Lifetime Medical Costs Of Obese People Actually Lower Than Costs For Healthy And Fit, Mathematical Model Shows

Daily Science Journal (Feb. 8, 2008) — A new research paper suggests that preventing obesity might result in increased public spending on medical care. Many countries are currently developing policies aimed at reducing obesity in the population. However, it is not currently clear whether successfully reducing obesity will also reduce national healthcare spending or not. Pieter van Baal and colleagues, from the National Institute for Public Health and the Environment in the Netherlands, created a mathematical model to try to answer this question.

Researchers found that the group of healthy, never-smoking individuals had the highest lifetime healthcare costs, because they lived the longest and developed diseases associated with aging; healthcare costs were lowest for the smokers, and intermediate for the group of obese never-smokers. (Credit: iStockphoto/Eliza Snow)

In their study, van Baal and his co-workers created three hypothetical populations of 1000 men and women, all aged 20 years at the start: a group of obese, never-smoking individuals; a group of healthy-never smoking individuals of normal weight; and a group of smokers of normal weight. The model produced an estimate of the likely proportion of each group who would encounter certain long term (chronic) diseases, and then estimated what the approximate cost of medical care associated with each disease was likely to be. The researchers found that the group of healthy, never-smoking individuals had the highest lifetime healthcare costs, because they lived the longest and developed diseases associated with aging; healthcare costs were lowest for the smokers, and intermediate for the group of obese never-smokers.

However, the authors argue that although obesity prevention may not be a cure for increasing expenditures, it may well be a cost-effective cure for much morbidity and mortality and importantly contribute to the health of nations.

A Perspective by Klim McPherson, from Oxford University in the UK, who was not involved in the study, discusses the implications of these findings and comments that "it would be wrong to interpret the findings as meaning that public-health prevention (e.g., to prevent obesity) has no benefits"; the quality of life experienced by individuals, and other factors, must also be taken into account when planning interventions aimed at improving public health.

Citation: van Baal PHM, Polder JJ, de Wit GA, Hoogenveen RT, Feenstra TL, et al. (2008) Lifetime medical costs of obesity: Prevention no cure for increasing health expenditure. PLoS Med 5(2): e29. doi:10.1371/journal.pmed.0050029 http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050029

Adapted from materials provided by Public Library of Science, via EurekAlert!, a service of AAAS.

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'Weight Training' Reduces Fat And Improve Metabolism In Mice

Daily Science Journal (Feb. 8, 2008) — Researchers from the Boston University School of Medicine (BUSM) have demonstrated that in mice, the use of barbells may be as important to losing weight and improving health as the use of running shoes. The discovery builds upon the fact that skeletal muscle consists of two types of fibers. Endurance training such as running increases the amount of type I muscle fibers, while resistance training such as weightlifting increases type II muscle fibers. Using a mouse genetic model, BUSM researchers demonstrated that an increase in type II muscle mass can reduce body fat which in turn reduces overall body mass and improves metabolic parameters such as insulin resistance. These studies indicate that weight bearing exercise, in addition to endurance training, may benefit overweight people.

Weight-lifting. "We've shown that type II muscle does more than allow you to pick up heavy objects," said Kenneth Walsh of Boston University School of Medicine. "It is also important in controlling whole-body metabolism." (Credit: iStockphoto/Sean Locke)

Researchers used a genetic trick in obese mice that caused the mice's muscles to bulk up as though they had been lifting weights. The researchers found that the "genetically reprogrammed" mice lost fat and showed other signs of metabolic improvement throughout the body. What's more, those benefits were seen even though the mice continued eating a diet high in both fat and sugar and didn't increase their physical activity at all.

The researchers genetically engineered a mouse, called the MyoMouse, to grow type II fibers by activating a muscle growth-regulating gene. The gene, called Akt1, was engineered in such a way that it could be turned on and off at will by researchers. Even without exercise, activating the gene made the MyoMouse physically stronger. When the gene was de-activated, the mouse returned to its original strength. While stronger and faster than a regular mouse, the MyoMouse did not run with as much endurance on a treadmill, a finding that is consistent with the growth of type II rather than type I muscle. These findings demonstrate that the mouse was genetically programmed to have the characteristics of a lean and powerful sprinter rather than those of a gaunt marathon runner.

"We've shown that type II muscle does more than allow you to pick up heavy objects," said Kenneth Walsh of Boston University School of Medicine. "It is also important in controlling whole-body metabolism."

In the study, the Akt1 gene was turned off and the MyoMice were fed a high fat/high sugar diet with a similar caloric composition as a meal from a fast food restaurant. Over an eight-week period, the mice became obese and insulin resistant and developed fatty acid deposits in their liver, a condition referred to as hepatic steatosis or fatty liver disease.

