Random Reading....

[Emma-Leigh]

Why I don't like using the HB equation...


Journal of the American Dietetic Association - September 2003 (Vol. 103, Issue 9, Pages 1152-1159, DOI: 10.1016/S0002-8223(03)00982-9)

Validation of several established equations for resting metabolic rate in obese and nonobese people

David C. Frankenfield, MS, RD, William A. Rowe, MD, J.Stanley Smith, MD, R.N. Cooney, MD

Objective
To evaluate several equations for predicting resting metabolic rate against measured values in obese and nonobese people.

Design
Resting metabolic rate was measured with indirect calorimetry. Four calculation standards using various combinations of weight, height, and age were used to predict resting metabolic rate: a) Harris-Benedict equation, b) Harris-Benedict equation using adjusted body weight in obese individuals, c) Owen, and d) Mifflin. Main outcome was percentage of subjects whose calculated metabolic rate was outside a ±10% limit from measured values.

Subjects/setting
130 nonhospitalized adult volunteers grouped by degree of obesity (range of body mass index, 18.8 to 96.8).

Statistical analysis performed
Analysis of proportions was used to determine differences in the percentage of subjects estimated accurately by each equation; α was set at 0.05.

Results
Calculated resting metabolic rate was more than 10% different from measured in 22% of subjects using the Mifflin equation, 33% using the Harris-Benedict equation (P=.05 vs Mifflin), and 35% using the Owen equation (P<.05 vs Mifflin). The error rate using Harris-Benedict with adjusted weight in obesity was 74% (vs 36% in obese subjects using actual weight in the standard Harris-Benedict equation).

Applications/conclusion
Of the calculation standards tested, the Mifflin standard provided an accurate estimate of actual resting metabolic rate in the largest percentage of nonobese and obese individuals and therefore deserves consideration as the standard for calculating resting metabolic rate in obese and nonobese adults. Use of adjusted body weight in the Harris-Benedict equation led to less overestimation by that equation in obese people at the expense of increased incidence of underestimation.

[Emma-Leigh]

Clinical Cardiology, Volume 32 Issue 3, Pages 121 - 124
Published Online: 19 Mar 2009
Copyright © 2010 Wiley Periodicals, Inc.

Cardiorespiratory Fitness and Sedentary Lifestyle in the Morbidly Obese
Thomas E. Vanhecke, MD *, Barry A. Franklin, PhD, Wendy M. Miller, MD, Adam T. deJong, MA, Catherine J. Coleman, RN, BSN, Peter A. McCullough, MD, MPH
Department of Medicine, Divisions of Cardiology, Nutrition, and Preventive Medicine, William Beaumont Hospital, Royal Oak, Michigan, USA
email: Thomas E. Vanhecke (tvanhecke@gmail.com)
*Correspondence to Thomas E. Vanhecke, Department of Internal Medicine Divisions of Cardiology, Nutrition, and Preventive Medicine William Beaumont Hospital 3601 W. 13 Mile Rd. Royal Oak, MI 48073, USA


Background
Sedentary lifestyles and poor physical fitness are major contributors to the current obesity and cardiovascular disease pandemic.

Hypothesis
Daily physical activity and cardiorespiratory fitness are correlated in morbidly obese individuals in their free-living environment.

Methods
Ten morbidly obese participants continuously wore an activity sensor that measured caloric expenditure, minute-by-minute physical activity, and steps/day over a 72-h period. Following collection of the device data, structured cardiorespiratory fitness testing was performed on each subject.

Results
Mean caloric expenditure for all individuals was 2,668 ± 481 kcal/d. On average, subjects took 3,763 ± 2,223 steps. On average 23 h and 51.6 min per d were spent sleeping or engaged in sedentary activity (<3 metabolic equivalents [METs]) and the remaining 8.4 min were spent in moderate activity (3-6 METs). Average peak VO2 was 16.8 ± 4.7 mL/kg/min. Higher peak VO2 correlated with higher total caloric expenditure (TCE; r = 0.628, p = 0.05) and trended with higher steps/day (r = 0.591, p = 0.07).

Conclusions
Most morbidly obese participants in this study were markedly sedentary. These study results may provide important links between obesity, poor fitness, and cardiovascular disease. Copyright © 2009 Wiley Periodicals, Inc.

[Emma-Leigh]

J Appl Physiol 107: 1308-1315, 2009. First published July 30, 2009; doi:10.1152/japplphysiol.00348.2009

TRANSLATIONAL PHYSIOLOGY

No major sex differences in muscle protein synthesis rates in the postabsorptive state and during hyperinsulinemia-hyperaminoacidemia in middle-aged adults

Gordon I. Smith,1 Philip Atherton,2 Dominic N. Reeds,1 B. Selma Mohammed,1 Hadia Jaffery,1 Debbie Rankin,2 Michael J. Rennie,2 and Bettina Mittendorfer1
1Washington University, School of Medicine, St. Louis, Missouri; and ; 2University of Nottingham, School of Graduate Entry Medicine and Health, Derby, United Kingdom

Submitted 2 April 2009 ; accepted in final form 29 July 2009

Men have more muscle than women, but most studies evaluating sex differences in muscle protein metabolism have been unable to discern sexual dimorphism in basal muscle protein turnover rates in young and middle-aged adults. We hypothesized that the anabolic response to nutritional stimuli (i.e., amino acids and insulin) would be greater in young/middle-aged men than women. We therefore measured the rates of muscle protein synthesis (MPS) in 16 healthy individuals [8 men and 8 women, matched for age (mean ± SE: 37.7 ± 1.5 yr) and body mass index (25.2 ± 0.7 kg/m2)] after an overnight fast (plasma insulin 5 µU/ml and plasma phenylalanine 60 µM) and during a hyperinsulinemic-hyperaminoacidemic-euglycemic clamp (plasma insulin 28 µU/ml; plasma phenylalanine 110 µM; plasma glucose 5.4 mM). The rates of MPS were not different between men and women (ANOVA main effect for sex; P = 0.49). During the clamp, the rate of MPS increased by 50% (P = 0.003) with no difference in the increases from basal values between men and women (+0.019 ± 0.004 vs. +0.018 ± 0.010%/h, respectively; P = 0.93). There were also no differences between men and women in the basal concentrations of muscle phosphorylated AktSer473, AktThr308, mTORSer2448, and p70s6kThr389 or in the hyperinsulinemia-hyperaminoacidemia-induced increases in phosphorylation of those signaling elements (P 0.25). We conclude that there are no major differences in the rate of MPS and its intracellular control during basal conditions and during hyperinsulinemia-hyperaminoacidema between young and middle-aged adult men and women.

signal transduction; protein metabolism

[Emma-Leigh]

J Gerontol A Biol Sci Med Sci (2008) 63 (11): 1209-1218.

