Posts Tagged ‘weight’

new-way-to-target-high-rates-of-obesity-307945
A UNSW-led team researching a drug to avoid insulin resistance was greeted with an unexpected result that could have implications for the nation’s rising rates of obesity and associated disease.

A novel drug is being touted as a major step forward in the battle against Australia’s escalating rates of obesity and associated metabolic diseases.

Two in three adults in Australia are overweight or obese. A long-term study between researchers at the Centenary Institute and UNSW Sydney has led to the creation of a drug which targets an enzyme linked to insulin resistance – a key contributor of metabolic diseases, such as type 2 diabetes.

The project has been a collaboration between the Centenary Institute’s Associate Professor Anthony Don, UNSW’s Metabolic research group and its leader Associate Professor Nigel Turner, and UNSW Professor Jonathan Morris’ synthetic chemistry group. Together, they set out to create a drug that targeted enzymes within the Ceramide Synthase family, which produce lipid molecules believed to promote insulin resistance in skeletal muscle, as well as liver and fat tissue.

The study has been published in the highly-regarded scientific journal Nature Communications. Surprisingly, although the drug was very effective at reducing the lipids of interest in skeletal muscle, it did not prevent mice (which had been fed a high-fat diet to induce metabolic disease) from developing insulin resistance. Instead, it prevented the mice from depositing and storing fat by increasing their ability to burn fat in skeletal muscle.

“We anticipated that targeting this enzyme would have insulin-sensitising, rather than anti-obesity, effects. However, since obesity is a strong risk factor for many different diseases including cardiovascular disease and cancer, any new therapy in this space could have widespread benefits,” says UNSW Associate Professor Nigel Turner.

While the study produced some unexpected results, it’s the first time scientists have been able to develop a drug that successfully targets a specific Ceramide Synthase enzyme in metabolic disease, making it a significant advancement in the understanding and prevention of a range of chronic health conditions.

“From here, I would like to develop drugs which target both the Ceramide Synthase 1 and 6 enzymes together, and see whether it produces a much stronger anti-obesity and insulin sensitising response. Although these drugs need more work before they are suitable for use in the clinic, our work so far has been a very important step in that direction,” says Centenary Institute’s Associate Professor Anthony Don.

https://newsroom.unsw.edu.au/news/health/surprise-result-researchers-targeting-high-rates-obesity

Advertisements


Adipose Connective Tissue Stores Fat in Our Body. Credit: Berkshire Community College Bioscience Image Library

A new technique to study fat stores in the body could aid efforts to find treatments to tackle obesity.

The approach focuses on energy-burning tissues found deep inside the body – called brown fat – that help to keep us warm when temperatures drop.

Experts are aiming to find it this calorie-burning power can be harnessed to stop weight gain, but little is known about how the process works.

Previous studies have mainly relied on a medical imaging technique called PET/CT to watch brown fat in action deep inside the body. But the method is unable to directly measure the chemical factors in the tissue.

Scientists at the University of Edinburgh developed a technique called microdialysis to measure how brown fat generates heat in people.

The approach involves inserting a small tube into an area of brown fat in the body and flushing it with fluid to collect a snapshot of the tissues’ chemical make-up.

The team tested the technique in six healthy volunteers, using PET/CT to guide the tube to the right location.

They discovered that in cold conditions, brown fat uses its own energy stores and other substances to generate heat.

Brown fat was active under warm conditions too, when the body does not need to generate its own heat, an outcome that had not been seen before.

Researchers hope the technique will help them to analyse the specific chemicals involved, so that they can better understand how brown fat works.

Most of the fat in our body is white fat, which is found under the skin and surrounding internal organs. It stores excess energy when we consume more calories than we burn.

Brown fat is mainly found in babies and helps them to stay warm. Levels can decrease with age but adults can still have substantial amounts of it, mainly in the neck and upper back region. People who are lean tend to have more brown fat.

