10/15/15

More than 300,000 women experience postpartum depression every year, but only 50 percent of cases are diagnosed

From: http://www.cbsnews.com/news/postpartum-depression-symptoms-experienced-by-nearly-20-percent-of-women/

Actress' struggle shines light on postpartum depression

Actress Hayden Pannettiere announced earlier this week that she's receiving treatment for postpartum depression

From: http://www.cbsnews.com/videos/actress-struggle-shines-light-on-postpartum-depression/

Seniors may face higher Medicare premiums

The Social Security Administration told nearly 65 million retirees they will not be getting a raise in their Social Security benefits next year due to low inflation

From: http://www.cbsnews.com/videos/seniors-may-face-higher-medicare-premiums/

Is modern life making us sleep deprived? Maybe not

Researchers compare the sleep patterns of our high-tech 21st century vs. people living a hunter-gatherer lifestyle

From: http://www.cbsnews.com/news/is-modern-life-making-us-sleep-deprived-maybe-not/

Millions could see their Medicare costs soar

Unless Congress acts, many of the more than 55 million on Medicare could see premiums rise as much as 50%

From: http://www.cbsnews.com/news/millions-could-see-their-medicare-costs-soar/

5 hidden health threats tripping up seniors

Loose rugs and slips in the shower aren't the only troublemakers that land hundreds of thousands of older Americans in the hospital every year

From: http://www.cbsnews.com/media/hidden-health-threats-tripping-up-seniors/

Fewer Teens Smoking Cigarettes, But More Using Pot

Meanwhile, more American adults are trying to break the tobacco habit, second government study shows

From: http://teens.webmd.com/news/20151015/fewer-teens-smoking-cigarettes-but-twice-as-many-using-pot-cdc?src=RSS_PUBLIC

Theranos disputes report that its tech has problems

Elizabeth Holmes' ballyhooed biotech startup says a Wall Street Journal article is "factually and scientifically erroneous"

From: http://www.cbsnews.com/news/theranos-disputes-report-that-its-tech-has-problems/

Things Americans fear most

A recent survey ranked what people across the country are most afraid of, and some of the answers may surprise you

From: http://www.cbsnews.com/media/things-americans-fear-most-2015/

PAR-2 activation enhances weak acid-induced ATP release through TRPV1 and ASIC sensitization in human esophageal epithelial cells

Esophageal visceral hypersensitivity has been proposed to be the pathogenesis of heartburn sensation in nonerosive reflux disease. Protease-activated receptor-2 (PAR-2) is expressed in human esophageal epithelial cells and is believed to play a role in inflammation and sensation. PAR-2 activation may modulate these responses through adenosine triphosphate (ATP) release, which is involved in transduction of sensation and pain. The transient receptor potential vanilloid receptor 1 (TRPV1) and acid-sensing ion channels (ASICs) are both acid-sensitive nociceptors. However, the interaction among these molecules and the mechanisms of heartburn sensation are still not clear. We therefore examined whether ATP release in human esophageal epithelial cells in response to acid is modulated by TRPV1 and ASICs and whether PAR-2 activation influences the sensitivity of TRPV1 and ASICs. Weak acid (pH 5) stimulated the release of ATP from primary human esophageal epithelial cells (HEECs). This effect was significantly reduced after pretreatment with 5-iodoresiniferatoxin (IRTX), a TRPV1-specific antagonist, or with amiloride, a nonselective ASIC blocker. TRPV1 and ASIC3 small interfering RNA (siRNA) transfection also decreased weak acid-induced ATP release. Pretreatment of HEECs with trypsin, tryptase, or a PAR-2 agonist enhanced weak acid-induced ATP release. Trypsin treatment led to the phosphorylation of TRPV1. Acid-induced ATP release enhancement by trypsin was partially blocked by IRTX, amiloride, or a PAR-2 antagonist. Conversely, acid-induced ATP release was augmented by PAR-2 activation through TRPV1 and ASICs. These findings suggested that the pathophysiology of heartburn sensation or esophageal hypersensitivity may be associated with the activation of PAR-2, TRPV1, and ASICs.

