12/01/15

Tuesday, December 1, 2015

Consumer Reports investigates prescription drug sticker shock

Americans spent $374 billion on prescription drugs last year, but only 17 percent of people shop around for a lower price

From: http://www.cbsnews.com/videos/consumer-reports-investigates-prescription-drug-sticker-shock/

Analyst: Drug companies have "moral obligation" to make meds affordable

Don Dahler has a look at the drug company practice of buying the rights to drugs and then drastically increasing their prices

From: http://www.cbsnews.com/videos/analyst-drug-companies-have-moral-obligation-to-make-meds-affordable/

High cost of Hep C drug a barrier to treatment

A new breakthrough drug that cures Hepatitis C is so expensive that many people cannot afford it -- even with a drug benefit on their health insurance

From: http://www.cbsnews.com/videos/high-cost-of-hep-c-drug-a-barrier-to-treatment/

Reining in the rising cost of some prescription drugs

Some pharmaceutical companies are making their own version of pricey prescriptions, saying they only want to make "an ethical profit"

From: http://www.cbsnews.com/news/reining-in-the-rising-cost-of-some-prescription-drugs/

VA can't afford drug for veterans suffering from hepatitis C

Up to 230,000 U.S. veterans are suffering from hepatitis C, but the Department of Veterans Affairs says it can't afford the antiviral drugs to cure them

From: http://www.cbsnews.com/news/va-cant-afford-drug-for-veterans-suffering-from-hepatitis-c/

Study: Higher cigarette taxes could save babies' lives

Researchers say an extra $1 a pack could lead to hundreds fewer infant deaths each year

From: http://www.cbsnews.com/news/higher-cigarette-taxes-save-babies-lives-study-finds/

Sleep Apnea Devices Lower Blood Pressure

Researchers find both common treatments, CPAP and MADs, produce modest decreases

From: http://www.webmd.com/sleep-disorders/sleep-apnea/news/20151201/sleep-apnea-devices-lower-blood-pressure?src=RSS_PUBLIC

Multiple Sclerosis: Questions to Ask Your Doctor

Questions to ask your doctor about multiple sclerosis.

From: http://www.webmd.com/multiple-sclerosis/features/10-questions?src=RSS_PUBLIC

Multiple Sclerosis: Planning for Your Future

Planning ahead, including for insurance and finances, is key when you have a chronic condition like multiple sclerosis (MS). Get tips to get started from WebMD.

From: http://www.webmd.com/multiple-sclerosis/features/live-better-with-ms?src=RSS_PUBLIC

What Isn’t Your Loved One Telling You About MS?

Multiple sclerosis can cause hidden symptoms. Here’s how to help your loved one.

From: http://www.webmd.com/multiple-sclerosis/features/loved-one-multiple-sclerosis?src=RSS_PUBLIC

1 in 8 Adults Still Have High Cholesterol: CDC

Many don't meet targets, and expert says even those targets aren't good enough to prevent heart attacks

From: http://www.webmd.com/cholesterol-management/news/20151201/1-in-8-american-adults-still-have-high-cholesterol-cdc?src=RSS_PUBLIC

HIV Prevention Pill May Not Need to Be Taken Daily

Research suggests Truvada still works when taken before and after sex

From: http://www.webmd.com/hiv-aids/news/20151201/hiv-prevention-pill-may-not-need-to-be-taken-daily?src=RSS_PUBLIC

The secret behind why knuckles crack

Ultrasound images reveal a bright flash, "like a firework exploding in the joint"

From: http://www.cbsnews.com/news/the-secret-behind-why-knuckles-crack-discovered/

Who should be taking the HIV prevention pill?

Experts say many of the people who could benefit from the medication aren't getting it

From: http://www.cbsnews.com/news/1-in-4-gay-and-bisexual-men-should-take-hiv-prevention-pill-cdc/

Mayo Clinic Minute: Lewy Body Dementia 101

From: Mayo Clinic http://www.youtube.com/watch?v=T57EM7GMSSI

Casein Compared with Whey Proteins Affects the Organization of Dietary Fat during Digestion and Attenuates the Postprandial Triglyceride Response to a Mixed High-Fat Meal in Healthy, Overweight Men [Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions]

Background: Postprandial lipemia is a risk factor for cardiovascular disease. The potential impacts of the type/nature of dietary protein on postprandial lipemia and associated dysregulations have been insufficiently investigated.

Objective: We investigated the postprandial effect of including in a high-fat meal some milk protein fractions that markedly differ in their physicochemical properties and composition [either casein (CAS), whey protein (WHE), or α-lactalbumin-enriched whey protein (LAC)].

