<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_431"
                     title="Down a Beer to Improve Bone Health? Not So Fast"
                     score="0.011"
                     href="http://www.medpagetoday.com/PrimaryCare/DietNutrition/tb/18347?impressionId=1265768442532"
                     
      &lt;p&gt;A flagon of ale may indeed be a good source of dietary silicon, a recent study showed, but experts say any attempt to link beer drinking to bone health is not based on scientific data.&lt;/p&gt;
&lt;p&gt;The study of 100 commercial beers in the February issue of the &lt;em&gt;Journal of the Science of Food and Agriculture&lt;/em&gt;, by Charles Bamforth, PhD, DSc, and Troy Casey, of the University of California Davis, examined the silicon content that results from different ingredients and brewing processes.&lt;/p&gt;
&lt;p&gt;Although a press release issued with the study prominently mentioned the link between silicon and bone health, the study itself did not look at bone mineral density or analyze any patient data at all, according to several researchers contacted by &lt;em&gt;MedPage Today&lt;/em&gt; and ABC News.&lt;/p&gt;
&lt;p&gt;The authors wrote that they explored the silicon content in beer because the popular beverage has been identified as one of the richest potential sources of dietary silicon in the Western diet. The average intake is 20 to 50 mg/day.&lt;/p&gt;
&lt;p&gt;The beers sampled contained an average of 29.4 mg/L of silicon, with a range of 6.4 to 56.4 mg/L. Beers made from a barley-based grist (as opposed to wheat-based beers ) and brews containing more hops had the highest silicon levels.&lt;/p&gt;
&lt;p&gt;The beer type with the overall highest silicon level was India Pale Ale, with an average of 41.2 mg/L. Other ales came in second with 32.8 mg/L.&lt;/p&gt;
&lt;p&gt;Nonalcoholic beers, light lagers, and wheat beers had the least silicon.&lt;/p&gt;
&lt;p&gt;In the end, the authors concluded that &quot;beer is a substantial source of silicon in the diet&quot; and that &quot;beers containing high levels of malted barley and hops are richest in silicon,&quot; but they did not attempt to establish a link between beer drinking and bone health.&lt;/p&gt;
&lt;p&gt;Experts contacted for comment on the study also cautioned the public against establishing any such connection.&lt;/p&gt;
&lt;p&gt;&quot;To conclude any bone health benefits from this study would require a great leap,&quot; Tim Byers, MD, MPH, deputy director of the University of Colorado Cancer Center in Aurora, wrote in an e-mail.&lt;/p&gt;
&lt;p&gt;Other researchers noted that previous studies have shown an association between alcohol consumption and an increased risk of fracture.&lt;/p&gt;
&lt;p&gt;That&apos;s probably because of a greater chance of falling after drinking, according to Walter Willett, MD, DrPH, of the Harvard School of Public Health.&lt;/p&gt;
&lt;p&gt;In fact, Stephen Richardson, MD, an endocrinologist at NYU Langone Medical Center, noted that &quot;alcohol consumption is a risk factor for osteoporosis.&quot;&lt;/p&gt;
&lt;p&gt;Still, there is some evidence supporting a positive link between overall dietary silicon and bone health.&lt;/p&gt;
&lt;p&gt;A 2004 cross-sectional study in the &lt;em&gt;Journal of Bone and Mineral Research&lt;/em&gt; that used data from the Framingham Offspring cohort found a significant association between greater dietary silicon intake, including that from beer, and higher bone mineral density in the hip in men and premenopausal women.&lt;/p&gt;
&lt;p&gt;The researchers concluded: &quot;These findings suggest that higher dietary silicon intake in men and younger women may have salutary effects on skeletal health, especially cortical bone health, that has not been previously recognized.&quot;&lt;/p&gt;
&lt;p&gt;Another study by the same group published last year in the &lt;em&gt;American Journal of Clinical Nutrition&lt;/em&gt; found that moderate consumption of alcohol, including beer, wine, and liquor, was associated with higher bone mineral density in men and postmenopausal women.&lt;/p&gt;
