DAILY NEWS BULLETIN LEADING HEALTH, POPULATION AND FAMILY WELFARE STORIES OF THE Day Thursday
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1 DAILY NEWS BULLETIN LEADING HEALTH, POPULATION AND FAMILY WELFARE STORIES OF THE Day Thursday Diabetes Extreme low-calorie diet leading to radical weight loss can reverse diabetes: Lancet study (Hindustan Times: ) Almost half of those who participated in the extreme low-calorie diet programme stayed in remission after a year. Losing weight has been linked to better management of type 2 diabetes but the study reported by The Lancet is the first to show that substantial weight loss leads to lasting remission. Losing weight has been linked to better management of type 2 diabetes but the study reported by The Lancet is the first to show that substantial weight loss leads to lasting remission.(representative photo) An extreme low-calorie diet that leads to an average weight loss of 10kg helps reverse type-2 diabetes, says a study reported in the journal, The Lancet. The weight-loss diet plan was a formula, drank mostly as a shake, of calories a day for three to five months, followed by a stepped reintroduction of solid food over two to eight weeks. Study participants were encouraged to be active, but were not asked to follow a structured exercise plan. Close to 70 million adults in India have diabetes in India, with another 10.2% of the population with glucose intolerance, a precursor to diabetes.
2 Studies show that south Asians develop diabetes a decade earlier than Caucasians at a lower weight, and those with prediabetes progress to overt diabetes at a faster rate. While losing weight has been linked to better management of type 2 diabetes, this is the first study to show that substantial weight loss leads to lasting remission without medication even in people who have had type-2 diabetes for six years. The Lancet study by researchers from Newcastle and Glasgow Universities showed almost half (45.6%) of those who took part in the programme stayed in remission after a year. This included 86% of people who lost more than 15kg, 57% of people who lost 10-15kg, and 34% who lost 5-10kg. In the comparison group, remission was seen in four per cent people with best available diabetes care but not the low-calorie diet. Worldwide, 425 million one in 11 adults -- have diabetes, of whom half million -- are undiagnosed. Untreated diabetes leads to irreversible complications, such as retinopathy that causes blindness, kidney damage, heart disease, slow-healing wounds and amputations. We are all immensely encouraged by these data and should try to achieve substantial weight loss early on after diagnosis for reversal, said Dr Anoop Misra, chairman, Fortis centre of excellence for diabetes, metabolic diseases and endocrinology. But, several roadblocks remained. Misra said the data didn t apply to non-obese individuals, in ethnic group like Indians where such reversal could be inherently difficult, and in many Indians who were non-compliant to basics of diet and exercise. Bariatric surgery that restricts stomach capacity has also been shown to reverse the disease. People with diabetes who lose 10-15% of their body weight show a very dramatic and significant change in their diabetes status, with some becoming diabetes free and others controlling blood glucose at lower medicinal doses, said Dr Pradeep Chowbey, chairman, Max institute of minimal access, metabolic and bariatric surgery, New Delhi. The benefits are most apparent in people who are morbidly obese, with a body mass index (ratio of the weight to height) of more than 30. Abdominal or belly fat was a risk factor for type-2 diabetes. Visceral fat, deep intraabdominal fat that s stored underneath subcutaneous belly fat, cells have an affinity for insulin, insulin gets fixed with fat cells and less is available for metabolism, Dr Chowbey said.
