Lose weight image via Shutterstock

Dr. Proietto runs a weight-loss clinic. In this most recent study, he recruited fifty obese individuals without diabetes or other serious illnesses into an intensive ten week weight loss program. After weight loss was achieved — study participants were required to lose ten percent of their body weight — they received dietary counseling to help them maintain their new weight. Dr. Proietto measured levels of a variety of hormones known to mediate appetite and got subjective ratings of appetite before the program began, immediately after it ended, and then again a year later.

Of the fifty people recruited, thirty-four were able to complete the study. Perhaps not surprisingly, Dr. Proietto found that the participants reported their “desire and urge to eat” as higher immediately after the weight loss regimen than it was before they had started. But distressingly, it was just as high a year later. What’s more, they reported being more preoccupied with thoughts of food, and less full, after a year than they had been just coming off of the diet.

The levels of nine different hormones were measured. Of these, leptin might be the best known. It is made by body fat, and thus functions as an indicator of energy stores. It acts in the brain to suppress hunger and increase metabolism. Leptin levels plummeted by 64% over the ten weeks that the study participants were dieting, and although they recovered somewhat over the course of the next year, they were still 35% lower than when the study began. The researchers noticed that as study participants put weight back on, their leptin levels rose. Ghrelin can be thought of as the opposite of leptin — whereas leptin suppresses feelings of hunger, ghrelin promotes them. And as such its levels were the opposite of leptin’s — for the ten weeks of the diet the participants’ ghrelin levels steadily rose, and although they fell over the course of the year, they ended up significantly higher than they were at the beginning of the study. The other hormones followed the same pattern established by these representatives; those that suppress appetite were reduced, while those that stimulate appetite were increased.

These hormonal changes indicate that a full year after these people lost weight, their bodies were trying to put it back on. Their bodies regarded this leaner state as akin to starvation, and treated their heavier body weights as normal. Their metabolism was not at all the same as that of someone who had always weighed this lower amount rather than achieving it by dieting.

A number of other studies have borne out this idea, that a weight-reduced body is quite different than one of the same size that had always been that way.

Last month, Tara Parker Pope expanded upon Dr. Proietto’s study in the in The New York Times Magazine. Ms. Parker Pope highlights some studies being done at Columbia University confirming that after people lose weight their muscles are more efficient — meaning that when doing the same activity as people who were always at that lower weight, they burn 20-25% fewer calories. And using brain scans, neuroscientists at Columbia have shown that images of food activate regions of the brain associated with reward more strongly in people after they have lost weight, while regions associated with control did not respond as strongly in these post dieters. Their brains are actively making food look more appealing, and undermining their will power, to get them to eat more — to get them back to their original weight.

The National Weight Control Registry tracks 10,000 people who have lost at least thirty pounds and kept it off for at least a year. Analysis of their habits reveals that to maintain their new lower weights, these individuals must in fact eat less, and exercise more, than those who naturally weigh the same amount. And that’s not really surprising: if you want to lose weight and keep it off, you have to permanently change your lifestyle. The lifestyle that you adopt to lose weight has to be one you’re prepared to maintain for the rest of your life. So as Ms. Parker-Pope notes in her article, it is not hopeless. It is not impossible to lose weight and then keep it off. It’s just really, really hard.

References

1. Sumithran P et al. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med. 2011 Oct 27; 365(17):1597-604.
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2. Rosenbaum M, Kissileff HR, Mayer LE, Hirsch J, Leibel RL. Energy intake in weight-reduced humans. Brain Res. 2010 Sep 2; 1350:95-102. Epub 2010 Jun 2.
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The campaign, launched in August 2011, features provocative television and outdoor advertisements around metro Atlanta seeking to raise public awareness of the childhood obesity crisis [1]. The hospital justifies the harsh nature of the ads by citing the many serious health issues associated with childhood obesity. These include heart disease, high blood pressure, and type 2 diabetes. Linda Matzigkeit, a senior vice president at Children’s Healthcare who leads the system’s wellness projects, told The Atlanta Journal-Constitution that the campaign’s harsh tone was necessary [2]:

We felt like we needed a very arresting, abrupt campaign that said: “Hey, Georgia! Wake up. This is a problem.”

