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“Childhood obesity is a significant public health issue in our country, with nearly one-third of all US children ages 2-17 overweight or obese,” says Rachel Kimbro, study co-author, associate professor of sociology at Rice University and director of the Kinder Institute Urban Health Program. “Despite this, very little research has been conducted to explore the impact of family structure on this epidemic.”

In a recent edition of the Journal of Applied Research on Children: Informing Policy for Children at Risk, research by Kimbro and colleagues examined the obesity rates of preschool children living in traditional and nontraditional family structures in the US.

Their research shows that children living in a traditional two-parent married household are less likely to be obese with a 17 percent obesity rate, than children living with cohabitating parents, who have a 31 percent obesity rate.

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Read the original study

The obesity rate for children living with an adult relative is 29 percent, with a single mother is 23 percent. Kids raised in a cohabitating stepparent family have a 23 percent obesity rate. The study did not evaluate children of same-sex couples, due to lack of available data.

The higher rates for nontraditional parent families were observed even after the researchers accounted for factors associated with childhood obesity, including diet, physical activity, and socioeconomic status.

The exception to this finding was children living with single fathers or in married stepparent households, who had an obesity rate of 15 percent.

“Previous research has shown that single-father households tend to have more socioeconomic resources than single-mother households,” Kimbro says. “And since socioeconomic status is the single greatest predictor of health, it serves to explain why children in single-father households may be less likely to be obese.”

‘Birth Cohort’ study

The research sample of 10,400 children comes from the Early Childhood Longitudinal Study–Birth Cohort, a nationally representative study of US children and their families designed to provide information on children’s development.

Data collection for the study began in 2001. The primary caregivers of the children participated in the first wave of the in-home interviews when their children were approximately 9 months old. Data was subsequently collected when the children were 2 years old, in preschool (approximately age 4) and in kindergarten.

The sample included children from diverse socioeconomic, racial, and ethnic backgrounds as well as an oversample of Asian, Pacific Islander, Alaska Native, American Indian, twins, and low-birth-weight children.

Forty-six percent of the children were racial or ethnic minorities, 25 percent were poor, and 16 percent of the children had mothers without high school diplomas.

The interviews included assessments of the children’s height, weight, and other measures of development, such as cognitive functioning. The children were organized in eight mutually exclusive categories designed to account for the children’s current family structure and the one they were born into.

Further exploration of family structure

The authors hope their research will inspire future studies of nontraditional family structures and their impact on health and weight.

“For reasons we cannot fully measure, there appears to be something about people who marry and have a child that is fundamentally different than the other groups, and these factors are also linked to children’s weight,” Kimbro says.

“Our hope is that this research will encourage further exploration of this topic,” says Kimbro’s co-author, Jennifer Augustine, professor of sociology at the University of Houston. “There is substantial research on how family structure matters to other domains of children’s development, yet little research on why marriage and other family structure types might matter for children’s obesity.”

Kimbro and Augustine have already begun to lead this charge with a new project that examines the household-level processes associated with different family structures that may explain differences in young children’s risk of obesity.

Rice University and the University of Houston funded the research.

Source: Rice University

Article source: http://www.futurity.org/health-medicine/lower-obesity-rates-for-kids-in-traditional-families/

At 129 kg, 32-year-old IT professional Rajdeep Roy (name changed to protect identity) had been battling not just obesity but even Type 2 diabetes for three years. “My pre-meal sugar count was 280 mg/ dL and post was 350 mg/dL. I felt perpetually tired and lethargic,” says Roy, a Kharghar resident. He had tried exercise, diet and pills to bring his weight and blood sugar level under control. Then, his doctor recommended bariatric surgery, a procedure where the stomach is stapled and a person’s appetite decreases, as a result. The procedure is used to treat morbid obesity.

“My doctor asked me to go in for bariatric surgery, which would help me in my battle against diabetes,” says Roy. “This sealed my decision.”