Adipose Endocrine Function, Insulin-Like Growth Factor-1 Axis, and Exceptional Survival Beyond 100 Years of Age
Yasumichi Arai, Michiyo Takayama, Yasuyuki Gondo, Hiroki Inagaki, Ken Yamamura, Susumu Nakazawa, Toshio Kojima, Yoshinori Ebihara, Kenichirou Shimizu, Yukie Masui, Koji Kitagawa, Toru Takebayashi and Nobuyoshi Hirose
+ Author Affiliations

1Division of Geriatric Medicine, Department of Internal Medicine, and 2Department of Preventive Medicine and Public Health, Keio University School of Medicine, Tokyo, Japan.
3Tokyo Metropolitan Institute of Gerontology, Japan.
4Mizuho Health Insurance Society, Tokyo, Japan.
5Health Care Center, Shoko Chukin Bank, Tokyo, Japan.
6Human Genome Research Group, Genomic Sciences Center, RIKEN, Yokohama, Japan.
7Tohoku Bunka Gakuen University, Miyagi, Japan.
Address correspondence to Yasumichi Arai, MD, PhD, Division of Geriatric Medicine, Keio University School of Medicine, 35, Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: yasumich@sc.itc.keio.ac.jp
Received July 17, 2007.
Accepted December 3, 2007.
Abstract

Background. Observational studies have demonstrated similarities between the underpinning of frailty and biological features of centenarians, suggesting that adaptability to age-related multiple physiological decline may be a core component of successful aging. The aim of this study is to determine whether hormonal pathways potentially involved in energy homeostasis contribute to survival beyond 100 years of age.

Methods. We assessed a total of 252 centenarians (mean [standard deviation (SD)] age, 101.5 (1.8) years, range 100–108 years) using a complete set of biomarkers of adipose endocrine function and the insulin-like growth factor-1 (IGF-1) axis. Conventional risk factors at baseline were also assessed. The participants were followed up for all-cause mortality every 12 months by telephone contact.

Results. During 2253 days of follow-up, 208 centenarians (82.5%) died. The lowest tertile of leptin and the highest tertile of tumor necrosis factor-α were associated with higher mortality risk among centenarians after adjusting for age (per 6-month increase), sex, education, smoking, activities of daily living (ADL), cognitive function, and comorbidities (hazard ratio [HR] 1.6; 95% confidence interval [CI], 1.14–2.35; and HR 1.45; 95% CI, 1.00–2.08, respectively). The lowest tertiles of both IGF-1 and IGF binding protein 3 (IGFBP3) were also associated with increased mortality. The adipose risk score, indicating cumulative effects of adipokine dysregulation, was strongly associated with increased mortality risk; ADL; cognitive function; and levels of albumin, cholinesterase, high-density lipoprotein-cholesterol, C-reactive protein, interleukin 6, and IGF-1 at baseline.

Conclusions. The results suggested that preservation of adipose endocrine function and the IGF-1 axis may be potentially important for maintaining health and function and promoting survival at an extremely old age.

[Emma-Leigh]

Nutrition
Volume 20, Issue 7, Pages 716-727 (July 2004)

Optimizing fat oxidation through exercise and diet

Juul Achten, PhDa, Asker E Jeukendrup, PhDa
Abstract
Interventions aimed at increasing fat metabolism could potentially reduce the symptoms of metabolic diseases such as obesity and type 2 diabetes and may have tremendous clinical relevance. Hence, an understanding of the factors that increase or decrease fat oxidation is important. Exercise intensity and duration are important determinants of fat oxidation. Fat oxidation rates increase from low to moderate intensities and then decrease when the intensity becomes high. Maximal rates of fat oxidation have been shown to be reached at intensities between 59% and 64% of maximum oxygen consumption in trained individuals and between 47% and 52% of maximum oxygen consumption in a large sample of the general population. The mode of exercise can also affect fat oxidation, with fat oxidation being higher during running than cycling. Endurance training induces a multitude of adaptations that result in increased fat oxidation. The duration and intensity of exercise training required to induce changes in fat oxidation is currently unknown. Ingestion of carbohydrate in the hours before or on commencement of exercise reduces the rate of fat oxidation significantly compared with fasted conditions, whereas fasting longer than 6 h optimizes fat oxidation. Fat oxidation rates have been shown to decrease after ingestion of high-fat diets, partly as a result of decreased glycogen stores and partly because of adaptations at the muscle level.

[atomdawgg]

Am J Clin Nutr. 2010 Apr 7. [Epub ahead of print]

Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index.
Jakobsen MU, Dethlefsen C, Joensen AM, Stegger J, Tjønneland A, Schmidt EB, Overvad K.

Department of Clinical Epidemiology Aarhus University Hospital Aalborg Denmark.

Abstract
BACKGROUND: Studies have suggested that replacing saturated fatty acids (SFAs) with carbohydrates is modestly associated with a higher risk of ischemic heart disease, whereas replacing SFAs with polyunsaturated fatty acids is associated with a lower risk of ischemic heart disease. The effect of carbohydrates, however, may depend on the type consumed. OBJECTIVES: By using substitution models, we aimed to investigate the risk of myocardial infarction (MI) associated with a higher energy intake from carbohydrates and a concomitant lower energy intake from SFAs. Carbohydrates with different glycemic index (GI) values were also investigated. DESIGN: Our prospective cohort study included 53,644 women and men free of MI at baseline. RESULTS: During a median of 12 y of follow-up, 1943 incident MI cases occurred. There was a nonsignificant inverse association between substitution of carbohydrates with low-GI values for SFAs and risk of MI [hazard ratio (HR) for MI per 5% increment of energy intake from carbohydrates: 0.88; 95% CI: 0.72, 1.07). In contrast, there was a statistically significant positive association between substitution of carbohydrates with high-GI values for SFAs and risk of MI (HR: 1.33; 95% CI: 1.08, 1.64). There was no association for carbohydrates with medium-GI values (HR: 0.98; 95% CI: 0.80, 1.21). No effect modification by sex was observed. CONCLUSION: This study suggests that replacing SFAs with carbohydrates with low-GI values is associated with a lower risk of MI, whereas replacing SFAs with carbohydrates with high-GI values is associated with a higher risk of MI.