The obesity epidemic in the United States isn’t limited to Georgia — or to children — but it’s more severe in the South than in other parts of the country. Further, while Americans are becoming fatter across age brackets, obesity in children is particularly problematic because it sets children up for a lifetime of health problems. According to the CDC, childhood obesity rates have been skyrocketing over the past two decades. In 1996, just over 20% of public school children in sixth grade were overweight. By 2003, this number had risen to 43%, half of whom were obese [3]. The report goes on to state that in the last five years, obesity rates have actually fallen a bit among school children, but that this trend is strongly associated with income and race. Minority children and those from poorest families have experienced the smallest drop in obesity.

Opponents of the Georgia ad campaign object to the ad’s negativity, claiming that they could impact the already low self-esteem of an overweight or obese child. However, proponents of the ads counter with the logic that a blow to the self-esteem is minor compared to the significant health consequences of childhood obesity. Children’s Healthcare of Atlanta explains that their targeted research shows children don’t see the ads as “bullying,” and want to be talked to directly about the problem.

References

1. Children’s Healthcare of Atlanta Launches Provocative Awareness Campaign to Combat Childhood Obesity. Children’s Healthcare of Atlanta. 2011 Aug 23.
2. Grim childhood obesity ads stir critics. Atlanta Journal-Constitution. 2012 Jan 1.
3. CDC. Obesity in K–8 Students — New York City, 2006–07 to 2010–11 School Years. MMWR Morb Mortal Wkly Rep. 2011 Dec 16;60:1673-8.
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Osteoblasts, or bone cells, have been shown to grow into mature bone when subjected to mechanical stress. Scientists hypothesized that the same might hold true for other cell types. Adipocytes seemed the ideal test system for a number of reasons. Firstly, they are derived from the same embryonic progenitor cells as osteoblasts, so they might share similar properties. Moreover, adipocytes in the buttocks are known to be exposed to a large mechanical strain in a physiological setting — when we sit down. And lastly, obesity is such an immense health problem that any insight into its development could be clinically valuable.

To test their theory, researchers created a unique experimental apparatus in which two groups of cells could be cultured under identical conditions, but one group would be stretched and the other would not. The stretching of the cells mimicked the about half the degree of tissue compression that occurs in weight bearing postures. All of the cells were induced to differentiate by the addition of insulin, and cells were inspected almost daily. The researchers measured the numbers and sizes of lipid droplets in the two cell populations every two to three days over the course of three to four weeks. Within the first ten days of culture, the stretched cells differentiated about twice as fast as the non-stretched cells. Thereafter, the stretched cells contained lipid droplets that were about one and a half times as large — 50% more fat — as those in the non-stretched cells.

This is the first study to look at fat cells as they develop under sustained mechanical loading. The authors are quick to point out that cyclic or intermediate stretching — such as that attained during physical motion — has been shown to have the opposite effect; it actually inhibits the differentiation of preadipocytes and lipid production. They also note that future studies should try to determine if these results hold true in a more physiological setting, and if the cells might respond differently to different concentrations of insulin and glucose such as those that might be representative of a high calorie diet.

Nevertheless, the study is highly suggestive of yet another damaging effect of a modern, sedentary lifestyle. Dr. Gefen notes [2]:

Obesity is more than just an imbalance of calories. Cells themselves are also responsive to their mechanical environment. Fat cells produce more triglycerides, and at a faster rate, when exposed to static stretching.

Indeed, the findings indicate that we need to take our cells’ mechanical environment into account as well as pay attention to calories consumed and burned. Even people that eat a healthy diet and exercise will be negatively impacted by long periods of inactivity.

References

1. Shoham et al. Static Mechanical Stretching Accelerates Lipid Production in 3T3-L1 Adipocytes by Activating the MEK Signaling Pathway. Am J Physiol Cell Physiol. 2011 Oct 19.

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2. ‘Just chill?’ Relaxing can make you fatter. EurekAlert. 2011 Dec 1.

Too much body fat, however, is associated with a number of negative health effects, including increased risk of heart disease, type 2 diabetes, arthritis, and apnea.

Fat in the diet can contribute to excess fat on the body, as dietary fat is a dense source of calories. This means that even small quantities of fatty food are very calorie-rich. However, too much body fat comes from too much food in general — regardless of whether it’s made up of fat, carbohydrate or protein — since the body converts excess protein and carbohydrate into stored fat. Further, appropriate quantities of fat are important in the diet; dietary fat serves as a satiety signal, increases the absorption of fat-soluble vitamins, and (depending upon the kind of fat) plays other roles as well.

