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    <recommendedItem id="20100101_19_394"
                     title="Even Normal Glucose in Kids Could Predict Diabetes Later (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Endocrinology/Diabetes/tb/18291?impressionId=1265785543553"
                     
      Increases in fasting plasma glucose during childhood  --  even though levels remain in the normal range  --  can predict adult prediabetes and type 2 diabetes later in life, a retrospective cohort study showed.&lt;br&gt;
&lt;br&gt;Among individuals with a fasting plasma glucose of less than 100 mg/dL as children, increasing levels were associated with greater risks of prediabetes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) and type 2 diabetes (&lt;em&gt;P&lt;/em&gt;=0.03) in adulthood, according to Gerald Berenson, MD, of Tulane University Health Sciences Center in New Orleans, and colleagues.&lt;br&gt;
&lt;br&gt;There appeared to be a threshold  --  85 mg/dL  --  above which the risk of adult problems began to increase, the researchers reported in the February issue of &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;It is not surprising that a higher fasting glucose level in childhood predicts prediabetes and diabetes in adulthood,&quot; Matthew Gillman, MD, of Harvard, wrote in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;More surprising, he said, was the existence of the apparent threshold, although &quot;the authors are appropriately circumspect about recommending lowering glucose cutoff points to diagnose children at risk of developing prediabetes or diabetes.&quot;&lt;/p&gt;
&lt;p&gt;&quot;Even if there is a threshold over which children are at substantially higher risk of later prediabetes, it is unclear exactly how high the risk should be to make changing guidelines a good thing,&quot; he wrote. &quot;After all, the right interventions for individuals with prediabetes are still obscure, so identifying more of them may be more trouble than it&apos;s worth.&quot;&lt;/p&gt;
&lt;p&gt;According to Berenson and colleagues, 19 million U.S. adults have type 2 diabetes. More common is a prediabetic state of impaired fasting glucose, affecting about 54 million.&lt;/p&gt;
&lt;p&gt;Previous studies have suggested that higher plasma glucose levels, even if still in the normal range, might be a predictor of diabetes.&lt;/p&gt;
&lt;p&gt;Berenson&apos;s group wanted to see whether elevated fasting plasma glucose in childhood would predict prediabetes or type 2 diabetes in adulthood.&lt;/p&gt;
&lt;p&gt;To find out, they turned to the Bogalusa Heart Study, which began tracking children from that Louisiana town in 1978. All had a fasting plasma glucose lower than 100 mg/dL.&lt;/p&gt;
&lt;p&gt;The current analysis included those same individuals assessed as adults after a mean follow-up of 21 years  --  1,723 were normoglycemic (99 mg/dL or lower), 79 were prediabetic (100 to 125 mg/dL), and 47 had type 2 diabetes.&lt;/p&gt;
&lt;p&gt;Using a childhood fasting plasma glucose of 86 mg/dL or higher as a predictor for prediabetes yielded a 76.9% sensitivity and 85.2% specificity. For diabetes, sensitivity was 75% and specificity was 76%.&lt;/p&gt;
&lt;p&gt;In a multivariate analysis controlling for anthropometric, hemodynamic, and metabolic variables from childhood to adulthood, as well as baseline fasting plasma glucose level, those individuals who had a childhood level 86 mg/dL or higher had increased risks of both prediabetes (OR 3.40, 95% CI 1.87 to 6.18) and type 2 diabetes (OR 2.06, 95% CI 1.01 to 4.23) as adults.&lt;/p&gt;
&lt;p&gt;The authors acknowledged some limitations of the study, including the lack of data on postchallenge glucose, in vivo insulin action and secretion, and glycosylated hemoglobin in childhood.&lt;/p&gt;
&lt;p&gt;Gillman, the editorialist, also noted that the findings&apos; generalizability to children today is unclear because obesity was much less prevalent when the adults in this study were children.&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 Institute on Aging and the American Heart Association.&lt;/p&gt;&lt;p&gt;The editorial was supported by a grant from the NIH.&lt;/p&gt;&lt;p&gt;Neither the study authors nor the editorialist reported any 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_391"
                     title="Rare Genetic Deletion Linked to Morbid Obesity (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Genetics/GeneralGenetics/tb/18286?impressionId=1265785543553"
                     
