Tuesday, November 30, 2010

New study reports effects of endurance running

New study reports effects of endurance running

Belly fat puts women at risk for osteoporosis, study finds

Belly fat puts women at risk for osteoporosis, study finds

The Worst Type of Fish You Can Eat


Congress Does Something: Food Safety Bill Passes Senate - Chris Good - Politics - The Atlantic

Congress Does Something: Food Safety Bill Passes Senate - Chris Good - Politics - The Atlantic

Moderate Alcohol Consumption Lowers the Risk of Metabolic Diseases, Study Suggests

Moderate alcohol consumption lowers the risk of metabolic diseases, study suggests
ScienceDaily (2010-11-29) -- With the emergence of an epidemic of obesity and type 2 diabetes (DM) throughout the world, the association of lifestyle habits that may affect the risk of metabolic diseases is especially important. ... > read full article

Sunday, November 28, 2010

Official Food, Inc. Movie Site - Hungry For Change?

Official Food, Inc. Movie Site - Hungry For Change?

Food, Inc. - The Passionate Eye | CBC News Network

Food, Inc. - The Passionate Eye CBC News Network

Does bicycling contribute to the risk of erectile dysfunction? Results from the Massachusetts Male Aging Study (MMAS).

Int J Impot Res. 2001 Oct;13(5):298-302.

Does bicycling contribute to the risk of erectile dysfunction? Results from the Massachusetts Male Aging Study (MMAS).

Marceau L, Kleinman K, Goldstein I, McKinlay J.

New England Research Institutes, Watertown, MA 02472, USA. lmarceau@neri.org


An association between bicycling and erectile dysfunction (ED) has been described previously, but there are limited data examining this association in a random population of men. Such data would incorporate bicyclists with varied types of riding and other factors. Data from the Massachusetts Male Aging Study (MMAS) were utilized to examine the association between bicycling and ED. Logistic regression was used to test for an association, controlling for age, energy expenditure, smoking, depression and chronic illness. Bicycling less than 3 h per week was not associated with ED and may be somewhat protective. Bicycling 3 h or more per week may be associated with ED. Data revealed that there may be a reduced probability of ED in those who ride less than 3 h per week and ED may be more likely in bikers who ride more than 3 h per week. More population-based research is needed to better define this relationship.

Does Bicycling Cause Erectile Dysfunction and Impotence in Men?


Thursday, November 25, 2010

Parents Failing To Recognize Their Children's Risk For Obesity May Be Contributing To Epidemic

Parents Failing To Recognize Their Children's Risk For Obesity May Be Contributing To Epidemic

ScienceDaily (2009-03-19) -- With 17 percent of US children between ages 2 and 19 classified as obese, new research shows that parents may not be recognizing their own children's risk factors. A new study shows that parents are likely to misperceive their child's weight -- especially those parents who are overweight themselves. ... > read full article

Why Are We Getting Fatter? Seeking a Mysterious Culprit

Why are we getting fatter? Seeking a mysterious culprit

ScienceDaily (2010-11-23) -- Researchers suggest there are multiple, still undiscovered causes for obesity, based observations of weight gain in controlled groups of animals that has no single explanation, such as diet or activity level. ... > read full article

How People Perceive Sour Flavors: Proton Current Drives Action Potentials in Taste Cells

How people perceive sour flavors: Proton current drives action potentials in taste cells

ScienceDaily (2010-11-25) -- Tart cranberry sauce is part of Thanksgiving, and a new study reveals a surprising mechanism for how we perceive sourness: a proton current in taste cells. ... > read full article

Wednesday, November 24, 2010

Study identifies foods that promote weight maintenance - latimes.com

Study identifies foods that promote weight maintenance - latimes.com

Combining aerobic and resistance training appears helpful for patients with diabetes


Danish researchers finally solve the obesity riddle


Obesity Riddle Finally 'Solved'

Obesity riddle finally 'solved'

ScienceDaily (2010-11-24) -- Researchers now unveil the results of the world's largest diet study and recommend: Eat more proteins and less refined starch. The study concludes that the official dietary recommendations are not sufficient for preventing obesity. ... > read full article

Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

Am J Clin Nutr. 2004 Apr;79(4):537-43.

Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity.

Bray GA, Nielsen SJ, Popkin BM.

Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA. brayga@pbrc.edu

Erratum in:

Am J Clin Nutr. 2004 Oct;80(4):1090.

Comment in:

Am J Clin Nutr. 2004 Nov;80(5):1446-7; author reply 1447-8.

Am J Clin Nutr. 2004 Oct;80(4):1081; author reply 1081-2.


Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.

Majority Of Americans Will Have Diabetes Or Pre-Diabetes By 2020 - With Huge Financial Costs

Imagine a society where over half its people, i.e. the majority of them, are diabetic or prediabetic. There is a good chance this will happen in the USA by 2020. The estimated $3.35 trillion cost over the coming ten years is massive. A study by The Center for Health Reform & Modernization of UnitedHealth Group, an insurance company, reveals that if the current pattern continues, those figures will be a reality within the next ten years. The report offers some suggestions which may slow things down, and perhaps even turn them round.

By 2020, diabetes and prediabetes will use up approximately 10% of health care spending, the authors estimate. The current annual health care bill of $194 billion will shoot up to nearly $500 billion.

UnitedHealth says it produced the report for November's National Diabetes Awareness month. Suggestions within it could save as much as $250 billion over the coming decade. Included are potential savings to the government in Medicare, Medicaid, and other programs of $144 billion.

It is vital that lifestyle interventions that address obesity and prevent prediabetes from developing into full blown diabetes are put into action. Medication programs to ensure proper diabetes control are also important.

Simon Stevens, executive vice president, UnitedHealth Group, and chairman of the UnitedHealth Center for Health Reform & Modernization, said:

"Our new research shows there is a diabetes time bomb ticking in America, but fortunately there are practical steps that can be taken now to defuse it. What is now needed is concerted, national, multi-stakeholder action. Making a major impact on the prediabetes and diabetes epidemic will require health plans to engage consumers in new ways, while working to scale nationally some of the most promising preventive care models. Done right, the human and economic benefits for the nation could be substantial."

Average healthcare costs in the USA for people without diabetes stand at approximately $4,400, compared to $11,700 for those with the disease. For diabetes patients with complications, the average annual cost rises to $20,700. Add to this the impact on work productivity and employer costs and the numbers increase considerably.

Diabetes rates in the USA are growing at such a rate that it is now "one of the fastest-growing diseases in the nation." 27 million Americans are known to have diabetes, and a further 67 million are thought to be prediabetic.

Diabetes Type 2 can sometimes have no symptoms at all. The same is the case with prediabetes. The percentage of babies born after the year 2000 who will probably have diabetes some time during their lives is extremely worrying. Diabetes significantly increases the risk of blindness, nerve damage, limb amputation, kidney disease, cancer, and heart disease.

The authors of the report explain the link between obesity and diabetes type 2 risk. Over two-thirds of US adults and 17% of children are overweight/obese. The report stresses that overweight/obesity rates are still rising, and consequently so are/will diabetes and prediabetes risk. The majority of American overweight/obese adults either have diabetes type 2 or prediabetes. The authors quote studies which have shown a doubling of type 2 diabetes risk when a person puts on 11-16 pounds of body weight. Those who gain 17 to 24 pounds triple their risk.

Deneen Vojta, M.D., senior vice president of the UnitedHealth Center for Health Reform & Modernization, who helped develop UnitedHealth Group's Diabetes Prevention and Control Alliance, said:

"Because diabetes follows a progressive course, often starting with obesity and then moving to prediabetes, there are multiple opportunities to intervene early and prevent this devastating disease before it's too late."

The report offers four solutions:

Lifestyle intervention - public health initiatives and more extensive use of wellness programs could reduce diabetes/prediabetes human totals by up to ten million.

Preventing prediabetes from becoming full blown diabetes - community-based intervention programs have been shown to reduce prediabetes rates, consequently lowering eventual diabetes rates.

Medication and care compliance programs - to achieve better diabetes control. Well controlled diabetes significantly lowers the risk of complications. Another word for compliance is adherence (sticking to the treatment plan).

Public-private partnerships for lifestyle intervention strategies - the authors explain that more extensive use of public-private partnerships to develop infrastructure would have a beneficial effect on prediabetes and diabetes rates.

"The United States of Diabetes: Challenges and Opportunities in the Decade Ahead" (PDF)

Source: UnitedHealth Center for Health Reform & Modernization (UnitedHealth Group)

Written by Christian Nordqvist

Copyright: Medical News Today

Overweight Primarily a Problem Among Wealthier Women in Low To Middle-Income Countries

Overweight primarily a problem among wealthier women in low- to middle-income countries

ScienceDaily (2010-11-23) -- A new study finds that high body mass index (BMI) in developing countries remains primarily a problem of the rich. ... > read full article

Depression May Be Both Consequence of and Risk Factor for Diabetes

Depression may be both consequence of and risk factor for diabetes

ScienceDaily (2010-11-22) -- Diabetes appears to be associated with the risk of depression and vice versa, suggesting the relationship between the two works in both directions, according to a new report. ... > read full article

Nearly 25 Percent of Overweight Women Misperceive Body Weight

Nearly 25 percent of overweight women misperceive body weight

ScienceDaily (2010-11-23) -- A startling number of overweight and normal weight women of reproductive age inaccurately perceive their body weight, affecting their weight-related behaviors and making many vulnerable to cardiovascular and other obesity-related diseases, according to new research. ... > read full article

Tuesday, November 23, 2010

Adiposity suppression effect in mice due to black pepper and its main pungent component, piperine.

Biosci Biotechnol Biochem. 2010 Aug 23;74(8):1545-9. Epub 2010 Aug 7.

Adiposity suppression effect in mice due to black pepper and its main pungent component, piperine.

Okumura Y, Narukawa M, Watanabe T.

Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, Suruga-ku, Shizuoka, Japan.