There are three basic categories of fat in the diet: saturated fats, trans fats and unsaturated fats. For a healthy diet, a growing body of research suggests that you should avoid saturated fats and trans fats, and focus on eating unsaturated fats.

What to avoid: saturated fats

Saturated fats come mainly from animal sources, though there are some plants (avocados and coconut, for instance) that contain saturated fat. Because of their chemical makeup, these fats have high melting points, and are solid at room temperature. Saturated fats contribute to heart disease by increasing low-density lipoprotein, also known as LDL (sometimes called “bad cholesterol”) and should be limited in the diet. According to the American Heart Association, an individual on a 2,000 calorie-per-day diet should limit saturated fat intake to no more than about 16 grams [2].

What to avoid: trans fats

Trans fats are common in the American diet, but they’re not found in nature to any significant extent. Instead, they come about by processing unsaturated oils (including corn and soybean oil). The processes used, called “partial hydrogenation” and “interesterification,” result in the production of plant-based fat that behaves in food like saturated fat. Shortening is an example of trans fat; it’s plant based, but it’s solid at room temperature. Trans fats act strangely in the body: they not only increase LDL, as saturated fat does, they also decrease high-density lipoprotein or HDL. This makes them particularly deleterious components of diet.

In addition to impacting cholesterol, trans fats appear to increase risk of type 2 diabetes. The American Heart Association recommends limiting the amount of trans fat in the diet as much as possible, and sets an upper recommended limit of 2 grams per day [4]. Nutrition labels on foods report how much trans fat is in a serving of the food; whole foods (which don’t have nutrition labels) don’t contain trans fat. One important point to remember is that manufacturers can report that a food contains zero grams of trans fat per serving as long as it contains no more than 0.49 grams per serving. Avoiding trans fat in the diet therefore requires reading ingredient lists as well as nutrition facts; if the words “partially-hydrogenated” or “interesterified” appear in the ingredients, there’s trans fat in the food. The most common sources of trans fat in the diet are processed foods and fast food.

Unsaturated fats are healthy fats

Unsaturated fats, which include both monounsaturated and polyunsaturated fats, come mainly from plant sources, though they’re also found in cold-water fish. Their chemical makeup is such that they have low melting points, and are liquid at room temperature. Some of them are even liquid in the refrigerator or freezer. They confer all the benefits of dietary fat (immune system support, increased fat-soluble vitamin absorption, and so forth) without increasing LDL concentration in the blood. The American Heart Association recommends that 25-35% of daily calories come from fat, the vast majority of which should be unsaturated [3].

Omega-3 fats and omega-6 fats are subcategories of unsaturated fat. They’re both essential in the human diet, but the typical Western diet is much too high in omega-6 fat relative to the amount of omega-3 fat. Generally speaking, omega-6 fat is pro-inflammatory, and increases risk of arthritis, asthma and heart disease when consumed out-of-proportion with omega-3 fat, which is generally anti-inflammatory. Omega-6 fat comes from plant sources, most notably from grains and grain-based oils like corn oil. Omega-3 fat is found in some plant sources (flax is a commonly-cited example), and in fish. Unfortunately, the majority of omega-3 fat in plant sources isn’t a type that humans can use, and has to be converted in the cells into usable omega-3 fats such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). Human cells are quite inefficient at this conversion, meaning most of the omega-3 fat from the majority of plant sources isn’t bioavailable. Fatty, cold-water fish are the best source of bioavailable omega-3 fat.

At the campaign website of MyPlate, which replaced the Food Pyramid to help consumers eat better, there are a number of nutrition education tips in an easy-to-follow, convenient format. One of the ten tips to making food choices for a healthy lifestyle in Choose MyPlate: 10 tips to a great plate focuses on “foods to eat less often”: these include foods high in solid fats, such as ice cream, pizza, ribs, sausages, bacon and hot dogs. Instead, choose lean, protein-rich foods such as soy, fish, skinless chicken and fat-free or 1% dairy products. Eat foods that are naturally low in fat such as whole grains, fruits and vegetables.