The study, published in Cell Metabolism, was funded by the Medical Research Council and Wellcome.

Lead researcher Dr Roland Stimson, of the British Heart Foundation Centre for Cardiovascular Science at the University of Edinburgh, said: “Understanding how brown fat is activated could reveal potential targets for therapies that boost its energy-burning power, which could help with weight loss.”

This article has been republished from materials provided by the University of Edinburgh. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference: Weir, G., Ramage, L. E., Akyol, M., Rhodes, J. K., Kyle, C. J., Fletcher, A. M., … Stimson, R. H. (2018). Substantial Metabolic Activity of Human Brown Adipose Tissue during Warm Conditions and Cold-Induced Lipolysis of Local Triglycerides. Cell Metabolism, 0(0). https://doi.org/10.1016/j.cmet.2018.04.020

https://www.technologynetworks.com/proteomics/news/how-brown-fat-keeps-us-warm-304351?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=63228690&_hsenc=p2ANqtz-9oqDIw3te1NPoj51s94kxnA1ClK8Oiecfela6I4WiITEbm_-SWdmw6pjMTwm2YP24gqSzRaBvUK1kkb2kZEJKPcL5JtQ&_hsmi=63228690

Want to prolong your life expectancy by more than a decade? A new study suggests that you can do just that by following these five healthy habits: never smoke, maintain a healthy body-mass index, keep up moderate to vigorous exercise, don’t drink too much alcohol, and eat a healthy diet.

Adhering to those five lifestyle factors at age 50, compared with not adhering to any of them, was associated with 14 additional years of life expectancy among women and 12.2 additional years among men in the study, published in the journal Circulation on Monday.

Each of those factors is significantly associated with a reduced risk of dying from the top two killers in the United States, cardiovascular disease and cancer, according to the study.
About 610,000 people die of heart disease in the US each year, which is about one in every four deaths, according to the US Centers for Disease Control and Prevention.
About 609,640 Americans are expected to die of cancer this year, according to the American Cancer Society.

“These are some of the leading causes of premature death, so by preventing or reducing the incidence of those diseases, it promotes longevity, and it also improves survival after diagnosis of those diseases,” said Dr. Meir Stampfer, a professor of medicine at Harvard Medical School and professor of epidemiology and nutrition at the Harvard T.H. Chan School of Public Health, who was a co-author of the study.

“We can do so much better for having a long healthy life by pretty simple minimal changes in our behavior, and only 8% of adults in our country are adhering to these,” he said. “The main take-home message is that there’s huge gains in health and longevity to be had just by simple changes in our behavior pattern, and as a country, I think we need to make it easier for ourselves to do this by promoting tobacco cessation, by providing better environments for physical activity and so on.”

Globally, the US ranks 43rd when it comes to life expectancy at birth, with an average life expectancy of 80, according to 2017 data from the Central Intelligence Agency’s World Factbook.
The three countries ranked highest for life expectancy at birth are Monaco, with 89.4 years; Japan, with 85.3 years; and Singapore, with 85.2 years, according to those data.

The countries with the lowest life expectancy at birth, based on that data, are Chad, with 50.6 years; Guinea-Bissau, with 51 years; and Afghanistan, with 51.7 years.

The ‘surprising’ impact of behaviors on longevity

For the new study, researchers measured the association between those five lifestyle factors and premature death using data from the national Nurses’ Health Study and the Health Professionals Follow-Up Study. The data came from 1980 to 2014 and included more than 122,000 people combined.

Then, the researchers used data from the National Health and Nutrition Examination Surveys to estimate the distribution of those modifiable lifestyle factors among adults in the United States. Those data, from 2013 to 2014, consisted of 2,128 adults, 50 to 80 years old.

The researchers also derived death rates of US adults using the CDC’s Wide-Ranging Online Data for Epidemiologic Research database.

After analyzing the data, the researchers found that, in 2014, the overall projected life expectancy at age 50 was to live 33.3 more years for women and 29.8 more years for men.