We investigated energy metabolism enhancement by pepper by examining suppression of body fat accumulation in mice due to piperine (PIP) and black pepper (BP) intake. To induce adiposity, mice were fed a high-fat, high-sucrose (HFS) diet as a control diet for 4 weeks. Visceral fat weights decreased significantly in the mice fed diets of 0.03% and of 0.05% PIP. Body weight in the 0.05% PIP group also decreased significantly. In the mice fed a diet of 1.0% BP, body weight and visceral fat weights decreased significantly. For all parameters tested, the 1.0% BP group tended to show values slightly lower than those of the 0.03% PIP group. Expression of thermogenic protein uncoupling protein 1 tended to increase in the mice on the 1.0% BP diet. These results indicate that BP suppresses the effect of body fat accumulation mainly through the action of PIP.

Synephrine: from trace concentrations to massive consumption in weight-loss.

Food Chem Toxicol. 2010 Nov 11. [Epub ahead of print]

Synephrine: from trace concentrations to massive consumption in weight-loss.

Rossato LG, Costa VM, Limberger RP, Bastos MD, Remião F.

REQUIMTE, Toxicology Department, Faculty of Pharmacy, University of Porto, Rua Aníbal Cunha 164, 4099-030 Porto, Portugal.


Synephrine is cited as 'the active component' of plants and dietary supplements used in weight loss. It became one of the most popular stimulants present in weight-loss products after the US Food and Drug Administration had interdicted the use of ephedrine-containing dietary supplements. Synephrine is also a trace amine that can be found in vertebrates and invertebrates. Synephrine acts on several adrenergic and serotonergic receptors and its activity on trace-amine associated receptors has long been discussed. Synephrine exists in three different positional isomers; however, only p- and m-synephrine have been described in weight-loss products. The alleged effectiveness of synephrine-containing supplements is attributed to the thermogenic effects arising from synephrine's adrenergic stimulation. The growing use of synephrine has raised concerns since it has been accompanied by reports of adverse effects. Cardiac adverse events, including hypertension, tachyarrhythmia, variant angina, cardiac arrest, QT prolongation, ventricular fibrillation, myocardial infarction, and sudden death, have been the most common adverse effects associated with synephrine intake. The mechanisms involved in synephrine-induced cardiotoxicity are still unknown since studies related to its safety are scarce. This review will address general aspects concerning the pharmacology of synephrine, but will focus on the efficacy and toxicity aspects related to the use of synephrine in weight-loss.

New Sleep Cycle Discovery Explains Why Fatty Diets During Pregnancy Make Kids Obese

New sleep cycle discovery explains why fatty diets during pregnancy make kids obese

ScienceDaily (2010-11-23) -- The link between sleeping and obesity is drawn tighter as a new research shows that what your mother ate when she was pregnant may make you obese or overweight by altering the function of genes (epigenetic changes) that regulate circadian rhythm. ... > read full article

Too Much Fructose Could Leave Dieters Sugar Shocked

Too Much Fructose Could Leave Dieters Sugar Shocked

ScienceDaily (2007-12-14) -- Dieters should focus on limiting the amount of fructose they eat instead of cutting out starchy foods such as bread, rice and potatoes, report researchers, who propose using new dietary guidelines based on fructose to gauge how healthy foods are. ... > read full article

Excess Fructose May Play Role in Diabetes, Obesity and Other Health Conditions

Excess fructose may play role in diabetes, obesity and other health conditions

ScienceDaily (2010-11-22) -- More and more people have become aware of the dangers of excessive fructose in diet. A new review on fructose indicates just how dangerous this simple sugar may be. ... > read full article

Aerobic exercise training-induced decrease in plasma visfatin and insulin resistance in obese female adolescents.

Int J Sport Nutr Exerc Metab. 2010 Aug;20(4):275-81.

Aerobic exercise training-induced decrease in plasma visfatin and insulin resistance in obese female adolescents.

Lee KJ, Shin YA, Lee KY, Jun TW, Song W.

Institute of Sports Science, Seoul National University, Seoul, Korea.


The purpose of this study was to assess differences in the levels of plasma visfatin among female adolescents and changes in plasma visfatin and insulin resistance in obese female adolescents after 12 wk of aerobic exercise training. Twenty normal-weight female students (body-mass index [BMI] < 22.9 kg/m² and body fat ≤ 29.9) and 18 obese female students (BMI ≥ 25 kg/ m² and body fat ≥ 30%) participated in this study. Eleven obese students were assigned to an exercise group and completed a 12-wk aerobic exercise-training program that included four 40- to 50-min sessions per wk with an energy expenditure of 300-400 kcal/d. Seven obese students were assigned to a control group that received no exercise sessions or dietary restriction. The plasma visfatin levels of obese female adolescents were significantly higher (p < .05) than those of the normal-weight female adolescents. The plasma visfatin levels (294.00 ± 124.74 ng/ml to 185.55 ± 67.30 ng/ml, p < .01) and insulin resistance (p < .05) were significantly reduced after 12 wk of aerobic exercise. The results suggest that aerobic exercise resulting in an energy expenditure of 1,200-1,600 kcal/wk for 12 wk decreases plasma visfatin and insulin resistance in obese female adolescents.

Factors influencing overweight children's commencement of and continuation in a resistance training program.

BMC Public Health. 2010 Nov 18;10(1):709. [Epub ahead of print]

Factors influencing overweight children's commencement of and continuation in a resistance training program.

Pescud M, Pettigrew S, McGuigan MR, Newton RU.



BACKGROUND: In light of the child overweight and obesity problem in Australia, resistance training programs have been trialled as an innovative way of assisting children increase lean body mass and reduce body fat. The purpose of this study was to investigate the factors influencing overweight children's participation in a resistance training trial program.

METHOD: Parent-child pairs who participated in the trial program were invited to take part in a follow-up individual interview to discuss their program experiences. In total, 22 semi-structured interviews were conducted with 11 parent-child pairs.

RESULTS: The factors found to be most relevant to program commencement among parents were a desire for their child to lose weight and gain confidence, the proximity of the venue, and no cost for participation. For children, the most relevant factors were the opportunity to build strength and improve fitness and having supportive parents who facilitated program initiation. The factors most relevant to continuation for parents were the quality of the program management, being able to stay for the sessions, the child's improved weight status, coordination, and confidence, and no cost for participation. Weight loss and improved confidence were also motivators for continuation among the children, along with pleasant social interaction with peers and trainers and ongoing parental support.

CONCLUSION: Different factors variably influence program commencement and program continuation in both parents and children. This has important implications for future interventions that aim to successfully recruit and retain intervention participants.

Resistance Exercise and Lipoproteins in Postmenopausal Women.

Int J Sports Med. 2010 Nov 17. [Epub ahead of print]

Resistance Exercise and Lipoproteins in Postmenopausal Women.

Wooten JS, Phillips MD, Mitchell JB, Patrizi R, Pleasant RN, Hein RM, Menzies RD, Barbee JJ.

Texas Woman's University, Institute for Women's Health, Denton, United States.


The specific aims of this study were to quantify the effects of 12 weeks of resistance training, as well as a single session of resistance exercise on lipids and lipoproteins in obese, postmenopausal women. 21 obese, postmenopausal women, not on hormone replacement therapy (age=65.9±0.5 yr; BMI=32.7±0.8 kg/m (2)), were randomly assigned to control (n=12) and exercise (n=9) groups matched for age and BMI. For 12 weeks, 3 days/week, the exercise group performed 10 whole body resistance exercises (3 sets at 8-RM). Fasting (10 h) blood samples were collected immediately prior to and 24 h after the first and last exercise and control session. Serum was assayed for concentrations of total cholesterol, triglycerides, LDL-C, HDL-C, HDL 2-C, HDL 3-C, non-HDL-C and TC:HDL and LDL:HDL ratios. The exercise group exhibited a significant (P<0.01) improvement in muscular strength, but no change in BMI, body mass or body composition post-training. Total cholesterol, LDL-C and non-HDL-C were significantly (P<0.05) lower in the exercise compared to the control group following the 12 weeks of resistance training. Whole body resistance training provides obese, postmenopausal women a non-pharmacological approach for the reduction of lipid and lipoprotein-cholesterol concentrations.

Sunday, November 21, 2010

Effects of dihydrocapsiate on adaptive and diet-induced thermogenesis with a high protein very low calorie diet: a randomized control trial.

Nutr Metab (Lond). 2010 Oct 6;7:78.

Effects of dihydrocapsiate on adaptive and diet-induced thermogenesis with a high protein very low calorie diet: a randomized control trial.

Lee TA, Li Z, Zerlin A, Heber D.

Center for Human Nutrition, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. dheber@mednet.ucla.edu.



BACKGROUND: Dihydrocapsiate (DCT) is a natural safe food ingredient which is structurally related to capsaicin from chili pepper and is found in the non-pungent pepper strain, CH-19 Sweet. It has been shown to elicit the thermogenic effects of capsaicin but without its gastrointestinal side effects.

METHODS: The present study was designed to examine the effects of DCT on both adaptive thermogenesis as the result of caloric restriction with a high protein very low calorie diet (VLCD) and to determine whether DCT would increase post-prandial energy expenditure (PPEE) in response to a 400 kcal/60 g protein liquid test meal. Thirty-three subjects completed an outpatient very low calorie diet (800 kcal/day providing 120 g/day protein) over 4 weeks and were randomly assigned to receive either DCT capsules three times per day (3 mg or 9 mg) or placebo. At baseline and 4 weeks, fasting basal metabolic rate and PPEE were measured in a metabolic hood and fat free mass (FFM) determined using displacement plethysmography (BOD POD).

RESULTS: PPEE normalized to FFM was increased significantly in subjects receiving 9 mg/day DCT by comparison to placebo (p < 0.05), but decreases in resting metabolic rate were not affected. Respiratory quotient (RQ) increased by 0.04 in the placebo group (p < 0.05) at end of the 4 weeks, but did not change in groups receiving DCT.

CONCLUSIONS: These data provide evidence for postprandial increases in thermogenesis and fat oxidation secondary to administration of dihydrocapsiate.

TRIAL REGISTRATION: clinicaltrial.govNCT01142687.

Brown fat thermogenesis and body weight regulation in mice: relevance to humans.

Int J Obes (Lond). 2010 Oct;34 Suppl 1:S23-7.

Brown fat thermogenesis and body weight regulation in mice: relevance to humans.