Across the world, bariatric surgery is used to tame diabetes, and doctors endorse it over pills and insulin injections. Now, city doctors too are recommending it. With India fast becoming the diabetic capital of the world (India and China account for more than half of the world’s diabetics), experts blame our sedentary lifestyle and easier access to nutritionally-poor, calorie-dense foods for the surge in type 2 diabetes cases. It doesn’t help that Indians are genetically prone to obesity and diabetes.

In bariatric surgery, the stomach is divided into two sections and food is directed into the smaller section, helping the patient feel full despite eating less. Studies have found that when a meal is digested in the stomach’s smaller section, the levels of insulin, hormones and amino acids are much higher, while levels of free fatty acids are lower. The surge in hormone levels help during digestion and make it easier for patients to regulate blood sugar.

Dr Jayashree Todkar, a bariatric surgeon at Kurla’s Kohinoor Hospital adds that with the presence of the hunger hormones in the body decreasing, the patient feels satiated more easily. “Diabetics find it easier to discipline their diet because with their hunger in check, they lose their cravings and don’t seek more food. Their body clock gets reset. They feel fresher and more energetic.” The surgery (costs between Rs 3-5 lakh) takes an hour and the patient is discharged in three days. The results in diabetic control are the first to show.

Endocrinologist Dr Altamash Shaikh says, “Even before you lose weight post-surgery, the patient’s requirement of tablets and insulin lowers drastically.”

Roy, who underwent the surgery in January can testify to that. “Now, my pre-meal blood sugar level is 91 mg/dL and post is 94 mg/dL. I had a chronic Urinary Tract Infection, which has disappeared. I’m off my daily dose of a dozen-odd diabetes pills,” says Roy, adding that he now eats one-sixth of what he would earlier. “I feel hungry more often, but I can’t eat more than a few spoons of dal-rice at one go. So, I eat six small meals through the day.”

In four months after the surgery, Roy lost 94 kg. “Earlier, I would struggle to walk even one kilometre. Today, I can easily walk four km without stopping.” Dr Shashank Shah, president of the Obesity Surgery Society of India, says that they are in the process of discussing guidelines to make this surgery a recommendation for diabetics, if they fulfill certain criteria.

Who’s eligible?
A Body Mass Index of 35 is the cutoff for bariatric surgery around the world. However, in India and other Asian countries, the cut-off is 32.5, as our bodies tend to have more fat. The surgery, warn doctors, is not for all who suffer from type 2 diabetes. They would recommend it only if the person has a BMI of 32.5 or more, and suffers from obesity related ailments like blood pressure, obstructive sleep apnea, high cholesterol, joint trouble, varicose veins and breathlessness. Roy, for instance, had a BMI of 37.

Dr Shaikh warns that the surgery is not a one-stop solution for diabetic cure. “Its success depends on lifestyle and food choices post-surgery, apart from how severe the patient’s diabetes is at the time of surgery. The ideal time to go for it is when your diabetes is in control and your organs are in good shape.”

Article source: http://timesofindia.indiatimes.com/life-style/health-fitness/health/Pinning-down-diabetes/articleshow/20200741.cms

A new UK study finds that children who have suffered maltreatment are 36 percent more likely to be obese in adulthood compared to non-maltreated children.

Researchers from King’s College London estimate that the prevention or effective treatment of seven cases of child maltreatment could prevent one case of adult obesity.

Experts analyzed data from 190,285 individuals across 41 studies worldwide, and have published their results in the journal Molecular Psychiatry.

Severe childhood maltreatment (physical, sexual or emotional abuse or neglect) affects approximately 1 in 5 children (under 18) in the UK and in the US.

Officials say that in addition to the long-term mental health consequences of maltreatment, there is increasing evidence that child maltreatment may affect physical health.

Dr. Andrea Danese, child and adolescent psychiatrist from King’s College London’s Institute of Psychiatry and lead author of the study says: “We found that being maltreated as a child significantly increased the risk of obesity in adult life.

“Prevention of child maltreatment remains paramount and our findings highlight the serious long-term health effects of these experiences.”

