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Showing posts from November, 2015

fructose restriction and cardiometabolic and weight improvement

There are several epidemiologic studies suggesting that fructose plays a role in the development of metabolic syndrome, as well as non-alcoholic fatty liver disease, type 2 diabetes, and cardiovascular disease. A small study just came out assessing 43 children with obesity and metabolic syndrome who were put on a 9 day fructose-restricted diet and then evaluated several metabolic parameters ( see  obesity and fructose restriction obesity2015  in dropbox, or doi:10.1002/oby.21371). this diet attempted to match each participant's prior macronutrient intake profile details: --27 Latino and 16 African-American children with obesity and metabolic syndrome (mean age 13.3, weight 93 kg, BMI 35.6) --a child-friendly diet: various no- or lower-sugar added processed foods including turkey hot dogs, pizza, bean burritos, baked potato chips, and popcorn results:     --mean caloric intake was 29 kcal/kg: 51% carbs, 16% protein, 33% fat (16% saturated, 9% polyunsat, 13% monounsat),

troubling microbiome changes

A couple of recent studies have found very troubling microbial changes, one dealing with the effect of PPIs on the gut microbiome, the other with the evolution of a very serious development in antibiotic resistance. 1. I sent out a blog in December 2014 on use of PPIs (proton-pump inhibitors) and changes in the microbiome (see  http://gmodestmedblogs.blogspot.com/2014/11/gastric-acid-suppression-and-microbiome_23.html   ), which noted that gastric acid suppression (mostly with PPIs) in kids led to pretty profound changes in both the lung and gut microbiomes. Another study just came out looking at the PPI-associated gut microbiome changes in adults, which could predispose people to C. difficile infections (see   ppi microbiome gastro2015  in dropbox, or Gastroenterology 2015;149:883). details: --background: C diff infections happen more often in those on PPIs. There are data showing that increases in gut Enterococcaceae and Streptococcaceae and decreases in Clostridiales taxa a

functional dyspepsia

New Engl J  Med just had a useful review of the remarkably common "functional dyspepsia" (see  functional dyspepsia NEJM2015  in dropbox, or N Engl J Med 2015;373:1853-63​) ​. their points: --Definition: Rome III criteria -- sensation of pain or burning in epigastrium, early satiety, fullness during or after a meal, or a combo of these symptoms; lasting at least 6 months and occurring at least weekly, and no organic explanation --but, symptoms above to not reliably distinguish "functional" from organic cause: <10% with dyspepsia have a peptic ulcer, <1% gastroesophageal cancer, and >70% have functional dyspepsia as determined by EGD (ie, nothing found) --one other overlapping diagnosis is GERD, but more than 50% of patients meeting functional dyspepsia criteria with symptoms of heartburn and regurgitation had normal 48-hour pH studies, and in these patients, heartburn/regurgitation was the predominant functional dyspepsia symptom in 30% --there i

inhaled steroids for COPD may increase pneumonia

The data are pretty mixed on the efficacy of inhaled corticosteroids (ICS) in patients with COPD, yet in some studies 85% of COPD patients are on them. in this light, there a recent large case-control study found that weaning some patients off ICS found a dramatic decrease in pneumonia cases !!! (see  copd inhaled steroid PNA chest2015 in dropbox, or CHEST2015; 148(5): 1177). details: --case-control study from Quebec, looking at a new-user cohort of patients with COPD ( mean age 78.6, 50% male ) put on ICS during 1990-2005, followed thru 2007 or until a serious pneumonia event (first hospitalization or death from pneumonia). --they compared those who discontinued ICS, vs those who continued, to assess development of a serious pneumonia event, adjusting for age, sex, comorbidities, and respiratory disease severity  (which they defined as: number of prescriptions for b-agonists, ipratropium and tiotropium, theophylline, oral steroids, and antibiotics; and if there were hospitaliza