3 Diabetes (Hindustan: ) Public Health Universal health coverage is the best prescription (The Hindu: ) UHC provides the framework in which the issues of access, quality and cost can be integrated Three recent incidents involving the health-care sector in Delhi have sparked widespread outrage over the alleged mercenary motives and callous conduct of high-profile corporate
4 hospitals. Two cases involved children with dengue who died soon after leaving these hospitals in a serious condition after their families were presented huge hospitalisation and treatment bills. The third case involved a live premature baby being declared dead and handed over to the parents wrapped in plastic. Distrust and despair Questions have been raised, and rightly so, about the lack of professional standards in terms of competence and compassion. The medical bills, running into huge figures, also stoked anger at perceived corporate addiction to profit maximisation. The government, the hospital managements and the Indian Medical Association have begun inquiries. Even as these go on, there is deep public distrust and despair over health care in private and public sector hospitals. Three major issues are involved when we assess health care: access, quality and cost. Each of these needs to be addressed with clarity, and not in isolation. Solutions have to be those that fit into a common system architecture, or a system best designed and delivered as Universal Health Coverage (UHC), now enshrined in the Sustainable Development Goals. Access to readily reachable, trustworthy and affordable health care is a major challenge before poorly served rural areas and overcrowded urban areas. Also, the inadequacy of organised primary health services here is compounded by a weakness at the intermediate level of care in many district hospitals and nursing homes. While corporate hospitals boast of high quality advanced care and compete with each other for a significant share of medical tourism, they are mostly inaccessible to the rural population and the urban poor. Government institutions of advanced care suffer from low budgets and a lack of managerial talent. Steps to improving access The pathway to improving access lies in expanding the network of public sector facilities at all levels. This calls for higher levels of public financing, investment in training and incentivised placements of more health personnel and improved management through the creation of a public health management cadre. These measures have been envisaged in the National Health Policy, 2017 and need urgent and earnest implementation. Health-care providers in the private and voluntary sectors should be empanelled to fill the gaps through carefully crafted contracting mechanisms that best serve public interest. Quality of care is determined by the extent to which appropriate care is provided in each clinical context. Here there must be an emphasis on the benefit and safety of tests and treatment, and ensuring that satisfaction levels of patients, families, care providers in the nature of institutional processes as well as human interactions are met. This requires ensuring conformity to accepted scientific and ethical standards. Here, the Clinical Establishments Act is a good beginning, in moving health-care facilities towards registration, ensuring compliance with essential standards of equipment and performance, adopting standard management guidelines, grievance redress mechanisms, and respecting encoded patient rights.
5 Managing cost Cost of care is a major challenge in a system where patients and families have to bear the burden. High out-of-pocket spending on health care leads to unacceptable levels of impoverishment. With high levels of poverty and a very large segment of the working population in the informal sector, both private insurance and employer provided insurance can cover only small population segments. With a small risk pool, these schemes can only provide limited cost coverage to subscribers. Government-funded social insurance schemes do increase access to advanced care. But they have not been shown to provide financial protection as they cover only part of the hospitalisation cost and none of the expenses of prolonged outpatient care which forms a higher percentage of out-of-pocket spending. The solution lies in doubling the level of public financing to at least 2.5% of GDP by 2019, rather than 2025, as proposed in the National Health Policy, and by pooling tax funding, all Central and State insurance schemes and employer-provided health insurance into a single payer system. That can be managed by an empowered autonomous authority which purchases services from a strengthened public sector and, as necessary, from empanelled private health-care providers. Quality is promoted through audited insistence on implementation of standard management guidelines by all service providers who enter this system, and cost is controlled by the negotiating power of the single payer. Since the risk pool is very large, there is a high level of cross- subsidisation of the sick by the healthy, the poor by the rich and the elderly retired by the young employed. The burden on an individual is greatly minimised. Implemented piecemeal, these three areas of action will yield only limited results as access alone cannot assure appropriate or affordable care and cost subsidy will be meaningless if there is limited access or undependable quality. The UHC provides the framework in which all three elements can be integrated. The cry for stronger regulation of quality and cost is justified but regulation will fail to deliver needed health care to all if the health system architecture does not adopt UHC. Similarly, the success of UHC depends on effective regulation. Now, there is a disconnect between these two in ongoing health system reforms. It is time to bridge that gap if tragic tales of terrible health care are not to cause recurring lament.