Methods: The protein fractions were incorporated as 15% energy in a high-fat meal in a 3-period, crossover postprandial study of 10 healthy overweight men with an elevated waist circumference (>94 cm). We measured postprandial changes in plasma lipids, amino acids, glucose, and oxidative stress markers, vascular function (using pulse contour analysis), and low-grade inflammation (using plasma markers). We also characterized in vitro the meal structures, including the size of the fat globule, and possible changes during digestion.

Results: The type of protein did not affect postprandial plasma glucose, amino acids, insulin, or nonesterified fatty acids, but, compared with WHE and LAC, which did not differ, CAS markedly reduced postprandial triglycerides (TGs), achieving a 22 ± 10% reduction in the 6-h area under the curve (P < 0.05). Similar trends were shown for plasma chylomicrons [apolipoprotein (apo)B-48; P < 0.05]. However, there were no significant differences between the meals regarding postprandial oxidative stress (plasma hydroperoxides and malondialdehyde), endothelial dysfunction (salbutamol-induced changes in pulse contour analysis), or low-grade inflammation. In vitro studies showed that when the pH of the meal decreased to stomach pH values, the reduction in the solubility of casein resulted in a phase separation between fat and protein, whereas the proteins in the other meals remained suspended with fat globules.

Conclusion: In healthy overweight men, casein has specific physical interactions with fat that affect postprandial TGs, leading to the formation of fewer chylomicrons or an increase in chylomicron clearance. This trial was registered at clinicaltrials.gov as NCT00931151.

From: Mariotti, F., Valette, M., Lopez, C., Fouillet, H., Famelart, M.-H., Mathe, V., Airinei, G., Benamouzig, R., Gaudichon, C., Tome, D., Tsikas, D., Huneau, J. F. http://jn.nutrition.org/cgi/content/short/145/12/2657?rss=1

Americans pay up to 10 times more for common drugs, survey shows

Consumer Reports uncovered striking price ranges for prescription drugs across the country, even retailers within the same zip code

From: http://www.cbsnews.com/news/consumer-reports-survey-finds-varying-prescription-drug-prices-across-country/

Increased IGF-IEc expression and mechano-growth factor production in intestinal muscle of fibrostenotic Crohn's disease and smooth muscle hypertrophy

The igf1 gene is alternatively spliced as IGF-IEa and IGF-IEc variants in humans. In fibrostenotic Crohn's disease, the fibrogenic cytokine TGF-β₁ induces IGF-IEa expression and IGF-I production in intestinal smooth muscle and results in muscle hyperplasia and collagen I production that contribute to stricture formation. Mechano-growth factor (MGF) derived from IGF-IEc induces skeletal and cardiac muscle hypertrophy following stress. We hypothesized that increased IGF-IEc expression and MGF production mediated smooth muscle hypertrophy also characteristic of fibrostenotic Crohn's disease. IGF-IEc transcripts and MGF protein were increased in muscle cells isolated from fibrostenotic intestine under regulation by endogenous TGF-β₁. Erk5 and MEF2C were phosphorylated in vivo in fibrostenotic muscle; both were phosphorylated and colocalized to nucleus in response to synthetic MGF in vitro. Smooth muscle-specific protein expression of α-smooth muscle actin, -smooth muscle actin, and smoothelin was increased in affected intestine. Erk5 inhibition or MEF2C siRNA blocked smooth muscle-specific gene expression and hypertrophy induced by synthetic MGF. Conditioned media of cultured fibrostenotic muscle induced muscle hypertrophy that was inhibited by immunoneutralization of endogenous MGF or pro-IGF-IEc. The results indicate that TGF-β₁-dependent IGF-IEc expression and MGF production in patients with fibrostenotic Crohn's disease regulates smooth muscle cell hypertrophy a critical factor that contributes to intestinal stricture formation.