drink coffee and live longer

An analysis of the Nurses' Health Studies (NHS, which began in 1976 with RNs aged 30-55 and  NHS2 which began in 1989 with RNs aged 25-42) and the Health Professionals Follow-up Study (HPFS, which began in 1986, with male health professionals aged 40-75) assessed total and cause-specific mortality in drinkers of caffeinated and decaffeinated coffee (see  coffee and mortality circ2015  in  dropbox , or  DOI : 10.1161/ CIRCULATIONAHA.115.017341).  details: --74,890 women in NHS, 93,054 women in NHS2, and 40,557 men in HPFS, with extensive semi-quantitative food frequency questionnaires (131 items, administered every 4 years), and 4,690,072 person-years of follow-up. 95% white. --up to 30 years of follow-up, with extensive data on known or suspected confounders (biennial questionnaires asking about age, weight, smoking, physical activity, medication use, fam history of diabetes, and self-reported diagnoses including hypertension, hypercholesterolemia, cardiovasc disease, and ca

longterm microbiome changes with antibiotics

a small study was done looking at antibiotic exposure and changes in both the salivary and gut microbiomes (see  microbiome antibiotics  longterm  change mBio  2015  in  dropbox , or  http:// mbio.asm.org /content/6/6/ e01693-15.full.pdf+html ,  or   doi:10.1128 / mBio.01693 -15​). this study involved 2 clinical sites, one in Sweden and one in the UK, randomly assigned to placebo vs different antibiotics, and looking at changes in the microbiomes both before  a single antibiotic exposure  and for up to one year after. details: --30 people in the Swedish site were randomized to placebo, ciprofloxacin, or clindamycin; 44 people in the UK were randomized to placebo, amoxicillin, or minocycline (dosage not stated) --for the Swedish site:         --the fecal microbiome diversity was significantly reduced for up to 4 months in the clindamycin group, and up to 12 months in the ciprofloxacin group         --the salivary microbiomes in the same groups showed only a short-term reducti

rotator cuff repair in the older people???

And yet another article suggests that we are doing too much surgery.  this one is on nontraumatic rotator cuff tears in older patients  ( see  rotator cuff tear nonsurg JBoneJointSurg2015  in dropbox, or  J Bone Joint Surg Am. 2015;97:1729). details: --160 patients (mean age 64, 50% female, 50% working, mean duration of symptoms 27 months) in Finland with 167 symptomatic, nontraumatic, isolated full-thickness supraspinatus tears were randomized into:     --group 1: physiotherapy-- patients given written info and guidance on home-based excercise program. first six weeks aimed at improving glenohumeral motion and active scapular retraction; then static and dynamic exercises to improve scapular and glenohumeral muscle function until 12 weeks, then increased resistance and strength training until 6 months. also 10 sessions of PT in outpatient facility to monitor progress.      --group 2: physiotherapy plus acromioplasty. PT as in group 1, plus arthroscopic acromioplasty (to reduce

central obesity

there are a plethora of older studies showing that central obesity has a much stronger association with cardiovascular and mortality outcomes than BMI. The role of BMI as a predictor of events is largely explained by the concomitant risk factors of hypertension, hyperlipidemia, glucose intolerance/diabetes. Central obesity, on the other hand, is associated with the more metabolically active visceral fat. Not surprisingly, several studies have shown that there is a strong correlation between an increased BMI and central obesity for most individuals. However, little attention is paid to people with normal BMI but central obesity, and the 2013 Am Heart Assn Obesity Society guidelines on obesity management only recommends checking waist circumference in those with high BMIs. In this context, there was a study looking at the clinical consequences of central obesity in individuals with normal weight (see  obesity central nl wt mortality AIM2015 in dropbox, or doi:10.7326/M14-2525​), using t

atrial fibrillation -- should we look harder for it?

over the years, I have had several patients who have presented with significant strokes related to previously-undetected atrial fibrillation (AF). I have also had a couple of patients with dementia and no evident prior stroke, who on workup have had multiple small infarcts, again possibly related to AF. in this light, there was an interesting editorial in JAMA (see  afib screening JAMA2015  in dropbox, or JAMA 2015; 314: 1911) raising the question of whether we should be screening regularly for AF. although not part of their argument, i think that the potential and not clearly well-defined relationship between AF and cognitive decline may be part of the incentive to screen (see below). their argument is basically (all references are in the text): --AF is really common (1 in 4 lifetime risk in those >40, with 0.5% age 40, increasing to up to 15% at age 80) --treatment is pretty effective: oral anticoagulation (OA) reduces stroke risk by 2/3 and mortality by 1/3, with relativel