References

1. Obesity and Overweight for Professionals: Data and Statistics: U.S. Obesity Trends. Centers for Disease Control and Prevention. Accessed 2011 Nov 15.
2. Saturated Fats. American Heart Association. Accessed 2011 Nov 15.
3. Know Your Fats. American Heart Association. Accessed 2011 Nov 15.
4. Trans Fats American Heart Association. Accessed 2011 Nov 15.

Saccharin is the oldest of the artificial sugars that’s still in use today. It was discovered in the late 19th century, completely by chance, when a chemistry student who was working with coal tar derivatives licked his fingers and found they tasted sweet [1]. Saccharin is about 500 times sweeter than sugar, and the human body can’t break it down to provide the cells with energy, which is why it contains no calories. While some research suggests that it can cause bladder cancer in lab rats, no research has linked saccharin to cancer in humans. Saccharin-containing foods once carried warning labels, but scientists have since determined that rats have specific features of their urinary system (which humans lack) that make them susceptible to bladder cancer from saccharine [2]. Warning labels have been removed from foods as of 2000. Sweet’N Low is a brand of artificial sweetener made from granulated saccharin, dextrose and cream of tartar.

Aspartame is another non-nutritive sweetener that was discovered serendipitously by Jim Schlatter in 1965, as he was attempting to synthesize an ulcer drug [3]. Aspartame is a modified dipeptide, whose full name is aspartyl-phenylalanine methyl ester. Equal is an example of an aspartame-based sweetener.

Like saccharin, aspartame is sweeter than table sugar (by a factor of about 200), and it’s not possible for the human body to break aspartame down, which explains its lack of calories. The reason artificial sweeteners are sweeter than table sugar is that they bind more tightly to sweetness receptors on the human tongue, which then sends a signal to the brain. Chemicals that don’t bind very tightly — like table sugar — send signals of mild sweetness. Chemicals like aspartame and saccharine bind much more tightly, meaning they stay in the sweetness receptor (and continue to trigger signals) for a longer period of time.

The sweetness receptor is a complex called a G-protein coupled receptor comprised of proteins encoded by the genes TAS1R2 taste receptor, type 1, member 2 (TAS1R2) and TAS1R3 taste receptor, type 1, member 3 (TAS1R3) [4].

While there’s no evidence linking aspartame to cancer or other major health problems in most people, it’s not safe for individuals with the disease phenylketonuria (PKU). PKU is a genetic, meaning inherited, disorder in which affected individuals can’t break down phenylalanine. Phenylalanine is one of the amino acids, which are components of protein. Because those with PKU can’t break phenylalanine down, it accumulates in the bloodstream, and negatively impacts brain development in babies and children. Babies with PKU (a disease that hospitals routinely test newborns for) must be kept on a phenylalanine-free diet in order to avoid impaired physical and mental function. Adults with PKU don’t have to follow as strict a diet, but generally benefit from diets with low phenylalanine. Because aspartame contains the amino acid phenylalanine, aspartame-containing foods carry a warning label.

Sucralose is yet another non-nutritive sweetener. Its chemical structure is quite similar to that of table sugar, but key differences (e.g. the presence of chlorine atoms, where table sugar has none) prevent the human body from breaking it down for energy. Like the other non-nutritive sweeteners, sucralose is much sweeter than table sugar. No research has yet linked sucralose to cancer or other major health problems, but as the newest of the popular non-nutritive sweeteners, it may be some time before long-term effects of routine consumption — if there are any — reveal themselves. Splenda is an example of a sucralose-based artificial sweetener.

While there isn’t reason to believe that non-nutritive sweeteners cause cancer, there is some research evidence to suggest that they aren’t as benign as manufacturers claim. Many individuals who use these calorie-free sweeteners do so in an attempt to avoid the weight gain associated with excess sugar consumption, since the body can convert sugar — but not non-nutritive sweeteners — into fat. However, research suggests that there are sweetness receptors in the gut as well as in the mouth [5], and that artificial sweeteners can bind to these receptors. Further, research reveals that when calorie-free sweeteners bind to gut sweetness receptors, physiological responses mimic those expected in the case of sugar binding to the same receptors: the cells take up glucose [6], and the gut releases digestive hormones [7]. In short, it appears that the human body has an ability to sense the sugar — and therefore caloric — content of foods based upon the binding of key nutrients in those foods to receptors in the gut, but that these receptors are fooled (just like receptors in the mouth) by substitute chemicals. This can disrupt the body’s ability to determine whether a given quantity of food is sufficient to meet energy needs [8]. Compare, for example, the quantity of salad necessary to stimulate a feeling of fullness to the quantity of cheesecake necessary to do the same; the average individual consumes a much greater quantity of salad than of cheesecake, because the gut senses the caloric density of the cheesecake and sends satiety signals after consumption of a smaller quantity.