From: Li, C., Vu, K., Hazelgrove, K., Kuemmerle, J. F. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G888?rss=1

CD44 and TLR4 mediate hyaluronic acid regulation of Lgr5+ stem cell proliferation, crypt fission, and intestinal growth in postnatal and adult mice

Hyaluronic acid, a glycosaminoglycan in the extracellular matrix, binds to CD44 and Toll-like receptor 4 (TLR4). We previously addressed the role of hyaluronic acid in small intestinal and colonic growth in mice. We addressed the role of exogenous hyaluronic acid by giving hyaluronic acid intraperitoneally and the role of endogenous hyaluronic acid by giving PEP-1, a peptide that blocks hyaluronic acid binding to its receptors. Exogenous hyaluronic acid increased epithelial proliferation but had no effect on intestinal length. PEP-1 resulted in a shortened small intestine and colon and diminished epithelial proliferation. In the current study, we sought to determine whether the effects of hyaluronic acid on growth were mediated by signaling through CD44 or TLR4 by giving exogenous hyaluronic acid or PEP-1 twice a week from 3–8 wk of age to wild-type, CD44^–/–, and TLR4^–/– mice. These studies demonstrated that signaling through both CD44 and TLR4 were important in mediating the effects of hyaluronic acid on growth in the small intestine and colon. Extending our studies to early postnatal life, we assessed the effects of exogenous hyaluronic acid and PEP-1 on Lgr5⁺ stem cell proliferation and crypt fission. Administration of PEP-1 to Lgr5⁺ reporter mice from postnatal day 7 to day 14 decreased Lgr5⁺ cell proliferation and decreased crypt fission. These studies indicate that endogenous hyaluronic acid increases Lgr5⁺ stem cell proliferation, crypt fission, and intestinal lengthening and that these effects are dependent on signaling through CD44 and TLR4.

From: Riehl, T. E., Santhanam, S., Foster, L., Ciorba, M., Stenson, W. F. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G874?rss=1

Apolipoprotein A-V is present in bile and its secretion increases with lipid absorption in Sprague-Dawley rats

Apolipoprotein (apo) A-V is a protein synthesized only in the liver that dramatically modulates plasma triglyceride levels. Recent studies suggest a novel role for hepatic apoA-V in regulating the absorption of dietary triglycerides, but its mode of action on the gut remains unknown. The aim of this study was to test for apoA-V in bile and to determine whether its secretion is regulated by dietary lipids. After an overnight recovery, adult male Sprague-Dawley bile fistula rats indeed secreted apoA-V into bile at a constant rate under fasting conditions. An intraduodenal bolus of intralipid (n = 12) increased the biliary secretion of apoA-V but not of other apolipoproteins, such as A-I, A-IV, B, and E. The lipid-induced increase of biliary apoA-V was abolished under conditions of poor lymphatic lipid transport, suggesting that the stimulation is regulated by the magnitude of lipids associated with chylomicrons transported into lymph. We also studied the secretion of apoA-V into bile immediately following bile duct cannulation. Biliary apoA-V increased over time (~6-fold increase at hour 16, n = 8) but the secretions of other apolipoproteins remained constant. Replenishing luminal phosphatidylcholine and taurocholate (n = 9) only enhanced apoA-V secretion in bile, suggesting that the increase was not due to depletion of phospholipids or bile salts. This is the first study to demonstrate that apoA-V is secreted into bile, introducing a potential route of delivery of hepatic apoA-V to the gut lumen. Our study also reveals the uniqueness of apoA-V secretion into bile that is regulated by mechanisms different from other apolipoproteins.

From: Zhang, L. S., Sato, H., Yang, Q., Ryan, R. O., Wang, D. Q.- H., Howles, P. N., Tso, P. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G918?rss=1

Despite sequence homologies to gluten, salivary proline-rich proteins do not elicit immune responses central to the pathogenesis of celiac disease

Celiac disease (CD) is an inflammatory disorder triggered by ingested gluten, causing immune-mediated damage to the small-intestinal mucosa. Gluten proteins are strikingly similar in amino acid composition and sequence to proline-rich proteins (PRPs) in human saliva. On the basis of this feature and their shared destination in the gastrointestinal tract, we hypothesized that salivary PRPs may modulate gluten-mediated immune responses in CD. Parotid salivary secretions were collected from CD patients, refractory CD patients, non-CD patients with functional gastrointestinal complaints, and healthy controls. Structural similarities of PRPs with gluten were probed with anti-gliadin antibodies. Immune responses to PRPs were investigated toward CD patient-derived peripheral blood mononuclear cells and in a humanized transgenic HLA-DQ2/DQ8 mouse model for CD. Anti-gliadin antibodies weakly cross-reacted with the abundant salivary amylase but not with PRPs. Likewise, the R5 antibody, recognizing potential antigenic gluten epitopes, showed negligible reactivity to salivary proteins from all groups. Inflammatory responses in peripheral blood mononuclear cells were provoked by gliadins whereas responses to PRPs were similar to control levels, and PRPs did not compete with gliadins in immune stimulation. In vivo, PRP peptides were well tolerated and nonimmunogenic in the transgenic HLA-DQ2/DQ8 mouse model. Collectively, although structurally similar to dietary gluten, salivary PRPs were nonimmunogenic in CD patients and in a transgenic HLA-DQ2/DQ8 mouse model for CD. It is possible that salivary PRPs play a role in tolerance induction to gluten early in life. Deciphering the structural basis for the lack of immunogenicity of salivary PRPs may further our understanding of the toxicity of gluten.