      &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_291"
                     title="Obese Kids at Risk for Adult CVD (CME/CE)"
                     score="0.005"
                     href="http://www.medpagetoday.com/Endocrinology/MetabolicSyndrome/tb/18153?impressionId=1265785543553"
                     
      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;
    </recommendedItem>
    <recommendedItem id="20100101_19_132"
                     title="Economic Burden of Diabetes Tops $200B"
                     score="-0.005"
                     href="http://www.medpagetoday.com/Endocrinology/Diabetes/tb/17950?impressionId=1265785543553"
                     
      &lt;p&gt;Medical costs and reduced work productivity associated with diabetes cost the U.S. $218 billion in 2007, researchers said.&lt;/p&gt;
&lt;p&gt;The annual average cost per patient was $9,975 for diagnosed diabetes and $2,864 for undiagnosed disease, according to Timothy M. Dall of the Lewin Group in Falls Church, Va., and colleagues.&lt;/p&gt;
&lt;p&gt;&quot;The burden of diabetes to society is even higher when one considers intangible costs from reduced quality of life,&quot; the researchers wrote online in &lt;em&gt;Health Affairs&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;The sobering statistics presented in this paper underscore the urgency to better understand the cost-mitigation potential of prevention and treatment strategies.&quot;&lt;/p&gt;
&lt;p&gt;Dall and his colleagues, working with funding from Novo Nordisk, developed the estimates from a proprietary economic model based on medical literature, government statistics, and insurance claims data.&lt;/p&gt;
&lt;p&gt;Results from the National Health Interview Survey, corrected with claims data, indicate that about one million Americans had type 1 diabetes and 16.5 million had type 2 diabetes in 2007.&lt;/p&gt;
&lt;p&gt;The economic model indicated that the per-patient economic burden was $14,856 for type 1 diabetes and $9,677 for type 2 disease.&lt;/p&gt;
&lt;p&gt;National Health and Nutrition Examination Survey findings indicate that some 57 million individuals had &quot;prediabetes,&quot; and another 6.3 million Americans had diabetes but have not been formally diagnosed.&lt;/p&gt;
&lt;p&gt;Their average costs were $443 for prediabetes (medical costs only) and $2,864 for undiagnosed diabetes, Dall and colleagues estimated.&lt;/p&gt;
&lt;p&gt;Compared to those with no diagnosis, people with known diabetes accounted for vastly more use of various services, including outpatient care, emergency visits, and hospitalization.&lt;/p&gt;
&lt;p&gt;For example, ambulatory visits for neurological symptoms were nearly eight times as common among among type 1 diabetics as among nondiabetics, and five times as common among those with type 2 diabetes.&lt;/p&gt;
&lt;p&gt;Inpatient days for cardiovascular problems were increased more than six-fold for both types of diabetes, and emergency visits for such problems were about three times as common.&lt;/p&gt;
&lt;p&gt;Undiagnosed diabetes had smaller but still detectable consequences for medical expenses. Compared with people with no history of diabetes, undiagnosed diabetics had 70% more outpatient visits and more than twice as many hospital inpatient days for cardiovascular complaints.&lt;/p&gt;
&lt;p&gt;Overall, the bill for medical services associated with diabetes was $153 billion, according to Dall and colleagues  --  about 7% of the total national healthcare expenditure.&lt;/p&gt;
&lt;p&gt;The researchers put the loss of work productivity at $65 billion, including absenteeism, reduced productivity while at work, disability, and premature death.&lt;/p&gt;
&lt;p&gt;Some of the data underlying the estimate came from National Health Interview Survey data on missed workdays and disability rates, reports in the literature, and CDC estimates of diabetes-related mortality.&lt;/p&gt;
&lt;p&gt;Dall and colleagues noted that patients and their families bear much of the burden in the form of out-of-pocket expenses and reduced earnings  --  not to mention the impaired quality of life and other intangibles.&lt;/p&gt;
&lt;p&gt;But everyone else shares the costs as well, they argued.&lt;/p&gt;
&lt;p&gt;&quot;This diabetes burden represents a hidden &apos;tax&apos; in the form of higher health insurance premiums and reduced disposable income,&quot; Dall and colleagues wrote.&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20090101_1_183"
                     title="Variant Gene Linked to Diabetes Is Carried by 38% of People"
                     score="-0.005"
                     href="