By disrupting the body’s ability to equate sweetness with calories, it appears that non-nutritive sweeteners can “teach” the body that sugar contains no calories. This can result in consumption of more total calories, which can lead to increased weight gain. In the end, consumption of sugar in moderate quantities may be more compatible with weight-loss or weight maintenance goals than consumption of artificial sweeteners.

References

1. Wotiz. The discovery of saccharin. J. Chem. Educ. 1978 55(3): 161.
2. Whysner et al. Saccharin mechanistic data and risk assessment: urine composition, enhanced cell proliferation, and tumor promotion. Pharmacol Ther. 1996;71(1-2):225-52.
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3. Mazur, R.H. (1984). Discovery of aspartame. In Aspartame: Physiology and Biochemistry (L. D. Stegink and L. J. Filer Jr., Eds.). Marcel Dekker, New York, pp. 3–9.
4. Li et al. Human receptors for sweet and umami taste. Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4692-6. Epub 2002 Mar 26.
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5. Jang et al. Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1. Proc Natl Acad Sci U S A. 2007 Sep 18;104(38):15069-74. Epub 2007 Aug 27.
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6. Mace et al. Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2. J Physiol. 2007 Jul 1;582(Pt 1):379-92. Epub 2007 May 10.
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7. Kokrashvili et al. Taste signaling elements expressed in gut enteroendocrine cells regulate nutrient-responsive secretion of gut hormones. Am J Clin Nutr. 2009 Sep;90(3):822S-825S. Epub 2009 Jul 1.
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8. Egan et al. Taste cells of the gut and gastrointestinal chemosensation. Mol Interv. 2008 Apr;8(2):78-81.
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Researchers at Princeton University examined the effect of HFCS and other sweeteners on the eating habits and weight gain of Sprague-Dawley rats, which are commonly used in nutrition studies because of their metabolic similarity to humans. In the first phase of the study, some male rats were given plain water to drink, while others consumed either water sweetened with HFCS or water sweetened with table sugar (sucrose). In all instances, rats had free access to rat chow. The rats were examined for weight gain and body changes after eight weeks. The scientists found that HFCS-consuming rats gained more total weight than sucrose-consuming rats. This was despite the fact that the two groups of rats consumed approximately equal total daily calories, and that the HFCS rats consumed fewer calories from HFCS than the sucrose rats consumed from sucrose. A little HFCS, it appears, goes a long way toward influencing weight gain.

In the second phase of the study, the researchers examined the effect of HFCS-sweetened water on the body weight and general constitution of male rats over the course of 6 months. Rats with free access to rat chow and plain water gained less weight, while rats with free access to rat chow and HFCS-sweetened water gained more. The fat pads on the HFCS-fed rats were much heavier than those of the rats who had access to only food and water, and specifically, the fat pads in the abdomen were much larger.

The investigators found similar long-term results in female rats, and additionally noted that among the females, access to long-term HFCS-sweetened water had a greater impact on total body weight gain and fat gain than access to long-term sucrose-sweetened water, echoing the results of the first phase of the study.

HFCS is a common additive to processed foods, and occurs in everything from packaged desserts to fast food meals to condiments like ketchup. Many nutrition researchers have speculated in recent years that it’s no coincidence that the American obesity rate has increased tremendously since the advent of HFCS in the American diet. However, there has been debate among scientists as to whether the increased obesity rate was due to increased caloric intake or was specific to HFCS.

On the surface, HFCS appears quite similar to sucrose. Sucrose is a disaccharide, made up of the smaller sugars glucose and fructose, chemically bonded together.

Because of its chemical makeup, sucrose contains 50% glucose and 50% fructose. Digestive enzymes in the intestine break sucrose into glucose and fructose, which are absorbed separately into the bloodstream. There are several types of HFCS, but the most prevalent in processed food is HFCS-55, which consists of 55% fructose and 42% glucose [2]. The chemical difference between HFCS and sucrose is significant because glucose stimulates the release of insulin and has been linked to higher circulating levels of leptin [3], and there’s a significantly higher proportion of glucose in sucrose than in HFCS-55.