&lt;p&gt;However, it also showed that men who drank too much liquor were more likely to have lower spine and hip bone mineral density.&lt;/p&gt;
&lt;p&gt;The relationship between beer and bone mineral density appeared to be mediated by silicon, the researchers concluded.&lt;/p&gt;
&lt;p&gt;Bottom line: considering the increased fracture risk and the various other problems associated with drinking too much alcohol, experts agree that guzzling beer is not strategy for improving bone health.&lt;/p&gt;
&lt;p&gt;&quot;In the absence of bone density values or preferably fracture incidence, it would be premature to tout beer as a preventative or treatment,&quot; Richardson said.&lt;/p&gt;
&lt;p&gt;David Katz, MD, MPH, of the Yale School of Public Health, agreed.&lt;/p&gt;
&lt;p&gt;&quot;This is NOT a reason to drink beer,&quot; he said in an e-mail. &quot;This is simply a bit of good news for those who do drink beer already  --  yours truly among them!&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 authors did not make any financial disclosures.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&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_428"
                     title="Blocking Serotonin in Gut Reverses Osteoporosis in Mice (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Endocrinology/Osteoporosis/tb/18346?impressionId=1265768442532"
                     
      &lt;p&gt;Blocking serotonin production in the intestine might help restore lost bone mass, rather than just preventing further loss like most current osteoporosis treatments, an animal study suggested.&lt;/p&gt;
&lt;p&gt;Once daily treatment with a novel serotonin inhibitor prevented development of osteoporosis and also fully reversed existing low bone mass in mice, according Gerard Karsenty, MD, PhD, of Columbia University in New York City, and colleagues.&lt;/p&gt;
&lt;p&gt;These proof-of-principle findings came without any impact on serotonin levels in the brain, the researchers reported in the Feb. 7 issue of &lt;em&gt;Nature Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Just two years ago, Karsenty&apos;s group discovered that the vast majority of serotonin in the body acts to regulate bone formation.&lt;/p&gt;
&lt;p&gt;Only 5% plays the chemical&apos;s better-known role as a brain neurotransmitter. The rest comes from the gut for circulation below the blood-brain barrier which, in this regard, Karsenty called &quot;more hermetic than the Berlin Wall was.&quot;&lt;/p&gt;
&lt;p&gt;So the gut treatment is unlikely to affect mood and other critical functions serotonin plays in the brain, he emphasized in an interview. But he acknowledged that much more proof is needed on the way to the clinic.&lt;/p&gt;
&lt;p&gt;The tip-off to bone effects of serum serotonin came from a group of patients with a syndrome that produced high bone mass when they were into their 60s.&lt;/p&gt;
&lt;p&gt;Usually, bone destruction outpaces formation after menopause, eventually leading to osteoporosis. But something different was happening in these patients, who never developed the condition.&lt;/p&gt;
&lt;p&gt;&quot;The only cause we could find was that it was due to a decrease in the synthesis of serotonin in the gut,&quot; Karsenty told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;After their initial experiments showed serotonin did indeed boost the pace of bone formation, the researchers found that a biotech company had already developed a compound that would reduce gut synthesis of the hormone. It had been tested in women with irritable bowel syndrome.&lt;/p&gt;
&lt;p&gt;So Karsenty&apos;s group examined its effects on bone in mice and found a dose-dependent reduction in serum serotonin.&lt;/p&gt;
&lt;p&gt;Mice that got 250 mg/kg body weight per day of this compound  --  known as LP533401, a small molecule inhibitor of Tph1, the initial enzyme in gut serotonin synthesis  --  produced 30% less serotonin than controls, without a change in brain serotonin levels.&lt;/p&gt;
&lt;p&gt;Then the researchers tested the compound on mice whose ovaries had been excised to simulate the dramatic drop-off in hormones women experience after menopause. That condition, in turn, leads to an imbalance in bone resorption versus formation.&lt;/p&gt;