Although experimental studies in animal models have previously suggested that early life stress is associated with an increased risk of obesity, evidence from population studies has been inconsistent.

Researchers believe the new meta review provides a comprehensive assessment of the evidence from all existing population studies.

From the analysis, the authors found that childhood maltreatment was associated with adult obesity.

This association was independent of the measures or definitions used for maltreatment or obesity, childhood or adult socioeconomic status, current smoking, alcohol intake, or physical activity.

Additionally, childhood maltreatment was not linked to obesity in children and adolescents, making it unlikely that the link was explained by reverse causality (i.e. children are maltreated because they were obese).

However, the analysis showed that when current depression was taken into account, the link between childhood maltreatment and adult obesity was no longer significant, suggesting that depression might help explain why some maltreated individuals become obese.

Previous studies offer possible biological explanations for this link.

Maltreated individuals may eat more because of the effects of early life stress on areas of the developing brain linked to inhibition of feeding, or on hormones regulating appetite.

Alternatively, maltreated individuals may burn fewer calories because of the effects of early life stress on the immune system leading to fatigue and reduced activity.

According to the study authors, future research will directly assess the link between maltreatment and adult obesity.

Source: King’s College London

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Article source: http://psychcentral.com/news/2013/05/22/abused-children-at-risk-for-adult-obesity/55125.html

Toking up may help marijuana users to stay slim and lower their risk of developing diabetes, according to the latest study, which suggests that cannabis compounds may help in controlling blood sugar.

Although marijuana has a well-deserved reputation for increasing appetite via what stoners call “the munchies,” the new research [PDF], which was published in the American Journal of Medicine, is not the first to find that the drug has a two-faced relationship to weight. Three prior studies have shown that marijuana users are less likely to be obese, have a lower risk for diabetes and have lower body mass index (BMI) measurements. And these trends occurred despite the fact that they seemed to take in more calories.

Why? “The most important finding is that current users of marijuana appeared to have better carbohydrate metabolism than non-users,” says Murray Mittleman, associate professor of medicine at Harvard Medical School and the lead author of the study. “Their fasting insulin levels were lower, and they appeared to be less resistant to the insulin produced by their body to maintain a normal blood sugar level.”

The research included over 4,600 men and women participating in the National Health and Nutrition Examination Survey between 2005 and 2010.  Among them, 48% had smoked marijuana at least once in their lives and 12% were current cannabis smokers. The authors controlled for other factors like age, sex, income, alcohol use, cigarette smoking and physical activity that could also affect diabetes risk.

Even after these adjustments, the current marijuana users showed fasting insulin levels that were 16% lower than those of former or never-users, along with a 17% reduction in another measure of insulin resistance as well. Higher levels on both tests are associated with Type II diabetes, which is linked with obesity. Marijuana users also had higher levels of HDL, the so-called “good” cholesterol, which can protect against heart disease. And the regular smokers also boasted smaller waistlines: on average, they were 1.5 inches slimmer than the former users and those who had never smoked cannabis.

Researchers don’t yet know how to explain these correlations — and since the study was not a controlled trial, it’s not clear whether marijuana or some other factor in marijuana users’ lifestyles actually accounted for the beneficial effects. Studies showed, however, that the cannabinoid brain receptors affected by marijuana are deeply involved in appetite and metabolism. But the exact details of how the compound alters the relationship between appetite, caloric intake and insulin response isn’t obvious yet.

One clue, however, may lie in the effects of a diet drug that was developed to have the opposite effect that marijuana has on the brain. That drug, rimonabant, produced significant weight loss and a drop in fasting insulin levels by affecting certain cannabinoid receptors in in the exact opposite way that THC, marijuana’s main psychoactive ingredient, does.  This action is complex:  rimonabant doesn’t simply block the receptor and keep the natural cannabinoids from activating it.  Instead, while the natural cannabinoids elevate the normal level of activity already going on in the system; rimonabant lowers it so the result is precisely the reverse of activating the receptor naturally. However, due to psychiatric side effects like increasing suicide risk, rimonabant was pulled from the European market and never approved in the U.S.