6 Alzheimer's disease Alzheimer's brain damage halved with gene-targeting compound (Medical News Today: ) More and more studies are starting to point to the APOE gene as a gateway to halting the progression of Alzheimer's disease. But few have actually targeted APOE in living animals. New research uses a molecule against APOE in mice, and the treatment could reduce brain damage by half. Targeting the APOE gene may one day prevent brain damage in people at risk of Alzheimer's. The APOE gene, responsible for encoding a protein called apolipoprotein E, is known to dramatically raise the risk of Alzheimer's. In fact, the E4 variant of the gene is "the most prevalent genetic risk factor" for Alzheimer's, with over half of people with the condition having this gene expressed. Also, studies show that people who have both copies of the gene have a 12-fold higher risk of developing Alzheimer's disease. Recent research has focused on understanding the role of APOE in Alzheimer's formation. For instance, Medical News Today have recently reported on a study led by Dr. David Holtzman, head of the Department of Neurology at the Washington University School of Medicine in St. Louis, MO. In that very study, Dr. Holtzman uncovered the mechanism by which the APOE protein amplifies Alzheimer's disease-related brain damage in mice, and he suggested that future research should focus on targeting the protein to nip the neurodegenerative process in the bud. Now, in the new study, Dr. Holtzman has done exactly that. Together with Ph.D. student Tien-Phat Huynh, Dr. Holtzman and colleagues reveal that a molecule called an "antisense oligonucleotide" interferes with the production of the APOE protein, which leads to significantly less brain damage. The DNA-based molecule was created by study co-author Tracy Cole, Ph.D., and the findings are now published in the journal Neuron. Antisense oligo halves brain damage in mice
7 Dr. Holtzman and his team used a mouse model of Alzheimer's disease. They injected the molecule into the brains of newborn mice that were genetically designed to be predisposed to the disease. A control group of newborn mice was administered either saltwater or a placebo "oligo." APOE protein levels were halved by the molecule in the mice that were given it, compared with control mice. After 2 months, the rodents received another boost of the treatment or another boost of saltwater depending on their group. Another 2 months later, the mice's brains were examined. By this point when the mice were 4 months old they would have developed plaques of the sticky amyloid-beta protein, a known hallmark of the disease. However, the mice that had been treated with the antisense molecule had half as many amyloid plaques as the mice that received saltwater. Additionally, each plaque caused only half as much neuronal damage in the intervention group compared with the saltwater group, suggesting the molecule successfully staved off Alzheimer's-related neurodegeneration. Given the success that the molecule had in prevention, the team also wanted to see whether the compound would yield any benefits if administered after the plaques had formed. APOE ideally targeted before plaques form Therefore, this time they administered the molecule to 6-week-old mice that had developed amyloid beta plaques, and they gave saltwater to a control group. Although the experiments revealed no reduction in the actual number of beta-amyloid plaques or in the amount of the damaging protein, the results did show that each plaque caused only half as much neuronal damage in the oligo compound group compared with the saltwater group. Dr. Holtzman comments on the findings, saying, "If you wanted to target APOE to affect the amyloid process, the best thing would be to start before the plaques form." "But even if you start later, you still may reduce the amount of damage caused by the plaques. Now that we have shown that it is possible to target APOE, we can start figuring out the best way to do it." Dr. David Holtzman "Our findings indicate that APOE is not just involved in Alzheimer's risk and disease progression, but it could potentially be a real target for treatment or prevention," concludes Dr. Holtzman.
8 Obesity A high-fat diet without the weight gain? Study says it's possible (Medical News Today: ) When it comes to gaining weight, a high-fat diet is a key culprit. New research, however, suggests that there may one day be a way to avoid piling on the pounds as a result of eating fatty foods. Researchers were able to prevent weight gain in mice fed a high-fat diet. In a newly published study, researchers reveal how activating a specific protein pathway can prevent the growth of fat cells in mice in response to a high-fat diet. Senior study investigator Fanxin Long, Ph.D. who works in the Washington University School of Medicine in St. Louis, MO and colleagues say that their findings could bring us closer to a new treatment strategy for obesity, which is, at present, thought to affect more than a third of adults in the United States. The researchers recently reported their results in the journal elife. Weight gain is most commonly caused by an energy imbalance, wherein the intake of calories is higher than the number of calories burned. Over time, an energy imbalance causes the body to store fat. This can lead to weight gain and obesity which is a risk factor for type 2 diabetes, heart disease, stroke, and some types of cancer. Foods high in fat, particularly saturated fats, are thought to be a main driver of obesity, especially when consumed in large amounts. But Long and colleagues suggest that there could be a way to prevent weight gain induced by a high-fat diet. Hedgehog signaling and fat cells For their study, the team focused on the Hedgehog signaling pathway, which is a complex network of proteins that play a role in various developmental processes. Previous research in mouse models has shown that the Hedgehog signaling pathway can also inhibit adipogenesis, or the formation of fat cells. According to Long and his team, the majority of studies have looked at the effects of Hedgehog signaling on adipogenesis during embryonic development, so it has been unclear as to whether activating this pathway in adulthood influences fat cell formation.