&lt;p&gt;Mice given the experimental drug at doses up to 10 mg/kg, starting the day after surgery, had elevated bone resorption but maintained higher bone mass than those that got placebo. The placebo group all developed osteopenia.&lt;/p&gt;
&lt;p&gt;Treated mice had a &quot;major&quot; increase in bone formation markers, including osteoblast numbers, bone formation rate, and osteocalcin serum levels. But again, brain serotonin remained unaffected.&lt;/p&gt;
&lt;p&gt;These benefits were achieved with a modest, roughly 30% reduction in serum serotonin  --  which appeared to be the threshold beyond which skeletal response increased only marginally.&lt;/p&gt;
&lt;p&gt;Some mice were left untreated for two weeks  --  &quot;a long time for a rodent,&quot; Karsenty noted  --  to develop osteopenia. Subsequently treated with a daily 250 mg/kg dose of LP533401, they had such an increase in bone formation over four weeks that it normalized their bone mass, the researchers noted.&lt;/p&gt;
&lt;p&gt;The same thing happened when researchers began treatment even longer after surgery, six or 12 weeks, when bone loss was already severe. Bone mass rose with serotonin inhibition in the vertebrae and long bones, but without a change in bone length or width.&lt;/p&gt;
&lt;p&gt;Nor were there effects on platelets, coagulation, or the GI tract with regard to the key measures of transit, colonic mobility, and gastric emptying.&lt;/p&gt;
&lt;p&gt;Serotonin inhibition in the gut as a potential anabolic treatment for osteopenia and osteoporosis appeared to work as well as the only currently available treatment that can increase bone formation sufficiently to compensate for the increased resorption caused by menopause  --  parathyroid hormone injections.&lt;/p&gt;
&lt;p&gt;Since serum serotonin inhibitors could be given in pill form, this pathway is much more attractive, Karsenty said.&lt;/p&gt;
&lt;p&gt;The specific agent used in this trial was designed for proof-of-principle and wouldn&apos;t necessarily be what is developed for clinical use, he cautioned.&lt;/p&gt;
&lt;p&gt;&quot;Although the data presented here are promising we remain fully aware that, since rodents do not remodel bones as much as humans do, our results will have to be confirmed in other species,&quot; the researchers also warned in the paper.&lt;/p&gt;
&lt;p&gt;Karsenty said the group plans to continue animal model studies for the time being, with no plans to move into clinical trials.&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 grants from the National Institutes of Health and a Gideon and Sevgi Rodan fellowship from the International Bone and Mineral Society.&lt;/p&gt;&lt;p&gt;The researchers reported no conflicts of interest or industry involvement in the study.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_391"
                     title="Rare Genetic Deletion Linked to Morbid Obesity (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Genetics/GeneralGenetics/tb/18286?impressionId=1265768442532"
                     
      &lt;p&gt;Missing sections of DNA may have a powerful impact on weight for a small segment of the population, researchers said.&lt;/p&gt;
&lt;p&gt;Nearly all teens and adults found to have a particular deletion of roughly 30-genes on chromosome 16p11.2 were obese  --  most morbidly so  --  with a body mass index of at least 40 kg/m&lt;sup&gt;2&lt;/sup&gt;, Philippe Froguel, MD, PhD, of Imperial College London, and colleagues reported in &lt;em&gt;Nature&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;While the variant appeared to explain only a small proportion of morbid obesity  --  0.7% in the study population  --  it was never present in healthy, normal-weight controls.&lt;/p&gt;
&lt;p&gt;&quot;Although the recent rise in obesity in the developed world is down to an unhealthy environment, with an abundance of unhealthy food and many people taking very little exercise, the difference in the way people respond to this environment is often genetic,&quot; Froguel said in a prepared statement.&lt;/p&gt;