[Emma-Leigh]

Appl Physiol Nutr Metab. 2009 Aug;34(4):632-9.
Does habitual dietary intake influence myofiber hypertrophy in response to resistance training? A cluster analysis.
Thalacker-Mercer AE, Petrella JK, Bamman MM.

UAB Department of Physiology, Birmingham, AL 35294, USA.
Abstract
Although resistance exercise training (RT) is a common intervention to stimulate muscle protein synthesis and increase skeletal muscle mass, the optimal daily protein and total energy intakes sufficient to support RT-mediated muscle growth are as yet unclear. Further, the efficacy of RT varies widely among adults of all ages and whether this is attributable to interindividual differences in nutrition is not known. To determine if self-selected daily intake of macronutrients and specific components of dietary protein and fat are predictive of the magnitude of RT-mediated muscle growth, detailed 4-day dietary records were analyzed on 60 subjects previously clustered (K-means cluster analysis) as non-, modest, and extreme responders (non, n = 16; mod, n = 29; xtr, n = 15), based on the magnitudes of change in vastus lateralis myofiber cross-sectional area following a 16-week, 3-day-per-week, high-intensity RT. Despite the marked contrast between 60% myofiber hypertrophy in xtr and zero growth in non, we found no differences among response clusters in daily intakes of energy (mean +/- SEM: non 102 +/- 8; mod 111 +/- 6; xtr 109 +/- 5 kJ.kg-1.day-1), protein (non 0.97 +/- 0.08; mod 1.07 +/- 0.07; xtr 1.05 +/- 0.06 g.kg-1.day-1), carbohydrate (non 3.02 +/- 0.24; mod 3.18 +/- 0.20; xtr 3.14 +/- 0.17 g.kg-1.day-1), and fat (non 0.95 +/- 0.09; mod 1.05 +/- 0.08; xtr 1.03 +/- 0.08 g.kg-1.day-1), which generally met or exceeded dietary recommendations. There were no cluster differences in intakes of branched chain amino acids known to stimulate muscle protein synthesis. Using the novel K-means clustering approach, we conclude from this preliminary study that protein and energy intakes were sufficient to facilitate modest and extreme muscle growth during RT and intrinsic or extrinsic factors other than nutrient ingestion apparently impaired the anabolic response in nonresponders.

[TheWaffleIron]

I've got a sh*tload. Here's a good start, relevant to the "clean" v. "dirty" debates.

http://www.ncbi.nlm.nih.gov/pubmed/17536194

Ann Nutr Metab. 2007;51(2):163-71. Epub 2007 May 29.

Hormonal responses to a fast-food meal compared with nutritionally comparable meals of different composition.

Bray GA, Most M, Rood J, Redmann S, Smith SR.

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

Abstract

BACKGROUND: Fast food is consumed in large quantities each day. Whether there are differences in the acute metabolic response to these meals as compared to 'healthy' meals with similar composition is unknown. DESIGN: Three-way crossover. METHODS: Six overweight men were given a standard breakfast at 8:00 a.m. on each of 3 occasions, followed by 1 of 3 lunches at noon. The 3 lunches included: (1) a fast-food meal consisting of a burger, French fries and root beer sweetened with high fructose corn syrup; (2) an organic beef meal prepared with organic foods and a root beer containing sucrose, and (3) a turkey meal consisting of a turkey sandwich and granola made with organic foods and an organic orange juice. Glucose, insulin, free fatty acids, ghrelin, leptin, triglycerides, LDL-cholesterol and HDL-cholesterol were measured at 30-min intervals over 6 h. Salivary cortisol was measured after lunch. RESULTS: Total fat, protein and energy content were similar in the 3 meals, but the fatty acid content differed. The fast-food meal had more myristic (C14:0), palmitic (C16:0), stearic (C18:0) and trans fatty acids (C18:1) than the other 2 meals. The pattern of nutrient and hormonal response was similar for a given subject to each of the 3 meals. The only statistically significant acute difference observed was a decrease in the AUC of LDL cholesterol after the organic beef meal relative to that for the other two meals. Other metabolic responses were not different. CONCLUSION: LDL-cholesterol decreased more with the organic beef meal which had lesser amounts of saturated and trans fatty acids than in the fast-food beef meal. Copyright 2007 S. Karger AG, Basel.

http://www.ncbi.nlm.nih.gov/pubmed/19064536

Am J Clin Nutr. 2008 Dec;88(6):1716S-1721S.

Straight talk about high-fructose corn syrup: what it is and what it ain't.

White JS.

White Technical Research, Argenta, IL 62501, USA. white.tech.res@gmail.com

Abstract

High-fructose corn syrup (HFCS) is a fructose-glucose liquid sweetener alternative to sucrose (common table sugar) first introduced to the food and beverage industry in the 1970s. It is not meaningfully different in composition or metabolism from other fructose-glucose sweeteners like sucrose, honey, and fruit juice concentrates. HFCS was widely embraced by food formulators, and its use grew between the mid-1970s and mid-1990s, principally as a replacement for sucrose. This was primarily because of its sweetness comparable with that of sucrose, improved stability and functionality, and ease of use. Although HFCS use today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened world: >90% of the nutritive sweetener used worldwide is sucrose. Here I review the history, composition, availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have been a source of confusion to health professionals and the general public alike. In particular, I evaluate the strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption. I conclude that the HFCS-obesity hypothesis is supported neither in the United States nor worldwide.

[Emma-Leigh]

Am J Clin Nutr. 2010 Apr;91(4):950-7. Epub 2010 Feb 24.
Effects of coffee consumption on subclinical inflammation and other risk factors for type 2 diabetes: a clinical trial.
Kempf K, Herder C, Erlund I, Kolb H, Martin S, Carstensen M, Koenig W, Sundvall J, Bidel S, Kuha S, Jaakko T.