MORE: Reverse Engineering the Marijuana ‘Munchies’: What Causes Binge Eating?

How could both marijuana and a compound that has the the opposite effect of pot act on the same brain receptors and lead to weight loss? Natural marijuana includes many different potentially active compounds, and one of them— rather than THC— could be responsible for this effect.  One potential candidate is a substance called cannabidiol or CBD, which also affects cannabinoid receptors, but in a different way than THC or rimonabant does.

Another possibility involves tolerance: repeated use of a drug can make receptors less sensitive over time. “The most likely explanation is that prolonged cannabis use causes the [receptors] to lose sensitivity and become inactive,” says Daniele Piomelli, a professor of pharmacology at the University of California-Irvine, who was not associated with the new research, “This has been shown to happen in people who smoke marijuana. This weakening of the [these receptors] translates into a lower risk for obesity and diabetes because the inactive receptor would be unable to respond to our own cannabis-like molecules, which we know are important in keeping us chubby.” While marijuana may initially promote appetite and overeating, in the long run it has the opposite effect because it desensitizes cannabinoid receptors and may even protect against obesity.

So don’t skip the gym and break out the bong just yet: there’s still not enough data to tell whether marijuana, like alcohol, could have health benefits in moderation. Mittleman says that the study relied on self-reported use of marijuana, which can be unreliable. However, he points out that since people are more likely to hide drug use than they are to falsely claim it, the findings could even underestimate marijuana’s effects.

MORE: Marijuana Slims? Why Pot Smokers Are Less Obese

But whether that’s true, and whether marijuana might be a window into understanding how to best control glucose and insulin to prevent diabetes, isn’t known yet. “It is much too early to say,” says Mittleman, “We need much more research to better understand the biologic responses to marijuana use. We really need more research to allow physicians and patients to make decisions based on solid evidence.” An editorial [PDF] that accompanied the study also urged government action to reduce barriers to such research.

Even with 18 states now approving marijuana for medical uses, the politics of pot will always shadow research efforts to understand how cannabinoids work in the brain—or affect disease. But, as Piomelli says, “The [new] study suggests that smoking marijuana [may] protect people against obesity and diabetes.” And following up on that finding could yield new insights into how to tackle one of our biggest public health issues.

Article source: http://healthland.time.com/2013/05/21/marijuana-the-next-diabetes-drug/

By Dennis Thompson

HealthDay Reporter

MONDAY, May 20 (HealthDay News) — Boys who are diagnosed with attention deficit-hyperactivity disorder (ADHD) are twice as likely to become obese adults as those who didn’t have the disorder when they were young, a new 30-year study shows.

Researchers found that men with childhood ADHD tended to have a higher body-mass index (BMI) and obesity, even if they no longer had symptoms of the disorder. Socioeconomics made no difference; well-off or poor, they tended toward obesity.

“The bottom line is, boys who were hyperactive when followed up for more than 30 years turn out to be more likely to be obese than comparable kids from their same communities,” said study co-author Dr. Francisco Xavier Castellanos, a professor of child and adolescent psychiatry in the Child Study Center at NYU Langone Medical Center in New York City.

“That really seems to be reflective of their early hyperactivity. It doesn’t matter what their current diagnosis is so much, so we think these are longstanding issues that likely arose in early adolescence,” he added.

A lack of impulse control and poor planning skills, symptoms often associated with ADHD, could lead to poor eating habits and food choices as well as the tendency to overeat, the study authors speculated.

“It fits with other studies, and suggests that the inability to control one’s impulses, the tendency to be relatively reward-driven, may represent a risk of obesity over time,” Castellanos said.

The study, published online May 20 and in the June print issue of Pediatrics, tracked 111 men diagnosed with childhood hyperactivity, touching base with them at ages 18, 25 and 41. By adulthood, 41 percent had become obese, compared with a non-hyperactive control group that had a 22 percent obesity rate.

The results are somewhat confounding, Castellanos said.