Yet among the adults who reported that they adopted all five healthy lifestyle factors, the researchers found, they lived 43.1 more years among women and 37.6 more years among men.

Among those adults who reported that they adhered to none of the five healthy lifestyle factors, the researchers found that they lived only 29 additional years among women and 25.5 additional years among men.

“To me, the surprising outcome was how strong it was: what a big impact these simple behaviors could have on life expectancy,” Stampfer said. “I was surprised that it was that pronounced.”

Among the women, on average, about 30.8% of the life expectancy at age 50 that they gained from adopting five, versus zero, of those lifestyle factors was attributed to a reduced risk of cardiovascular disease death; 21.2% was attributed to a reduced risk of cancer and 48% to other causes of death.

Among the men, those percentages were 34.1% attributed to a reduced risk of cardiovascular disease death, 22.8% attributed to a reduced risk of cancer and 43.1% to other causes.

The study had some limitations, including that the data on adherence to the five lifestyle factors were all self-reported, making outcome vulnerable to measurement errors.

Also, the data analysis did not include measures of certain health conditions that are risk factors for a shorter life expectancy, such as diabetes or high blood pressure.

That limitation, however, “is both a strength and a limitation, in a way … because what we’re estimating here is the prolongation of life expectancy just based on behaviors,” Stampfer said.
“Obviously, it’s much better to do these healthy behaviors from childhood, really, but if you’re beyond age 50, beyond age 60, beyond age 70, it’s not too late,” he added.

The factor that was seen as more ‘powerful’

The findings should encourage and motivate people to adopt a healthier lifestyle, said Dr. Douglas Vaughan, chairman of the department of medicine in Northwestern University’s Feinberg School of Medicine, who was not involved in the study.

Though the study highlighted how the combination of all five lifestyle factors could help prolong life expectancy, Vaughan pointed out how each individual factor also was tied to a reduced risk of premature death.

“It looks like cigarette smoking has a more powerful effect than the other lifestyle changes or behaviors. Certainly, maintaining a reasonable body-mass index is a great way to protect oneself against the development of diabetes,” Vaughan said.

Body-mass index, a calculation derived from a person’s weight and height, is used as a screening tool for body fatness. A normal or healthy body-mass index is typically said to be between 18.5 and 24.9.

“So, in aggregate, we see the effect on longevity, but you can imagine it’s largely through effects on cardiovascular risk and metabolic risk,” Vaughan said. “It suggests potentially at a defined point in life, say age 50, if you adhere to a healthy paradigm like this, you can have an impact on your longevity and on your health span.”

Dr. Jack Der-Sarkissian, a family medicine physician and assistant area medical director of Kaiser Permanente Los Angeles Medical Center, called smoking “the least-debated health risk factor.”

“Beyond cancer risk, smoking contributes to lung disease, heart disease and diabetes. The study shows that even minimal smoking — from one to 14 cigarettes a day — is associated with increased death due to cancer and heart disease,” said Der-Sarkissian, who was not involved in the new study.

As for some of the other lifestyle factors, “getting weight below a BMI of 30 appears to help considerably, according to the study. A higher body weight is linked to increased risk of diabetes and cancer, among other obesity-related conditions,” he said. “The study suggests physical activity of at least 30 minutes a day of moderate or vigorous activities, including brisk walking.”

https://www.cnn.com/2018/04/30/health/life-expectancy-habits-study/index.html

With the pressure for a certain body type prevalent in the media, eating disorders are on the rise. But these diseases are not completely socially driven; researchers have uncovered important genetic and biological components as well and are now beginning to tease out the genes and pathways responsible for eating disorder predisposition and pathology.

As we enter the holiday season, shoppers will once again rush into crowded department stores searching for the perfect gift. They will be jostled and bumped, yet for the most part, remain cheerful because of the crisp air, lights, decorations, and the sound of Karen Carpenter’s contralto voice ringing out familiar carols.