Institute of Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich, Heine University Düsseldorf, Düsseldorf, Germany.
Abstract
BACKGROUND: Coffee consumption is associated with a decreased risk of type 2 diabetes. Suggested mechanisms underlying the association have included attenuation of subclinical inflammation and a reduction in oxidative stress. OBJECTIVE: The aim was to investigate the effects of daily coffee consumption on biomarkers of coffee intake, subclinical inflammation, oxidative stress, glucose, and lipid metabolism. DESIGN: Habitual coffee drinkers (n = 47) refrained for 1 mo from coffee drinking; in the second month they consumed 4 cups of filtered coffee/d and in the third month 8 cups of filtered coffee/d (150 mL/cup). Blood samples were analyzed by gas chromatography-mass spectrometry, bead-based multiplex technology, enzyme-linked immunosorbent assay, or immunonephelometry. RESULTS: Coffee consumption led to an increase in coffee-derived compounds, mainly serum caffeine, chlorogenic acid, and caffeic acid metabolites. Significant changes were also observed for serum concentrations of interleukin-18, 8-isoprostane, and adiponectin (medians: -8%, -16%, and 6%, respectively; consumption of 8 compared with 0 cups coffee/d). Serum concentrations of total cholesterol, HDL cholesterol, and apolipoprotein A-I increased significantly by 12%, 7%, and 4%, respectively, whereas the ratios of LDL to HDL cholesterol and of apolipoprotein B to apolipoprotein A-I decreased significantly by 8% and 9%, respectively (8 compared with 0 cups coffee/d). No changes were seen for markers of glucose metabolism in an oral-glucose-tolerance test. CONCLUSIONS: Coffee consumption appears to have beneficial effects on subclinical inflammation and HDL cholesterol, whereas no changes in glucose metabolism were found in our study. Furthermore, many coffee-derived methylxanthines and caffeic acid metabolites appear to be useful as biomarkers of coffee intake.

PMID: 20181814 [PubMed - indexed for MEDLINE]

[Emma-Leigh]

Mood Food
Chocolate and Depressive Symptoms in a Cross-sectional Analysis

Natalie Rose, MD; Sabrina Koperski, BS; Beatrice A. Golomb, MD, PhD
Arch Intern Med. 2010;170(8):699-703.

Background Much lore but few studies describe a relation of chocolate to mood. We examined the cross-sectional relationship of chocolate consumption with depressed mood in adult men and women.

Methods A sample of 1018 adults (694 men and 324 women) from San Diego, California, without diabetes or known coronary artery disease was studied in a cross-sectional analysis. The 931 subjects who were not using antidepressant medications and provided chocolate consumption information were the focus of the analysis. Mood was assessed using the Center for Epidemiologic Studies Depression Scale (CES-D). Cut points signaling a positive depression screen result (CES-D score, 16) and probable major depression (CES-D score, 22) were used. Chocolate servings per week were provided by 1009 subjects. Chocolate consumption frequency and rate data from the Fred Hutchinson Food Frequency Questionnaire were also available for 839 subjects. Chocolate consumption was compared for those with lower vs higher CES-D scores. In addition, a test of trend was performed.

Results Those screening positive for possible depression (CES-D score 16) had higher chocolate consumption (8.4 servings per month) than those not screening positive (5.4 servings per month) (P = .004); those with still higher CES-D scores (22) had still higher chocolate consumption (11.8 servings per month) (P value for trend, <.01). These associations extended to both men and women. These findings did not appear to be explained by a general increase in fat, carbohydrate, or energy intake.

Conclusion Higher CES-D depression scores were associated with greater chocolate consumption. Whether there is a causal connection, and if so in which direction, is a matter for future prospective study.


^^
mmmmm... chocolate...

[blumnblam]

http://www.sciencenews.org/view/gene...C_then_muscles

Gargling Gatorade could clinch the gold for future Olympians. A new study establishes a neural link between mouth and muscles that slips right past the gut, producing additional power output with nothing more than the promise of an impending nutritional boost.

“What we’ve uncovered is a way in which we can shortcut our sensory circuitry, and to fool our body, maybe, briefly, into thinking the tank is full,” says study coauthor Nicholas Gant of the University of Auckland in New Zealand. The study will appear in an upcoming issue of Brain Research.

Earlier studies had shown that swishing and spitting an energy drink made study subjects sprint or cycle faster than swishing a placebo — even though the sugar never made it to the muscles. This effect could be the brain’s signal to the body that “help is on the way, fuel is in the mouth,” Gant says. But scientists weren’t sure whether there is a neural pathway that goes directly from the taste buds to the muscles, or if it’s all in athletes’ heads.

To find evidence of a mouth-to-muscle pathway, Gant and colleagues had 16 healthy men between the ages of 21 and 36 flex their biceps while electrodes on their arms measured the electrical energy in their muscles.

After wearing out their biceps for 11 minutes, the participants swished and swallowed a bright green Gatorade-like beverage sweetened with an artificial sugar called acesulfame K. In half the trials, the drink also contained a colorless, flavorless carbohydrate called maltodextrin.

Not surprisingly, the men’s muscles perked up in response to carbs. But measurements of their blood sugar at four-minute intervals showed that the response began even before the nutrition entered the men’s systems.

The electrical energy in the muscles of athletes who drank the maltodextrin-containing drink increased by 30 percent, and the maximum amount of force they exerted went up by 2 percent. By contrast, the energy-free drink had no effect on muscle performance; maximum force actually went down by 3 percent as subjects who drank it got more tired.

“We were really surprised by the magnitude of increase in force production,” says Gant, whose research has been used to advise Olympic athletes. “It’s less than a percent of your total output that will decide whether you got the gold. We’re seeing improvements that are far greater than that.”

To see if the trick worked even if the subjects never swallowed and their muscles were fresh, the researchers asked 17 different participants to rinse their mouths with either the carb drink or the placebo. The researchers then measured the electrical energy in the participants’ hand muscles. Swishing the carb drink increased the muscular energy by 9 percent.

“This clearly shows that you change something in the brain which directly affects the muscle,” comments Asker Jeukendrup of the University of Birmingham in England. “It’s quite an important piece of the puzzle.”

To see which part of the brain was responsible, the researchers applied a magnetic jolt to the subjects’ scalps in both experiments to probe activity in the primary motor cortex, a region of the brain associated with planning and executing movements. Surprisingly, the extra electrical boost in the muscles did not come from the motor cortex. The signals may come from a deeper, less consciously controlled part of the brain, Gant suggests.

In addition to helping sprinters and shot-putters improve their game, these results could help develop physical therapy treatments for people who have trouble controlling their muscles, Jeukendrup speculates.

This study supports earlier evidence that the taste receptor for sweetness is different from the part of the mouth that detects carbohydrates. But “whatever that is, that has not been detected yet,” Jeukendrup says. “That’s definitely something that someone should do at some point, try to identify that.”

Cliffs:
-body can think it has had carbs even without swallowing them.

Makes sense to me, for a couple reasons...

[L.1.3]

Cliffs:
-body can think it has had carbs even without swallowing them.