“The pattern of results to a certain extent was counterintuitive,” he said. “We thought we would get the strongest effect in those men who manifested ADHD as adults, and that wasn’t the case. That suggests that it’s not something that is very tightly related to the current diagnosis, but the tendency to have the diagnosis.”

The findings run counter to an earlier study that showed that hyperactive adult men had a greater tendency for obesity than men who left childhood ADHD behind, said Dr. Craig Surman, scientific coordinator for the Adult ADHD Research Program at Massachusetts General Hospital in Boston.

“So, the simple story here would be we don’t know, because you have to replicate studies to know,” he said. “The question now becomes why the findings are different.”

Future research also needs to consider whether women with childhood ADHD are as likely as men with childhood ADHD to become obese, and whether controlling hyperactivity through the use of medication can have an impact, Surman said.

ADHD is more common in boys than girls, with 12 percent of U.S. boys aged 3 to 17 receiving the diagnosis, according to the U.S. Centers for Disease Control and Prevention.

The link between ADHD and obesity has become a topic of great interest as elevated rates of obesity have been reported in children with the disorder, Surman said. Obesity can lead to heart disease and diabetes later in life.

“It’s very important to understand the ways ADHD affects life and self-care,” Surman said. “We’ve known for some time that it’s not just people’s desks and houses that are messy. For some people, it’s a lack of ability to control how to care for themselves as well.”

Article source: http://www.webmd.com/add-adhd/childhood-adhd/news/20130520/adhd-in-childhood-may-raise-risk-for-obesity-in-adulthood

]]> http://www.celebrities-with-diseases.com/obesity-fat/adhd-in-childhood-may-raise-risk-for-obesity-in-adulthood-30132.html/feed 0 http://www.celebrities-with-diseases.com/diabetes-2/protein-that-can-stop-diabetes-in-its-tracks-identified-30131.html http://www.celebrities-with-diseases.com/diabetes-2/protein-that-can-stop-diabetes-in-its-tracks-identified-30131.html#comments Tue, 21 May 2013 02:38:41 +0000 Lee http://www.celebrities-with-diseases.com/diabetes-2/protein-that-can-stop-diabetes-in-its-tracks-identified-30131.html Scientists have identified an immune protein that has the potential to stop or reverse the development of Type-1 diabetes in its early stages, before insulin-producing cells have been destroyed.

The discovery has wider repercussions, as the protein is responsible for protecting the body against excessive immune responses, and could be used to treat, or even prevent, other immune disorders such as multiple sclerosis and rheumatoid arthritis.

Professor Len Harrison, Dr. Esther Bandala-Sanchez and Dr. Yuxia Zhang led the research team from Australia’s Walter and Eliza Hall Institute’s Molecular Medicine division that identified the immune protein CD52 as responsible for suppressing the immune response, and its potential for protecting against autoimmune diseases.

Autoimmune diseases develop when the immune system goes awry and attacks the body’s own tissues. Mr. Harrison said CD52 held great promise as a therapeutic agent for preventing and treating autoimmune diseases such as Type-1 diabetes.

“Immune suppression by CD52 is a previously undiscovered mechanism that the body uses to regulate itself, and protect itself against excessive or damaging immune responses,” Mr. Harrison said.

“We are excited about the prospect of developing this discovery to clinical trials as soon as possible, to see if CD52 can be used to prevent and treat Type-1 diabetes and other autoimmune diseases. This has already elicited interest from pharmaceutical companies,” Mr. Harrison said.

Type-1 diabetes is an autoimmune disease that develops when immune cells attack and destroy insulin-producing beta cells in the pancreas.

Harrison said that T cells that have or release high levels of CD52 are necessary to maintain normal balance in the immune system.

“In a preclinical model of Type-1 diabetes, we showed that removal of CD52-producing immune cells led to rapid development of diabetes,” he said.

“We think that cells that release CD52 are essential to prevent the development of autoiummune disease, and that CD52 has great potential as a therapeutic agent,” he added.