&lt;p&gt;But with further findings like these, it may be possible to identify such individuals through genetic testing, he said.&lt;/p&gt;
&lt;p&gt;If so, &quot;We can then offer them appropriate support and medical interventions, such as the option of weight-loss surgery, to improve their long-term health,&quot; Froguel declared.&lt;/p&gt;
&lt;p&gt;Although researchers speculate that one in 20 cases of obesity may have a genetic cause, the genetic component remains largely elusive.&lt;/p&gt;
&lt;p&gt;Even accounting for such a small fraction of cases, the newly discovered 16p11.2 variant would be the second most frequent known genetic cause of obesity, Froguel&apos;s group said.&lt;/p&gt;
&lt;p&gt;Extensive genome-wide association studies have linked numerous single nucleotide polymorphisms (SNPs) to obesity, but added all together they account for only a small fraction of the known heritable component, the researchers said.&lt;/p&gt;
&lt;p&gt;&quot;The &apos;common disease, common variant&apos; hypothesis is increasingly coming under challenge,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Their team first identified the genetic deletion in teen and adults with learning difficulties or delayed development.&lt;/p&gt;
&lt;p&gt;Because the 31 individuals who had the nearly identical deletions of at least 593 kilobases at chromosome 16p11.2 in one copy of their DNA all had a BMI of over 30 kg/m&lt;sup&gt;2&lt;/sup&gt;, the researchers decided to dig a little deeper.&lt;/p&gt;
&lt;p&gt;&quot;Cohorts with extreme phenotypes that include obesity may be enriched for rare but very potent risk variants,&quot; making them easier to discover, they wrote.&lt;/p&gt;
&lt;p&gt;So they undertook a case-control study among 312 patients at three centers in Britain and France who presented with congenital malformations, developmental delay, or both, in addition to obesity.&lt;/p&gt;
&lt;p&gt;The same deletions were seen in 2.9% of these individuals.&lt;/p&gt;
&lt;p&gt;The function of the missing genes are not well known, but some have previously been associated with delayed development, autism, and schizophrenia.&lt;/p&gt;
&lt;p&gt;Notably, though, the frequency of deletion of these genes in the obese case-control cohort was &quot;appreciably higher&quot; than the less than 1% seen in the autism and other studies that didn&apos;t include obesity as an inclusion criteria, the researchers said.&lt;/p&gt;
&lt;p&gt;A second independent survey of genetic data at eight cytogenetic centers in France, Switzerland, and Estonia turned up a 0.6% rate among 3,947 people with developmental delay, malformations, or both, but who were not selected for obesity (&lt;em&gt;P&lt;/em&gt;=0.00022 versus the cohort selected for obesity).&lt;/p&gt;
&lt;p&gt;Analysis of those with the missing genes revealed an age-dependent link to weight: All four teens and adults were obese. Children were often obese (four of 15) or overweight (two of 15). Children under 2 years all had normal weight.&lt;/p&gt;
&lt;p&gt;So to see whether the deletion was independent of neurodevelopmental problems, Froguel&apos;s group examined genome-wide association study data from general population cohorts totaling 11,856 individuals along with 2,772 from childhood obesity and adult morbid obesity case-control studies, 931 in an extreme early-onset obesity study, and 141 who had bariatric weight-loss surgery.&lt;/p&gt;
&lt;p&gt;All adult carriers of the deletion were obese with the exception of one who was apparently diabetic. Each of the seven children and adolescents who carried the variant had a BMI in the top 0.1% for their age and gender.&lt;/p&gt;
&lt;p&gt;None had any reported developmental or cognitive problems. Four had reported hyperphagia with excessive hunger and food intake.&lt;/p&gt;
&lt;p&gt;Altogether, the 16p11.2 deletions predicted 29.8-fold elevated risk of obesity (&lt;em&gt;P&lt;/em&gt;=0.00000058) and 43.0-fold elevated risk of morbid obesity (&lt;em&gt;P&lt;/em&gt;=0.000000064) compared with lean or normal weight.&lt;/p&gt;
&lt;p&gt;By extrapolation, the researchers extrapolated that about 0.4% of all morbidly obese cases are attributable to an inherited 16p11.2 deletion, with 0.3% arising from a de novo deletion in the same genetic region.&lt;/p&gt;
