt;
&lt;p&gt;Their &lt;em&gt;JACC&lt;/em&gt; article listed 15 common herbal medicines known to interact adversely with conventional cardiovascular drugs.&lt;/p&gt;
&lt;p&gt;In many cases, the herbal products compete with the regular medicines for the same drug-metabolizing cytochrome P450 enzymes, potentiating the latter&apos;s effects. In other cases, the herbal products have their own cardiovascular effects.&lt;/p&gt;
&lt;p&gt;Many physicians already know that grapefruit juice occupies the CYP3A4 enzyme, leading to slower-than-expected metabolism and, therefore, higher blood levels of a host of pharmaceuticals.&lt;/p&gt;
&lt;p&gt;These include the statins, calcium channel antagonists, several common anti-arrhythmic drugs, and the angiotensin receptor blocker irbesartan (Avapro), Jahangir and colleagues noted.&lt;/p&gt;
&lt;p&gt;Garlic is one of several common herbal remedies with specific cardiovascular effects in its own right (others include ginkgo biloba, ginseng, and saw palmetto). Garlic inhibits platelet aggregation and thus can lead to increased bleeding risks when combined with aspirin, clopidogrel (Plavix), or warfarin (Coumadin), the researchers noted.&lt;/p&gt;
&lt;p&gt;The Mayo group identified 10 herbal products that increase bleeding risks with anticoagulant and antiplatelet drugs, as well as 14 that can induce arrhythmias.&lt;/p&gt;
&lt;p&gt;In all, Jahangir and colleagues listed 27 herbal products that patients with cardiovascular diseases would do well to avoid. These include such common and harmless-seeming products as green tea, capsicum pepper, licorice, and kelp, as well as grapefruit juice and garlic.&lt;/p&gt;
&lt;p&gt;&quot;We need to check with our patients what type of products they are using, to identify these potential interactions,&quot; Jahangir told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;He cited the previously reported figure of 100,000 deaths annually from drug interactions, adding, &quot;We don&apos;t even know how many of these are due to use of compounds that we are not aware that our patients are taking.&quot;&lt;/p&gt;
&lt;p&gt;Jahangir said he was surprised, in preparing the review, at the scale of hebal medicine use in the U.S.&lt;/p&gt;
&lt;p&gt;He and his colleagues found data from the 1990s suggesting that more patients consult complementary and alternative medicine providers than regular physicians.&lt;/p&gt;
&lt;p&gt;The total annual out-of-pocket expenditure on complementary and alternative medicine services and products also was greater than for conventional physician services.&lt;/p&gt;
&lt;p&gt;&quot;The surprise for me was . . . how much people are willing to spend on a type of therapy which has not shown, in any scientific way, to be effective or safe,&quot; Jahangir said.&lt;/p&gt;
&lt;p&gt;He added that the trend may reflect shortcomings of the conventional medical system.&lt;/p&gt;
&lt;p&gt;&quot;What is the reason people are going there? Is it because there is some unmet type of need that we are not recognizing as practitioners of conventional medicine?&quot;&lt;/p&gt;
&lt;p&gt;Jahangir said it may be that physicians aren&apos;t spending enough time with patients to understand their true needs. He said it appears that, &quot;despite the advancement in our technology and new medicines, there is a demand for alternative therapies that is increasing.&quot;&lt;/p&gt;
&lt;p&gt;He recommended that, in addition to asking patients in detail about herbal and other alternative therapies they may be using, physicians should educate themselves on what these therapies purport to do and what is known about their real biological effects.&lt;/p&gt;
&lt;p&gt;The &lt;a href=&quot;http://nccam.nih.gov&quot; mce_href=&quot;http://nccam.nih.gov&quot; target=&quot;_blank&quot;&gt;National Center for Complementary and Alternative Medicine&lt;/a&gt; at the National Institutes of Health is a good starting point for such information, both for physicians and for patients, Jahangir said.&lt;/p&gt;
&lt;p&gt;Lenox Hill&apos;s Steinbaum said it was important that conventional physicians &quot;become more open-minded and accepting&quot; of alternative medicine, if only because so many of their patients are already practicing it.&lt;/p&gt;
&lt;p&gt;David Meyerson, MD, JD, a Johns Hopkins University cardiologist, told &lt;em&gt;MedPage Today&lt;/em&gt; and ABC News in an e-mail that he advises patients to limit their use of &quot;unstudied and unproven and FDA-unregulated herbal medications.&quot;&lt;/p&gt;
&lt;p&gt;&quot;It&apos;s unfortunately very big business, and potential drug interactions and potential harmful effects abound,&quot; he wrote.&lt;/p&gt;
&lt;p&gt;But another physician criticized the Mayo physicians&apos; emphasis on adverse effects in their review.&lt;/p&gt;
&lt;p&gt;&quot;For many of products listed, evidence for side effects seems to be minimal,&quot; Scott Grundy, MD, of the University of Texas Southwestern Medical Center in Dallas, argued in an e-mail.&lt;/p&gt;
&lt;p&gt;He agreed that the efficacy and safety of such drugs remains largely unproven, but added, &quot;It is mainly for these reasons that they cannot be recommended for use.&quot;&lt;/p&gt;