Kozak LP, Koza RA, Anunciado-Koza R.

Pennington Biomedical Research Center, Baton Rouge, LA, USA. kozaklp@pbrc.edu


Physiological, pharmacological and genetic studies in dogs, mice and rats have established that the uncoupling protein-1 (UCP1)-based brown adipose tissue system has an important role in the regulation of body temperature. Although it may be possible to create laboratory conditions in which mice with inactivated Ucp1 can survive in a modestly cooled environment, data overwhelmingly support the conclusion that the UCP1/BAT system has evolved to maintain body temperature at 37 °C. The corollary to this conclusion is that any influence UCP1/BAT might have on body weight regulation is a secondary function. The idea that BAT prevents obesity by burning off excess energy to maintain energy balance seems incompatible with evolutionary biology. Premodern humans spent an enormous amount of energy either running to catch their meal or avoiding becoming a meal themselves; consequently, there was no obesity. Nevertheless, although secondary to body temperature regulation, UCP1/BAT is extraordinarily effective at reducing adiposity and insulin resistance in mice and rats. Variation among mice in susceptibility to diet-induced obesity is correlated with the induction of brown adipocytes in traditional white fat depots (wBAT). Both genetic and cell biology-based experimentation have shown that the cellular origins of wBAT are different from those of interscapular-like brown adipocytes (iBAT). Do they have different functions? We have analyzed the effects of the early nutritional environment on the induction of brown adipocytes in inguinal fat to test the hypothesis that wBAT is primarily involved in body weight regulation. Although undernutrition during lactation severely suppresses wBAT at 21 days of age, undernourished mice fed a normal chow diet ad libitum at weaning recovered their normal wBAT and iBAT systems as young adults. The function of wBAT does not seem to be uniquely devoted to body weight regulation.

MSG: The Hidden Cause for Weight Gain


The Surprising Ingredient Causing Weight Gain


Say it isn't so! A recent study out of the University of North Carolina at Chapel Hill cites what animal studies have hinted at for years: MSG (aka monosodium glutamate) could be a factor in weight gain.

The study focused on 750 Chinese men and women, ages 40-59, living in 3 rural villages in north and south China. Most of the study subjects prepared their meals at home without commercially processed foods and roughly 82 percent used MSG. Those participants who used the highest amounts of MSG had nearly 3 times the incidence of overweight as those who did not use MSG, even when physical activity, total caloric intake, and other possible explanations for body mass differences were accounted for. The positive correlation between MSG and higher weight confirmed what animal studies have been suggesting for years.

Maybe you're wondering what monosodium glutamate is exactly, and what you can do to avoid it in your diet. MSG is a flavor enhancer in foods—some believe it may even provide a fifth basic taste sensation (in addition to sweet, sour, salt, and bitter), what the Japanese call "umami" (roughly translated as "tastiness"). MSG is considered an "excitotoxin," since its action in the body is to excite neurotransmitters (important brain chemicals), causing nerve cells to discharge and also exciting nerves related to taste. Perhaps this ability to excite these nerves is a factor in an association between increased MSG usage and weight gain.

How prevalent is MSG in the U.S. diet? Americans consumed about 1 million pounds of MSG in 1950, and today that number has increased by a factor of 300!

The Food and Drug Administration (FDA) describes MSG as "naturally occurring," and has it on the GRAS ("generally regarded as safe") list. However, not only could MSG be causing us to gain weight, but some studies also reveal that as many as 25 to 30 percent of Americans have adverse reactions to it (e.g., palpitations and migraine headaches), and as many as 30 percent are extra sensitive to it if they consume more than 5 grams at one sitting.

OK, if you're an MSG user who could stand to lose a little weight (or know someone who is), what should you do?

Unfortunately, eliminating MSG from the diet is much easier said than done, since—given the fact that food processors often change recipes—there's no list of "safe" foods that never contain MSG. A good start is to avoid anything with MSG anywhere in the ingredient list, but there will still be many foods that have MSG hidden inside other ingredients. Likewise, even products labeled "no MSG added" can still contain these hidden sources.

Best bets for avoiding MSG

•Buy organic produce whenever possible.

•Make things from scratch, avoiding processed ingredients as much as possible.

•Limit making stews or soups in a crock pot, since slow-cooking tends to cause small amounts of glutamic acid to be released from the protein sources (e.g., meat, chicken) in the recipe.

What are your thoughts on MSG? I'd love to hear from you!

A high fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload.

Am J Physiol Heart Circ Physiol. 2010 Oct 22. [Epub ahead of print]

A high fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload.

Bouchard-Thomassin AA, Lachance D, Drolet MC, Couet J, Arsenault MC.

1Centre de recherche Institut universitaire de cardiologie et pneumologie de Québec.


Aims: The development of left ventricular hypertrophy (LVH) can be affected by diet manipulation. Concentric LVH resulting from pressure overload can be worsened by feeding rats with a high-fructose diet. Eccentric LVH is a different type of hypertrophy and is associated with volume overload (VO) diseases. The impact of an abnormal diet on the development of eccentric LVH and on ventricular function in chronic volume overload is unknown. This study therefore examined the effects of a fructose-rich diet on left ventricular eccentric hypertrophy, ventricular function and myocardial metabolic enzymes in rats with chronic VO caused by severe aortic valve regurgitation (AR). Methods: Wistar rats were divided in four groups: Sham-operated on control or fructose-rich diet (SC (n=13) and SF (n=12)) and severe aortic regurgitation fed with the same diets (ARC (n=16) and ARF (n=13)). Fructose-rich diet (F) was started one week before surgery and the animals were sacrificed 9 weeks later. Results: SF and ARF had high circulating triglycerides. ARC and ARF developed significant LV eccentric hypertrophy after 8 weeks as expected. However ARF developed more LVH than ARC. LV ejection fraction was slightly lower in the ARF compared to ARC. The increased LVH and decreased ejection fraction could not be explained by differences in hemodynamic load. SF, ARC and ARF had lower phosphorylation levels of the AMP kinase compared to SC. Conclusion: A fructose-rich diet worsened LV eccentric hypertrophy and decreased LV function in a model of chronic VO caused by AR in rats. Normal animals fed the same diet did not develop these abnormalities. Hypertriglyceridemia may play a central role in this phenomenon as well as AMP kinase activity.

Fructose-Rich Beverages and Risk of Gout in Women.

JAMA. 2010 Nov 10. [Epub ahead of print]

Fructose-Rich Beverages and Risk of Gout in Women.

Choi HK, Willett W, Curhan G.

Boston University School of Medicine (Dr Choi), Channing Laboratory (Drs Choi, Willett, and Curhan), Department of Epidemiology, Harvard School of Public Health (Drs Willett and Curhan), and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (Dr Curhan), Boston, Massachusetts.


CONTEXT: Fructose-rich beverages such as sugar-sweetened soda and orange juice can increase serum uric acid levels and, thus, the risk of gout, but prospective data on the relationship are limited.

OBJECTIVE: To examine the relationship between intake of fructose-rich beverages and fructose and the risk of incident gout among women.

DESIGN, SETTING, AND PARTICIPANTS: In the Nurses' Health Study, a US prospective cohort study spanning 22 years (1984-2006), we analyzed data from 78 906 women with no history of gout at baseline who provided information on intake of beverages and fructose through validated food frequency questionnaires.

MAIN OUTCOME MEASURE: Incident cases that met the American College of Rheumatology survey criteria for gout.

RESULTS: During 22 years of follow-up, we documented 778 confirmed incident cases of gout. Increasing intake of sugar-sweetened soda was independently associated with increasing risk of gout. Compared with consumption of less than 1 serving per month of sugar-sweetened soda, the multivariate relative risk of gout for 1 serving per day was 1.74 (95% confidence interval [CI], 1.19-2.55) and for 2 or more servings per day was 2.39 (95% CI, 1.34-4.26) (P<.001 for trend). The corresponding relative risks for orange juice were 1.41 (95% CI, 1.03-1.93) and 2.42 (95% CI, 1.27-4.63) (P = .02 for trend). The absolute risk differences corresponding to these relative risks were 36 and 68 cases per 100 000 person-years for sugar-sweetened soda and 14 and 47 cases per 100 000 person-years for orange juice, respectively. Diet soft drinks were not associated with the risk of gout (P = .27 for trend). Compared with the lowest quintile of fructose intake, the multivariate relative risk of gout in the top quintile was 1.62 (95% CI, 1.20-2.19; P = .004 for trend) (risk difference of 28 cases per 100 000 person-years).

CONCLUSION: Among this cohort of women, consumption of fructose-rich beverages is associated with an increased risk of incident gout, although the contribution of these beverages to the risk of gout in the population is likely modest given the low incidence rate among women.

Do all sedentary activities lead to weight gain: sleep does not.

Curr Opin Clin Nutr Metab Care. 2010 Nov;13(6):601-7.

Do all sedentary activities lead to weight gain: sleep does not.

Chaput JP, Klingenberg L, Sjödin A.

Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Copenhagen, Denmark. jepc@life.ku.dk


PURPOSE OF REVIEW: To discuss the benefits of having a good night's sleep for body weight stability.

RECENT FINDINGS: Experimental studies have shown that short-term partial sleep restriction decreases glucose tolerance, increases sympathetic tone, elevates cortisol concentrations, decreases the satiety hormone leptin, increases the appetite-stimulating hormone ghrelin, and increases hunger and appetite. Short sleep duration might increase the risk of becoming obese, because it does not allow the recovery of a hormonal profile facilitating appetite control. Lack of sleep could also lead to weight gain and obesity by increasing the time available for eating and by making the maintenance of a healthy lifestyle more difficult. Furthermore, the increased fatigue and tiredness associated with sleeping too little could lessen one's resolve to follow exercise regimens.

SUMMARY: Short sleep duration appears to be a novel and independent risk factor for obesity. With the growing prevalence of chronic sleep restriction, any causal association between reduced sleep and obesity would have substantial importance from a public health standpoint. Future research is needed to determine whether sleep extension in sleep-deprived obese individuals will influence appetite control and/or reduce the amount of body fat.

Physical activity plays an important role in body weight regulation.