While Carpenter is mainly remembered for her musical talents, unfortunately, she is also known for introducing the world to anorexia nervosa (AN), a severe life-threatening mental illness characterized by altered body image and stringent eating patterns that claimed her life just before her 33rd birthday in 1983.

Even though eating disorders (ED) carry one of the highest mortality rates of any mental illness, many researchers and clinicians still view them as socially reinforced behaviors and diagnose them based on criteria such as “inability to maintain body weight,” “undue influence of body weight or shape on self-evaluation,” and “denial of the seriousness of low body weight” (1). This way of thinking was prevalent when Michael Lutter, then an MD/PhD student at the University of Texas Southwestern Medical Center, began his psychiatry residency in an eating disorders unit. “I just remember the intense fear of eating that many patients exhibited and thought that it had to be biologically driven,” he said.

Lutter carried this impression with him when he established his own research laboratory at the University of Iowa. Although clear evidence supports the idea that EDs are biologically driven—they predominantly affect women and significantly alter energy homeostasis—a lack of well-defined animal models combined with the view that they are mainly behavioral abnormalities have hindered studies of the neurobiology of EDs. Still, Lutter is determined to find the biological roots of the disease and tease out the relationship between the psychiatric illness and metabolic disturbance using biochemistry, neuroscience, and human genetics approaches.

We’ve Only Just Begun

Like many diseases, EDs result from complex interactions between genes and environmental risk factors. They tend to run in families, but of course, for many family members, genetics and environment are similar enough that teasing apart the influences of nature and nurture is not easy. Researchers estimate that 50-80% of the predisposition for developing an ED is genetic, but preliminary genome-wide analyses and candidate gene studies failed to identify specific genes that contribute to the risk.

According to Lutter, finding ED study participants can be difficult. “People are either reluctant to participate, or they don’t see that they have a problem,” he reported. Set on finding the genetic underpinnings of EDs, his team began recruiting volunteers and found 2 families, 1 with 20 members, 10 of whom had an ED and another with 5 out of 8 members affected. Rather than doing large-scale linkage and association studies, the team decided to characterize rare single-gene mutations in these families, which led them to identify mutations in the first two genes, estrogen-related receptor α (ESRRA) and histone deacetylase 4 (HDAC4), that clearly associated with ED predisposition in 2013 (1).

“We have larger genetic studies on-going, including the collection of more families. We just happened to publish these two families first because we were able to collect enough individuals and because there is a biological connection between the two genes that we identified,” Lutter explained.

ESRRA appears to be a transcription factor upregulated by exercise and calorie restriction that plays a role in energy balance and metabolism. HDAC4, on the other hand, is a well-described histone deacteylase that has previously been implicated in locomotor activity, body weight homeostasis, and neuronal plasticity.

Using immunoprecipitation, the researchers found that ESRRA interacts with HDAC4, in both the wild type and mutant forms, and transcription assays showed that HDAC4 represses ESRRA activity. When Lutter’s team repeated the transcription assays using mutant forms of the proteins, they found that the ESRRA mutation seen in one family significantly reduced the induction of target gene transcription compared to wild type, and that the mutation in HDAC4 found in the other family increased transcriptional repression for ESRRA target genes.

“ESRRA is a well known regulator of mitochondrial function, and there is an emerging view that mitochondria in the synapse are critical for neurotransmission,” Lutter said. “We are working on identifying target pathways now.”

Bless the Beasts and the Children

Finding genes associated with EDs provides the groundwork for molecular studies, but EDs cannot be completely explained by the actions of altered transcription factors. Individuals suffering these disorders often experience intense anxiety, intrusive thoughts, hyperactivity, and poor coping strategies that lead to rigid and ritualized behaviors and severe crippling perfectionism. They are less aware of their emotions and often try to avoid emotion altogether. To study these complex behaviors, researchers need animal models.