From: Wu, L., Oshima, T., Shan, J., Sei, H., Tomita, T., Ohda, Y., Fukui, H., Watari, J., Miwa, H. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G695?rss=1

Variants in pancreatic carboxypeptidase genes CPA2 and CPB1 are not associated with chronic pancreatitis

Genetic alterations in the carboxypeptidase A1 gene (CPA1) are associated with early onset chronic pancreatitis (CP). Besides CPA1, there are two other human pancreatic carboxypeptidases (CPA2 and CPB1). Here we examined whether CPA2 and CPB1 alterations are associated with CP in Japan and Germany. All exons and flanking introns of CPA2 and CPB1 were sequenced in 477 Japanese patients with CP (234 alcoholic, 243 nonalcoholic) and in 497 German patients with nonalcoholic CP by targeted next-generation sequencing and/or Sanger sequencing. Secretion and enzymatic activity of CPA2 and CPB1 variants were determined after transfection into HEK 293T cells. We identified six nonsynonymous CPA2 variants (p.V67I, p.G166R, p.D168E, p.D173H, p.R237W, and p.G388S), eight nonsynonymous CPB1 alterations (p.S65G, p.N120S, p.D172E, p.R195H, p.D208N, p.F232L, p.A317V, and p.D364Y), and one splice-site variant (c.687+1G>T) in CPB1. Functional analysis revealed essentially complete loss of function in CPA2 variants p.R237W and p.G388S and CPB1 variants p.R110H and p.D364Y. None of the CPA2 or CPB1 variants, including those resulting in a marked loss of function, were overrepresented in patients with CP. In conclusion, CPA2 and CPB1 variants are not associated with CP.

From: Nakano, E., Geisz, A., Masamune, A., Niihori, T., Hamada, S., Kume, K., Kakuta, Y., Aoki, Y., Matsubara, Y., Ebert, K., Ludwig, M., Braun, M., Groneberg, D. A., Shimosegawa, T., Sahin-Toth, M., Witt, H. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G688?rss=1

Short- and long-term regulation of intestinal Na+/H+ exchange by Toll-like receptors TLR4 and TLR5

Inappropriate activation of pattern recognition receptors has been described as a potential trigger in the development of inflammatory bowel disease (IBD). In this study, we evaluated the activity and expression of Na⁺/H⁺ exchanger (NHE) subtypes in T84 intestinal epithelial cells during Toll-like receptor 4 (TLR4) activation by monophosphoryl lipid A and TLR5 by flagellin. NHE activity and intracellular pH were evaluated by spectrofluorescence. Additionally, kinase activities were evaluated by ELISA, and siRNA was used to specifically inhibit adenylyl cyclase (AC). Monophosphoryl lipid A (MPLA) (0.01–50.00 μg/ml) and flagellin (10–500 ng/ml) inhibited NHE1 activity in a concentration-dependent manner (MPLA short term –25.2 ± 5.0%, long term –31.9 ± 4.0%; flagellin short term –14.9 ± 2.0%, long term –19.1 ± 2.0%). Both ligands triggered AC3, PKA, PLC, and PKC signal molecules. Long-term exposure to flagellin and MPLA induced opposite changes on NHE3 activity; flagellin increased NHE3 activity (~10%) with overexpression of membrane protein, whereas MPLA decreased NHE3 activity (–17.3 ± 3.0%). MPLA and flagellin simultaneously had synergistic effects on NHE activity. MPLA and flagellin impaired pH_i recovery after intracellular acidification. The simultaneous exposure to MPLA and flagellin induced a substantial pH_i reduction (–0.55 ± 0.03 pH units). Activation of TLR4 and TLR5 exerts marked inhibition of NHE1 activity in intestinal epithelial cells. Transduction mechanisms set into motion during TLR4-mediated and long-term TLR5-mediated inhibition of NHE1 activity involve AC3, PKA, PLC, and PKC. However, short- and long-term TLR4 activation and TLR5 activation might use different signaling pathways. The physiological alterations on intestinal epithelial cells described here may be useful in the development of better IBD therapeutics.