J Obes. 2011;2011. pii: 360257. Epub 2010 Aug 12.

Physical activity plays an important role in body weight regulation.

Chaput JP, Klingenberg L, Rosenkilde M, Gilbert JA, Tremblay A, Sjödin A.

Department of Human Nutrition, Faculty of Life Sciences, University of Copenhagen, Rolighedsvej 30, DK-1958 Frederiksberg C, Copenhagen, Denmark.


Emerging literature highlights the need to incorporate physical activity into every strategy intended to prevent weight gain as well as to maintain weight loss over time. Furthermore, physical activity should be part of any plan to lose weight. The stimulus of exercise provides valuable metabolic adaptations that improve energy and macronutrient balance regulation. A tight coupling between energy intake and energy expenditure has been documented at high levels of physical exercise, suggesting that exercise may improve appetite control. The regular practice of physical activity has also been reported to reduce the risk of stress-induced weight gain. A more personalized approach is recommended when planning exercise programs in a clinical weight loss setting in order to limit the compensatory changes associated to exercise-induced weight loss. With modern environment promoting overeating and sedentary behavior, there is an urgent need for a concerted action including legislative measures to promote healthy active living in order to curb the current epidemic of chronic diseases.

Anti-inflammatory effect of resveratrol on adipokine expression and secretion in human adipose tissue explants.

Int J Obes (Lond). 2010 Oct;34(10):1546-53. Epub 2010 Jun 8.

Anti-inflammatory effect of resveratrol on adipokine expression and secretion in human adipose tissue explants.

Olholm J, Paulsen SK, Cullberg KB, Richelsen B, Pedersen SB.

Department of Endocrinology and Metabolism C, Aarhus University Hospital, Aarhus C, Denmark. jens.olholm@ki.au.dk


OBJECTIVE: Human obesity is closely associated with a state of chronic low-grade inflammation, which also involves the adipose tissue with enhanced production of bioactive substances (adipokines). Calorie restriction (CR) reduces adipocytokine production and improves metabolic profile in rodents. Some of these effects are mediated through activation of the sirtuin 1 (Sirt1) enzyme, and in this study, we investigate whether the natural phytoalexin, resveratrol (RSV), which is a potent Sirt1 activator, has anti-inflammatory effects in human adipose tissue explants.

DESIGN: The effect of RSV on interleukin 1β (IL1β)-induced change of adipokine mRNA gene expression and secretion were measured in human adipose tissue explants.

RESULTS: Exposure of human adipose tissue in vitro to IL1β for 24 h increased secretion of the proinflammatory adipokines IL6, IL8 and monocyte chemoattractant protein 1 (MCP-1) 3-7.7-fold (P<0.05) and increased IL6, IL8, MCP-1, IL1β and PAI-1 mRNA expression 1.3-7.2-fold (P<0.05) accordingly. Concomitant incubations with RSV reversed the IL1β-stimulated secretion (16-36%) and gene expression (25-48%) of these adipokines. IL1β reduced adiponectin mRNA expression (40%), a decrement that was reversed by RSV treatment. Similar effects were observed in differentiated human preadipocytes in primary culture, indicating that human adipocytes are a potential target for RSV effects. Finally, the effects were neutralized by sirtinol, a Sirt1 inhibitor.

CONCLUSION: This study is the first to show anti-inflammatory effects of RSV on adipokine expression and secretion in human adipose tissue in vitro through the SIRT1 pathway. Thus, RSV is hypothesized to possess beneficial effects and might improve the metabolic profile in human obesity.

Regulation of energy metabolism by inflammation: a feedback response in obesity and calorie restriction.

Aging (Albany NY). 2010 Jun;2(6):361-8.

Regulation of energy metabolism by inflammation: a feedback response in obesity and calorie restriction.

Ye J, Keller JN.

Pennington Biomedical Research Center, Louisiana State University System, LA 70808, USA.


Caloric restriction (CR), in the absence of malnutrition, delays aging and prevents aging-related diseases through multiple mechanisms. A reduction in chronic inflammation is widely observed in experimental models of caloric restriction. The low inflammation status may contribute to the reduced incidence of osteoporosis, Alzheimer's disease, cardiovascular diseases and cancer in the aging subjects. The association of caloric restriction with low inflammation suggests a role of energy accumulation in the origin of the chronic inflammation. This point is enforced by recent advances in obesity research. Abundant literature on obesity suggests that chronic inflammation is a consequence of energy accumulation in the body. The emerging evidence strongly supports that the inflammatory response induces energy expenditure in a feedback manner to fight against energy surplus in obesity. If this feedback system is deficient (Inflammation Resistance), energy expenditure will be reduced and energy accumulation will lead to obesity. In this perspective, we propose that an increase in inflammation in obesity promotes energy expenditure with a goal to get rid of energy surplus. A decrease in inflammation under caloric restriction contributes to energy saving. Inflammation is a mechanism for energy balance in the body. Inflammation resistance will lead to obesity. We will review the recent literature in support of the viewpoints.

Insufficient sleep undermines dietary efforts to reduce adiposity.

Ann Intern Med. 2010 Oct 5;153(7):435-41.

Insufficient sleep undermines dietary efforts to reduce adiposity.

Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.

The University of Chicago, Illinois, USA.

Comment in:

Ann Intern Med. 2010 Oct 5;153(7):475-6.

Summary for patients in:

Ann Intern Med. 2010 Oct 5;153(7):I28.


BACKGROUND: Sleep loss can modify energy intake and expenditure.

OBJECTIVE: To determine whether sleep restriction attenuates the effect of a reduced-calorie diet on excess adiposity.

DESIGN: Randomized, 2-period, 2-condition crossover study.

SETTING: University clinical research center and sleep laboratory.

PATIENTS: 10 overweight nonsmoking adults (3 women and 7 men) with a mean age of 41 years (SD, 5) and a mean body mass index of 27.4 kg/m² (SD, 2.0).

INTERVENTION: 14 days of moderate caloric restriction with 8.5 or 5.5 hours of nighttime sleep opportunity.

MEASUREMENTS: The primary measure was loss of fat and fat-free body mass. Secondary measures were changes in substrate utilization, energy expenditure, hunger, and 24-hour metabolic hormone concentrations.

RESULTS: Sleep curtailment decreased the proportion of weight lost as fat by 55% (1.4 vs. 0.6 kg with 8.5 vs. 5.5 hours of sleep opportunity, respectively; P = 0.043) and increased the loss of fat-free body mass by 60% (1.5 vs. 2.4 kg; P = 0.002). This was accompanied by markers of enhanced neuroendocrine adaptation to caloric restriction, increased hunger, and a shift in relative substrate utilization toward oxidation of less fat.

LIMITATION: The nature of the study limited its duration and sample size.

CONCLUSION: The amount of human sleep contributes to the maintenance of fat-free body mass at times of decreased energy intake. Lack of sufficient sleep may compromise the efficacy of typical dietary interventions for weight loss and related metabolic risk reduction.

PRIMARY FUNDING SOURCE: National Institutes of Health.

Reduction in the Incidence of Type 2-Diabetes with the Mediterranean Diet: Results of the PREDIMED-Reus Nutrition Intervention Randomized Trial.

Diabetes Care. 2010 Oct 13. [Epub ahead of print]

Reduction in the Incidence of Type 2-Diabetes with the Mediterranean Diet: Results of the PREDIMED-Reus Nutrition Intervention Randomized Trial.

Salas-Salvadó J, Bulló M, Babio N, Martínez-González MA, Ibarrola-Jurado N, Basora J, Estruch R, Covas MI, Corella D, Arós F, Ruiz-Gutiérrez V, Ros E; For the PREDIMED Study investigators.

From the Human Nutrition Unit, Hospital Universitari de Sant Joan, Departament de Bioquímica i Biotecnologia, IISPV, Universitat Rovira i Virgili, Reus (J.S., M.B., N.B., N.I., J.B.); Department of Preventive Medicine and Public Health, University of Navarra, Pamplona (M.A.M.); SAP Reus-Altebrat, Institut Català de la Salut, Reus (J.B.); Department of Internal Medicine, Institut d'Investigacions Biomèdiques August Pi Sunyer (IDIBAPS), Hospital Clínic, Barcelona (R.E.); Cardiovascular Risk and Nutrition Research Group, Institut Municipal d'Investigació Mèdica (IMIM), Barcelona (M.I.C); Department of Preventive Medicine and Public Health, University of Valencia, Valencia (D.C); Department of Cardiology, University Hospital Txagorritxu, Vitoria (F.A.); Instituto de la Grasa, CSIC, Sevilla (V.R); Lipid Clinic, Service of Endocrinology and Nutrition, IDIBAPS, Hospital Clínic, Barcelona (E.R.); and CIBER Fisiopatologia de la Obesidad y Nutrición (CIBERObn), Instituto de Salud Carlos III, Spain (J.S.; M.B., N.B., M.A.M., N.I., J.B., R.E., M.I.C., D.C., F.A., E.R.).


AbstractObjective - To test the effects of two Mediterranean-diet interventions versus a low-fat diet on incidence of diabetes. Research Design and Methods - Three-arm randomized trial in 418 nondiabetic subjects aged 55-80 years recruited in one center (PREDIMED-Reus, North-Eastern Spain) of the PREDIMED study, a large nutrition-intervention trial for primary cardiovascular prevention in persons at high cardiovascular risk. Participants were randomized to education on a low-fat diet (control group) or one of two Mediterranean diets, supplemented with either free virgin olive oil (1 liter/week) or nuts (30 g/day). Diets were ad libitum and no advice on physical activity was given. The main outcome was diabetes incidence diagnosed by the 2009 American Diabetes Association criteria. Results - After a median follow-up of 4.0 years, diabetes incidence was 10.1% (95% confidence interval [CI], 5.1-15.1), 11.0% (5.9-16.1), and 17.9% (11.4-24.4) in the Mediterranean-diet with olive oil group, the Mediterranean-diet with nuts group, and the control group, respectively. Multivariable-adjusted hazard ratios of diabetes were 0.49 (0.25-0.97) and 0.48 (0.24-0.96) in the Mediterranean-diet groups supplemented with olive oil and nuts, respectively, compared to the control group. When pooling the two Mediterranean-diet groups compared to the control group, diabetes incidence was reduced by 52% (27-86). In all study arms, increased adherence to the Mediterranean-diet was inversely associated with diabetes incidence. Diabetes risk reduction occurred in the absence of significant changes in body weight or physical activity. Conclusion - Mediterranean diets without calorie restriction appear to be effective in the prevention of diabetes in subjects at high cardiovascular risk. Trial Registration: www.controlled-trials.com Identifier: ISRCTN35739639.