CD52 appears to play a dominant role in controlling or suppressing immune activity in the early stages of the immune response, Mr. Harrison said.

“We identified a specialised population of immune cells (T cells) that carry high levels of CD52, which they release to dampen the activity of other T cells and prevent uncontrolled immune responses. The cells act as an early ‘braking’ mechanism,” Mr. Harrison said.

“In animal models we can prevent and cure Type-1 diabetes. I am hopeful that these results will be translatable into humans, hopefully in the not-too-distant future,” Mr. Harrison said.

The study was published in the journal Nature Immunology.

Article source: http://www.thehindu.com/sci-tech/health/medicine-and-research/protein-that-can-stop-diabetes-in-its-tracks-identified/article4733290.ece

]]> http://www.celebrities-with-diseases.com/diabetes-2/protein-that-can-stop-diabetes-in-its-tracks-identified-30131.html/feed 0 http://www.celebrities-with-diseases.com/obesity-fat/futurity-org-vicious-cycle-in-brain-keeps-obesity-going-30130.html http://www.celebrities-with-diseases.com/obesity-fat/futurity-org-vicious-cycle-in-brain-keeps-obesity-going-30130.html#comments Mon, 20 May 2013 20:38:54 +0000 Anna A. http://www.celebrities-with-diseases.com/obesity-fat/futurity-org-vicious-cycle-in-brain-keeps-obesity-going-30130.html Share this article

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The root cause appears to be a breakdown in the protein-processing mechanism of the cells, according to the researchers, who also found that they could intervene to break that cycle by fixing the core protein-processing problem.

Before the study, scientists knew that one mechanism in which obesity perpetuates itself was by causing resistance to leptin, a hormone that signals the brain about the status of fat in the body.

Straight from the Source

Read the original study

DOI: 10.1074/jbc.M113.475343

But years ago, senior author Eduardo A. Nillni, professor of medicine at Brown University and a researcher at Rhode Island Hospital, observed that after meals obese rats had a dearth of another key hormone—alpha-MSH—compared to rats of normal weight.

Alpha-MSH has two jobs in parts of the hypothalamus region of the brain. One is to suppress the activity of food-seeking brain cells. The second is to signal other brain cells to produce the hormone TRH, which prompts the thyroid gland to spur calorie-burning activity in the body.

In the obese rats alpha-MSH was low, despite an abundance of leptin and despite normal levels of gene expression both for its biochemical precursor protein called pro-opiomelanocortin (POMC) and for a key enzyme called PC2 that processes POMC in brain cells. There had to be more to the story than just leptin, and it wasn’t a problem with expressing the needed genes.

Nillni and his co-authors conducted the new study, published in the Journal of Biological Chemistry, to find out where the alpha-MSH deficit was coming from. Nillni says he suspected that the problem might lie in the brain cells’ mechanism for processing the POMC protein to make alpha-MSH.

Protein processing trouble

To do their work, the team fed some rats a high-calorie diet and fed others a normal diet for 12 weeks. The overfed rats developed the condition of “diet-induced obesity.” The team then studied the hormone levels and brain cell physiology of the rats. They also tested their findings by experimenting with the biochemistry of key individual cells on the lab bench.

They found that in the obese rats, a key “machine” in the brain cells’ assembly line of protein-making, called the endoplasmic reticulum (ER), becomes stressed and overwhelmed. The overloaded ER apparently fumbles the proper handling of PC2, perhaps discarding it because it can’t be folded up properly. The PC2 levels they measured in obese rats, for example, were 53 percent lower than in normal rats. Alpha-MSH peptides were also barely more than half as abundant in obese rats as they were in healthy rats.

“In our study we showed that what actually prevents the production of more alpha-MSH peptide is that ER stress was decreasing the biosynthesis of POMC by affecting one key enzyme that is essential for the formation of alpha-MSH,” Nillni says. “This is so novel. Nobody ever looked at that.”

Novel as it was, the story—a stressed ER mishandles PC2, which leaves POMC unfolded, which impedes alpha-MSH production—needed experimental confirmation.