Consuming a meal high in fructose (one sweetened with HFCS, for instance) results in lower circulating insulin and leptin, which can cause a reduced sense of satisfaction and stimulate overeating. Moreover, high fructose diets can induce leptin resistance, accelerating high-fat induced obesity [4].

A recent study demonstrated this by offering different groups of rats either plain water or water sweetened with a variety of compounds, including both sucrose and HFCS [5]. The rats that drank sweetened water, regardless of sweetener type, consumed more total calories than those that drank plain water. This result suggests that consumption of sweetened beverages may increase the risk of obesity, as appetite doesn’t completely accommodate for calories consumed in the form of liquid. Further, however, rats consuming HFCS-sweetened water had the greatest final weight and fat mass, despite the fact that all the rats drinking sweetened water took in approximately the same number of total calories. This suggests once again that HFCS influences fat accumulation to a disproportionately large extent per calorie consumed, compared to other sweeteners.

While researchers haven’t completely elucidated the mechanism through which HFCS promotes rapid fat gain — particularly in the abdominal region — accumulating evidence suggests that avoiding HFCS in the diet might help reduce the risk of obesity and obesity-related disease.

References

1. Bocarsly et al. High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels. Pharmacol Biochem Behav. 2010 Nov;97(1):101-6. Epub 2010 Feb 26.
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2. White JS. Straight talk about high-fructose corn syrup: what it is and what it ain’t. Am J Clin Nutr. 2008 Dec;88(6):1716S-1721S.
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3. Teff et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72.
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4. Shapiro et al. Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding. Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1370-5. Epub 2008 Aug 13.
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5. Light et al. The type of caloric sweetener added to water influences weight gain, fat mass, and reproduction in growing Sprague-Dawley female rats. Exp Biol Med (Maywood). 2009 Jun;234(6):651-61. Epub 2009 Apr 9.
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More than one-third of adults in the United States and nearly 17 percent of the nation’s children are now obese, which increases a person’s chance of developing many health problems, including type 2 diabetes, heart disease, high blood pressure, fatty liver disease, and some cancers. Although American obesity rates leveled off in 2007, in 2008, obesity-related medical costs were an estimated $147 billion. Government, nonprofit and community groups, businesses, health care professionals, schools, families, and individuals are taking action to address this public health problem — and research can provide the foundation for these efforts.

NIH funds research to reduce the prevalence of obesity and its health consequences, an investment of $824 million in fiscal year 2010, plus awards totaling $147 million made in the same year through the Recovery Act. This NIH strategic plan, developed by the NIH Obesity Research Task Force, recognizes that eating less and exercising more is easier said than done. Highlighting the crucial role of research in efforts to reduce obesity, the plan emphasizes moving science from laboratory to clinical trials to practical solutions, and is designed to help target efforts and resources in areas most likely to help [1].

NIH Director Francis S. Collins, M.D., Ph.D. said:

Obesity has many causes and contributing factors. This plan is a bold blueprint that will encourage the research community to examine the epidemic of obesity from diverse perspectives. Through the scientific opportunities outlined in the strategic plan, researchers can work together toward the goals of preventing and treating obesity, to help people lead healthier and more fulfilling lives.

The task force is co-chaired by Griffin P. Rodgers, M.D., director of the National Institute of Diabetes and Digestive and Kidney Diseases; Susan B. Shurin, M.D., acting director of the National Heart, Lung, and Blood Institute; and Alan E. Guttmacher, M.D., director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. These three institutes, along with the National Cancer Institute, led in the plan’s development.

The research recommendations include:

• Discover key processes that regulate body weight and influence behavior
• Understand the factors that contribute to obesity and its consequences
• Design and test new approaches for achieving and maintaining a healthy weight
• Evaluate promising strategies to prevent and treat obesity in real-world settings and diverse populations
• Use technology to advance obesity research and improve healthcare delivery

To increase the reach of research and improve public health, the plan also highlights education and outreach to move proven strategies into community programs and medical practice.

Since the release of the first strategic plan in 2004, research produced many advances, including:

• Lifestyle interventions for weight loss reduce risk for heart disease and type 2 diabetes. NIH-funded studies are testing ways to bring these proven strategies to more people.
• When a woman with obesity or diabetes becomes pregnant, her child’s risk of developing obesity may increase, suggesting a critical period to intervene. Researchers can study approaches to help women achieve a healthy weight before and during pregnancy.
• Many genes and other aspects of our biology, from body fat to the gastrointestinal system and brain, influence whether we’re likely to become obese. Researchers are delving deeper into these pathways and how they’re affected by our environment.