From: Cabral, J. M., Gracio, D., Soares-da-Silva, P., Magro, F. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G703?rss=1

Phenotypic divergence in two lines of L-Fabp-/- mice reflects substrain differences and environmental modifiers

Phenotypic divergence in diet-induced obesity (DIO) and hepatic steatosis has been reported in two independently generated lines of L-Fabp^–/– mice [New Jersey (NJ) L-Fabp^–/– vs. Washington University (WU) L-Fabp^–/– mice]. We performed side-by-side studies to examine differences between the lines and investigate the role of genetic background, intestinal microbiota, sex, and diet in the divergent phenotypes. Fasting-induced steatosis was attenuated in both L-Fabp^–/– lines compared with C57BL/6J controls, with restoration of hepatic triglyceride levels following adenoviral L-Fabp rescue. Both lines were protected against DIO after high-saturated-fat diet feeding. Hepatic steatosis was attenuated in WU but not NJ L-Fabp^–/– mice, although this difference between the lines disappeared upon antibiotic treatment and cohousing. In contrast, there was phenotypic divergence in L-Fabp^–/– mice fed a high cocoa butter fat diet, with WU L-Fabp^–/– mice, but not NJ L-Fabp^–/– mice, showing protection against both DIO and hepatic steatosis, with some sex-dependent (female > male) differences. Dense mapping revealed no evidence of unintended targeting, duplications, or deletions surrounding the Fabp1 locus in either line and only minor differences in mRNA expression of genes located near the targeted allele. However, a C57BL/6 substrain screen showed that the NJ L-Fabp^–/– line contains ~40% C57BL/6N genomic DNA, despite reports that these mice were backcrossed six generations. Overall, these findings suggest that some of the phenotypic divergence between the two L-Fabp^–/– lines may reflect unanticipated differences in genetic background, underscoring the importance of genetic background in phenotypic characterization.

From: Newberry, E. P., Kennedy, S., Xie, Y., Luo, J., Jiang, H., Ory, D. S., Davidson, N. O. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G648?rss=1

Intestinal DMT1 is critical for iron absorption in the mouse but is not required for the absorption of copper or manganese

Divalent metal-ion transporter-1 (DMT1) is a widely expressed iron-preferring membrane-transport protein that serves a critical role in erythroid iron utilization. We have investigated its role in intestinal metal absorption by studying a mouse model lacking intestinal DMT1 (i.e., DMT1^int/int). DMT1^int/int mice exhibited a profound hypochromic-microcytic anemia, splenomegaly, and cardiomegaly. That the anemia was due to iron deficiency was demonstrated by the following observations in DMT1^int/int mice: 1) blood iron and tissue nonheme-iron stores were depleted; 2) mRNA expression of liver hepcidin (Hamp1) was depressed; and 3) intraperitoneal iron injection corrected the anemia, and reversed the changes in blood iron, nonheme-iron stores, and hepcidin expression levels. We observed decreased total iron content in multiple tissues from DMT1^int/int mice compared with DMT1^+/+ mice but no meaningful change in copper, manganese, or zinc. DMT1^int/int mice absorbed ⁶⁴Cu and ⁵⁴Mn from an intragastric dose to the same extent as did DMT1^+/+ mice but the absorption of ⁵⁹Fe was virtually abolished in DMT1^int/int mice. This study reveals a critical function for DMT1 in intestinal nonheme-iron absorption for normal growth and development. Further, this work demonstrates that intestinal DMT1 is not required for the intestinal transport of copper, manganese, or zinc.

From: Shawki, A., Anthony, S. R., Nose, Y., Engevik, M. A., Niespodzany, E. J., Barrientos, T., Ohrvik, H., Worrell, R. T., Thiele, D. J., Mackenzie, B. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G635?rss=1