9 To find out, the researchers engineered adult mice to possess genes that activated the Hedgehog signaling in response to a high-fat diet. These rodents were fed a high-fat diet for a total of 8 weeks. While a control group of mice whose Hedgehog signaling pathways were not activated when they ate fatty foods became obese after 8 weeks of a high-fat diet, the genetically engineered mice gained no more weight than control mice that consumed standard chow. "More importantly," notes Long, "when we did metabolic studies, we found that the animals with the active Hedgehog pathway not only were leaner, they also had lower blood glucose levels and were more sensitive to insulin." A new way to fight obesity? The researchers explain that by activating the Hedgehog signaling pathway in the rodents upon consumption of a high-fat diet, they were able to reduce the size of fat cells. "Fat gain is due mainly to increased fat cell size," explains Long. "Each fat cell grows bigger so that it can hold larger fat droplets. We gain weight mainly because fat cells get bigger, as opposed to having more fat cells." But the researchers note that applying their results to humans will be challenging; heightened Hedgehog signaling has been linked to increased cancer risk, so any strategy that targets this pathway would need to be approached with caution. That said, the team believes that its results show promise for a new approach to preventing weight gain. "If we can come up with strategies to carefully target fat cells, then I think activating this pathway could be effective in the fight against obesity." Fanxin Long, Ph.D. "What's particularly important," Long adds, "is that the animals in our study ate a high-fat diet but didn't gain weight, and in people, too much fat in the diet is a common cause of obesity."
10 Skin Cancer Common blood pressure drug raises skin cancer risk (Medical News Today: ) A new study, led by Danish-based researchers, shows that one of the most popular drugs used worldwide in the treatment of hypertension raises the risk of skin cancer by seven times. Hydrochlorothiazide users may be at a much higher risk of developing skin cancer, according to new research. The study was led by Anton Pottegård, associate professor of clinical pharmacology at the University of Southern Denmark in Odense, and the findings were published in the Journal of the American Association of Dermatology. Pottegård and colleagues examined the link between the common drug hydrochlorothiazide (HCTZ) and the risk of non-melanoma skin cancer. HCTZ is a popular diuretic used to treat water retention and high blood pressure. In fact, according to some studies, it is "the most commonly prescribed antihypertensive drug worldwide." The researchers were prompted in their endeavor by the fact that HCTZ has been linked with an increased risk of lip cancer in the past. In fact, a study led by Pottegård attributed 11 percent of lip cancer cases to the drug. Moreover, HCTZ, the authors explain, makes the skin more sensitive to the damage of ultraviolet (UV) rays, due to its photosensitizing effects. This was a further reason for the researchers to examine the drug. HCTZ raises skin cancer risk Using national databases, Pottegård and colleagues examined the use of HCTZ in over 80,000 patients who had been diagnosed with non-melanoma skin cancer, and compared it with its use in a group of 1.5 million healthy controls. Additionally, the researchers considered the use of other antihypertensive medication. The research revealed that those who took HCTZ were up to seven times more likely to develop skin cancer. More specifically, the antihypertensive drug raised the risk of both squamous cell carcinoma and basal cell carcinoma a less serious form of skin cancer. By contrast, none of the other antihypertensive drugs examined seemed to raise skin cancer risk.