Makes sense to me, for a couple reasons...[/QUOTE]

Very interesting

[Emma-Leigh]

Nutrition & Metabolism 2010, 7:39doi:10.1186/1743-7075-7-39

New Fat Free Mass - Fat Mass Model for use in Physiological Energy Balance Equations
Diana Thomas , Sai Krupa Das , James A Levine , Corby K Martin , Laurel Mayer , Andrew McDougall , Boyd J Strauss and Steven B Heymsfield

Published: 9 May 2010
Abstract (provisional)

Background
The Forbes equation relating fat-free mass (FFM) to fat mass (FM) has been used to predict longitudinal changes in $FFM$ during weight change but has important limitations when paired with a one dimensional energy balance differential equation. Direct use of the Forbes model within a one dimensional energy balance differential equation requires calibration of a translate parameter for the specific population under study. Comparison of translates to a representative sample of the US population indicate that this parameter is a reflection of age, height, race and gender effects.

Results
We developed a class of fourth order polynomial equations relating FFM to FM that consider age, height, race and gender as covariates eliminating the need to calibrate a parameter to baseline subject data while providing meaningful individual estimates of FFM. Moreover, the intercepts of these polynomial equations are nonnegative and are consistent with observations of very low FM measured during a severe ****li famine. The models preserve the predictive power of the Forbes model for changes in body composition when compared to results from several longitudinal weight change studies.

Conclusions
The newly developed FFM-FM models provide new opportunities to compare individuals undergoing weight change to subjects in energy balance, analyze body composition for individual parameters, and predict body composition during weight change when pairing with energy balance differential equations.

[Emma-Leigh]

Nutrition Bulletin
Issue: Volume 35(2), June 2010, p 102–112


The gut, immunoregulation and micro-organisms from man's evolutionary past
Rook, G. A. W.
University College London, London, UK
Correspondence: Professor Graham A. W. Rook, Researcher in Medical Microbiology and Immunology, Department of Infection, Windeyer Institute for Medical Sciences, University College London, 46 Cleveland Street, London W1T 4JF, UK. E-mail: g.rook@ucl.ac.uk


Summary
Man has moved rapidly from the hunter-gatherer environment to the living conditions of the rich industrialised countries. The hygiene hypothesis suggests that the resulting changed and reduced pattern of exposure to certain critical micro-organisms, mostly derived from mud, animals and faeces, has led to disordered regulation of the immune system and, hence, to increases in chronic inflammatory disorders such as allergies, inflammatory bowel diseases and autoimmunity. Epidemiology, backed up by laboratory models, indicates that the relevant organisms are those that have very long associations with the mammalian immune system, traceable back to the Palaeolithic or earlier. Often, these organisms have been present as commensals (notably in the intestinal microbiota), environmental ‘pseudocommensals’, sub-clinical infections or asymptomatic carrier states, and the mammalian immune system is in a state of ‘evolved dependence’ on their continued presence. Several of these ‘Old Friends’, often operating primarily in the gut, act as modulators of dendritic cells and T cells, leading to the establishment of immunoregulatory circuits. Clinical trials are in progress to test living helminths (Trichuris suis and Necator americanus) in allergies, inflammatory bowel disease and multiple sclerosis. We can anticipate rapid increases in the use of these and other organisms or their components in novel types of therapy with applications in several branches of medicine. Probiotics tested in clinical trials targeting chronic inflammatory disorders have so far given unconvincing results, but if strains for these indications are selected on the basis of their ability to induce immunoregulation, and not merely imposed by companies that have intellectual property rights, we can anticipate rapid progress.

[Emma-Leigh]

LOL - >> just for kicks:

Journal of Food Science
Volume 67 Issue 8, Pages 2945 - 2951
Published Online: 20 Jul 2006
© 2010 Institute of Food Technologists®

Heat-induced Changes in Angel Food Cakes Containing Egg-white Protein or Whey Protein Isolate
C.W. Pernell 1 , P.J. Luck 1 , E. AllenFoegeding 1 , C.R. Daubert 1
1 Authors Pernell, Luck, Foegeding, and Daubert are with the Dept. of Food Science, Box 7624, 236 Schaub Hall, North Carolina State Univ., Raleigh, NC 27695. Direct inquiries to author Foegeding (E-mail: allen_foegeding@ncsu.edu)
Paper nr FSR-02-8 of the Journal Series of the Dept. of Food Science, NCSU, Raleigh, NC 27695-7624. Support from the North Carolina Agricultural Research Service and Dairy Management Inc. The use of trade names in this publication does not imply endorsement by the North Carolina Agricultural Research Service of the products named nor criticism of similar ones not mentioned.

ABSTRACT: Angel food cakes made from egg white or whey protein foams were compared. Cakes were evaluated based on final volume, dynamic volume change, and rheological transitions during baking. Cake expansion during baking was a function of protein concentration regardless of protein type. Cakes containing whey proteins had a lower ability to prevent collapse once starch gelatinization started during baking. Heat-treating whey proteins or adding xanthan gum increases cake volume, but not to the extent of egg-white proteins. Cakes containing egg-white proteins became more elastic at 60 to 85 °C than those containing whey proteins, indicating physical differences in the heat-set protein foam network associated with protein type.

MS 20020136 Submitted 2/27/02, Revised 4/11/02, Accepted 7/9/02, Received 7/ 10/02

[Emma-Leigh]

Am J Physiol Endocrinol Metab 298: E449-E466, 2010. First published November 24, 2009; doi:10.1152/ajpendo.00559.2009

Predicting metabolic adaptation, body weight change, and energy intake in humans
Kevin D. Hall
Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland

Submitted 8 September 2009 ; accepted in final form 16 November 2009

Complex interactions between carbohydrate, fat, and protein metabolism underlie the body's remarkable ability to adapt to a variety of diets. But any imbalances between the intake and utilization rates of these macronutrients will result in changes in body weight and composition. Here, I present the first computational model that simulates how diet perturbations result in adaptations of fuel selection and energy expenditure that predict body weight and composition changes in both obese and nonobese men and women. No model parameters were adjusted to fit these data other than the initial conditions for each subject group (e.g., initial body weight and body fat mass). The model provides the first realistic simulations of how diet perturbations result in adaptations of whole body energy expenditure, fuel selection, and various metabolic fluxes that ultimately give rise to body weight change. The validated model was used to estimate free-living energy intake during a long-term weight loss intervention, a variable that has never previously been measured accurately.