Saturday, November 20, 2010

The association of television and video viewing with fast food intake by preschool-age children.

Obesity (Silver Spring). 2006 Nov;14(11):2034-41.

The association of television and video viewing with fast food intake by preschool-age children.

Taveras EM, Sandora TJ, Shih MC, Ross-Degnan D, Goldmann DA, Gillman MW.

Center for Child Health Care Studies, Department of Ambulatory Care and Prevention, Harvard Pilgrim Health Care and Harvard Medical School, 133 Brookline Avenue, 6th floor, Boston, MA 02215, USA. Elsie.Taveras@childrens.harvard.edu


OBJECTIVE: To examine the extent to which television (TV) and video viewing is associated with consumption of fast food by preschool-age children.

RESEARCH METHODS AND PROCEDURES: In a cross-sectional study of 240 parents of children ages 2.0 to 5.9 years, parents reported the number of hours their child watched TV/videos on an average weekday and weekend day in the past month; a daily, weighted average of TV/video viewing was then calculated. The main outcome was parents' report of their children's fast food intake, using the question, "How many times a week does your child eat at fast food restaurants such as McDonald's, Burger King, or Kentucky Fried Chicken?" dichotomized to (never/<1 vs. > or =1 time/wk). The association of TV/video viewing with fast food intake was evaluated by multiple logistic regression before and after adjusting for several potential confounders.

RESULTS: Twenty-two percent of parents reported that their child ate at fast food restaurants at least once per week. After adjusting for parents' age, race/ethnicity, and household income as well as child's age and sex, for each 1-hour increase of TV/video watched per day, the odds ratio (OR) for consuming fast food > or =1 time per week was 1.60 (95% confidence interval, 1.03 to 2.49). After further adjustment for socio-environmental factors that might serve as proxies for the availability of healthy food options, such as parental time constraints and the availability and high cost of fresh fruits and vegetables in their neighborhoods, the OR for consuming fast food > or =1 time per week was minimally attenuated (OR, 1.55; 95% confidence interval, 1.04 to 2.31).

DISCUSSION: TV/video viewing was correlated with fast food consumption among preschool children in this study. Our findings raise the possibility that greater exposure to TV and videos may influence preschool children's consumption of unhealthful foods.

Excessive recreational computer use and food consumption behaviour among adolescents.

Ital J Pediatr. 2010 Aug 5;36(1):52.

Excessive recreational computer use and food consumption behaviour among adolescents.

Shi L, Mao Y.

Department of Health Services, 650 Charles E, Young Drive S, 61-253 CHS, University of California Los Angeles, Los Angeles, CA 90095, USA. lushi.pku@gmail.com


INTRODUCTION: Using the 2005 California Health Interview Survey (CHIS) data, we explore the association between excessive recreational computer use and specific food consumption behavior among California's adolescents aged 12-17.

METHOD: The adolescent component of CHIS 2005 measured the respondents' average number of hours spent on viewing TV on a weekday, the average number of hours spent on viewing TV on a weekend day, the average number of hours spent on playing with a computer on a weekday, and the average number of hours spent on playing with computers on a weekend day. We recode these four continuous variables into four variables of "excessive media use," and define more than three hours of using a medium per day as "excessive." These four variables are then used in logistic regressions to predict different food consumption behaviors on the previous day: having fast food, eating sugary food more than once, drinking sugary drinks more than once, and eating more than five servings of fruits and vegetables. We use the following variables as covariates in the logistic regressions: age, gender, race/ethnicity, parental education, household poverty status, whether born in the U.S., and whether living with two parents.

RESULTS: Having fast food on the previous day is associated with excessive weekday TV viewing (O.R.=1.38, p<0.01). Having sugary food more than once is associated with excessive weekend TV viewing (O.R.=1.50, p<0.001). Having sugary drinks more than once is associated with excessive weekday TV viewing (O.R.=1.41, p<0.01), excessive weekday recreational computer use (O.R.=1.38, p<0.05), and excessive weekend TV viewing (O.R.=1.43, p<0.001). Finally, having more than five servings of fruits and vegetables on the previous day is negatively associated with all four media use variables: excessive weekday TV viewing (O.R.=0.64, p<0.001), excessive weekday recreational computer use (O.R.=0.68, p<0.01), excessive weekend TV viewing (O.R.=0.80, p<0.05), and excessive weekend recreational computer use (O.R.=0.78, p<0.05).

CONCLUSION: Excessive recreational computer use independently predicts undesirable eating behaviors that could lead to overweight and obesity. Preventive measures ranging from parental/youth counseling to content regulations might be addressing the potential undesirable influence from excessive computer use on eating behaviors among children and adolescents.

The combined influence of genetic factors and sedentary activity on body mass changes from adolescence to young adulthood: the National Longitudinal Adolescent Health Study.

Diabetes Metab Res Rev. 2010 Nov 14. [Epub ahead of print]

The combined influence of genetic factors and sedentary activity on body mass changes from adolescence to young adulthood: the National Longitudinal Adolescent Health Study.

Graff M, North KE, Monda KL, Lange EM, Lange LA, Guo G, Gordon-Larsen P.

Department of Nutrition, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.


BACKGROUND: An increase in sedentary activities is likely a major contributor to the rise in obesity over the last three decades. Little research has examined interactions between genetic variants and sedentary activity on obesity phenotypes. High levels of sedentary activity during adolescence may interact with genetic factors to influence body mass changes between adolescence and young adulthood, a high risk period for weight gain.

METHODS: In the National Longitudinal Study of Adolescent Health, siblings and twin pairs (16.5 ± 1.7 years) were followed into young adulthood (22.4 ± 1.8 years). Self-reported screen time (TV, video, and computer use in h/week) and body mass index (kg/m(2)), calculated from measured height and weight at adolescence and at young adulthood, were available for 3795 participants. We employed a variance component approach to estimate the interaction between genotype and screen time for body mass changes. Additive genotype-by-screen time interactions were assessed using likelihood-ratio tests. Models were adjusted for race, age, sex, and age-by-sex interaction.

RESULTS: The genetic variation in body mass changes was significantly larger in individuals with low ($\sigma_{{{\rm G}}} = 27.59 \pm 1.58$) compared with high ($\sigma_{{{\rm G}}} = 18.76 \pm 2.59$) levels of screen time (p < 0.003) during adolescence.

CONCLUSIONS: Our findings demonstrate that sedentary activities during adolescence may interact with genetic factors to influence body mass changes between adolescence and young adulthood. Accounting for obesity-related behaviours may improve current understanding of the genetic variation in body mass changes. Copyright © 2010 John Wiley & Sons, Ltd.

Greater Consumption of Sweetened Beverages and Added Sugars Is Associated with Obesity among US Young Adults.

Ann Nutr Metab. 2010 Nov 19;57(3-4):211-218. [Epub ahead of print]

Greater Consumption of Sweetened Beverages and Added Sugars Is Associated with Obesity among US Young Adults.

Bermudez OI, Gao X.

Tufts University School of Medicine, Boston, Mass., USA.


Background/Aims: This study sought to examine the associations of the consumption of sugar-sweetened beverages and of added sugars with total and abdominal obesity in American adults aged 20-39 years who participated in the 1999-2000 National Health and Nutrition Examination Survey in the U.S. Methods: This was a cross-sectional study based on a sample of 947 adults (aged 20-39 years): 424 non-Hispanic whites, 222 non-Hispanic blacks, and 301 Mexican-Americans. Obesity was defined as a body mass index ≥30 and abdominal obesity as a waist circumference >102 cm in men or >88 cm in women. The use of sweetened beverages and added sugars was stratified into quartiles of intake. Odds ratios (ORs) for total and abdominal obesity were estimated with logistic regression models. Results: Compared to the lowest intake quartile of sweetened beverages, those with the highest intake had a higher intake of energy, added sugars, and carbohydrates, as well as a lower intake of fiber, orange juice, and low-fat milk. A greater intake of sweetened beverages was associated with a higher risk of total and abdominal obesity (p(trend) <0.02 for both). The adjusted ORs comparing 2 extreme quartiles of sweetened beverages were 2.1 (95% CI 1.2-3.7) for total obesity and 2.0 (95% CI 1.1-3.6) for abdominal obesity. Conclusions: An increased consumption of sweetened beverages was associated with total and abdominal obesity in US adults aged 20-39 years. Further investigation of the potential role of sweetened beverages and other dietary components, and of the mechanisms by which these intakes contribute to weight gain, is needed to accelerate our efforts to halt or somewhat alleviate the current obesity epidemic facing the American population.

Sarcopenic obesity: a new category of obesity in the elderly.

Nutr Metab Cardiovasc Dis. 2008 Jun;18(5):388-95. Epub 2008 Apr 18.

Sarcopenic obesity: a new category of obesity in the elderly.

Zamboni M, Mazzali G, Fantin F, Rossi A, Di Francesco V.

Geriatric Medicine, Cattedra di Geriatria, University of Verona, Ospedale Maggiore, Piazzale Stefani 1, 37126 Verona, Italy. mauro.zamboni@univr.it


BACKGROUND AND AIM: In elderly patients, age-related changes in body composition, as well as the increased prevalence of obesity, determine a combination of excess weight and reduced muscle mass or strength, recently defined as sarcopenic obesity (SO). This review examines the main studies regarding sarcopenic obesity in the elderly.