Until recently, scientists relied on mice with access to a running wheel and restricted access to food. Under these conditions, the animals quickly increase their locomotor activity and reduce eating, frequently resulting in death. While some characteristics of EDs—excessive exercise and avoiding food—can be studied in these mice, the model doesn’t allow researchers to explore how the disease actually develops. However, Lutter’s team has now introduced a promising new model (3).

Based on their previous success with identifying the involvement of ESRRA and HDAC4 in EDs, the researchers wondered if mice lacking ESRRA might make suitable models for studies on ED development. To find out, they first performed immunohistochemistry to understand more about the potential cognitive role of ESRRA.

“ESRRA is not expressed very abundantly in areas of the brain typically implicated in the regulation of food intake, which surprised us,” Lutter said. “It is expressed in many cortical regions that have been implicated in the etiology of EDs by brain imaging like the prefrontal cortex, orbitofrontal cortex, and insula. We think that it probably affects the activity of neurons that modulate food intake instead of directly affecting a core feeding circuit.”

With these data, the team next tried providing only 60% of the normal daily calories to their mice for 10 days and looked again at ESRRA expression. Interestingly, ESRRA levels increased significantly when the mice were insufficiently fed, indicating that the protein might be involved in the response to energy balance.

Lutter now believes that upregulation of ESRRA helps organisms adapt to calorie restriction, an effect possibly not happening in those with ESRRA or HDAC4 mutations. “This makes sense for the clinical situation where most individuals will be doing fine until they are challenged by something like a diet or heavy exercise for a sporting event. Once they start losing weight, they don’t adapt their behaviors to increase calorie intake and rapidly spiral into a cycle of greater and greater weight loss.”

When Lutter’s team obtained mice lacking ESRRA, they found that these animals were 15% smaller than their wild type littermates and put forth less effort to obtain food both when fed restricted calorie diets and when they had free access to food. These phenotypes were more pronounced in female mice than male mice, likely due to the role of estrogen signaling. Loss of ESRRA increased grooming behavior, obsessive marble burying, and made mice slower to abandon an escape hole after its relocation, indicating behavioral rigidity. And the mice demonstrated impaired social functioning and reduced locomotion.

Some people with AN exercise extensively, but this isn’t seen in all cases. “I would say it is controversial whether or not hyperactivity is due to a genetic predisposition (trait), secondary to starvations (state), or simply a ritual that develops to counter the anxiety of weight related obsessions. Our data would suggest that it is not due to genetic predisposition,” Lutter explained. “But I would caution against over-interpretation of mouse behavior. The locomotor activity of mice is very different from people and it’s not clear that you can directly translate the results.”

For All We Know

Going forward, Lutter’s group plans to drill down into the behavioral phenotypes seen in their ESRRA null mice. They are currently deleting ESRRA from different neuronal cell types to pair individual neurons with the behaviors they mediate in the hope of working out the neural circuits involved in ED development and pathology.

In addition, the team has created a mouse line carrying one of the HDAC4 mutations previously identified in their genetic study. So far, this mouse “has interesting parallels to the ESRRA-null mouse line,” Lutter reported.

The team continues to recruit volunteers for larger-scale genetic studies. Eventually, they plan to perform RNA-seq to identify the targets of ESRRA and HDAC4 and look into their roles in mitochondrial biogenesis in neurons. Lutter suspects that this process is a key target of ESRRA and could shed light on the cognitive differences, such as altered body image, seen in EDs. In the end, a better understanding of the cells and pathways involved with EDs could create new treatment options, reduce suffering, and maybe even avoid the premature loss of talented individuals to the effects of these disorders.

References

1. Lutter M, Croghan AE, Cui H. Escaping the Golden Cage: Animal Models of Eating Disorders in the Post-Diagnostic and Statistical Manual Era. Biol Psychiatry. 2015 Feb 12.