The team provided that confirmation in several ways: In obese rats they measured elevated levels of known markers of ER stress. They also purposely induced ER stress in cells using pharmacological agents and saw that both PC2 and Alpha-MSH levels dropped.

Breaking the cycle?

Next they conducted an experiment to see if fixing ER stress would improve alpha-MSH production. They treated lean and obese rats for two days with a chemical called TUDCA, which is known to alleviate ER stress. If ER stress is responsible for alpha-MSH production problems, the researchers would see alpha-MSH recover in obese rats treated with TUDCA. Sure enough, while TUDCA didn’t increase alpha-MSH production in normal rats, it increased it markedly in the obese rats.

Similarly on the benchtop they took mouse neurons that produce PC2 and POMC and pretreated some with a similar chemical called PBA that prevents ER stress. They left others untreated. Then they induced ER stress in all the cells. Under that ER stress, those that had been pretreated with PBA produced about twice as much PC2 as those that had not.

Nillni cautions that although his team found ways to restore PC2 and alpha-MSH by treating ER stress in living rats and individual cells, the agents used in the study are not readily applicable as medicines for treating obesity in humans. There could well be unknown and unwanted side effects, for example, and TUDCA is not approved for human use by the US Food and Drug Administration.

But by laying out the exact mechanism responsible for why the brains of the obese rats failed to curb appetite or spur greater calorie burning, Nillni says, the study points drug makers to several opportunities where they can intervene to break this new, vicious cycle that helps obesity to perpetuate itself.

“Understanding the central control of energy-regulating neuropeptides during diet-induced obesity is important for the identification of therapeutic targets to prevent and or mitigate obesity pathology,” the authors write.

The National Institute of Diabetes and Digestive and Kidney Diseases supported the research.

Source: Brown University

Article source: http://www.futurity.org/health-medicine/vicious-cycle-in-brain-keeps-obesity-going/

The Summit also announced Cycle-III of the Certificate Course in Evidence Based Diabetes Management (CCEBDM), a unique training program on diabetes care for Primary Care physician’s pan-India.

The event had participation of experts in the field of diabetes, academics, and scientific research which included Padma Shri Dr. V. Mohan President, DMDEA and Chairman Chief Diabetologist, Dr. Mohan’s Diabetes Specialties Centre, Chennai, Dr S S Gill, vice chancellor Baba Farid University of Health Sciences, Faridkot Punjab, Dr A.K. Das, Senior Prof. Medical Superintendent, JIPMER, Pondicherry Dr. Anil Bhansali (Head of Department, Endocrinology, PGIMER, Chandigarh, Mr. K. G. Ananthakrishnan, Managing Director, MSD India, Dr Sandeep Bhalla, Public Health Expert, PHFI and National Programme Manager, CCEBDM and Dr. Geeta Sharma, Director Principal, Sri Guru Ram Das Institute of Medical Sciences and Research, Amritsar along with around 300 doctors and general practitioners from the four states of Punjab, Haryana, Himachal Pradesh and Jammu Kashmir.

In his address, Dr V Mohan said, “Education, for both physicians and patients is important because one cannot have good control without education in the management of diabetes. The CCEBDM course jointly organised by PHFI and DMEDA with educational grant by MSD Pharmaceuticals Pvt. Ltd. (“MSD India”) has been received very well and is making rapid progress in training doctors in diabetes pan-India. A program which can increase the number of physicians equipped, trained and empowered to manage the disorder in a better way is highly warranted.”

Article source: http://timesofindia.indiatimes.com/city/chandigarh/National-Diabetes-Summit-2013-held-in-Amritsar/articleshow/20136694.cms

The Summit also announced Cycle-III of the Certificate Course in Evidence Based Diabetes Management (CCEBDM), a unique training program on diabetes care for Primary Care physician’s pan-India.