DATA SYNTHESIS: Definition of SO necessarily combines those of sarcopenia and obesity. The prevalence of sarcopenia and SO increases with age. Muscle and fat mass are strongly interconnected from a pathogenetic point of view. A better understanding of the mechanisms which lead from loss of muscle mass to fat gain or vice versa from fat gain to muscle loss seems to be crucial. Recent data suggest that peptides produced by adipose tissue may play an important role in the pathophysiology of SO, thus more research is needed to better characterize this new area. Obesity and sarcopenia in the elderly may potentiate each other maximizing their effects on disability, morbidity and mortality. Identifying elderly subjects with SO should be mandatory; effective treatment of sarcopenia and SO may attenuate its clinical impact.

CONCLUSION: The concept of SO may help to clarify the relationship between obesity, morbidity and mortality in the elderly.

Sarcopenic obesity: satellite cells in the aging muscle.

Curr Opin Clin Nutr Metab Care. 2010 Nov 17. [Epub ahead of print]

Sarcopenic obesity: satellite cells in the aging muscle.

Thornell LE.

Department of Integrative Medical Biology, Section for Anatomy, Umea University, Umea, Sweden.


PURPOSE OF REVIEW: Current knowledge on satellite cells in relation to suggested mechanisms of loss of muscle mass and strength, induction of fat infiltration, and countermeasures is highlighted.

RECENT FINDINGS: Consensus on the definition of sarcopenia and sarcopenic obesity is proposed. Human satellite cell heterogeneity has now unequivocally been verified in situ as well as an adipogenic potential, though in mice other muscle stem cells are the hot topic to induce adipogenesis upon muscle damage. Inflammation, oxidative stress, proteolytic degradation, and nuclear apoptosis are discussed as pathogenetic mechanisms of sarcopenia, although little evidence exists that they are important in human muscle. In rodents, exercise-induced muscle injury is a hallmark for sequential events leading to muscle fiber necrosis and sarcopenia. Exercise in humans, on the contrary, is the key event to countermeasure sarcopenia. Cautions to extrapolate observation in rodents to explain human conditions have been presented.

SUMMARY: Human satellite cells are indispensable for maintenance of human muscle mass, but their implications in the pathogenesis of sarcopenia and sarcopenic obesity are still under debate. Nevertheless, satellite cell activation upon exercise seems unequivocally together with adequate nutrition to be the most effective countermeasure for sarcopenia and sarcopenic obesity.

Friday, November 19, 2010

Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise.

Am J Physiol. 1997 Oct;273(4 Pt 1):E768-75.

Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise.

Horowitz JF, Mora-Rodriguez R, Byerley LO, Coyle EF.

Department of Kinesiology and Health Education, The University of Texas at Austin, 78712, USA.


This study determined if the suppression of lipolysis after preexercise carbohydrate ingestion reduces fat oxidation during exercise. Six healthy, active men cycled 60 min at 44 +/- 2% peak oxygen consumption, exactly 1 h after ingesting 0.8 g/kg of glucose (Glc) or fructose (Fru) or after an overnight fast (Fast). The mean plasma insulin concentration during the 50 min before exercise was different among Fast, Fru, and Glc (8 +/- 1, 17 +/- 1, and 38 +/- 5 microU/ml, respectively; P < 0.05). After 25 min of exercise, whole body lipolysis was 6.9 +/- 0.2, 4.3 +/- 0.3, and 3.2 +/- 0.5 micromol x kg(-1) x min(-1) and fat oxidation was 6.1 +/- 0.2, 4.2 +/- 0.5, and 3.1 +/- 0.3 micromol x kg(-1) x min(-1) during Fast, Fru, and Glc, respectively (all P < 0.05). During Fast, fat oxidation was less than lipolysis (P < 0.05), whereas fat oxidation approximately equaled lipolysis during Fru and Glc. In an additional trial, the same subjects ingested glucose (0.8 g/kg) 1 h before exercise and lipolysis was simultaneously increased by infusing Intralipid and heparin throughout the resting and exercise periods (Glc+Lipid). This elevation of lipolysis during Glc+Lipid increased fat oxidation 30% above Glc (4.0 +/- 0.4 vs. 3.1 +/- 0.3 micromol x kg(-1) x min(-1); P < 0.05), confirming that lipolysis limited fat oxidation. In summary, small elevations in plasma insulin before exercise suppressed lipolysis during exercise to the point at which it equaled and appeared to limit fat oxidation.

Effects of dietary fructose on plasma lipids in healthy subjects.

Am J Clin Nutr. 2000 Nov;72(5):1128-34.

Effects of dietary fructose on plasma lipids in healthy subjects.

Bantle JP, Raatz SK, Thomas W, Georgopoulos A.

Department of Medicine, the General Clinical Research Center, the Division of Biostatistics, and the School of Public Health, the University of Minnesota, Minneapolis, MN 55455, USA. bantl001@tc.umn.edu


BACKGROUND: About 9% of average dietary energy intake in the United States comes from fructose. Such a high consumption raises concern about the metabolic effects of this sugar.

OBJECTIVE: The objective of this study was to determine the effect of dietary fructose on plasma lipids.

DESIGN: The study was conducted in the General Clinical Research Center at Fairview-University of Minnesota Medical Center. The participants were 24 healthy adult volunteers (12 men and 12 women; 6 of each sex were aged <40 y and 6 of each sex were aged >/=40 y). All subjects received 2 isoenergetic study diets assigned by using a randomized, balanced crossover design. One diet provided 17% of energy as fructose. The other diet was sweetened with glucose and was nearly devoid of fructose. Each diet was fed for 6 wk. Both diets were composed of common foods and contained nearly identical amounts of carbohydrate, protein, fat, fiber, cholesterol, and saturated, monounsaturated, and polyunsaturated fatty acids. All meals were prepared in the metabolic kitchen of the General Clinical Research Center.

RESULTS: The responses to the study diets differed by sex. In men, the fructose diet produced significantly higher fasting, postprandial, and daylong plasma triacylglycerol concentrations than did the glucose diet. The daylong plasma triacylglycerol concentration after 6 wk of the fructose diet was 32% greater in men than the corresponding concentration during the glucose diet (P: < 0.001). The fructose diet had no significant effect on fasting or postprandial plasma triacylglycerol concentrations in women. The fructose diet also had no persistent effect on fasting plasma cholesterol, HDL cholesterol, or LDL cholesterol in either men or women.

CONCLUSIONS: Dietary fructose was associated with increased fasting and postprandial plasma triacylglycerol concentrations in men. Diets high in added fructose may be undesirable, particularly for men. Glucose may be a suitable replacement sugar.

EC must reverse decision on out-of-quota sugar and release internally, CIUS

EC must reverse decision on out-of-quota sugar and release internally, CIUS: "The CIUS is calling for the European Commission to act now to keep sugar supplies within the EU market rather than export the sweetener, with it claiming that EU based confectioners and other food and drink manufacturers are facing sugar"

Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats.

Br J Nutr. 2005 Nov;94(5):714-9.

Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats.

Fushimi T, Sato Y.

Central Research Institute, Mizkan Group Corporation, 2-6 Nakamura-cho, Handa, Aichi 475-8585, Japan. tfushimi@mizkan.co.jp


The aim of the present study is to investigate the effect of acetic acid feeding on the circadian changes in glycogen concentration in liver and skeletal muscle. Rats were provided meal once daily (09.00-13.00 hours) for 10 d. On the 11th day, they were either killed immediately or given 9 g diet containing either 0 (control) or 0.7 g/kg-diet acetic acid beginning at 09.00 hours for 4 h, as in the previous regimen. Rats in the fed group were killed at 4, 8 or 24 h after the start of feeding. At 4 h after the start of feeding, the acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentrations (P<0.05). Also, at this same point, liver xylulose-5-phosphate, a key stimulator of glycolysis, the ratio of fructose-1,6-bisphosphate to fructose-6-phosphate in skeletal muscle, which reflects phosphofructokinase-1 activity, and liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, were significantly lower in the acetic acid group than in the control group (P<0.05). In addition, the acetic acid group had a significantly lower serum lactate concentration and lower ratio of insulin to glucagon than the control group at the same point (P<0.05). We conclude that a diet containing acetic acid may enhance glycogen repletion but not induce supercompensation, a large increase in the glycogen level that is beneficial in improving performance, in liver and skeletal muscle by transitory inhibition of glycolysis. Further, we indicate the possibility of a transient enhancement of fatty acid oxidation in liver by acetic acid feeding.

A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans.

Am J Clin Nutr. 2006 Dec;84(6):1374-9.

A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans.

Lê KA, Faeh D, Stettler R, Ith M, Kreis R, Vermathen P, Boesch C, Ravussin E, Tappy L.

Department of Physiology, University of Lausanne, Lausanne, Switzerland.


BACKGROUND: High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated.

OBJECTIVE: We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7).

DESIGN: IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a high-fructose diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy.

RESULTS: Fructose caused significant (P < 0.05) increases in fasting plasma concentrations of triacylglycerol (36%), VLDL-triacylglycerol (72%), lactate (49%), glucose (5.5%), and leptin (48%) without any significant changes in body weight, IHCL, IMCL, or IS. IHCL were negatively correlated with triacylglycerol after 4 wk of the high-fructose diet (r = -0.78, P < 0.05).

CONCLUSION: Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.

Appetite hormones and energy intake in obese men after consumption of fructose, glucose and whey protein beverages.

Int J Obes (Lond). 2007 Nov;31(11):1696-703. Epub 2007 Jun 26.

Appetite hormones and energy intake in obese men after consumption of fructose, glucose and whey protein beverages.

Bowen J, Noakes M, Clifton PM.

Commonwealth Scientific and Industrial Research Organisation, Human Nutrition, Adelaide, Australia. jane.bowen@csiro.au


OBJECTIVE: To investigate appetite responses over 4 h to fructose beverages in obese men, relative to glucose and whey protein. Second, to investigate the effect of combining whey and fructose on postprandial appetite hormones.

DESIGN: Randomized, double-blind crossover study of four beverages (1.1 MJ) containing 50 g of whey, fructose, glucose or 25 g whey+25 g fructose. Blood samples and appetite ratings were collected for 4 h then a buffet meal was offered.

SUBJECTS: Twenty-eight obese men (age: 57.0+/-1.6 years, body mass index: 32.5+/-0.6 kg/m(2)).