The researchers then activated the Akt1 gene in the animals which led to the growth of type II muscle fibers. "Remarkably, type II muscle growth was associated with an overall reduction in body mass, due to a large decrease in fat mass. In addition, blood tests showed that these mice became metabolically normal and their fatty liver disease rapidly resolved," said senior author Kenneth Walsh, PhD, a professor of medicine and head of Molecular Cardiology at the Whitaker Cardiovascular Institute at BUSM.

The beneficial changes occurred despite the fact that the mice continued to eat the same high-calorie diet and did not display any increase in physical activity. "This work shows that type II muscle just doesn't allow you to pick up heavy objects, it is also important in controlling whole body metabolism," added Walsh.

Further analysis found that the mice burned fat because of changes in the physiology and gene expression of their fat and liver cells. "Thus, it appears that the increase in type II muscle fiber orchestrates changes in the body through its ability to communicate with these other tissues," he said.

These findings indicate that type II muscle has a previously unappreciated role in regulating whole body metabolism through its ability to alter the metabolic properties of remote tissues. These data also suggest that strength training, in addition to the widely-prescribed therapy of endurance training, may be of particular benefit to overweight individuals

Finally, these findings may be relevant for understanding aspects of the aging process. "Beyond the age of thirty, humans lose approximately 6 lbs of muscle mass per decade. Surprisingly, aging individuals predominantly lose type II muscle. Thus a 50 year old may be relatively good at playing tennis or jogging because type I muscle is preserved, but a measurement of grip strength or core body strength could show appreciable declines," explained Walsh. Therefore, this new study suggests that the loss of type II muscle contributes to the development of obesity and diabetes as we age.

The BUSM researchers suspect that the beneficial effects of muscle growth seen in the MyoMouse are mediated through the production and secretion of a variety of signaling factors. Walsh and his colleagues are currently identifying the novel proteins in muscle that communicate with other tissues. These new proteins, referred to as "myokines" from the Greek words "muscle" and "motion," may represent new targets for therapies that mimic the benefits of weight training for the treatment of obesity and diabetes as well as muscle wasting disorders.

"The work of [Walsh and his colleagues] reveals the intricate interplay between diet, energy balance, and the function/morphology of diverse tissue systems such as skeletal muscle and liver," said Brooke Harrison and Leslie Leinwand of the University of Colorado at Boulder in a commentary in the journal Cell Metabolism. "These findings indicate that interventions designed to increase skeletal muscle mass in at-risk human populations may prove to be critical weapons in the fight against obesity and obesity-related comorbidities including diabetes, heart disease, stroke, hypertension, and cancer."

The study appears in the February 6th issue of Cell Metabolism. The researchers include Yasuhiro Izumiya, Teresa Hopkins, Carl Morris, Kaori Sato, Ling Zeng, Jason Viereck, James A. Hamilton, Noriyuki Ouchi, Nathan K. LeBrasseur, and Kenneth Walsh, of Boston University School of Medicine, Boston, MA.

Adapted from materials provided by Boston University, via EurekAlert!, a service of AAAS.

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Sugary Soft Drinks Linked To Increased Risk Of Gout In Men

Daily Science Journal (Feb. 1, 2008) — Consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased risk of gout in men, finds a study published by the British Medical Journal.

Gout is a joint disease which causes extreme pain and swelling. It is most common in men aged 40 and older. It is caused by excess uric acid in the blood (hyperuricaemia) which leads to uric acid crystals collecting around the joints.

In the United States, levels of gout have doubled over the last few decades, which coincided with a substantial increase in the consumption of soft drinks and fructose (a simple sugar and the only carbohydrate known to increase uric acid levels).

Conventional dietary recommendations for gout have focused on the restriction of purines (found in high levels in meat and meat products, especially liver and kidney) and alcohol but with no restriction of sugar sweetened soft drinks.

So researchers in the US and Canada examined the relation between intake of sugar sweetened soft drinks and fructose and the risk of gout.

They followed over 46,000 men aged 40 years and over with no history of gout. The men completed regular questionnaires on their intake of more than 130 foods and beverages, including sugar sweetened soft drinks and diet soft drinks, over a period of 12 years. Different types of fruits and fruit juices (high in natural fructose) were also assessed.

At the start of the study, and every two years thereafter, information on weight, regular use of medications and medical conditions were also recorded. Gout was diagnosed according to American College of Rheumatology criteria.

During 12 years of follow-up, the researchers documented 755 newly diagnosed cases of gout.

