Thursday, 28 March 2013


A study conducted in collaboration with researchers at Harvard-affiliated Massachusetts General Hospital hints at a future where doctors could deliver the weight-loss benefits of gastric bypass surgery without the surgery. In a study described in a March 27 paper in Science Translational Medicine, researchers found that the surgery caused drastic changes to microbes in the guts of mice. When those microbes were transferred into the guts of sterile mice, the result was rapid weight loss.
“Simply by colonizing mice with the altered microbial community, the mice were able to maintain a lower body fat, and lose weight — about 20 percent as much as they would if they underwent surgery,” said Peter Turnbaugh, a Bauer Fellow at the Faculty of Arts and Sciences’ Center for Systems Biology, and one of two senior authors of the paper.
As striking as the results were, they weren’t as dramatic as they might have been.
“In some ways we were biasing the results against weight loss,” Turnbaugh said, explaining that the mice used in the study hadn’t been given a high-fat, high-sugar diet to increase their weight beforehand. “The question is whether we might have seen a stronger effect if they were on a different diet.”
“Our study suggests that the specific effects of gastric bypass on the microbiota contribute to its ability to cause weight loss, and that finding ways to manipulate microbial populations to mimic those effects could become a valuable new tool to address obesity,” said the other senior author, Lee Kaplan, director of the Obesity, Metabolism & Nutrition Institute at MGH.
“We need to learn a good deal more about the mechanisms by which a microbial population changed by gastric bypass exerts its effects, and then we need to learn if we can produce these effects — either the microbial changes or the associated metabolic changes — without surgery,” added Kaplan, an associate professor of medicine at Harvard Medical School. “The ability to achieve even some of these effects without surgery would give us an entirely new way to treat the critical problem of obesity, one that could help patients unable or unwilling to have surgery.”
Turnbaugh warned that it could be years before the research contributes to treatment, and that any procedure tied to it would likely not be for someone looking to lose those stubborn last 10 pounds. Rather, the technique may one day help dangerously obese people who want to lose weight without the trauma of surgery.
“It may not be that we will have a magic pill that will work for everyone who’s slightly overweight,” he said. “But if we can, at a minimum, provide some alternative to gastric bypass surgery that produces similar effects, it would be a major advance.”
While there had been hints that the microbes in the gut might change after bypass surgery, the speed and extent of the change came as a surprise.
In earlier experiments, researchers had shown that the guts of both lean and obese mice were populated by varying amounts of two types of bacteria — firmicutes and bacteroidetes. When mice undergo gastric bypass surgery, however, it “resets the whole picture,” Turnbaugh said.
“The post-bypass community was dominated by proteobacteria and verrucomicrobia, and had relatively low levels of firmicutes,” he said. What’s more, Turnbaugh said, those changes occurred within a week of the surgery, and were lasting — the altered gut microbial community remained stable for months afterward.
There is plenty left to uncover about what exactly is driving the weight loss in mice, the researchers said.
“A major gap in our knowledge is the underlying mechanism linking microbes to weight loss,” Turnbaugh said. “There were certain microbes that we found at higher abundance after surgery, so we think those are good targets for beginning to understand what’s taking place.”
In fact, he said, the answer may not be the specific types of microbes, but a by-product they excrete.
In addition to changes in the microbes found in the gut, researchers found changes in the concentration of certain short-chain fatty acids. Other studies have suggested that those molecules may be critical in signaling to the host to speed up metabolism.
“To some degree, what we’re learning is a comfort for people who have an issue with their weight, because more and more we’re learning that the story is more complicated than just how much you exercise and how much you eat,” Kaplan said.