The role of apolipoprotein A-IV in regulating glucagon-like peptide-1 secretion

Both glucagon-like peptide-1 (GLP-1) and apolipoprotein A-IV (apoA-IV) are produced from the gut and enhance postprandial insulin secretion. This study investigated whether apoA-IV regulates nutrient-induced GLP-1 secretion and whether apoA-IV knockout causes compensatory GLP-1 release. Using lymph-fistula-mice, we first determined lymphatic GLP-1 secretion by administering apoA-IV before an intraduodenal Ensure infusion. apoA-IV changed neither basal nor Ensure-induced GLP-1 secretion relative to saline administration. We then assessed GLP-1 in apoA-IV–/– and wild-type (WT) mice administered intraduodenal Ensure. apoA-IV–/– mice had comparable lymph flow, lymphatic triglyceride, glucose, and protein outputs as WT mice. Intriguingly, apoA-IV–/– mice had higher lymphatic GLP-1 concentration and output than WT mice 30 min after Ensure administration. Increased GLP-1 was also observed in plasma of apoA-IV–/– mice at 30 min. apoA-IV–/– mice had comparable total gut GLP-1 content relative to WT mice under fasting, but a lower GLP-1 content 30 min after Ensure administration, suggesting that more GLP-1 was secreted. Moreover, an injection of apoA-IV protein did not reverse the increased GLP-1 secretion in apoA-IV–/– mice. Finally, we assessed gene expression of GLUT-2 and the lipid receptors, including G protein-coupled receptor (GPR) 40, GPR119, and GPR120 in intestinal segments. GLUT-2, GPR40 and GPR120 mRNAs were unaltered by apoA-IV knockout. However, ileal GPR119 mRNA was significantly increased in apoA-IV–/– mice. GPR119 colocalizes with GLP-1 in ileum and stimulates GLP-1 secretion by sensing OEA, lysophosphatidylcholine, and 2-monoacylglycerols. We suggest that increased ileal GPR119 is a potential mechanism by which GLP-1 secretion is enhanced in apoA-IV–/– mice.

From: Wang, F., Yang, Q., Huesman, S., Xu, M., Li, X., Lou, D., Woods, S. C., Marziano, C., Tso, P. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G680?rss=1

"Store-operated" cAMP signaling contributes to Ca2+-activated Cl- secretion in T84 colonic cells

Apical cAMP-dependent CFTR Cl^– channels are essential for efficient vectorial movement of ions and fluid into the lumen of the colon. It is well known that Ca²⁺-mobilizing agonists also stimulate colonic anion secretion. However, CFTR is apparently not activated directly by Ca²⁺, and the existence of apical Ca²⁺-dependent Cl^– channels in the native colonic epithelium is controversial, leaving the identity of the Ca²⁺-activated component unresolved. We recently showed that decreasing free Ca²⁺ concentration ([Ca²⁺]) within the endoplasmic reticulum (ER) lumen elicits a rise in intracellular cAMP. This process, which we termed "store-operated cAMP signaling" (SOcAMPS), requires the luminal ER Ca²⁺ sensor STIM1 and does not depend on changes in cytosolic Ca²⁺. Here we assessed the degree to which SOcAMPS participates in Ca²⁺-activated Cl^– transport as measured by transepithelial short-circuit current (I_sc) in polarized T84 monolayers in parallel with imaging of cAMP and PKA activity using fluorescence resonance energy transfer (FRET)-based reporters in single cells. In Ca²⁺-free conditions, the Ca²⁺-releasing agonist carbachol and Ca²⁺ ionophore increased I_sc, cAMP, and PKA activity. These responses persisted in cells loaded with the Ca²⁺ chelator BAPTA-AM. The effect on I_sc was enhanced in the presence of the phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX), inhibited by the CFTR inhibitor CFTR_inh-172 and the PKA inhibitor H-89, and unaffected by Ba²⁺ or flufenamic acid. We propose that a discrete component of the "Ca²⁺-dependent" secretory activity in the colon derives from cAMP generated through SOcAMPS. This alternative mode of cAMP production could contribute to the actions of diverse xenobiotic agents that disrupt ER Ca²⁺ homeostasis, leading to diarrhea.

From: Nichols, J. M., Maiellaro, I., Abi-Jaoude, J., Curci, S., Hofer, A. M. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G670?rss=1

Neuropeptide S inhibits gastrointestinal motility and increases mucosal permeability through nitric oxide