From: Tian, N., Leffler, D. A., Kelly, C. P., Hansen, J., Marietta, E. V., Murray, J. A., Schuppan, D., Helmerhorst, E. J. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G910?rss=1

Krüppel-like factor KLF10 deficiency predisposes to colitis through colonic macrophage dysregulation

Krüppel-like factor (KLF)-10 is an important transcriptional regulator of TGF-β₁ signaling in both CD8⁺ and CD4⁺ T lymphocytes. In the present study, we demonstrate a novel role for KLF10 in the regulation of TGFβRII expression with functional relevance in macrophage differentiation and activation. We first show that transfer of KLF10^–/– bone marrow-derived macrophages into wild-type (WT) mice leads to exacerbation of experimental colitis. At the cell biological level, using two phenotypic strategies, we show that KLF10-deficient mice have an altered colonic macrophage phenotype with higher frequency of proinflammatory LyC6⁺MHCII⁺ cells and a reciprocal decrease of the anti-inflammatory LyC6^–MHCII⁺ subset. Additionally, the anti-inflammatory CD11b⁺CX3CR1^hi subset of colonic macrophages is significantly decreased in KLF10^–/– compared with WT mice under inflammatory conditions. Molecularly, CD11b⁺ colonic macrophages from KLF10^–/– mice exhibit a proinflammatory cytokine profile with increased production of TNF-α and lower production of IL-10 in response to LPS stimulation. Because KLF10 is a transcription factor, we explored how this protein may regulate macrophage function. Consequently, we analyzed the expression of TGFβRII expression in colonic macrophages and found that, in the absence of KLF10, macrophages express lower levels of TGFβRII and display an attenuated Smad-2 phosphorylation following TGF-β₁ stimulation. We further show that KLF10 directly binds to the TGFβRII promoter in macrophages, leading to enhanced gene expression through histone H3 acetylation. Collectively, our data reveal a critical role for KLF10 in the epigenetic regulation of TGFβRII expression in macrophages and the acquisition of a "regulatory" phenotype that contributes to intestinal mucosal homeostasis.

From: Papadakis, K. A., Krempski, J., Svingen, P., Xiong, Y., Sarmento, O. F., Lomberk, G. A., Urrutia, R. A., Faubion, W. A. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G900?rss=1

Ischemia reperfusion of the hepatic artery induces the functional damage of large bile ducts by changes in the expression of angiogenic factors

Liver transplantation and cholangiocarcinoma induce biliary dysfunction following ischemia reperfusion (IR). The function of the intrahepatic biliary tree is regulated by both autocrine and paracrine factors. The aim of the study was to demonstrate that IR-induced damage of cholangiocytes is associated with altered expression of biliary angiogenic factors. Normal and bile duct ligation rats underwent 24-h sham or hepatic reperfusion after 30 min of transient occlusion of the hepatic artery (HAIR) or portal vein (PVIR) before collecting liver blocks and cholangiocyte RNA or protein. We evaluated liver histology, biliary apoptosis, proliferation and expression of VEGF-A/C, VEGFR-2/3, Ang-1/2, and Tie-1/2 in liver sections and isolated small and large cholangiocytes. Normal rat intrahepatic cholangiocyte cultures (NRICC) were maintained under standard conditions in normoxic or under a hypoxic atmosphere for 4 h and then transferred to normal conditions for selected times. Subsequently, we measured changes in biliary proliferation and apoptosis and the expression of VEGF-A/C and VEGFR-2/3. In vivo, HAIR (but not PVIR) induced damage of large bile ducts and decreased proliferation and secretin-stimulated cAMP levels. HAIR-induced damage of large bile ducts was associated with increased expression of VEGF-A/C, VEGFR-2/3, Ang-1/2, and Tie-1/2. In vitro, under hypoxic conditions, there was increased apoptosis and reduced proliferation of NRICC concomitant with enhanced expression of VEGF-A/C and VEGFR-2/3. The functional damage of large bile ducts by HAIR and hypoxia is associated with increased expression of angiogenic factors in small cholangiocytes, presumably due to a compensatory mechanism in response to biliary damage.