The event had participation of experts in the field of diabetes, academics, and scientific research which included Padma Shri Dr. V. Mohan President, DMDEA and Chairman Chief Diabetologist, Dr. Mohan’s Diabetes Specialties Centre, Chennai, Dr S S Gill, vice chancellor Baba Farid University of Health Sciences, Faridkot Punjab, Dr A.K. Das, Senior Prof. Medical Superintendent, JIPMER, Pondicherry Dr. Anil Bhansali (Head of Department, Endocrinology, PGIMER, Chandigarh, Mr. K. G. Ananthakrishnan, Managing Director, MSD India, Dr Sandeep Bhalla, Public Health Expert, PHFI and National Programme Manager, CCEBDM and Dr. Geeta Sharma, Director Principal, Sri Guru Ram Das Institute of Medical Sciences and Research, Amritsar along with around 300 doctors and general practitioners from the four states of Punjab, Haryana, Himachal Pradesh and Jammu Kashmir.

In his address, Dr V Mohan said, “Education, for both physicians and patients is important because one cannot have good control without education in the management of diabetes. The CCEBDM course jointly organised by PHFI and DMEDA with educational grant by MSD Pharmaceuticals Pvt. Ltd. (“MSD India”) has been received very well and is making rapid progress in training doctors in diabetes pan-India. A program which can increase the number of physicians equipped, trained and empowered to manage the disorder in a better way is highly warranted.”

Article source: http://timesofindia.indiatimes.com/city/chandigarh/National-Diabetes-Summit-2013-held-in-Amritsar/articleshow/20136694.cms

Dr. Robert Shin, with CAMC, says the epidemic is continuing to grow. That’s why he took part in Friday’s 2013 West Virginia Obesity Conference. More then 120 medical professionals from around the state attended the one-day event at the Charleston Marriott.

Jennifer Smith/MetroNews

Those at Friday’s conference were asked to do some stretching of their own.

Shin says one problem they’re dealing with is the lack of physical activity among children and teens. They just don’t go outside and play anymore. Instead the doctor says kids are glued to a TV, computer screen or joy stick.

“The average kid spends more than 40-hours a week, playing those games! That’s more than full-time work,” says Shin.

The goal of the conference is to come up with a plan to attack the problem. Shin says the first place they start is with the parents.

“Parents are the ones that are going to shape the kids,” Shin stressed. “If as a parent, I eat the wrong things and I say to my kids, ‘You have a weight problem. You have to eat this.’ It’s not going to work.”

Shin says other factors come into play like accessibility to healthy foods, how the community views overweight children and self-image.

Nationally-recognized speakers from across the country took part in the conference. Shin says it’s important to hear success stories from other states to see what they’re doing right and how West Virginia might use those strategies here at home.

Shin says it is imperative that the medical community reach out to obese children now. He says there’s no time to wait.

“If you are obese as a child, there’s an 80 percent chance the obese child will develop into the obese adult.”

Shin says that leads to health problems like diabetes, heart disease and lung issues. But the doctor stresses there is reason for hope. Obesity is not an incurable disease. Children and adults can change their eating and exercising habits and lose weight, giving themselves a chance at a longer life.

Jennifer Smith

Comments

• C.Hoffman

  Children are no getting enough to eat so schooling suffers so let’s feed all the children. Now the children are too obese. Which is it? I see the problem as the myriad of agencies, consultants and pols that make a living off of creating problems and then providing the solution to solving the problems except the solution is never to stop listening to us. Come on WV wake up to this madness.

• What happened to wv?

  Bottom line is that parents need to take care of their children and feed them. It should not be the governments responsibility. I would be intrigued to see how many parents of the 25% are obese?

• Charles Pingley

  Too much pop and candy ,cakes to much food stamps and the wrong thing being purchased with them

  • wvtd

    I could not agree more. candy, pop and other junk food paid for with money taken from the hard working people of our state should end. make those able to work, work for food.

• Doug M

  Stop building restaurants and build more gyms, and playgrounds. Educate the the kids about eating right. Serve better food in school instead of crap. Make gym class mandatory all the way through their Senior Year.

Article source: http://wvmetronews.com/fighting-childhood-obesity/