Showing posts with label Health Obesity. Show all posts
Showing posts with label Health Obesity. Show all posts

October 25, 2015

Does Being Fat Matters? One Study said it helps



                                                                               

When it comes to nutrition, public health professionals seem to agree on very little, from whether coffee is a vice or a virtue to if red wine is a life extender. Yet for decades, they could agree on one thing: Being fat is bad for you. Everyone seems to know that carrying too much weight can lead to diabetes and heart disease, as well as increase some potentially hazardous biomarkers.
But recent research suggests that being fat might, in fact, be good for you. In 2013, a massive scientific review found that being in the least-severe overweight category — above “normal weight” but not by much — actually reduces your chances of dying in the future, aka “all-cause mortality.” Meanwhile, being in the lowest obesity category seems to have no effect on risk of death whatsoever. So if being overweight lowers your risk of dying, then being overweight is good for you … right? Time for doctors to prescribe Oreos? (Please, God.)
Note on figure 1 to left and center where all the major organs are covered in fat including the arteries, plus the strain on the spinal chord from the accumulating weight on the front part of the torso.
                                                
Not so fast. That review had more than a few critics. For instance, some scientists say that the sick, who are at a higher risk of death, tend to lose weight — that might make it look like people who are heavier are staying alive, when really it’s that sick people lose a lot of weight before they die. Another theory that could explain the paradox is that obese patients get more attentive care from doctors. Also, that review was based on a huge group of people, including smokers, gym rats, and the elderly, so it’s hard to translate its findings into medical recommendations for any single person.
So if benefits of being heavier were limited to reducing the risk of all-cause mortality, we might be able to put this idea in the “interesting but inconclusive” category and move on. But it turns out it’s even more complicated than that. Beyond the potentially protective effects of a little belly, being obese can also help you survive certain health problems. For example, being very obese has been linked to higher survival rates for people who have heart failure and other cardiovascular problems. 
The source of much of this confusion is this: When researchers talk about obesity, they are rarely talking only about fat. Studies that are allegedly about obesity tend to feature a host of other chronic health conditions, like type 2 diabetes and cardiovascular disease. This paper, for instance, claims to project the economic burden of obesity in the near future. It’s actually telling us how much it will cost to treat new cases of type 2 diabetes and cardiovascular disease if they continue to increase at present-day rates.
The problem here is that we are not distinguishing between symptom and cause. Obesity is caused by the same behaviors that cause cardiovascular disease and type 2 diabetes. This means that obesity is just the most visible and, to some, the most alarming symptom of unhealthy eating and sitting around too much. This is why some researchers think it’s possible to be fit and fat at the same time — obesity itself is not the problem, but the consequences of doing the things that make people obese, like diabetes and cardiovascular disease, are.
So is obesity actually good for you? Or is obesity a big fat villain? On the one hand, the mixed evidence is hard to parse. On the other hand, the answer to this question doesn’t actually matter. In fact, we shouldn’t even be talking about obesity. We need to focus on poor nutrition and inadequate exercise instead. Instead of worrying about our collective waistlines, we need to focus on making it possible, if not fun and easy, for everyone to eat well and move around. If we do that, obesity and its related health conditions should take care of themselves.

BENJAMIN SPOER

OZY AUTHOR
Benjamin Spoer is a Ph.D. student at NYU's Global Institute of Public Health obsessed with urbanism, obesity and community health. He considers himself one of the top three influential redheads in history, along with Thomas Jefferson and Carrot Top. After entering the world in a back alley in Hong Kong, he's now exiled to Harlem, where he finds solace in running long distances and baking pies.
Benjamin Spoer is a Ph.D. student at NYU’s College of Global Public Health and is obsessed with urbanism, obesity, and community health.              Published by OZY
Pictures, editing, titles by adamfoxie*blog International 

August 14, 2015

(NIH):Restricting Dietary Fats Makes You Loose Weight Better than Carb Redux


                                                                        