From: Mancinelli, R., Glaser, S., Francis, H., Carpino, G., Franchitto, A., Vetuschi, A., Sferra, R., Pannarale, L., Venter, J., Meng, F., Alpini, G., Onori, P., Gaudio, E. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G865?rss=1

Loss of NHE8 expression impairs intestinal mucosal integrity

The newest member of the Na⁺/H⁺ exchanger (NHE) family, NHE8, is abundantly expressed at the apical membrane of the intestinal epithelia. We previously reported that mucin 2 expression was significantly decreased in the colon in NHE8^–/– mice, suggesting that NHE8 is involved in intestinal mucosal protection. In this study, we further evaluated the role of NHE8 in intestinal epithelial protection after dextran sodium sulfate (DSS) challenge. Compared with wild-type mice, NHE8^–/– mice have increased bacterial adhesion and inflammation, especially in the distal colon. NHE8^–/– mice are also susceptible to DSS treatment. Real-time PCR detected a remarkable increase in the expression of IL-1β, IL-6, TNF-α, and IL-4 in DSS-treated NHE8^–/– mice compared with DSS-treated wild-type littermates. Immunohistochemistry showed a disorganized epithelial layer in the colon of NHE8^–/– mice. Periodic acid-Schiff staining showed a reduction in the number of mature goblet cells and the area of the goblet cell theca in NHE8^–/– mice. Phyloxine/tartrazine staining revealed a decrease in functional Paneth cell population in the NHE8^–/– small intestinal crypt. The expression of enteric defensins was also decreased in NHE8^–/– mice. The reduced mucin production in goblet cells and antimicrobial peptides production in Paneth cells lead to disruption of the intestinal mucosa protection. Therefore, NHE8 may be involved in the establishment of intestinal mucosal integrity by regulating the functions of goblet and Paneth cells.

From: Wang, A., Li, J., Zhao, Y., Johansson, M. E. V., Xu, H., Ghishan, F. K. http://ajpgi.physiology.org/cgi/content/abstract/309/11/G855?rss=1

Insurer Offering Life Insurance To People With HIV

The move signals growing recognition of HIV/AIDS’ transformation from a death sentence to a serious but manageable disease.

From: http://www.webmd.com/hiv-aids/news/20151201/major-insurer-says-it-will-offer-individual-life-insurance-coverage-to-people-with-hiv?src=RSS_PUBLIC

Express Scripts offers $1 alternative to $750 pill

After drug company's owner announced a 5,000-percent price hike earlier this year, a less expensive option will soon be available

From: http://www.cbsnews.com/news/express-scripts-will-offer-1-alternative-to-750-daraprim-pill/

New diabetes cases drop for first time in decades

After tripling over the last quarter century, a deadly trend shows signs of progress

From: http://www.cbsnews.com/news/new-diabetes-cases-are-dropping-a-first-in-decades/

Chronic Traumatic Encephalopathy (CTE) in Amateur Athletes - Mayo Clinic

From: Mayo Clinic http://www.youtube.com/watch?v=_hHV3QEvA5M

Possible Weight-Loss Tool: Blocking Stomach Artery

Experimental procedure tested in 4 morbidly obese patients so far

From: http://www.webmd.com/diet/obesity/20151201/possible-new-weight-loss-tool-blocking-stomach-artery?src=RSS_PUBLIC

USDA Begins 49th Enrollment Period for the Conservation Reserve Program

WASHINGTON, Dec. 1, 2015 – Agriculture Secretary Tom Vilsack today reminded farmers and ranchers that the next general enrollment period for the Conservation Reserve Program (CRP) begins today, Dec. 1, 2015, and ends on Feb. 26, 2016.

From: http://www.usda.gov/wps/portal/usda/usdahome?contentid=2015/12/0332.xml&contentidonly=true

Sugar-Free Sodas, Candy Can Still Damage Teeth

But, researchers add that there are easy ways to prevent lasting harm

From: http://www.webmd.com/oral-health/news/20151130/sugar-free-sodas-candy-can-still-damage-your-teeth?src=RSS_PUBLIC

Brain Gains for Older Adults Who Start Exercising

Besides improved heart and lung health, study detected growth in cerebral cortex

From: http://www.webmd.com/healthy-aging/news/20151130/brain-gains-for-older-adults-who-start-exercising?src=RSS_PUBLIC

Woman undergoing surgery after finding kidney donor on Craigslist

New Jersey man is being credited for saving her life after accidentally coming across an ad searching for a kidney donor