Neuropeptide S (NPS) receptor (NPSR1) polymorphisms are associated with enteral dysmotility and inflammatory bowel disease (IBD). This study investigated the role of NPS in conjunction with nitrergic mechanisms in the regulation of intestinal motility and mucosal permeability. In rats, small intestinal myoelectric activity and luminal pressure changes in small intestine and colon, along with duodenal permeability, were studied. In human intestine, NPS and NPSR1 were localized by immunostaining. Pre- and postprandial plasma NPS was measured by ELISA in healthy and active IBD humans. Effects and mechanisms of NPS were studied in human intestinal muscle strips. In rats, NPS 100-4,000 pmol·kg^–1·min^–1 had effects on the small intestine and colon. Low doses of NPS increased myoelectric spiking (P < 0.05). Higher doses reduced spiking and prolonged the cycle length of the migrating myoelectric complex, reduced intraluminal pressures (P < 0.05-0.01), and increased permeability (P < 0.01) through NO-dependent mechanisms. In human intestine, NPS localized at myenteric nerve cell bodies and fibers. NPSR1 was confined to nerve cell bodies. Circulating NPS in humans was tenfold below the ~0.3 nmol/l dissociation constant (K_d) of NPSR1, with no difference between healthy and IBD subjects. In human intestinal muscle strips precontracted by bethanechol, NPS 1–1,000 nmol/l induced NO-dependent muscle relaxation (P < 0.05) that was sensitive also to tetrodotoxin (P < 0.01). In conclusion, NPS inhibits motility and increases permeability in neurocrine fashion acting through NO in the myenteric plexus in rats and humans. Aberrant signaling and upregulation of NPSR1 could potentially exacerbate dysmotility and hyperpermeability by local mechanisms in gastrointestinal functional and inflammatory reactions.

From: Wan Saudi, W. S., Halim, M. A., Rudholm-Feldreich, T., Gillberg, L., Rosenqvist, E., Tengholm, A., Sundbom, M., Karlbom, U., Naslund, E., Webb, D.-L., Sjoblom, M., Hellstrom, P. M. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G625?rss=1

Glial cell line-derived neurotrophic factor promotes barrier maturation and wound healing in intestinal epithelial cells in vitro

Recent data suggest that neurotrophic factors from the enteric nervous system are involved in intestinal epithelial barrier regulation. In this context the glial cell line-derived neurotrophic factor (GDNF) was shown to affect gut barrier properties in vivo directly or indirectly by largely undefined processes in a model of inflammatory bowel disease (IBD). We further investigated the potential role and mechanisms of GDNF in the regulation of intestinal barrier functions. Immunostaining of human gut specimen showed positive GDNF staining in enteric neuronal plexus and in enterocytes. In Western blots of the intestinal epithelial cell lines Caco2 and HT29B6, significant amounts of GDNF were detected, suggesting that enterocytes represent an additional source of GDNF. Application of recombinant GDNF on Caco2 and HT29B6 cells for 24 h resulted in significant epithelial barrier stabilization in monolayers with immature barrier functions. Wound-healing assays showed a significantly faster closure of the wounded areas after GDNF application. GDNF augmented cAMP levels and led to significant inactivation of p38 MAPK in immature cells. Activation of p38 MAPK signaling by SB-202190 mimicked GDNF-induced barrier maturation, whereas the p38 MAPK activator anisomycin blocked GDNF-induced effects. Increasing cAMP levels had adverse effects on barrier maturation, as revealed by permeability measurements. However, increased cAMP augmented the proliferation rate in Caco2 cells, and GDNF-induced proliferation of epithelial cells was abrogated by the PKA inhibitor H89. Our data show that enterocytes represent an additional source of GDNF synthesis. GDNF contributes to wound healing in a cAMP/PKA-dependent manner and promotes barrier maturation in immature enterocytes cells by inactivation of p38 MAPK signaling.

From: Meir, M., Flemming, S., Burkard, N., Bergauer, L., Metzger, M., Germer, C.-T., Schlegel, N. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G613?rss=1

Effects of birth asphyxia on the modulation of pharyngeal provocation-induced adaptive reflexes

Perinatal asphyxia and aerodigestive symptoms are troublesome. We tested the hypothesis that pharyngeal provocation alters proximal and distal aerodigestive reflex coordination and kinetics in infants with hypoxic ischemic encephalopathy (HIE), compared with healthy controls. Specifically, we characterized the sensory-motor properties of pharyngeal provocation-induced effects on upper esophageal sphincter (UES) and lower esophageal sphincter (LES) reflexes. Ten orally fed controls (32.0 ± 1.5 wk gestation) and 25 infants with HIE (38.1 ± 0.4 wk gestation) were evaluated at 39.7 ± 0.9 and 41.9 ± 0.6 wk postmenstrual age respectively. Pharyngo-esophageal reflexes evoked upon graded water stimuli were tested using water-perfusion micromanometry methods. Analysis included sensory-motor characteristics of pharyngeal reflexive swallow (PRS), pharyngo-UES-contractile reflex (PUCR), esophageal body-waveform kinetics, and pharyngo-LES-relaxation reflex (PLESRR). For controls vs. infants with HIE, median appearance, pulse, grimace, activity, respiration (APGAR) scores were 6 vs. 1 at 1 min (P < 0.001) and 8 vs. 3 at 5 min (P < 0.001). Upon pharyngeal- stimulation, HIE infants (vs. controls) had frequent PUCR (P = 0.01); increased UES basal tone (P = 0.03); decreased LES basal tone (P = 0.002); increased pharyngeal-waveforms per stimulus (P = 0.03); decreased frequency of LES relaxation (P = 0.003); and decreased proximal esophageal contractile amplitude (P = 0.002), with prolonged proximal esophageal contractile duration (P = 0.008). Increased tonicity and reactivity of the UES and dysregulation of LES may provide the pathophysiological basis for pooling of secretions, improper bolus clearance, and aspiration risk. Deficits in function at the nuclear or supranuclear level involving glossopharyngeal and vagal neural networks and respiratory regulatory pathways involved with aerodigestive protection may be contributory.