mathematical model; energy metabolism; macronutrient metabolism; body composition

Abbreviations: BM, Bone mineral mass in g • BW, Body weight in g • CarbOx, Rate of carbohydrate oxidation in kcal/day • CI, Carbohydrate intake rate in kcal/day • DF, Rate of endogenous lipolysis in g/day • DG, Rate of glycogenolysis in g/day • DNL, Rate of de novo lipogenesis in kcal/day • DP, Rate of proteolysis in g/day • ECF, Extracellular fluid mass in g • ECP, Extracellular protein mass in g • EI, Energy intake in kcal/day • FM, Body fat mass in g • FatOx, Rate of fat oxidation in kcal/day • fC, Carbohydrate oxidation fraction • fF, Fat oxidation fraction • FFM, Fat-free body mass in g • FI, Fat intake rate in kcal/day • fP, Protein oxidation fraction • G, Body glycogen mass in g • G3P, Rate of glycerol 3-phosphate synthesis in kcal/day • GNGF, Rate of gluconeogenesis from glycerol in kcal/day • GNGP, Rate of gluconeogenesis from protein in kcal/day • ICS, Intracellular solid mass in g • ICW, Intracellular water mass in g • KetOx, Rate of ketone oxidation in kcal/day • KTG, Rate of ketogenesis in kcal/day • KUexcr, Rate of ketone excretion in kcal/day • LCM, Lean tissue cell mass in g • Nexcr, Nitrogen excretion rate in g/day • NPRQ, Nonprotein respiratory quotient • P, Intracellular protein mass in g • PAE, Physical activity energy expenditure in kcal/day • PI, Protein intake rate in kcal/day • ProtOx, Rate of protein oxidation in kcal/day • RMR, Resting metabolic rate in kcal/day • RQ, Respiratory quotient • SynthF, Rate of fat synthesis in g/day • SynthG, Rate of glycogen synthesis in g/day • SynthP, Rate of protein synthesis in g/day • T, Adaptive thermogenesis • TEE, Total energy expenditure in kcal/day • TEF, Thermic effect of feeding in kcal/day • TG, Triacylglyceride • CO2, Rate of carbon dioxide production in liters/day • O2, Rate of oxygen consumption in liters/day

[Emma-Leigh]

Am J Clin Nutr 90: 519-526, 2009. First published July 29, 2009; doi:10.3945/ajcn.2009.27834
American Journal of Clinical Nutrition, doi:10.3945/ajcn.2009.27834
Vol. 90, No. 3, 519-526, September 2009

Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet1,2,3
Margriet AB Veldhorst, Margriet S Westerterp-Plantenga and Klaas R Westerterp
1 From the NUTRIM School for Nutrition, Toxicology and Metabolism, Department of Human Biology, Maastricht University Medical Centre, Maastricht, Netherlands, and the Top Institute Food and Nutrition, Wageningen, Netherlands.
2 Supported by the Top Institute Food and Nutrition, Wageningen, Netherlands.
3 Address correspondence to MAB Veldhorst, Maastricht University, Department of Human Biology, PO Box 616, 6200 MD Maastricht, Netherlands. E-mail: m.veldhorst@hb.unimaas.nl.


Background: High-protein diets have been shown to increase energy expenditure (EE).

Objective: The objective was to study whether a high-protein, carbohydrate-free diet (H diet) increases gluconeogenesis and whether this can explain the increase in EE.

Design: Ten healthy men with a mean (±SEM) body mass index (in kg/m2) of 23.0 ± 0.8 and age of 23 ± 1 y received an isoenergetic H diet (H condition; 30%, 0%, and 70% of energy from protein, carbohydrate, and fat, respectively) or a normal-protein diet (N condition; 12%, 55%, and 33% of energy from protein, carbohydrate, and fat, respectively) for 1.5 d according to a randomized crossover design, and EE was measured in a respiration chamber. Endogenous glucose production (EGP) and fractional gluconeogenesis were measured via infusion of [6,6-2H2]glucose and ingestion of 2H2O; absolute gluconeogenesis was calculated by multiplying fractional gluconeogenesis by EGP. Body glycogen stores were lowered at the start of the intervention with an exhaustive glycogen-lowering exercise test.

Results: EGP was lower in the H condition than in the N condition (181 ± 9 compared with 226 ± 9 g/d; P < 0.001), whereas fractional gluconeogenesis was higher (0.95 ± 0.04 compared with 0.64 ± 0.03; P < 0.001) and absolute gluconeogenesis tended to be higher (171 ± 10 compared with 145 ± 10 g/d; P = 0.06) in the H condition than in the N condition. EE (resting metabolic rate) was greater in the H condition than in the N condition (8.46 ± 0.23 compared with 8.12 ± 0.31 MJ/d; P < 0.05). The increase in EE was a function of the increase in gluconeogenesis (EE = 0.007 x gluconeogenesis ***8211; 0.038; r = 0.70, R2 = 0.49, P < 0.05). The contribution of gluconeogenesis to EE was 42%; the energy cost of gluconeogenesis was 33% (95% CI: 16%, 50%).

Conclusions: Forty-two percent of the increase in energy expenditure after the H diet was explained by the increase in gluconeogenesis. The cost of gluconeogenesis was 33% of the energy content of the produced glucose.

[Emma-Leigh]

IUBMB Life. 2010 Jun;62(6):477-9.
Protein causes a glycemic response.
Whelan WJ, Ghanchi H, Ricciardi M.

Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL, USA. wwhelan@miami.edu

Abstract
The glycemic index is used to compare the extent to which the blood glucose level increases following the consumption of foods containing digestible carbohydrate and is considered to be zero, or not measurable, if the food, such as protein, is carbohydrate-free. We have found that after overnight fasting, the consumption of several varieties of meat caused significant increases in blood glucose levels. We consider these possibly to be because of gluconeogenesis from the digested protein. It is a curious feature that in two instances the response was inversely related to the amount of meat consumed, over the range from 26 to 78 g of protein.

PMID: 20503441 [PubMed - in process]

[Emma-Leigh]

just got this. the guy who did it, wj whelan, is a professor from my school. apparently he's known for being somewhat of a fructose alarmist, so know what his agenda is. i haven't gone through the whole thing yet.

^
Yup => you can see his 'general feeling on things' by going through some of his other papers.

http://lib.bioinfo.pl/pmid:20503441
^
although a few have some good info in them....

[tubalard]

Hmm, this is most interesting.