In a recent study, restricting dietary fat led to body fat loss at a rate 68 percent higher than cutting the same number of carbohydrate calories when adults with obesity ate strictly controlled diets.  Carb restriction lowered production of the fat-regulating hormone insulin and increased fat burning as expected, whereas fat restriction had no observed changes in insulin production or fat burning. The research was conducted at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. Results were published August 13 in Cell Metabolism External Web Site Policy.
“Compared to the reduced-fat diet, the reduced-carb diet was particularly effective at lowering insulin secretion and increasing fat burning, resulting in significant body fat loss,” said Kevin Hall, Ph.D., NIDDK senior investigator and lead study author. “But interestingly, study participants lost even more body fat during the fat-restricted diet, as it resulted in a greater imbalance between the fat eaten and fat burned. These findings counter the theory that body fat loss necessarily requires decreasing insulin, thereby increasing the release of stored fat from fat tissue and increasing the amount of fat burned by the body.” 
The researchers studied 19 non-diabetic men and women with obesity in the Metabolic Clinical Research Unit at the NIH Clinical Center in Bethesda, Maryland. Participants stayed in the unit 24 hours per day for two extended visits, eating the same food and doing the same activities. For the first five days of each visit they ate a baseline balanced diet. Then for six days, they were fed diets containing 30 percent fewer calories, achieved by cutting either only total carbs or total fat from the baseline diet, while eating the same amount of protein. They switched diets during the second visit. 
Image of a scale
A scale shows pasta/carbs weighed against butter/fat. Courtesy Dr. Kevin Hall, NIDDK
The researchers had previously simulated the study with a math model of human metabolism, whose body fat predictions matched the data later collected in the study. When simulating what might happen over longer periods, the model predicted relatively small differences in body fat loss with widely varying ratios of carbs to fat. Those results suggest the body may eventually minimize differences in body fat loss when diets have the same number of calories. More research is needed to assess the physiological effects of fat and carb reduction in the long term.
“This NIH study provides invaluable evidence on how different types of calories affect metabolism and body composition,” said NIDDK Director Griffin P. Rodgers, M.D.  “The more we learn about the complicated topic of weight loss, the better we can find ways to help people manage their health.” 
More than two-thirds of American adults are overweight or obese. Maintaining a healthy weight can help prevent complications related to overweight and obesity such as heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.
“Our data tell us that when it comes to body fat loss, not all diet calories are exactly equal,” Hall said. “But the real world is more complicated than a research lab, and if you have obesity and want to lose weight, it may be more important to consider which type of diet you’ll be most likely to stick to over time.” 
The NIDDK, a component of the NIH, conducts and supports research on diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition and obesity; and kidney, urologic and hematologic diseases. Spanning the full spectrum of medicine and afflicting people of all ages and ethnic groups, these diseases encompass some of the most common, severe and disabling conditions affecting Americans. For more information about the NIDDK and its programs, visit http://www.niddk.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

March 25, 2015

Cholesterol might no longer be enemy no.1


                                                                         

Today I would like to talk about a small revolution that's brewing in the dietary recommendations for the American population. An expert panel has released its new recommendations to the US Departments of Health and Human Services and Agriculture, which will draft the final US dietary guidelines later this fall.[1]Those guidelines, which are updated every 5 years, will likely no longer set an upper limit for cholesterol intake for people with hypercholesterolemia.
Is saying that dietary cholesterol is not enemy number one for human health really something new? Not at all.
To explain this, I would first like to go over three distinct concepts that need to be kept in mind when discussing cholesterol.
1. The cholesterol molecule is unique to the animal kingdom. In humans, cholesterol is primarily endogenous in origin—that is, manufactured by our bodies. There is also exogenous cholesterol, which comes from fatty foods of animal origin.
2. The second concept is that of intestinal cholesterol, the cholesterol that passes into the intestine. Some of it is reabsorbed and some is eliminated in the feces. In intestinal cholesterol, a distinction should therefore be made between the cholesterol manufactured in the body and excreted in bile, and dietary cholesterol, which comes from the food we eat.
3. The third concept is that of the lipoproteins that transport cholesterol. We simplistically talk about bad cholesterol, or low-density lipoprotein (LDL) cholesterol, because these lipoproteins are atherogenic, and conversely about good cholesterol, or high-density lipoprotein (HDL) cholesterol, because these lipoproteins protect against atherosclerosis.
Most of the debates over cholesterol arise from the confusion between these different concepts.
Let's get back to the news—that is, to the change in the dietary recommendations concerning cholesterol. I ask the following question: What is the impact of dietary cholesterol on cardiovascular (CV) risk?
This question can be answered in two ways:
  • First, by examining the effect of a high-cholesterol diet on the level of one of the main CV risk factors: LDL cholesterol. The impact of dietary cholesterol on LDL levels is variable. It depends on both the individual and his or her underlying diet. While it may have an impact, we know that the most important thing for reducing plasma LDL levels is to reduce saturated fat intake in favor of unsaturated fats. In this context, reducing dietary cholesterol is not useless, but neither is it the most important thing.
  • And second, by examining the relationship between the consumption of the food with the highest cholesterol content, eggs, and the risk for coronary events or stroke. For this, we only have observational studies, but overall, eggs do not promote the occurrence of CV disease. Be careful, though, because according to some of the meta-analyses of these observational studies, dietary cholesterol could have a harmful effect, specifically in people with type 2 diabetes, although the reason for this is not really known.
Moreover, I would like to look at findings from two studies published in late 2014 concerning intestinal cholesterol.
One was a genetic study that found that the CV risk was higher in people who absorbed intestinal cholesterol especially well because of a specific form of the intestinal cholesterol transporter.[2]
The other was the IMPROVE-IT study, which showed that the risk for CV events was reduced by inhibiting cholesterol absorption in the intestine with ezetimibe (Zetia®).[3]
It is important to understand that these two studies mainly concerned the absorption of endogenous cholesterol. Consequently, one cannot draw any conclusions about dietary cholesterol, which accounts for only a small portion of intestinal cholesterol.
In practice, these new recommendations are perfectly in line with current scientific knowledge. They relativize the impact of dietary cholesterol on CV risk and will probably bring eggs back into favor, which, as has long been known, can be safely included in a balanced diet (with one possible exception, however, for diabetics).
Editor's Note: This commentary is an edited transcript of a video presentation published on Medscape France on February 24, 2015.