Sunday, 10 February 2013

VITAMIN D AND OBESITY ..Obesity causes vit D deficiency and not the other way around

6 February 2013 Last updated at 01:45 GMT

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Study finds obesity can 'lead to lack of vitamin D'

ObeseShould obese people be treated for vitamin D deficiency?
Obesity can lower vitamin D levels in the body, a study suggests.
The report, in the journal PLOS Medicine, analysed genetic data from 21 studies - a total of 42,000 people.
It found every 10% rise in body mass index (BMI) - used as an indicator of body fat - led to a 4% drop of available vitamin D in the body.
As vitamin D is stored in fatty tissue, the authors suggest the larger storage capacity in obese people may prevent it from circulating in the bloodstream.
BMI it is calculated by taking weight (in kilograms) and dividing it by height (in metres) squared. Those with a BMI of 30 or above are considered obese.
Lead author Dr Elina Hypponen, from the University College London Institute of Child Health, said the study "highlights the importance of monitoring and treating vitamin D deficiency in people who are overweight or obese".
Vitamin D is made in the skin after sun exposure and can be taken in dietary supplements.
Healthy levels are about 50 nanomole per litre - less than 30 nanomole per litre can cause the softening and weakening of bones, leading to rickets in children and osteomalacia in adults.
Prof David Haslam, from the National Obesity Forum, said: "Food intake and genetics all play a part in obesity - but this research is a reminder that physical activity, like walking the dog or going for a run out in the sunshine, shouldn't be forgotten and can help correct both weight and lack of vitamin D."

Friday, 25 January 2013

I dont use Diuretics for HTN among Native Americans

Mechanistic Insights into Diuretic-Induced Insulin Resistance
Author Affiliations