The risk of gout increased with increasing intake of sugar sweetened soft drinks. The risk was significantly increased with an intake level of 5-6 servings per week and the risk was 85% higher among men who consumed two or more servings of sugar-sweetened soft drinks per day compared to those who consumed less than one serving per month.

These associations were independent of other risk factors for gout such as body mass index, age, diuretic use, high blood pressure, alcohol intake, and dietary factors.

Diet soft drinks were not associated with the risk of gout.

Fruit juice and fructose rich fruits (apples and oranges) were associated with a higher risk of gout. However, the authors stress that this finding needs to be balanced against the benefit of fruit and vegetable intake to prevent other chronic disorders like high blood pressure, coronary heart disease, stroke and certain types of cancer.

In conclusion, our findings provide prospective evidence that consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased risk of gout, say the authors. Furthermore, fructose rich fruits and fruit juices may also increase the risk. In contrast, diet soft drinks were not associated with the risk of gout.

Adapted from materials provided by BMJ-British Medical Journal, via EurekAlert!, a service of AAAS.

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Omega-3 Fatty Acids: A Way To Improve Heart Health, Eating Oily Fish May Reduce Inflammation

Daily Science Journal (Aug. 13, 2007) — While a heart-healthy diet has become synonymous with plenty of fruits and vegetables and little fat and cholesterol, there’s more to the story. Omega-3 fatty acids should be part of a heart-healthy diet, too, according to the August issue of Mayo Clinic Health Letter.

Omega-3 fatty acids are a form of polyunsaturated fat important to overall health. As it pertains to heart disease, their main benefit is their ability to reduce the risk of heart rhythm problems in certain groups of people, thus reducing the risk of sudden cardiac death. In addition, omega-3s may help reduce triglycerides, lower blood pressure slightly and reduce blood clotting.

The best source of omega-3s is fatty, cold water fish such as herring, mackerel, salmon and tuna. Plant oils, such as canola and flaxseed oils, also are sources of omega-3s.

For heart disease prevention, near-maximum benefit comes from eating two 3-ounce servings of cold water fish a week. More than that doesn’t appear to offer any additional preventive benefit.

Higher amounts of two kinds of omega-3, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), may benefit some people with established heart disease or high triglyceride levels and can have an anti-inflammatory effect for people with rheumatoid arthritis. In addition, DHA is being studied to see if it can slow the progression of Alzheimer’s disease.

For those who don’t eat fish, a fish oil supplement or an algae supplement can provide omega-3 fatty acids. However, supplements aren’t cheap, and the amount of DHA and EPA in supplements varies widely. Except for people who have established heart disease, the evidence of heart disease prevention is stronger when one eats fish instead of taking supplements. Supplements can pose risks, too. Taking more than 3 grams of fish oil a day may increase the risk of bleeding, worsen heart rhythm problems in those who have arrhythmias or cause other side effects.

Adapted from materials provided by Mayo Clinic, via Newswise.

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Eating Oily Fish May Reduce Inflammation

A new study explains how a diet high in oily fish like salmon and mackerel improves inflammatory conditions, particularly in combination with low doses of aspirin. In a study in the March 7 issue of The Journal of Experimental Medicine, Arita and colleagues identify an anti-inflammatory lipid in humans that is derived from an essential fatty acid in fish oil.

Sockey Salmon. (Photo courtesy of Washington State Department of Fish and Wildlife)

Fatty fish contain large amounts of omega-3 fatty acids--diet-derived essential fatty acids known to benefit patients with cardiovascular disease and arthritis. This research group recently identified a new class of aspirin-triggered bioactive lipids, called resolvins, the activity of which may in part explain the beneficial effects of omega-3 fatty acids. Resolvins are made from the omega-3 fatty acids by cellular enzymes and can reduce inflammation in mice. The main bioactive component of this class of lipids was identified in mice and named resolvin E1.

The researchers have now identified this lipid in plasma taken from volunteers given omega-3 fatty acids and aspirin. Human resolvin E1, the authors show, inhibits both the migration of inflammatory cells to sites of inflammation and the turning on of other inflammatory cells.

This study also reveals a potential pitfall of COX-2 inhibitors, drugs designed to block inflammation, which have been shown to have negative cardiovascular side effects. COX-2 is involved in making resolvin E1 and the authors suggest that inhibition of vascular COX-2 by these inhibitors might block the synthesis of resolvin E1, which would eliminate an important anti-inflammatory pathway. The experiment to prove this idea, however, has yet to be done.

Adapted from materials provided by Journal Of Experimental Medicine.

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