11 "We knew that hydrochlorothiazide made the skin more vulnerable to damage from the sun's UV rays, but what is new and also surprising is that long-term use of this blood pressure medicine leads to such a significant increase in the risk of skin cancer," comments Pottegård. Choosing a different drug might be advisable Dr. Armand B. Cognetta Jr., chief division of dermatology at Florida State University in Tallahassee and a co-author on the study, weighs in on the findings, saying, "We have seen and followed many patients with different skin cancers where the only risk factor apart from exposure to sunlight seems to be hydrochlorothiazide." "The combination of living and residing in sunny Florida while taking hydrochlorothiazide seems to be very serious and even life-threatening for some patients," he adds. "The study carried out by Pottegård and his colleagues will have [a] great impact on skin cancer prevention and public health worldwide," Dr. Cognetta explains. However, Pottegård cautions against dismissing the use of HCTZ altogether as a result of his study, saying, "The risk of skin cancer must, of course, be weighed against the fact that hydrochlorothiazide is an effective and otherwise safe treatment for most patients." "Nevertheless," he continues, "our results should lead to a reconsideration of the use of hydrochlorothiazide. Hopefully, with this study, we can contribute towards ensuring safer treatment of high blood pressure in the future." "You should not interrupt your treatment without first consulting your doctor. However, if you use hydrochlorothiazide at present, it may be a good idea to talk to your doctor to see if it is possible to choose a different medicine."
12 Parkinsons Disease (Hindustan: )
13 Air Pollution (Hindustan: )
14 Healthcare (Dainik Jagran: )
15 ȡ ए नई ज च Ȣē बत एग ȡ ए ȧकम (Dainik Jagran: ) एक भ रत य सम त Ȱ ȡǓ ɉ क दल न È ज च ȧनई ȧ ह कम ल गत ȡ ȣ इस ज च स महज 15 Ʌ ȣ ȣ Ʌ ȡ ए और आयरन ȧकम क पत चल सकत ह Ȫ ȡ[j Ȳक अन स र, ल च ȨÈ क आक र क इस Ȫ ȶ ȡ^Ê Ȫǔè è Ʌ ȡ ǒ ȣ ȧ ज च Ʌ^è ȯ ȡ ह न ȡ ȣǔè ǗǓ [ ȣ क f ȣ Ȣएक Þ ɇ ȯè ǔè रहत ह \ ȯǐ ȡ ȧ ȡ ȶ Ȫ f Ĥ Ȫ ȯ स रभ म हत न कह, ȡ ए और आयरन ȧ कम स ǓǕ ȡ ȧएक Ǔ ȡ_ स Ï ȡ ȡ] ȡ ȣĥ ȡ ह ^ ȧकम क चलत ख सत र स Í ɉऔर Ǒ ȡj Ȳ ɅǺǔç ȣ ȡ, f Ȣ ȡऔर असमय म त क खतर रहत ह Ï ȡ ȡ ȡ Ȣ ȯ ɉ Ʌइस तरह क ` Û ` ɉक अभ व ह जसस इन ɉक झटपट पत लग य ज सक Ĥ ȯě f भ रत य सम त Ȱ ȡǓ ɉक दल न È ज च ȧनई ȧह कम ल गत ȡ ȣ इस ज च स महज 15 Ʌ ȣ ȣ Ʌ ȡ ए और आयरन ȧकम क पत चल सकत ह Ȫ ȡ[j Ȳक अन स र, ल च ȨÈ क आक र क इस Ȫ ȶ ȡ^Ê Ȫǔè è Ʌ ȡ ǒ ȣ ȧ ज च Ʌ^è ȯ ȡ ह न ȡ ȣǔè ǗǓ [ ȣ क f ȣ Ȣएक Þ ɇ ȯè ǔè रहत ह \ ȯǐ ȡ ȧ ȡ ȶ Ȫ f Ĥ Ȫ ȯ स रभ म हत न कह, ȡ ए और आयरन ȧ कम स ǓǕ ȡ ȧएक Ǔ ȡ_ स Ï ȡ ȡ] ȡ ȣĥ ȡ ह ^ ȧकम क चलत ख सत र स Í ɉऔर Ǒ ȡj Ȳ ɅǺǔç ȣ ȡ, f Ȣ ȡऔर असमय म त क खतर रहत ह Ï ȡ ȡ ȡ Ȣ ȯ ɉ Ʌइस तरह क ` Û ` ɉक अभ व ह जसस इन ɉक झटपट पत लग य ज सक Ĥ ȯě
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