  • From the Pritzker School of Medicine, Department of Medicine, Hypertensive Diseases Unit, Section of Endocrinology, Diabetes, and Metabolism, University of Chicago, Chicago, Ill.
  • Correspondence to George L. Bakris, Hypertensive Diseases Unit, University of Chicago School of Medicine, 5841 S Maryland Ave, MC 1027, Chicago, IL 60637. E-mail
The incidence of diabetes mellitus and hypertension continues to rise worldwide. The proportion of patients with hypertension at risk for developing diabetes mellitus is also growing secondary to aging and increased obesity rates.1 Several guidelines recommend thiazide diuretics as either first-line or add-on antihypertensive therapy to achieve blood pressure goals.2 Concern over negative metabolic effects associated with thiazide diuretics, however, dates back >3 decades.3 A substantial fraction of patients with hypertension have additional cardiovascular risk factors, and many have elevated fasting glucose and are at risk for developing diabetes mellitus.4 Impaired fasting glucose itself increases the risk for cardiovascular events.5
Any medication that worsens insulin sensitivity, ie, thiazide diuretics or most β-blockers will hasten the development of diabetes mellitus in those with impaired fasting glucose.6 Large observational studies demonstrate that thiazide diuretics and most β-blockers increase the incidence of new-onset diabetes mellitus compared with renin-angiotensin system (RAS) blockers or calcium channel blockers.7 To further support this observation, a network-based meta-analysis of hypertensive agents showed that RAS blockers were the agents least likely to be associated with the development of diabetes mellitus, whereas thiazides had a higher incidence of diabetes mellitus compared with placebo.7
The mechanism traditionally associated with this increased risk of diuretic-associated diabetes mellitus is a reduction in serum potassium. A meta-analysis of 59 studies involving 83 thiazide diuretic treatment arms found a significant correlation between the degree of diuretic-induced hypokalemia and an increase in plasma glucose.8 Moreover, there is evidence that prevention of hypokalemia with K+ supplementation or potassium-sparing agents lessens the degree to which plasma glucose is increased consequent to diuretic therapy.8 The mechanism of this glucose increase by diuretics may relate to insulin secretion. Mechanisms related to insulin release were reviewed recently, and it was noted that hyperkalemia stimulates insulin secretion and induces cellular uptake of potassium.9 This suggests that low plasma potassium could impair insulin secretion and thereby increase plasma glucose. Ironically, the significant hypokalemia associated with hyperaldosteronism is not associated with hyperglycemia. The presence of insulin resistance and an impaired glucose response to an oral glucose load, however, are reported in hyperaldosteronism.9 Thus, the exact relationship between hypokalemia and worsening of insulin resistance is unclear but appears most pronounced in those with preexisting impaired glucose tolerance and not all people.
Given this background, combining an agent that reduces potassium loss, ie, an RAS blocker with a thiazide diuretic, should reduce the risk of new-onset diabetes mellitus. Unfortunately, the Study of Trandolapril/Verapamil SR and Insulin Resistance failed to support this hypothesis. It demonstrated a 4-fold increase in diabetes mellitus at 1 year in comparison with a fixed-dose combination of an RAS blocker with a calcium channel blocker.10 This result was not attributable to differences in serum potassium between groups, because serum potassium values were >4.0 mEq/L in both groups. Thus, mechanisms other than changes in potassium may be operative to worsen glycemic control and are summarized elsewhere.9
One mechanism proposed for the prevention of worsening glycemic control by RAS blockers is their peroxisome proliferator-activated receptor-γ stimulating effects; however, this was not observed in this or any other trial, because candesartan had a neutral effect on glucose.11 Moreover, the peroxisome proliferator-activated receptor-γ stimulating effect observed by some RAS blockers appears relevant only in animal models or at a cellular level.12
The current study by Eriksson et al13 provides a potentially novel mechanism by which diuretics worsen insulin resistance. Twenty-six obese, hypertensive subjects were randomly assigned to candesartan, hydrochlorothiazide (HCTZ), or placebo (in random sequence), each for 12 weeks, using a 3-way crossover design. Insulin sensitivity and secretion, hepatic fat accumulation, inflammatory markers, and the ratio of subcutaneous:visceral abdominal fat were measured. Insulin sensitivity was assessed using a hyperinsulinemic, euglycemic clamp. Significant reductions in insulin sensitivity were present with HCTZ compared with candesartan. Serum potassium levels were within the normal range in all of the groups but 0.3 mEq/L lower among those randomly assigned to HCTZ. The authors reported that differences in potassium level between groups did not correlate with changes in insulin sensitivity. The epidemiological data, however, suggest that the risk for new-onset diabetes mellitus is increased if the serum potassium levels fall below 3.5 mEq/L7,9; levels in the current study were well above this value.
Perhaps the most interesting finding in this study was the increase in hepatic fat content after treatment with HCTZ; this fat increase correlated with the magnitude of insulin sensitivity decrease. Insulin secretion was not affected by HCTZ or candesartan, despite older studies implying decreased insulin secretion with HCTZ as the mechanism for worsened metabolic control.9
Given this new information, an additional mechanism to explain why thiazide diuretics worsen insulin resistance needs consideration. Before we embrace this concept, however, one needs to ask why this occurred. The increased shift of fat in liver, with resultant relative increases in visceral adiposity, is an intriguing perspective of this study. Hepatic fat accumulation is associated with insulin resistance, at the level of liver and skeletal muscle.14 The changes in content of visceral and hepatic fat could contribute to worsening of insulin sensitivity, but which occurs first? Is it possible that decreased insulin sensitivity and elevated insulin levels promote hepatic fat storage and visceral fat accumulation? In the Mechanisms for the Diabetes Preventing Effect of Candesartan Study, there was some correlation (r2=0.26; P=0.04) between the increased hepatic fat content and the observed decrease in insulin sensitivity.13
Other possible mechanisms that contributed to decreases in insulin sensitivity include increased inflammatory response or oxidative stress with diuretics, resulting in altered adipocyte activity.15 Inflammatory markers, such as high-sensitivity C-reactive protein and serum amyloid A, were higher in the diuretic group compared with the other groups. Changes in adiponectin levels may have also contributed to this shift in fat; however, adiponectin levels were not different between groups. Thus, there is no clear reason why this shift in fat occurred with HCTZ, but, if confirmed, this would provide another reason for the higher risk of new-onset diabetes.
Apart from the cost and inconvenience of new medications now required to treat the diabetes mellitus, the main concern is whether the cardiovascular risk–reduction that diuretics confer is lost in this subgroup of obese older patients who prematurely develop diabetes mellitus. Three posthoc analyses of large cardiovascular outcome trials evaluated whether the development of new-onset diabetes mellitus predicted a higher cardiovascular event rate.16–18 The results of 2 these analyses demonstrated no significant increase in risk, whereas another showed that those who developed diabetes mellitus had an intermediate cardiovascular risk less than those with diabetes mellitus but higher than those who did not develop diabetes mellitus.18 These analyses have major limitations, however, not the least of which is that they are posthoc, and most people in the analysis were not obese. There is, however, one ongoing trial that will address this issue and is due to be completed by 2010.19
In short, thiazide diuretics are associated with decreased insulin sensitivity over a relatively short time period in obese subjects with impaired fasting glucose. The mechanisms by which this occurs appear to be multifactorial. The current study provides new data to help us understand the interaction between thiazide diuretics and the adipocyte. This information, coupled with the results of a large multicentered cardiovascular outcome study that favors RAS blockade combined with a calcium channel blocker rather than a diuretic, may provide an option other than diuretics as initial agents in high-risk patients.20 Nevertheless, more detailed mechanistic studies are needed to explain further why insulin resistance is worsened with thiazide diuretics.