&lt;p&gt;&quot;Although they may be heterogeneous in nature, these deletions are highly likely to be the causal variants,&quot; they wrote.&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 &quot;Le Conseil Regional Nord Pas de Calais/FEDER&quot; along with various governmental and industry supporters for the various component studies.&lt;/p&gt;&lt;p&gt;The researchers reported no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_301"
                     title="Tight Glucose Control Fails in Septic Shock (CME/CE)"
                     score="0.003"
                     href="http://www.medpagetoday.com/CriticalCare/Sepsis/tb/18160?impressionId=1265768442532"
                     
      Septic shock patients treated with a corticosteroid get no survival advantage from tight glucose control or addition of a second corticosteroid to provide more mineralocorticoid activity, according to results of a randomized trial.&lt;br&gt;
&lt;br&gt;Aiming for normoglycemia at 80 to 110 mg/dL rather than the standard 150 mg/dL had no impact on inhospital mortality rates (45.9% versus 42.9%, &lt;em&gt;P&lt;/em&gt;=0.50), Djillali Annane, MD, of H&amp;#244;pital Raymond Poincar&amp;#233; in Garches, France, and colleagues found.&lt;br&gt;
&lt;br&gt;Inhospital mortality was likewise similar whether patients got hydrocortisone (Solu-Cortef) alone or with the addition of fludrocortisone ([Florinef] 42.9% versus 45.8%, &lt;em&gt;P&lt;/em&gt;=0.50), they reported in the Jan. 27 issue of the &lt;em&gt;Journal of the American Medical Association&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;This aggressive treatment strategy should not be routine, the researchers recommended.&lt;/p&gt;
&lt;p&gt;These findings largely match the general lack of benefit seen with tight glycemic control in recent studies with ICU patients overall.&lt;/p&gt;
&lt;p&gt;The prematurely terminated &lt;a href=&quot;http://www.medpagetoday.com/MeetingCoverage/SCCM/5096&quot; mce_href=&quot;http://www.medpagetoday.com/MeetingCoverage/SCCM/5096&quot; target=&quot;_blank&quot;&gt;European Glucontrol Trial&lt;/a&gt; found no mortality benefit but a seven-fold higher risk of hypoglycemia with an 80 to 110 mg/dL target in the ICU.&lt;/p&gt;
&lt;p&gt;In the &lt;a href=&quot;http://www.medpagetoday.com/CriticalCare/Intensivists/13397&quot; mce_href=&quot;http://www.medpagetoday.com/CriticalCare/Intensivists/13397&quot; target=&quot;_blank&quot;&gt;NICE-SUGAR&lt;/a&gt; study, 90-day mortality was actually higher in the tight glucose control group (27.9% versus 24.9%, &lt;em&gt;P&lt;/em&gt;=0.02), although there was a trend for benefit in patients who got corticosteroids (&lt;em&gt;P&lt;/em&gt;=0.06).&lt;/p&gt;
&lt;p&gt;Glucose targets are being re-evaluated across medicine as the &quot;lower is better&quot; paradigm has had a safety asterisk added everywhere from diabetes care to the ICU, noted Richard Bergenstal, MD, American Diabetes Association president for medicine and science.&lt;/p&gt;
&lt;p&gt;&quot;All of a sudden it&apos;s becoming more than a single number,&quot; he told &lt;em&gt;MedPage Today&lt;/em&gt;. &quot;Now be it inpatient or outpatient, we&apos;re realizing that ... you have to do it while you&apos;re minimizing hypoglycemia.&quot;&lt;/p&gt;
&lt;p&gt;A more nuanced and &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Diabetes/13818&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Diabetes/13818&quot; target=&quot;_blank&quot;&gt;individualized&lt;/a&gt; strategy is prudent, Bergenstal agreed.&lt;/p&gt;
&lt;p&gt;The current clinical uncertainty underscores the need for large-scale international cooperation to get adequately powered trials, according to an accompanying editorial.&lt;/p&gt;
&lt;p&gt;In it, Greet Van den Berghe, MD, PhD, of the Catholic University of Leuven, Belgium, cautioned that Annane&apos;s Corticosteroids and Intensive Insulin Therapy for Septic Shock (COIITSS) study was grossly underpowered.&lt;/p&gt;
&lt;p&gt;The initial studies that led to rapid adoption of intensive insulin therapy in ICUs around the world had suggested an absolute reduction in mortality of only 3%, whereas the COIITSS study projected a 12.5% absolute benefit.&lt;/p&gt;