From: Gulati, I. K., Shubert, T. R., Sitaram, S., Wei, L., Jadcherla, S. R. http://ajpgi.physiology.org/cgi/content/abstract/309/8/G662?rss=1

Size of These Brain Parts Tied to Dementia Risk

When brain structures called hippocampi are smaller, that may point to a higher risk of getting Alzheimer's disease and other types of dementia, new research suggests. WebMD has the details.

From: http://www.webmd.com/alzheimers/news/20151015/hippocampus-dementia-brain?src=RSS_PUBLIC

Do you really need an annual physical?

Research shows regular checkups do little to improve health, but many doctors and patients still think they're important

From: http://www.cbsnews.com/news/do-you-really-need-an-annual-physical-doctors-disagree/

Postpartum Depression: What You Need to Know

From: Mayo Clinic http://www.youtube.com/watch?v=fBYYr_kEjmo

Calcium, vitamin D don't cut colon cancer risk: Study

A new study presents a setback for efforts to prevent the disease through vitamin supplements

From: http://www.cbsnews.com/news/calcium-vitamin-d-do-not-lower-colon-cancer-risk-study/

Life-Threatening Vaccine Reactions Rare: CDC

Just 33 people from 25 million immunized were affected, researchers report

From: http://www.webmd.com/children/vaccines/news/20151015/vaccines-rarely-cause-life-threatening-allergic-reactions-cdc?src=RSS_PUBLIC

Vitamin D, Calcium May Not Prevent Colon Cancer

Large study finds supplements no better than placebo at warding off recurring polyps

From: http://www.webmd.com/colorectal-cancer/news/20151014/vitamin-d-calcium-may-not-prevent-colon-cancer-after-all?src=RSS_PUBLIC

Mom's pregnancy stress may affect kids years later

Researchers say a woman who has a stressful pregnancy may see impact on children's coordination later in life

From: http://www.cbsnews.com/news/pregnancy-stress-tied-to-teens-coordination-problems/

Straight Talk About Diabetes

WebMD shares tips on how to let friends and family know what kind of help you need when you have diabetes.

From: http://www.webmd.com/diabetes/features/straight-talk-diabetes?src=RSS_PUBLIC

USDA to Invest $30 million to Help Protect Wetlands in Six States

DES MOINES, Iowa, Oct. 15, 2015 – Agriculture Secretary Tom Vilsack today announced that the U.S. Department of Agriculture will award $30 million to projects in six states to protect, restore and enhance wetlands on private and tribal agricultural lands. The projects are being funded under the Wetland Reserve Enhancement Partnership (WREP), a program authorized by the 2014 Farm Bill.

From: http://www.usda.gov/wps/portal/usda/usdahome?contentid=2015/10/0288.xml&contentidonly=true

Fact Sheet: Impact of USDA Investments to Protect and Sustain America’s Water Supply

Over the past six years, USDA has worked with private landowners to implement voluntary conservation practices that conserve and clean the water we drink. USDA support—leveraged with historic outside investments—boosts producer incomes and rewards them for their good work.

From: http://www.usda.gov/wps/portal/usda/usdahome?contentid=2015/10/0287.xml&contentidonly=true

Ebola virus can stick around up to 9 months in men

Semen samples reveal presence of virus even longer than previously believed

From: http://www.cbsnews.com/news/ebola-virus-can-stick-around-up-to-9-months-in-men/

Could the benefits of exercise be packed into a pill?