Tips and tools

While research continues, NIH resources can help people achieve or maintain a healthy weight now. You can find tips and tools from the following resources:

The Weight-control Information Network provides up-to-date, science-based information on weight control, obesity, physical activity and related nutritional issues.

Aim for a Healthy Weight from the National Heart, Lung and Blood Institute offers the Aim for a Healthy Weight booklet includes portion and serving size information, sample reduced calorie menus, tips on dining out, a sample walking program, a weekly food and activity diary and more.

We Can! (Ways to Enhance Children’s Activity & Nutrition) from the National Heart, Lung and Blood Institute is a national movement designed to give parents, caregivers, and entire communities a way to help children 8 to 13 years old stay at a healthy weight.

The Let’s Move campaign, led by the White House, is dedicated to solving the problem of obesity within a generation, so that children born today will grow up healthier and able to pursue their dreams. It combines comprehensive strategies with common sense, putting children on the path to a healthy future during their earliest months and years, and giving parents helpful information and fostering environments that support healthy choices.

Learn more about obesity research at NIH, see a video about the plan from Collins, and view or request a free copy of the summary or complete Strategic Plan for NIH Obesity Research at www.obesityresearch.nih.gov.

Source: NIH News

References

1. Strategic Plan for NIH Obesity Research. NIH Obesity Research. Accessed 2010 Mar 31.

Although getting your five-a-day is important for promoting good health, overindulging on anything is bad for you. Indeed, overindulgence — consuming more calories than your body requires — is one of the main factors contributing to weight gain. Many of us love sweets during the holidays, but large portions won’t do anything but add surplus calories that get converted into fat.

Consider Santa Claus. One of the benefits of being “good St. Nick” is eating all the holiday cookies left by children around the world on Christmas eve.

Lee Biosolutions, a producer of enzymes, glycoprotein hormones and related reagents for the diagnostic and life science industries, realized that, given all the houses Santa must visit, he would put on more than the usual holiday weight. They recently did the math to determine just how much Santa would weight [1].

To calculate the number of households Santa must visit, they took the world population of 6.8 billion people and divided it by the average of 2.5 people per family. Thus, Santa would visit approximately 2.7 billion households on Christmas eve. Now, this number over-estimates the number of Christians in the world who would be celebrating Christmas by about 3-fold [2]. However, many people celebrate Christmas that aren’t Christian and we’re already talking ridiculously huge numbers here, so we’re not going to argue.

To continue the calculation: assuming that every household leaves Santa two chocolate chip cookies, Kris Kringle would eat about 5.4 billion cookies (or 473 million pounds of cookies) and consume 936 billion calories, far exceeding a 2,000 calorie-a-day diet.

Given these numbers, Santa would have or be at risk for a number of health issues, including heart disease, high blood pressure, diabetes, stroke and cancer.

This holiday season, take responsibility for your diet. Small portions of the “bad stuff” will make very little difference in your health, but going on a cookie binge very well could.

References

1. Santa’s Massive Weight Gain After Christmas Eve Cookie Binge: Local Company Estimates Santa Claus’ Weight and Health Problems from Cookies Consumed. PRWeb. 2010 Dec 17.
2. Christianity by country. Wikipedia. Accessed 2010 Dec 22.

The study, conducted by researchers at the Scripps Research Institute, was released on March 28th in the online version of Nature Neuroscience and will also appear in the journal’s May 2010 print issue. When investigators gave rats access to varying levels of high-fat foods, they found unrestricted availability alone can trigger addiction-like responses in the brain, leading to compulsive eating behaviors and the onset of obesity.

“Drug addiction and obesity are two of the most challenging health problems in the United States,” said Dr. Nora D. Volkow, director of NIDA. “This research opens the door for us to apply some of the knowledge we have gathered about drug addiction to the study of overeating and obesity.”

Both obesity and drug addiction have been linked to a dysfunction in the brain’s reward system. In both cases overconsumption can trigger a gradual increase in the reward threshold — requiring more and more palatable high fat food or reinforcing drug to satisfy the craving over time.