August 30, 2014

A Study Shows There is ‘No Metabolically Healthy Obese people’


 

The absence of additional metabolic risk factors does not protect overweight or obese young men from developing type 2 diabetes, a new study finds.
Gilad Twig, MD, PhD, of the department of medicine at Sheba Medical Center, Tel Hashomer, Israel, and colleagues published the results from the Metabolic, Lifestyle and Nutrition Assessment in Young Adults (MELANY) study online August 19 in Diabetes Care.
"Our findings primarily suggest that obesity, even when accompanied by an intact metabolic profile, is not a benign condition. Physicians should be aware of this, especially among young adults," Dr. Twig told Medscape Medical News.
The researchers enrolled 33,939 men aged 25 and older who were in the Israel Defense Forces (IDF). They followed the participants from 1995 through 2011. At baseline, 49% were of normal weight (body mass index [BMI] < 25 kg/m2), 38% were overweight (BMI 25 to 30 kg/m2), and 13% were obese (BMI > 30 kg/m2).
Over a median 6-year follow-up, 734 (2.2%) were diagnosed with type 2 diabetes.
Dr. Twig and colleagues also divided the subjects according to how many baseline metabolic abnormalities they had, including:
  • Triglyceride level of 150 mg/dL or greater or use of lipid-lowering drugs.
  • Glucose level of 100 mg/dL or greater.
  • Systolic blood pressure 130 mm Hg or greater or diastolic blood pressure 85 mm Hg or above or use of antihypertensive drugs.
  • HDL cholesterol less than 40 mg/dL.
Only 14.7% of the obese group were "metabolically healthy," defined as having none of the additional risk factors, compared with 55% of the normal-weight group and 32% of the overweight group.
The investigators found that each 1-unit increase in BMI was associated with a 10.6% increased risk of developing diabetes (P < .001), after adjusting for age, family history of diabetes, country of origin, physical activity, fasting plasma glucose, triglycerides, and white blood cell count.
Among the "metabolically healthy," the hazard ratios for development of diabetes compared with normal-weight subjects were 1.89 for overweight individuals and 3.88 for obese ones ( P < .001). The rates for development of diabetes among the metabolically healthy were 4.34 cases per 1000 per person-years for the obese group vs 1.15/1000 person-years for the normal-weight group (P < .001).
The increase in risk for each additional risk factor was far greater among those who were obese than those of normal weight. Among those with at least 3 risk factors, the difference in diabetes incidence was 19.17 per 1000 person-years for the obese group vs 3.17 for the normal-weight group.
When the risk factors were analyzed as continuous variables, diabetes risk increased by more than 3-fold in the obese group both among the “metabolically healthy" and among those with 3 metabolic abnormalities. 
This study differs from others that identified a "metabolically healthy obese" group in that "metabolically healthy" was defined as having no additional risk factors. By contrast, other studies have included those with 1 or 2 risk factors in the metabolically healthy group, Dr. Twig and colleagues note.
In addition, the subjects in this study were younger at baseline and were thus likely to develop more risk factors in the future. Moreover, previous studies have not carefully adjusted for the various risk factors as continuous variables, which is particularly important in young adults, the authors note.
While they acknowledge one limitation of this study is that it was only done in men, Dr. Twig toldMedscape Medical News that the findings should be extrapolatable to other populations. "The MELANY cohort of the IDF has been shown to be similar to many European and US cohorts of young adults....We analyzed these results by country of origin and show that our findings are independent of this variable."
Dr. Twig was partially supported by a grant from the Pinchas Borenstein Talpiot Medical Leadership Program, Chaim Sheba Medical Center, Tel Hashomer, Israel. Disclosures for the coauthors are listed in the article.
Diabetes Care. Published online August 19, 2014. Abstract

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