Scientists are in the early stages of developing so-called "exercise pills"

From: http://www.cbsnews.com/news/could-the-benefits-of-exercise-be-packed-into-a-pill/

Study sheds new light on effects of standing versus sitting

A new study has added another perspective to the health debate over the benefits of sitting versus standing

From: http://www.cbsnews.com/videos/study-sheds-new-light-on-effects-of-standing-versus-sitting/

Scientists unveil "breakthrough" exercise pill

Claiming a breakthrough, a group of scientists believe they have found the future of weight loss in a so-called "exercise pill"

From: http://www.cbsnews.com/videos/scientists-unveil-breakthrough-exercise-pill/

Harmful effects of supplements can send you to the emergency department

For many people, a healthy lifestyle means more than eating good diet and getting enough exercise — vitamins, supplements, and complementary nutritional products are also part of the plan. But though there is much publicity about their potential benefits, there is less awareness of their possible harmful effects.

In fact, using these products can land you in the emergency department.

A study published yesterday in The New England Journal of Medicine found that adverse effects of supplements were responsible for an average of about 23,000 emergency department (ED) visits per year. That’s a lot for something that is supposed to be good for you.

In this 10-year study, researchers looked at surveillance data from 63 hospital emergency departments to estimate the annual number of ED visits associated with adverse effects from dietary supplements. The authors defined “dietary supplements” as herbal or complementary products, and vitamin or amino acid micronutrients. Patients visiting the ED for symptoms related to supplement use were an average of 32 years old, and women made up more than half of all visits. Just over 10% of these visits resulted in admission to the hospital, especially among adults older than 65.

Weight-loss products accounted for one quarter of all single-product ED visits and disproportionately affected women, while men were more likely to experience adverse effects from products advertised for sexual enhancement and body building. Energy-boosting products made up another 10% of these visits.

Young adults weren’t the only ones affected. Many children under 4 years of age suffered allergic reactions or digestive symptoms (nausea, vomiting, abdominal pain) from unsupervised, accidental ingestion of vitamins. Patients older than 65 were more likely to have trouble swallowing after taking vitamins or micronutrients of large pill size.

Although the study’s findings are annual estimates based on ED visits to a relatively small number of hospitals, they reflect the growing use of dietary supplements and micronutrients. These products are widely available without prescription and are advertised as alternatives or complements to therapeutically prescribed pharmaceutical drugs. As a result, dietary or herbal supplements are widely perceived to be natural and safe. The most recent figures indicate that there are more than 55,000 such products available in the United States.

What you need to know before you take a supplement

While the Food and Drug Administration (FDA) is charged with overseeing dietary supplements, there is no safety testing or FDA approval required before a new supplement goes on the market. In addition, there are no requirements that dietary supplement packaging list potential adverse effects, nor are there standards for maximum pill size (a clear risk for older people).

Health care providers also may neglect to ask patients about the use of over-the-counter or natural dietary supplements. Without that information, they may not recognize that any signs and symptoms their patients may be experiencing could be related to these products.

To be sure, some dietary supplements can be beneficial. That’s because these products contain active ingredients — molecules that interact at receptors in our body and cause physiological changes. However, because they contain active ingredients, they can also cause unwanted effects, such as elevated blood pressure, racing or irregular heartbeat, headache, dizziness, or digestive symptoms.

What is the safe approach to the use of these dietary supplements? Staying healthy requires a multifaceted approach to self-care. Being aware and knowledgeable about any supplement—whether it is advertised as natural, herbal, or non-drug — is part of that care.

If you do take vitamins, supplements, or herbal products, always read any safety labels that are included with the packaging. Ask a pharmacist, your doctor, or a nurse to review everything you take to ensure that supplements will not cause harmful effects, either alone or in combination with regularly prescribed or over-the-counter drugs. If you do develop concerning symptoms after taking a dietary supplement, stop taking it and call your doctor.

The post Harmful effects of supplements can send you to the emergency department appeared first on Harvard Health Blog.

From: Susan Farrell, MD http://www.health.harvard.edu/blog/harmful-effects-of-supplements-can-send-you-to-the-emergency-department-201510158434

Thursday, October 15, 2015

What you need to know before you take a supplement

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