2. Cui H, Moore J, Ashimi SS, Mason BL, Drawbridge JN, Han S, Hing B, Matthews A, McAdams CJ, Darbro BW, Pieper AA, Waller DA, Xing C, Lutter M. Eating disorder predisposition is associated with ESRRA and HDAC4 mutations. J Clin Invest. 2013 Nov;123(11):4706-13.

3. Cui H, Lu Y, Khan MZ, Anderson RM, McDaniel L, Wilson HE, Yin TC, Radley JJ, Pieper AA, Lutter M. Behavioral disturbances in estrogen-related receptor alpha-null mice. Cell Rep. 2015 Apr 21;11(3):344-50.

http://www.biotechniques.com/news/Exploring-the-Biology-of-Eating-Disorders/biotechniques-361522.html


Dr. Justin Grobe, PhD


Dr. Michael Lutter, MD PhD

In a study that seems to defy conventional dietary wisdom, University of Iowa scientists have found that adding high salt to a high-fat diet actually prevents weight gain in mice.

As exciting as this may sound to fast food lovers, the researchers caution that very high levels of dietary salt are associated with increased risk for cardiovascular disease in humans. Rather than suggest that a high salt diet is suddenly a good thing, the researchers say these findings really point to the profound effect non-caloric dietary nutrients can have on energy balance and weight gain.

“People focus on how much fat or sugar is in the food they eat, but [in our experiments] something that has nothing to do with caloric content – sodium – has an even bigger effect on weight gain,” say Justin Grobe, PhD, assistant professor of pharmacology at the UI Carver College of Medicine and co-senior author of the study, which was published in the journal Scientific Reports on June 11.

The UI team started the study with the hypothesis that fat and salt, both being tasty to humans, would act together to increase food consumption and promote weight gain. They tested the idea by feeding groups of mice different diets: normal chow or high-fat chow with varying levels of salt (0.25 to 4 percent). To their surprise, the mice on the high-fat diet with the lowest salt gained the most weight, about 15 grams over 16 weeks, while animals on the high-fat, highest salt diet had low weight gain that was similar to the chow-fed mice, about 5 grams.

“We found out that our ‘french fry’ hypothesis was perfectly wrong,” says Grobe, who also is a member of the Fraternal Order of Eagles Diabetes Research Center at the UI and a Fellow of the American Heart Association. “The findings also suggest that public health efforts to continue lowering sodium intake may have unexpected and unintended consequences.”

To investigate why the high salt prevented weight gain, the researchers examined four key factors that influence energy balance in animals. On the energy input side, they ruled out changes in feeding behavior – all the mice ate the same amount of calories regardless of the salt content in their diet. On the energy output side, there was no difference in resting metabolism or physical activity between the mice on different diets. In contrast, varying levels of salt had a significant effect on digestive efficiency – the amount of fat from the diet that is absorbed by the body.

“Our study shows that not all calories are created equal,” says Michael Lutter, MD, PhD, co-senior study author and UI assistant professor of psychiatry. “Our findings, in conjunction with other studies, are showing that there is a wide range of dietary efficiency, or absorption of calories, in the populations, and that may contribute to resistance or sensitivity to weight gain.”

“This suppression of weight gain with increased sodium was due entirely to a reduced efficiency of the digestive tract to extract calories from the food that was consumed,” explains Grobe.

It’s possible that this finding explains the well-known digestive ill effects of certain fast foods that are high in both fat and salt, he adds.

Through his research on hypertension, Grobe knew that salt levels affect the activity of an enzyme called renin, which is a component in the renin- angiotensin system, a hormone system commonly targeted clinically to treat various cardiovascular diseases. The new study shows that angiotensin mediates the control of digestive efficiency by dietary sodium.

The clinical usefulness of reducing digestive efficiency for treating obesity has been proven by the drug orlistat, which is sold over-the-counter as Alli. The discovery that modulating the renin-angiotensin system also reduces digestive efficiency may lead to the developments of new anti-obesity treatments.