&lt;p&gt;Creating alarm about side effects &quot;may not be the appropriate way to discourage their use,&quot; Grundy said.&lt;/p&gt;
&lt;p&gt;&lt;em&gt;This article was developed in collaboration with ABC News. &lt;/em&gt;&lt;img src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; mce_src=&quot;http://www.medpagetoday.com/upload/2009/10/1/14357_1.jpg&quot; alt=&quot;&quot;&gt;&lt;/p&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_315"
                     title="A Few Extra Pounds May Benefit Older People (CME/CE)"
                     score="0.005"
                     href="http://www.medpagetoday.com/Geriatrics/GeneralGeriatrics/tb/18183?impressionId=1265786391074"
                     
      &lt;p&gt;A little excess weight after age 70 could do the body some good, according to results of a study involving 9,000 older patients.&lt;/p&gt;
&lt;p&gt;Overweight participants in the cohort study had the lowest 10-year mortality. Normal-weight and obese participants ages 70 to 75 had a similar and slightly higher risk of death, Leon Flicker, PhD, of the Western Australian Center for Health and Aging in Perth, and colleagues found.&lt;/p&gt;
&lt;p&gt;The findings add to evidence suggesting that being overweight in older age is not such a bad thing and might even be beneficial.&lt;/p&gt;
&lt;p&gt;&quot;These results lend further credence to claims that the body mass index [BMI] thresholds for overweight and obese are overly restrictive for older people,&quot; the researchers concluded in an article in the &lt;em&gt;Journal of the American Geriatrics Society&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The authors also found that a sedentary lifestyle doubled the mortality risk for older women but did not affect survival of older men.&lt;/p&gt;
&lt;p&gt;The World Health Organization has established four BMI thresholds to characterize body weight: &lt;ul&gt; &lt;li&gt;&amp;lt;18.5 kg/m&lt;sup&gt;2&lt;/sup&gt;, underweight&lt;/li&gt; &lt;li&gt;18.5 to 24.9 kg/m&lt;sup&gt;2&lt;/sup&gt;, normal weight&lt;/li&gt; &lt;li&gt;25 to 29.9 kg/m&lt;sup&gt;2&lt;/sup&gt;, overweight&lt;/li&gt; &lt;li&gt;&amp;#8805;30 kg/m&lt;sup&gt;2&lt;/sup&gt;, obese&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The authors noted that the thresholds were derived primarily from studies of younger and middle-age adults. Whether the cut points for overweight and obese are appropriate for older individuals has remained unclear.&lt;/p&gt;
&lt;p&gt;Two systematic reviews and a meta-analysis showed no increased mortality risk associated with a BMI in the overweight range for older people (&lt;em&gt;Arch Intern Med&lt;/em&gt; 2001; 161: 1194-1203, &lt;em&gt;Obesity Rev&lt;/em&gt; 2007; 8: 41-59). However, methodologic differences complicated the comparison of different studies, Flicker and colleagues wrote.&lt;/p&gt;
&lt;p&gt;So they sought to address some of the uncertainty by analyzing data from two large Australian cohort studies involving more than 9,000 individuals ages 70 to 75 (4,677 men, 4,563 women).&lt;/p&gt;
&lt;p&gt;The principal objectives were to determine the BMI threshold associated with the lowest mortality in older people and to determine whether the relationship between BMI and mortality differed between men and women.&lt;/p&gt;
&lt;p&gt;Data for the analysis came from self-reported measures of height and weight, which the authors used to calculate BMI for the study participants. Participants also provided demographic, lifestyle, and health information.&lt;/p&gt;
&lt;p&gt;Using the WHO criteria for BMI, the authors found that 1.3% of men and 3.1% of women were underweight; 43.5% of men and 50.3% of women were normal weight; 44.3% of men and 33.5% of women were overweight; and 11% of men and 13.1% of women were obese.&lt;/p&gt;
&lt;p&gt;During 10 years of follow-up, overweight study participants had a 13% lower risk of death compared with normal-weight participants (HR 0.87, 95% CI 0.78 to 0.94). Obese participants had a mortality risk similar to that of normal-weight participants (HR 0.98, 95% CI 0.85 to 1.11).&lt;/p&gt;
&lt;p&gt;Self-reported sedentary lifestyle doubled the mortality risk for women across all BMI categories (HR 2.08, 95% CI 1.79 to 2.41). In contrast, sedentary lifestyle increased the mortality risk for men by 28% (HR 1.28, 95% CI 1.14 to 1.44).&lt;/p&gt;
&lt;p&gt;Separate analyses involving common causes of death, such as cardiovascular disease and cancer, showed similar relationships between BMI and mortality risk.&lt;/p&gt;
&lt;p&gt;&quot;Even after removing the effects of early mortality, those who were overweight were still at lowest risk, a finding consistent with the observation that weight loss in older age groups is associated with greater mortality,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;Overweight older people are not at greater mortality risk, and there is little evidence that dieting in this age group confers any benefit,&quot; they added.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The authors had no relevant disclosures&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
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