We've known for ever and a day that protein consumption elicits an insulin response (well, ok, those of us who aren't carbo-phobes have known this), so it shouldn't come as a great shock that it also elicits a rise in blood sugar (therefore giving the insulin something to do in terms of energy storage and glycemic regulation).

Still, questions remain. What is the magnitude of the glycemic response per gram of protein versus per gram of carbohydrate (i.e.what is the dose dependance ratio)? Can we provoke hyperinsulinemia and/or insulin resistance by overfeeding with protein as per over-feeding with carbohydrate? If not, why not?

There's clearly a difference in the way our glycemic regulation systems deal with predominantly carbohydrate overfeeds and predominantly protein overfeeds (I emphasise overfeeds since underfeeds tend to produce healthy glycemic control irrespective of macro-nutrient composition). This kind of study makes that difference appear mysterious...I'm watching this space with much interest.

Thanks for posting the article, Emma.

Cheers
Tubs

[Emma-Leigh]

just got this. the guy who did it, wj whelan, is a professor from my school. apparently he's known for being somewhat of a fructose alarmist, so know what his agenda is. i haven't gone through the whole thing yet.

^
also - seems study was: n = 2 [and for one of the test meats - n = 1]. Hmmm.... now that is useful.....!!

BUT =>> puts forward some interesting points:
- AUC varied a LOT depending on the meat consumed
- Substantial amounts of glucose was formed when fasted - up to 50-60% of equivalent amount of ingested glucose
- Only happened when fasted ->> as when the same dose of protein was consumed after a carb (75g glucose) the protein didn't cause a glucaemic response
- Peak blood glucose of glucose: ~ 30 mins
- Peak blood glucose of protein: ~ 30-45 mins
- Inverse dose effect: the smaller the dose of protein - the higher the glucaemic response (that is: 4 oz meat created more blood glucose than 8 oz)
[QUOTE=tubalard;501790251]Hmm, this is most interesting.

We've known for ever and a day that protein consumption elicits an insulin response (well, ok, those of us who aren't carbo-phobes have known this), so it shouldn't come as a great shock that it also elicits a rise in blood sugar (therefore giving the insulin something to do in terms of energy storage and glycemic regulation).

Sort of... but not really.
^ insulin is stimulated by amino acids AND glucose, not just glucose << reason being is that it is part of the process of amino acid uptake into cells (for the anabolic response).
Just that amino acids also release glucagon (where glucose not so much of that effect) - this is such that they don't cause hypoglycaemic.

This 'glycaemic response' of protein is somewhat different >> because if, when fasted, protein is simply taken up and converted into carbs (at a rate of nearly 50-60%) -> it begs the question as to why one simply would not consume a carb.....

Still, questions remain. What is the magnitude of the glycemic response per gram of protein versus per gram of carbohydrate (i.e.what is the dose dependance ratio)? Can we provoke hyperinsulinemia and/or insulin resistance by overfeeding with protein as per over-feeding with carbohydrate? If not, why not?

>> as above -> seems to be... abnormal.
First: 50-60% of ingested protein =>> carbs via gluconeogenesis, and response/ rise in blood glucose is almost as fast as if you ingested carbs.

BUT - grams protein ingested is INVERSE dose response -> 4 oz meat => greater blood glucose response than 8 oz meat (anyone who can suggest a reason? feel free... ? perhaps by a larger insulin release created by the larger dose of protein => leading to a faster uptake of glucose / amino acids without an increase in the rate of gluconeogenesis?)....

[Quikfeet509]

Now I haven't seen the original article (since I've had issues with my school login for medical journals...should be resolved tomorrow) and the BP reductions are quite modest, but I think it is interesting that the BP reduction is even there at all:

http://www.ncbi.nlm.nih.gov/pubmed/20497980

Circulation. 2010 Jun 8;121(22):2398-406. Epub 2010 May 24.

Reducing consumption of sugar-sweetened beverages is associated with reduced blood pressure: a prospective study among United States adults.... See More
Chen L, Caballero B, Mitchell DC, Loria C, Lin PH, Champagne CM, Elmer PJ, Ard JD, Batch BC, Anderson CA, Appel LJ.

Program of Epidemiology, School of Public Health, Louisiana State University Health Science Center, New Orleans, LA 70112, USA. lchen@lsuhsc.edu

Abstract
BACKGROUND: Increased consumption of sugar-sweetened beverages (SSBs) has been associated with an elevated risk of obesity, metabolic syndrome, and type II diabetes mellitus. However, the effects of SSB consumption on blood pressure (BP) are uncertain. The objective of this study was to determine the relationship between changes in SSB consumption and changes in BP among adults. METHODS AND RESULTS: This was a prospective analysis of 810 adults who participated in the PREMIER Study (an 18-month behavioral intervention trial). BP and dietary intake (by two 24-hour recalls) were measured at baseline and at 6 and 18 months. Mixed-effects models were applied to estimate the changes in BP in responding to changes in SSB consumption. At baseline, mean SSB intake was 0.9+/-1.0 servings per day (10.5+/-11.9 fl oz/d), and mean systolic BP/diastolic BP was 134.9+/-9.6/84.8+/-4.2 mm Hg. After potential confounders were controlled for, a reduction in SSB of 1 serving per day was associated with a 1.8-mm Hg (95% confidence interval, 1.2 to 2.4) reduction in systolic BP and 1.1-mm Hg (95% confidence interval, 0.7 to 1.4) reduction in diastolic BP over 18 months. After additional adjustment for weight change over the same period, a reduction in SSB intake was still significantly associated with reductions in systolic and diastolic BPs (P<0.05). Reduced intake of sugars was also significantly associated with reduced BP. No association was found for diet beverage consumption or caffeine intake and BP. These findings suggest that sugars may be the nutrients that contribute to the observed association between SSB and BP. CONCLUSIONS: Reduced consumption of SSB and sugars was significantly associated with reduced BP. Reducing SSB and sugar consumption may be an important dietary strategy to lower BP.