From: http://www.cbsnews.com/news/nina-saria-finds-kidney-donor-glenn-calderbank-through-misplaced-ad-on-craigslist/

Consumer Reports investigates prescription drug sticker shock

Craigslist mistake leads New Jersey man to donate kidney

Glenn Calderbank from New Jersey is donating one of his kidneys to Nina Saria, a woman he met just months ago through a Craigslist ad

From: http://www.cbsnews.com/videos/craigslist-mistake-leads-new-jersey-man-to-donate-kidney/

Beyond the 2-hour screen rule: 10 tips for parenting in the digital age

(Follow me at @drClaire)

For years, the recommendation of the American Academy of Pediatrics (AAP) when it came to media and kids was pretty straightforward: limit the TV to 2 hours a day, and don’t let children under the age of 2 watch it. As the Internet emerged and new devices arrived, the recommendation was tweaked to 2 hours of “entertainment media,” with the recommendation that the under-2 crowd stay screen-free.

But these days, even that has gotten hard. Is doing a math game on an iPad entertainment? How do you do the 2-hour rule if your teen intermittently checks social media while doing online homework? What about texting — that’s media and screen-based, but a lot of it is conversations between friends, instead of tying up the home phone for hours, like teens used to do. And if you let your toddler watch a video on your phone to keep them quiet on a crowded bus (so that you don’t get the evil eye from everyone around you), is that terrible?

Our children are growing up in a digital age, and parenting needs to reflect that. The AAP understands this, and is working hard to understand the ongoing research about the effects of media on children, so as to give the best recommendations to parents. In the meantime, they have released Ten Tips for Parents in the Digital Age:

Treat media as you would any other environment in your child’s life. You want to know what your children do at school and with friends — you should want to know what they do online, too. And just like you have rules about behavior at school and with friends, you should have rules about online life as well.
Set limits and encourage playtime. The AAP recommends setting “reasonable limits” on media use, which will vary with the child and the situation. It’s also important that children get plenty of time away from media, using their brains and bodies in different ways and interacting with the three-dimensional world around them.
Families who play together learn together. This is particularly important for younger children — if you are going to let them use media, do it with them so that they get the back-and-forth that is so crucial for early brain development. And instead of using media as a babysitter, use it as a way to have fun together.
Be a good role model. If you are on your phone or laptop all the time, or turn on the TV as soon as you sit down on the couch, what kind of message are you sending?
Know the value of face-to-face communication. Not only is it crucial for the developing brains of babies, it’s crucial for relationships and mental health. Media can sometimes help with this, like with video chats with far-flung relatives, but for the most part, the take-home is: everyone needs to put down the devices and talk to each other on a regular basis.
Create tech-free zones. Sometimes technology can truly get in the way — of relationships (so the dinner table is a good place to make a tech-free zone) or sleep (this is becoming a big problem with teens — phones should be charged outside the bedroom). It’s also a safety issue: texting and driving (or walking down the street) can be fatal.
Don’t use tech as an emotional pacifier. Yes, it can come in handy with the toddler on that crowded bus. But kids also need to learn to handle emotions — and boredom — without the help of a device. It’s an important life skill.
Do your homework when it comes to apps for kids. They are absolutely not all created equal. A great resource is Common Sense Media, which has reviews on apps as well as all sorts of other media like movies and TV shows.
It’s okay for your teen to be online. It really is where teens connect these days, and it’s not a good idea to keep them off. They do, however, need to learn to be good and responsible digital citizens: online time shouldn’t crowd out offline activities and relationships; they need to be kind; and they need to remember that nothing they do online is truly private — and everything they do is potentially permanent.
Kids will make mistakes. Because that’s what kids do. They fall off bikes, they kick the ball into the other team’s goal, they break rules, they hurt feelings. They can make mistakes online, too. The AAP recommends trying to approach mistakes with empathy, and turning them into teachable moments. But if the “mistakes” continue, especially if you have concerns about bullying, sexting, or signs of depression, let your doctor know.

The AAP has lots of great resources to help families make healthy media decisions — as does the Center on Media and Child Health of Boston Children’s Hospital.

The post Beyond the 2-hour screen rule: 10 tips for parenting in the digital age appeared first on Harvard Health Blog.

From: Claire McCarthy, MD http://www.health.harvard.edu/blog/beyond-the-2-hour-screen-rule-10-tips-for-parenting-in-the-digital-age-201512018667

Tuesday, December 1, 2015

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