  • The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. 

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Friday, 4 January 2013

Corn syrup/Fructose Eat it and be FAT

Consuming fructose appears to cause changes in the brain that may lead to overeating, a new study suggests.
"Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance," lead author Kathleen A. Page, MD, and colleagues from Yale University in New Haven, Connecticut, write.
In this study, they showed in healthy volunteers that although glucose ingestion resulted in reduced activation of the hypothalamus, insula, and striatum on MRI — areas that regulate appetite, motivation, and reward processing — as well as increased functional connections between the hypothalamic striatal network and increased satiety. Fructose ingestion had none of these effects.
"The disparate responses to fructose were associated with reduced systemic levels of the satiety-signaling hormone insulin and were not likely attributable to an inability of fructose to cross the blood-brain barrier into the hypothalamus or to a lack of hypothalamic expression of genes necessary for fructose metabolism," they conclude.
Their findings are published in the January 2 issue of the Journal of the American Medical Association.
Glucose vs Fructose
Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety, the authors write. "Thus, fructose possibly increases food-seeking behavior and increases food intake."
In this study, the researchers used arterial spin labeling MRI to quantify regional cerebral blood flow in 20 healthy normal-weight adult volunteers before and after drinking a 75-g beverage of pure glucose or fructose.
They observed that glucose (but not fructose) ingestion reduced activation of the hypothalamus, insula, and striatum. Glucose ingestion also increased functional connections between the hypothalamic-striatal network and increased ratings of satiety and fullness.
Brain responses were markedly different after ingestion of an equal amount of fructose. Not only did fructose fail to diminish hypothalamic activity, but it also induced a small, transient increase in hypothalamic activity.
The striatum, as with the hypothalamus, also did not deactivate with fructose ingestion, which may cause decreased inhibitory responses. Fructose ingestion was also associated with reduced systemic levels of the satiety-signaling hormone insulin.
Appetite Regulation
"These findings support the conceptual framework that when the human brain is exposed to fructose, neurobiological pathways involved in appetite regulation are modulated, thereby promoting increased food intake," Jonathan Q. Purnell, MD, and Damien A. Fair, PhD, from Oregon Health & Science University, Portland, write in an accompanying editorial.
They say the implications of this study, coupled with mounting evidence from epidemiologic, metabolic feeding, and animal studies, are that the "advances in food processing and economic forces leading to increased intake of added sugar and accompanying fructose in U.S. society are indeed extending the supersizing concept to the population's collective waistlines."
The study was supported in part by grants from the National Institutes of Health and the Yale Center for Clinical Investigation. The authors and editorialists have disclosed no relevant financial relationships.