&lt;p&gt;More importantly, the study achieved mean glucose levels of only between 120 and 130 mg/dL in the intervention group for whom the aim was 80 to 110 mg/dL, which resulted in considerable overlap with the standard care group for whom mean levels were about 145 mg/dL.&lt;/p&gt;
&lt;p&gt;This could account for the lack of difference in outcome, Van den Berghe said.&lt;/p&gt;
&lt;p&gt;But the intensive insulin group did have &quot;markedly&quot; lower blood glucose levels for the duration of their ICU stay and spent more time in the 80 to 110 mg/dL range compared with the standard care group (both &lt;em&gt;P&lt;/em&gt;&amp;lt;0.00001), the researchers noted.&lt;/p&gt;
&lt;p&gt;Because corticosteroids further aggravate the &quot;diabetes of injury&quot; seen with septic shock, Annane&apos;s group undertook a multicenter trial of 509 adults treated for septic shock with multiple organ dysfunction over a three year period at 11 ICUs in France.&lt;/p&gt;
&lt;p&gt;Patients were randomly assigned to tight glucose control using continuous intravenous insulin infusion to target a glucose level of 80 to 110 mg/dL or conventional insulin therapy targeted to guidelines-recommended 150 mg/dL or under. They were additionally randomized to receive hydrocortisone alone (50-mg bolus every six hours) or in combination with fludrocortisone (50-&amp;#956;g tablets once daily) for seven days.&lt;/p&gt;
&lt;p&gt;Aside from the lack of inhospital mortality advantage, tight glucose control also failed to produce a benefit for the following secondary endpoints: &lt;ul&gt; &lt;li&gt;Overall survival (hazard ratio 1.04, &lt;em&gt;P&lt;/em&gt;=0.78) &lt;/li&gt; &lt;li&gt; ICU length of stay for survivors (median 10 versus nine days, &lt;em&gt;P&lt;/em&gt;=0.68)&lt;/li&gt; &lt;li&gt;Duration of hospital stay overall (24 versus 22 days, &lt;em&gt;P&lt;/em&gt;=0.87)&lt;/li&gt; &lt;li&gt;Median vasopressor-free days (four for both, P=0.58)&lt;/li&gt; &lt;li&gt;Median mechanical ventilation-free days (10 versus 13, &lt;em&gt;P&lt;/em&gt;=0.51)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Nor was there evidence for interaction with fludrocortisone in the primary endpoint (relative risk 0.89 versus 0.91 hydrocortisone alone, &lt;em&gt;P&lt;/em&gt;=0.31) or benefit in any other endpoint.&lt;/p&gt;
&lt;p&gt;The one effect of intensive insulin appeared to be an increase in episodes of severe hypoglycemia, defined by glucose falling below 40 mg/dL (mean 0.29 versus 0.14 episodes per patient, &lt;em&gt;P&lt;/em&gt;=0.003).&lt;/p&gt;
&lt;p&gt;However, having hypoglycemia did not increase the risk of death in intervention group patients compared with controls (45.2% versus 50%).&lt;/p&gt;
&lt;p&gt;The researchers cautioned that the study did not rule out a benefit from some degree of glucose control compared with none.&lt;/p&gt;
&lt;p&gt;They also noted that healthcare providers were not blinded to administration of fludrocortisone, for which no placebo was available.&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 funded by the Assistance Publique&amp;#8211;H&amp;#244;pitaux de Paris. The researchers reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;Van den Berghe, through the Catholic University of Leuven, reported receiving structural research financing from the Methusalem program, funded by the Flemish government.&lt;/p&gt;&lt;p&gt;Bergenstal reported receiving research funding and serving on advisory boards for various pharmaceutical companies related to novel diabetes drugs but without any personal financial compensation.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_291"
                     title="Obese Kids at Risk for Adult CVD (CME/CE)"
                     score="0.002"
                     href="http://www.medpagetoday.com/Endocrinology/MetabolicSyndrome/tb/18153?impressionId=1265768442532"
                     
      Obesity in children as young as 7 years old may put them at higher risk of heart disease and stroke later in life, even if they lack other cardiovascular risk factors such as high blood pressure, a new study found.&lt;br&gt;