MEASUREMENTS: Plasma ghrelin (total), glucagon-like peptide-1 (GLP-1 7-36), cholecystokinin-8, glucose, insulin and appetite ratings were assessed at baseline and 30, 45, 60, 90, 120, 180, 240 min after beverages, followed by measurement of ad libitum energy intake.

RESULTS: Fructose produced lower glycaemia and insulinaemia compared to the glucose treatment (P<0.0001); whereas postprandial ghrelin, GLP-1 and cholecystokinin responses were similar after both treatments. Whey protein produced a prolonged (2-4 h) suppression of ghrelin (P=0.001) and elevation of GLP-1 (P=0.002) and cholecystokinin (P=0.003) that were reduced when combined with fructose, while glucose and insulin responses were similar. Energy intake after 4 h was independent of beverage type (glucose 4.7+/-0.2 MJ; fructose 4.9+/-0.3 MJ; whey 4.6+/-0.3 MJ; whey/fructose 4.8+/-0.3 MJ; P>0.05).

CONCLUSION: In obese men, fructose- and glucose-based beverages had similar effects on appetite and associated regulatory hormones, independent of the differing glycaemic and insulinaemic responses. The contrasting profile of plasma ghrelin, GLP-1 and cholecystokinin after whey protein consumption did not impact on ad libitum intake 4 h later and was attenuated when 50% of whey was replaced with fructose.

Fructose, but not dextrose, accelerates the progression of chronic kidney disease.

Am J Physiol Renal Physiol. 2007 Oct;293(4):F1256-61. Epub 2007 Aug 1.

Fructose, but not dextrose, accelerates the progression of chronic kidney disease.

Gersch MS, Mu W, Cirillo P, Reungjui S, Zhang L, Roncal C, Sautin YY, Johnson RJ, Nakagawa T.

Division of Nephrology, Dialysis and Transplantation, University of Florida, Gainesville, Florida 32610-0224, USA. gerscms@medicine.ufl.edu


The metabolic syndrome has recently been recognized as a risk factor for kidney disease, but the mechanisms mediating this risk remain unclear. High fructose consumption by animals produces a model of the metabolic syndrome with hypertension, hyperlipidemia, and insulin resistance. The present study was conducted to test the hypothesis that consumption of a high-fructose diet could accelerate the progression of chronic kidney disease. Three groups of 14 male Sprague-Dawley rats were pair fed a specialized diet containing 60% fructose (FRU) or 60% dextrose (DEX) or standard rat chow (CON). After the animals were fed their assigned diet for 6 wk, five-sixths nephrectomy was performed, and the assigned diet was continued for 11 wk. Proteinuria was significantly increased and creatinine clearance was decreased in the FRU group compared with the CON and DEX groups, and blood urea nitrogen was higher in the FRU group than in the CON and DEX groups. Kidneys from the FRU group were markedly larger than kidneys from the CON and DEX groups. Glomerular sclerosis, tubular atrophy, tubular dilatation, and cellular infiltration appeared markedly worse in kidneys from the FRU group than in kidneys from the DEX and CON groups. Monocyte chemoattractant protein-1 (MCP-1) was measured in renal tissue homogenate and found to be increased in the FRU group. In vitro studies were conducted to determine the mechanism for increased renal MCP-1, and fructose stimulation of proximal tubular cells resulted in production of MCP-1. In conclusion, consumption of a high-fructose diet greatly accelerates progression of chronic kidney disease in the rat remnant kidney model.

Effects of acute and chronic protein intake on metabolism, appetite, and ghrelin during weight loss.

Obesity (Silver Spring). 2007 May;15(5):1215-25.

Effects of acute and chronic protein intake on metabolism, appetite, and ghrelin during weight loss.

Leidy HJ, Mattes RD, Campbell WW.

Department of Foods and Nutrition, Ingestive Behavior Research Center, Purdue University, 700 West State Street, West Lafayette, IN 47907, USA. hleidy@purdue.edu


OBJECTIVE: This study evaluated the effects of acute and chronic consumption of higher dietary protein on energy expenditure, macronutrient use, appetite, and appetite-regulating hormones during weight loss in women.

RESEARCH METHODS AND PROCEDURES: Thirty-eight women chronically consuming a 750 kcal/d energy-deficit diet with a protein content of 30% (higher protein-chronic diet, HP-CD, n = 21) or 18% (normal protein-chronic diet, NP-CD, n = 17) for 9 weeks were tested. On separate days, metabolic, appetite, and hormonal responses were measured over 4 hours when the women consumed a higher protein-acute meal (HP-AM) (30% of energy as protein) or a normal protein-acute meal (NP-AM) (18% of energy as protein).

RESULTS: With chronic diet groups combined, HP-AM led to lower respiratory exchange ratio (0.829 +/- 0.005 vs. 0.843 +/- 0.008; p < 0.05), lower carbohydrate oxidation (p < 0.05), and higher fat oxidation (p < 0.05) compared with NP-AM. HP-AM also led to reduced self-reported postprandial hunger (p < 0.001) and desire to eat (p < 0.001) and lower postprandial ghrelin (252 +/- 16 vs. 274 +/- 18 ng/mL x 240 minutes, p < 0.05) compared with NP-AM. No differences in postprandial energy expenditure (PPEE) occurred between meals. When combining acute meals, respiratory exchange ratio was lower (p < 0.05) and protein oxidation (p < 0.001) was higher in the HP-CD vs. NP-CD. An acute meal-by-chronic diet interaction was observed with PPEE such that HP-AM led to greater PPEE in the HP-CD vs. NP-CD (28.7 +/- 2.7 vs. 19.9 +/- 2.7 kcal/min for 195 minutes; p < 0.05).

CONCLUSIONS: During weight loss, thermogenesis and protein use appear to be influenced by chronic protein intake, while appetite and ghrelin are more responsive to acute protein intake.

How bad is fructose?

How bad is fructose?1,2

George A Bray

1 From the Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA

2 Reprints not available. Address correspondence to GA Bray, Boyd Professor, Pennington Biomedical Research Center, LSU System, 6400 Perkins Road, Baton Rouge, LA 70808. E-mail: brayga@pbrc.edu.

See corresponding article on page 1174.

This issue of the Journal contains another disturbing article on the biology of fructose (1). Why is fructose of concern? First, it is sweeter than either glucose or sucrose. In fruit, it serves as a marker for foods that are nutritionally rich. However, in soft drinks and other "sweets," fructose serves to reward sweet taste that provides "calories," often without much else in the way of nutrition. Second, the intake of soft drinks containing high-fructose corn syrup (HFCS) or sucrose has risen in parallel with the epidemic of obesity, which suggests a relation (2). Third, the article in this issue of the Journal (1) and another article published elsewhere last year (3) implicate dietary fructose as a potential risk factor for cardiovascular disease.

The intake of dietary fructose has increased significantly from 1970 to 2000. There has been a 25% increase in available "added sugars" during this period (4). The Continuing Survey of Food Intake by Individuals from 1994 to 1996 showed that the average person had a daily added sugars intake of 79 g (equivalent to 316 kcal/d or 15% of energy intake), approximately half of which was fructose. More important, persons who are ranked in the top one-third of fructose consumers ingest 137 g added sugars/d, and those in the top 10% consume 178 g/d, with half of that amount being fructose. If there are health concerns with fructose, then this increased intake could aggravate those problems.

Before the European encounter with the New World 500 y ago and the development of the worldwide sugar industry, fructose in the human diet was limited to a few items. For example, honey, dates, raisins, molasses, and figs have a content of >10% of this sugar, whereas a fructose content of 5–10% by weight is found in grapes, raw apples, apple juice, persimmons, and blueberries. Milk, the main nourishment for infants, has essentially no fructose, and neither do most vegetables and meats, which indicates that human beings had little dietary exposure to fructose before the mass production of sugar.

Most fructose in the American diet comes not from fresh fruit, but from HFCS or sucrose (sugar) that is found in soft drinks and sweets, which typically have few other nutrients (2). Soft drink consumption, which provides most of this fructose, has increased dramatically in the past 6 decades, rising from a per-person consumption of 90 servings/y (≈2 servings/wk) in 1942 to that of 600 servings/y (≈2 servings/d) in 2000 (5). More than 50% of preschool children consume some calorie-sweetened beverages (6). Children of this age would not normally be exposed to fructose, let alone in these high amounts. Because both HFCS and sucrose are "delivery vehicles for fructose," the load of fructose has increased in parallel with the use of sugar.

Fructose is an intermediary in the metabolism of glucose, but there is no biological need for dietary fructose. When ingested by itself, fructose is poorly absorbed from the gastrointestinal tract, and it is almost entirely cleared by the liver—the circulating concentration is ≈0.01 mmol/L in peripheral blood, compared with 5.5 mmol/L for glucose.

Fructose differs in several ways from glucose, the other half of the sucrose (sugar) molecule (4). Fructose is absorbed from the gastrointestinal tract by a different mechanism than that for glucose. Glucose stimulates insulin release from the isolated pancreas, but fructose does not. Most cells have only low amounts of the glut-5 transporter, which transports fructose into cells. Fructose cannot enter most cells, because they lack glut-5, whereas glucose is transported into cells by glut-4, an insulin-dependent transport system. Finally, once inside the liver cell, fructose can enter the pathways that provide glycerol, the backbone for triacylglycerol. The growing dietary amount of fructose that is derived from sucrose or HFCS has raised questions about how children and adults respond to fructose alone or when it is accompanied by glucose. In one study, the consumption of high-fructose meals reduced 24-h plasma insulin and leptin concentrations and increased postprandial fasting triacylglycerols in women, but it did not suppress circulating ghrelin, a major appetite-stimulating hormone (4).