Thursday, 3 January 2013


Cuba Maintains Infant Mortality Rate under Five  

HAVANA, Cuba, Jan 3 (ACN) For five years in a row, Cuba has reported its infant mortality rate at less than five deaths in every one thousand live births, with 4.6 in 2012. The achievement reveals the human development level reached by the country.

According to Granma newspaper, the important indicator reached only 4.7 in 2008; 4.8 in 2010; 4.5 in 2011 and 4.6 in 2012.

This public health achievement makes Cuba one of the countries with the lowest infant mortality rates in the Americas and it is the result of the Cuban government’s political will and decision to maintain free of charge and accessible health services for all citizens, the paper explains.

The lowest infant mortality level was reported in central Sancti Spiritus province, with only 2.8, while another four territories reported indicators below the 4.6 national rate, such as Artemisa (west), 3.8; Holguin (east) and Cienfuegos (Center) both with 3.9; and Granma (east), 4.1.

Preliminary statistics released on Wednesday by the Public Health Ministry say that some 125 thousand 661 births took place in 2012, seven thousand 406 less births than in 2011.

The major cause for death in children below one year of age is the infection during the delivery process, particularly infections linked to premature babies, who are born before the 34th week.

Medical specialists told Granma newspaper that the rate of low weight at birth was kept at 6 percent in 2012, which is a favorable level, they said. This means that only six babies in every 100 births weigh less than 2500 grams (5.5 pounds). However, 3.8 percent of children still are born before complete pregnancy period.

The infant mortality rate is a demographic indicator telling the number of deaths of children before the first year of living, which is the most critical period in human survival. The indicator is an international tool to measure the quality of the assistance given to children in every country.


Energy Drinks

Janet M. Torpy, MD; Edward H. Livingston, MD
JAMA. 2012;():1. doi:10.1001/jama.2012.170614.
Text Size: A A A
Published online December 19, 2012
Beverages called energy drinks are popular, especially with teenagers and young adults. These energy drinks are advertised to give individuals a higher energy level, to make a person feel more awake, and to boost attention span.
Energy drinks are marketed in different serving sizes and have varying amounts of caffeine. Sodas (also known as pop, colas, or soft drinks) may contain sugar and caffeine, although most sodas contain less caffeine than energy drinks on an ounce-by-ounce basis. As a comparison, an 8-oz cup of coffee has about 100 mg of caffeine (see table at right, and expanded table online at The January 16, 2013, issue of JAMA contains 2 articles discussing the harms associated with energy drinks.
Image not available.


  • Caffeine
  • Sugar
  • Guarana (a plant with seeds that contain caffeine)
  • Cocoa
  • B vitamins
  • Herbs, including ginseng, licorice, and kola nut


  • Increased heart rate
  • Irregular heart rate and palpitations
  • Increased blood pressure
  • Sleep disturbances, including insomnia
  • Diuresis (increased urine production)
  • Hyperglycemia (increased blood sugar) is related to all beverages with high sugar content. This can be harmful for individuals with diabetes or other metabolic health problems.
The American Academy of Pediatrics recommends that young children should not consume energy drinks. Caffeine may be especially harmful for children. Adolescents should not have more than 100 mg of caffeine each day. Parents should monitor how much soda or coffee (or other beverages containing caffeine, including energy drinks of any kind) their teenagers drink and help them understand the risks associated with taking in large amounts of caffeine.
Adults should limit their caffeine intake to 500 mg per day. Individuals who have heart problems, high blood pressure, or trouble sleeping or who are taking medications should be careful to limit the amount of caffeine they drink. Older persons may be more sensitive to the effects of caffeine.
Energy drinks are not regulated by the US Food and Drug Administration. However, the ingredients in energy drinks may be harmful to some individuals. It is important to read labels for any food or drink product that you consume. If you choose to use energy drinks, make sure you understand the ingredients and serving sizes listed on the label.