&lt;br&gt;Obese children had higher levels of biomarkers for inflammation and prothrombosis than thin children. These included 10 times higher concentrations of high sensitivity C-reactive protein, a marker associated with increased risk of developing heart disease, cardiovascular disease, or other processes involving inflammation (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01), according to an online report published Jan. 26 in the &lt;em&gt;Journal of Clinical Endocrinology and Metabolism&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Fibrinogen, interleukin-6 (IL-6) and plasminogen activator inhibitor 1 (PAI-1), other markers associated with inflammation and elevated blood clotting risk, were also elevated in obese children (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01).&lt;p&gt;&lt;/p&gt;
&lt;p&gt;&quot;These observations reflect the unhealthy status of many youth at risk for adult cardiovascular disease in our catchment area in the southeastern U.S.,&quot; Nelly Mauras, MD, of Nemours Children&apos;s Clinic in Jacksonville, Fla., and colleagues wrote.&lt;/p&gt;
&lt;p&gt;The number of overweight children in the U.S. has tripled in the last 30 years, and more than 17% of children between the ages of 6 and 19 are overweight, according to the authors.&lt;/p&gt;
&lt;p&gt;Overweight children often develop metabolic syndrome, a collection of findings that includes abdominal obesity, elevated triglyceride and decreased HDL concentrations, hypertension, and impaired glucose tolerance. These put the youngsters at risk for early adult cardiovascular disease. Yet the exact definition of metabolic syndrome is a matter of ongoing debate.&lt;/p&gt;
&lt;p&gt;While children are typically considered to be at low risk of tissue damage if they show no signs of carbohydrate intolerance, hypertension, and dyslipidemia, Mauras and colleagues theorized that obese children without other risk factors for metabolic syndrome could still be at risk for later cardiovascular disease.&lt;/p&gt;
&lt;p&gt;To test this, they compared markers for inflammation and prothrombosis in 115 obese children and 88 lean children between the ages of 7 and 18 years. The study was conducted at Wolfson Children&apos;s Hospital, in Jacksonville, Fla.&lt;/p&gt;
&lt;p&gt;&quot;Children with obesity show a marked increase in the concentrations of hsCRP, 351 fibrinogen, IL-6 and PAI-1, reflective of a proinflammatory and prothrombotic state, even before the comorbidities of the Metabolic Syndrome are present, and even before the onset of puberty,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;&quot;These data support the need for more aggressive interventions in very young children with obesity regardless of the absence of associated comorbidities.&quot;&lt;/p&gt;
&lt;p&gt;They also found that elevated levels of hsCRP and fibrinogen correlated with a wider waist circumference (R=0.73 and 0.40, respectively) and the percent of fat mass (r= 0.76 and 0.47) (&lt;em&gt;P&lt;/em&gt;=0.0001). Prepubertal obese children were taller than their lean counterparts (&lt;em&gt;P&lt;/em&gt;=0.005) and had higher systolic blood pressure.&lt;/p&gt;
&lt;p&gt;The authors noted that their study did not address whether the abnormalities they found are reversible with early therapeutic interventions.&lt;/p&gt;
&lt;p&gt;&quot;Weight reduction (or weight maintenance in many growing children) remains the cornerstone of any intervention in childhood obesity,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;&quot;However, further longitudinal studies adding pharmacological interventions, in addition to lifestyle changes, will soon offer much needed insight as to whether a decrease in the proinflammatory and prothrombotic state will improve long-term cardiovascular risk of obese children, even in preadolescence and before the development of the Metabolic Syndrome.&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 authors reported no sources of funding for the study and no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
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