Fructose is metabolized, primarily in the liver, by phosphorylation on the 1-position, a process that bypasses the rate-limiting phosphofructokinase step (4). Hepatic metabolism of fructose thus favors lipogenesis, and it is not surprising that several studies have found changes in circulating lipids when subjects eat high-fructose diets (4). In the study conducted by Aeberli et al (1), dietary factors, especially fructose, were examined in relation to body mass index, waist-to-hip ratio, plasma lipid profile, and LDL particle size in 74 Swiss schoolchildren who were 6–14 y old. In that study, plasma triacylglycerols were higher, HDL-cholesterol concentrations were lower, and lipoprotein (LDL) particle size was smaller in the overweight children than in the normal-weight children. Fatter children had smaller LDL particle size, and, even after control for adiposity, dietary fructose intake was the only dietary factor related to LDL particle size. In this study, it was the free fructose, and not sucrose, that was related to the effect of LDL particle size. Studies in rodents, dogs, and nonhuman primates eating diets high in fructose or sucrose consistently show hyperlipidemia (4). The current report by Aeberli et al suggests that the higher intake of fructose by school-age children may have detrimental effects on their future risk of cardiovascular disease by reducing LDL particle size. It is interesting that this study did not find a relation of dietary fructose with triacylglycerols but did find a relation with the more concerning lipid particle, LDL cholesterol. Another recent report has proposed a hypothesis relating fructose intake to the long-known relation between uric acid and heart disease (3). The ADP formed from ATP after phosphorylation of fructose on the 1-position can be further metabolized to uric acid. The metabolism of fructose in the liver drives the production of uric acid, which utilizes nitric oxide, a key modulator of vascular function (3). The studies by Aeberli et al and Nakagawa et al suggest that the relation of fructose to health needs reevaluation.


The author had no personal or financial conflict of interest.


1.1. Aeberli I, Zimmermann MB, Molinari L, et al. Fructose intake is a predictor of LDL particle size in overweight schoolchildren. Am J Clin Nutr 2007;86:1174–8.[Abstract/Free Full Text]

•2. Bray GA, Nielsen SJ, Popkin BM. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004;79:537–43.[Abstract/Free Full Text]

•3. Nakagawa T, Hu H, Zharikov S, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol (Renal Physiol) 2006;290:F625–31.[Abstract/Free Full Text]

•4. Havel PJ. Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005;63:133–57.[Medline]

•5. Vartanian LR, Schwartz MB, Brownell KD. Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health 2007;97:667–75.[Abstract/Free Full Text]

•6. Harnack L, Stang J, Story M. Soft drink consumption among US children and adolescents: nutritional consequences. J Am Diet Assoc 1999;99:436–41.[Medline]

Dietary fructose consumption among US children and adults: the Third National Health and Nutrition Examination Survey.

Medscape J Med. 2008 Jul 9;10(7):160.

Dietary fructose consumption among US children and adults: the Third National Health and Nutrition Examination Survey.

Vos MB, Kimmons JE, Gillespie C, Welsh J, Blanck HM.

Department of Pediatrics, Gastroenterology, Hepatology and Nutrition, Graduate Division of Biological and Biomedical Sciences, Nutrition and Health Science Program, Emory University, Atlanta, Georgia, USA. Miriam_Vos@oz.ped.emory.edu

Comment in:

Medscape J Med. 2008;10(7):159.


CONTEXT: High fructose intake has been associated with increased de novo lipogenesis in the liver as well as increased plasma triglycerides, insulin resistance, and obesity. Fructose occurs naturally in fruits and vegetables; however, it is added to many processed foods as table sugar (sucrose) and high-fructose corn syrup. Dietary data from a nationally representative sample in 1977-1978 estimated that mean consumption of fructose was 37 g/day (8% of total intake). Little is known about more recent fructose consumption patterns.

OBJECTIVE: We determined the amount and sources of dietary fructose among US adults and children.

DESIGN: We examined fructose consumption patterns by sex, age group, race/ethnicity, socioeconomic status, and body mass index for 21,483 children and adults. We used a single 24-hour dietary recall administered in the third National Health and Examination Survey (NHANES).

MAIN OUTCOME MEASURE: Weighted estimates of fructose intake were tested for significant differences (P < .05) between groups.

RESULTS: The mean consumption of fructose was estimated to be 54.7g/day (range, 38.4-72.8) and accounted for 10.2% of total caloric intake. Consumption was highest among adolescents (12-18 years) at 72.8 g/day (12.1% of total calories). One fourth of adolescents consumed at least 15% of calories from fructose. The largest source of fructose was sugar-sweetened beverages (30%) followed by grains (22%) and fruit or fruit juice (19%).

CONCLUSIONS: Over 10% of Americans' daily calories were from fructose. These results, when compared with a previous nationally representative study, suggest that fructose consumption has increased. Further research is needed to understand the impact of increased intake of fructose on human health.

Fructose consumption and the risk of kidney stones.

Kidney Int. 2008 Jan;73(2):207-12. Epub 2007 Oct 10.

Fructose consumption and the risk of kidney stones.

Taylor EN, Curhan GC.

Renal Division and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. entaylor@partners.org

Comment in:

Kidney Int. 2008 Jan;73(2):139-40.


Fructose consumption has markedly increased over the past decades. This intake may increase the urinary excretion of calcium, oxalate, uric acid, and other factors associated with kidney stone risk. We prospectively examined the relationship between fructose intake and incident kidney stones in the Nurses' Health Study I (NHS I) (93,730 older women), the Nurses' Health Study II (NHS II) (101,824 younger women), and the Health Professionals Follow-up Study (45,984 men). Food frequency questionnaires were used to assess free fructose and sucrose intake every 4 years. Total-fructose intake was calculated as free fructose plus half the intake of sucrose, and expressed as percentage of total energy. Cox proportional hazard regressions were adjusted for age, body mass index (BMI), thiazide use, caloric intake, and other dietary factors. We documented 4902 incident kidney stones during a combined 48 years of follow-up. The multivariate relative risks of kidney stones significantly increased for participants in the highest compared to the lowest quintile of total-fructose intake for all three study groups. Free-fructose intake was also associated with increased risk. Non-fructose carbohydrates were not associated with increased risk in any cohort. Our study suggests that fructose intake is independently associated with an increased risk of incident kidney stones.

Effects of seafood consumption and weight loss on fasting leptin and ghrelin concentrations in overweight and obese European young adults.

Eur J Nutr. 2009 Mar;48(2):107-14. Epub 2009 Jan 13.

Effects of seafood consumption and weight loss on fasting leptin and ghrelin concentrations in overweight and obese European young adults.

Ramel A, Parra D, Martinéz JA, Kiely M, Thorsdottir I.

Faculty of Food Science and Nutrition, Unit for Nutrition Research, Landspitali-University Hospital, University of Iceland, 101 Reykjavik, Iceland.


BACKGROUND: Energy restriction affects circulating leptin and ghrelin concentrations.

THE AIM OF THIS STUDY: To investigate whether seafood consumption affects fasting leptin and ghrelin concentrations in addition to weight loss.

METHODS: In this 8-week dietary intervention, subjects (324 Icelandic, Spanish and Irish subjects, 20-40 years, BMI 27.5-32.5 kg/m(2)) were randomized to energy-restricted diets (-30%) of identical macronutrient composition but different amount of seafood: control (no seafood); lean fish (150 g cod, three times per week); fatty fish (150 g salmon, three times per week); EPA&DHA [daily docosahexaenoic (DHA)/eicosapentaenoic acid (EPA) capsules]. Anthropometric data, ghrelin, leptin, and insulin were measured at baseline and endpoint. Linear models investigated the effects of seafood on fasting leptin, ghrelin and insulin.

RESULTS: Body weight (-5.2 +/- 3.0 kg), leptin (-34.8%) and insulin (-13.5%) decreased, while ghrelin increased (5.6%) (all P < 0.001). According to linear models endpoint insulin was significantly lower in the EPA&DHA group (-16.4%, P = 0.025) compared to control, endpoint leptin in men was lower in the salmon group (-22.9%, P = 0.026), and the EPA&DHA group tended to have higher endpoint ghrelin (5.6%, P = 0.060), an effect seen only in women indicated by a significant gender x EPA&DHA interaction. Weight loss explained the effects of fatty seafood on leptin and ghrelin, but not insulin.

CONCLUSIONS: Consumption of fatty seafood can modulate fasting insulin, ghrelin and leptin during an 8-week intervention. Effects are partly gender specific and are partly explained by weight loss. Consumption of lean fish does not affect circulating hormones in comparison to control. The most consistent effect on circulating hormones is mediated by weight loss.

Appetite responds to changes in meal content, whereas ghrelin, leptin, and insulin track changes in energy availability.

J Clin Endocrinol Metab. 2009 Jul;94(7):2290-8. Epub 2009 Apr 28.

Appetite responds to changes in meal content, whereas ghrelin, leptin, and insulin track changes in energy availability.

Borer KT, Wuorinen E, Ku K, Burant C.

School of Kinesiology, The University of Michigan, Ann Arbor, Michigan 48109, USA. Katarina@umich.edu


CONTEXT: It is uncertain how between-meal variations in energy availability and physiological changes in ghrelin, leptin, and insulin affect appetite. Objective: The aim of the study was to examine the influence on human appetite of the meal size and its nutrient content or changes in energy availability and concentrations of ghrelin, leptin, and insulin.

DESIGN: We conducted a crossover study manipulating meal size and energy availability through exercise energy expenditure and iv nutrient replacement (TPN). Setting: The study was performed at a Clinical Research Center.

PARTICIPANTS: Ten healthy postmenopausal women (age, 59.7 +/- 1.5 yr; mean body mass index, 26 kg/m(2)) were studied. Interventions: We conducted trials based on different morning meal size (418 vs. 2090 KJ), presence or absence of exercise energy expenditure (2273 to 2361 KJ), energy replacement by TPN (1521 to 1538 KJ), and a midday ad libitum meal. Main Outcome Measures: Changes in hunger, fullness, midday ad libitum food consumption, and concentrations of ghrelin, leptin, insulin, and metabolic fuels were measured. We also performed midday meal tests for the presence of caloric compensation.

RESULTS: Appetite was influenced by the size and energy content of the meals, but not by variation in energy availability which also did not trigger consummatory compensation. Exercise reduced hunger and increased fullness. Ghrelin, leptin, and insulin responded to changes in energy availability but not to meal size. Appetite was unaffected by physiological changes in ghrelin, leptin, or insulin.

CONCLUSIONS: During rest, appetite is influenced by the size and energy content of meals, but it bears no homeostatic relationship to between-meal changes in energy availability due to small meals, exercise, or TPN, or concentrations of ghrelin, leptin, and insulin.