Lutter, who also is an eating disorders specialist with UI Health Care, notes that another big implication of the findings is that we are just starting to understand complex interactions between nutrients and how they affect calorie absorption, and it is important for scientists investigating the health effects of diet to analyze diets that are more complex than those currently used in animal experiments and more accurately reflect normal eating behavior.

“Most importantly, these findings support continued and nuanced discussions of public policies regarding dietary nutrient recommendations,” Grobe adds.

http://www.eurekalert.org/pub_releases/2015-06/uoih-hsp061115.php

There’s been a fast growing body of evidence in the last several years that lack of exercise – or sedentariness – is a major risk factor in health. It’s been linked to heart disease, cancer, and to an early death. And now, a new study finds that lack of exercise may actually be even more of a risk than obesity in early mortality: The researchers calculate that a sedentary lifestyle may actually confer twice the risk of death as being obese. That said, the two are both important and, luckily, closely related: So if you start getting active, you’ll probably lose a little weight along the way, which itself is a very good thing.

The new study looked at data from over 334,000 people who participated in the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Over a period of 12 years, the participants’ height, weight, and waist circumferences were tracked, along with self-reports of activity levels, both at work and in free time. All-cause mortality (i.e., death from any cause) was the main outcome of interest.

It turned out that lack of physical activity was linked to the greatest risk of death – and the greatest reduction in death risk was in the difference between the lowest two activity groups. In other words, just moving from “inactive” to “moderately inactive” showed the largest reduction in death risk, especially for normal weight people, but true for people of all body weights. And, the authors say, just taking a brisk 20-minute walk per day can move you from one category to the other, and reduce the risk of death anywhere from 16% to 30%.

Using a statistical model, the team also calculated that being sedentary may account for double the death risk of obesity. According to their math, of the 9.2 million deaths in Europe in 2008, about 337,000 were attributable to obesity, whereas 676,000 were attributable to sedentariness.

Another takeaway from the study, however, is that waist circumference is a bigger player in mortality risk than overall body weight, which has certainly been suggested by previous studies. Belly fat seems to be disproportionately linked to chronic health issues like heart disease, stroke, diabetes, cancer, and of course, early mortality. So reducing belly fat is always a significant benefit to one’s health.

“This large study is rather complex in its details, but the take-away messages are actually both clear and simple,” says David L, Katz, Director of the Yale University Prevention Research CenterGriffin Hospital. “At any given body weight, going from inactive to active can reduce the risk of premature mortality substantially. At any given level of activity, going from overweight to a more optimal weight can do the same. We have long known that not all forms of obesity are equally hazardous, and this study reaffirms that. Losing weight if you have an excess around the middle, where it is most dangerous, exerts an influence on mortality comparable to physical activity. Losing excess weight that is not associated with a high waist circumference reduces mortality risk, but less — as we would expect.”

But perhaps the main point in all of this is that being active and being a healthy weight are inextricably linked. Though activity by itself can offer an immediate health benefit if you remain overweight, getting active also leads naturally to loss of body weight. “This study reminds that being both fit and unfat are good for health,” says Katz, “and can add both life to years, and years to life. These are not really disparate challenges, since the physical activity that leads to fitness is on the short list of priorities for avoiding fatness as well. The challenge before us now is for our culture to make it easier to get there from here.”

Earlier this month a study showed that the concept of “healthy obesity” may be very misleading, since health markers in an obese person tend to deteriorate over time. Though the current study suggests that fitness may matter more than fatness, the two are really two sides of a coin: It would be silly to become active and not lose weight — and it would be very hard to do, since the one leads to the other. But perhaps given the great benefits of exercise alone, public health campaigns should focus not just on losing weight, but on encouraging people to add just small amounts physical activity to their lives right off the bat, and to see where it goes from there.

http://www.forbes.com/sites/alicegwalton/2015/01/15/is-lack-of-exercise-worse-for-your-health-than-obesity/