[coals]

"Testosterone levels in healthy men and the relation to
behavioural and physical characteristics: facts and constructs"
http://www.eje-online.org/cgi/reprint/144/3/183

Abstract
This review summarises the correlations between testosterone levels and male physical appearance and behaviour. Methodological shortcomings concerning the measurement of testosterone could limit the value of these findings. In addition, testosterone measured in body fluids represents only one step in the cascade of action from production to biological effect, and could therefore provide only a limited view of the complexity of physiological events. Testosterone levels are influenced by conditions that are partly controlled or initiated by the hormone itself, but also by circumstances beyond hormonal or
individual control. Different kinds of behaviour are not only subject to influence by environment, but also androgens can reinforce the particular kind of conduct and the behavioural impact can wield negative or positive feedback on testosterone secretion. Therefore, both generalisation and individualisation of study results will lead to doubtful conclusions and prejudices. Results of such studies must be viewed with caution, and over-simplification as well as over-interpretation should be avoided.
European Journal of Endocrinology 144 183±197

Too long to post here, found this excellent 2001 journal review describing testosterone levels in healthy men of varying ages and activities that can influence / are influenced by testosterone. I'm sure it's nothing new for most of you here but it was an easy read and i reccomend it. May be repost. Discuss.

[Emma-Leigh]

interesting debate on IGF-1 and requirement for muscle growth:
http://jap.physiology.org/cgi/pdf_extract/108/6/1825

[Emma-Leigh]

and some good info here: http://www.nap.edu/catalog.php?record_id=9620
And here: http://jap.physiology.org/cgi/reprint/106/5/1692

[Emma-Leigh]

Int J Obes (Lond). 2008 Mar;32(3):573-6. Epub 2007 Sep 11.
What is the required energy deficit per unit weight loss?
Hall KD.

Laboratory of Biological Modeling, National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-5621, USA. kevinh@niddk.nih.gov
Abstract
One of the most pervasive weight loss rules is that a cumulative energy deficit of 3500 kcal is required per pound of body weight loss, or equivalently 32.2 MJ kg(-1). Under what conditions is it appropriate to use this rule of thumb and what are the factors that determine the cumulative energy deficit required per unit weight loss? Here, I examine this question using a modification of the classic Forbes equation that predicts the composition of weight loss as a function of the initial body fat and magnitude of weight loss. The resulting model predicts that a larger cumulative energy deficit is required per unit weight loss for people with greater initial body fat-a prediction supported by published weight loss data from obese and lean subjects. This may also explain why men can lose more weight than women for a given energy deficit since women typically have more body fat than men of similar body weight. Furthermore, additional weight loss is predicted to be associated with a lower average cumulative energy deficit since a greater proportion of the weight loss is predicted to result from loss of lean body mass, which has a relatively low energy density in comparison with body fat. The rule of thumb approximately matches the predicted energy density of lost weight in obese subjects with an initial body fat above 30 kg but overestimates the cumulative energy deficit required per unit weight loss for people with lower initial body fat. International Journal of Obesity (2008) 32, 573-576; doi:10.1038/sj.ijo.0803720; published online 11 September 2007.

[Emma-Leigh]

PLoS Comput Biol. 2008 Mar 28;4(3):e1000045.
The dynamics of human body weight change.
Chow CC, Hall KD.

Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America. carsonc@mail.nih.gov
Abstract
An imbalance between energy intake and energy expenditure will lead to a change in body weight (mass) and body composition (fat and lean masses). A quantitative understanding of the processes involved, which currently remains lacking, will be useful in determining the etiology and treatment of obesity and other conditions resulting from prolonged energy imbalance. Here, we show that a mathematical model of the macronutrient flux balances can capture the long-term dynamics of human weight change; all previous models are special cases of this model. We show that the generic dynamic behavior of body composition for a clamped diet can be divided into two classes. In the first class, the body composition and mass are determined uniquely. In the second class, the body composition can exist at an infinite number of possible states. Surprisingly, perturbations of dietary energy intake or energy expenditure can give identical responses in both model classes, and existing data are insufficient to distinguish between these two possibilities. Nevertheless, this distinction has important implications for the efficacy of clinical interventions that alter body composition and mass.

[isdatzo]

For years, BB-forums have discussed the possible negative effects of egg consumption on cholesterol and risk of heart disease. Until now, no systematic review was published on the direct relation between egg consumption and CVD. So I created one myself:

BACKGROUND: Consumption of dietary cholesterol from eggs has shown to increase the ratio of total to HDL cholesterol in humans, which has been suggested to increase the risk of CHD (a). However, until now no systematic review has been published about the direct effects between egg consumption and CHD/CVD.
OBJECTIVES:
-To review all prospective studies which published information about eggs in relationship with total cardiovascular disease, heart disease, or stroke.
-To define the amount of consumption found to be related with possible effects on these diseases.
-To define possible effect modification by confounders.
DATA SOURCE: The Pubmed database was searched (No start date - May 25th, 2010) for relevant articles using the keywords "dietary cholesterol, dietary fat, egg, or eggs" combined with "prospective, cohort, follow-up, or longitudinal". The exact search term is described Here.
Prospective studies published in the English language were included. Reference lists were searched for additional articles.
RESULTS: 23 articles were found which provided information about 19 different cohorts. Of these, 0 articles were excluded.
Disease risk.
-2 cohorts provided information about total CVD risk. Suggestive evidence was found for an increased CVD risk of egg consumption among subjects with pre-existing type 2 diabetes.
-10 cohorts provided information about CHD risk, including 5,678+ cases. No evidence was found for an association with any level of egg consumption. However, suggestive evidence was found for an increased CHD risk of high egg consumption among subjects with pre-existing type 2 diabetes.
-2 cohorts provided information about heart failure, including 2,224 cases. Suggestive evidence was found for an increased heart failure risk of high egg consumption.
-4 cohorts provided information about stroke risk, including 2,818 cases. No evidence was found for an association with any level of egg consumption.
Mortality risk.
-No data was found about the relation with total CVD mortality.
-8 cohorts provided information about CHD mortality, including 3,757+ cases. No evidence was found for an association with any level of egg consumption.
-4 cohorts provided information about stroke mortality, including 3,978 cases. Inconclusive evidence was found for an association.
CONCLUSION: No evidence was found for an overall association between any level of egg consumption and total CVD risk, CHD risk, stroke risk, CHD mortality, and stroke mortality. However, suggestive evidence was found for an increased heart failure risk of high egg consumption, and suggestive evidence was found for an increased total CVD- and CHD risk of high egg consumption (≥ 6-7 eggs/week) among subjects with type 2 diabetes.
Any increased risks were practically restricted to findings from Western cohorts, and any protective effects were practically restricted to findings from Asian cohorts. No other effect modification was found by any variables, including baseline cholesterol levels and hypertension.
LIMITATIONS: No evidence was found for an overall association between any level of egg consumption and any CVD end point, except for a possible association with the condition called heart failure. But since the amount of evidence is limited, and no results from cohorts of very large size were included, the possibility of an effect on CVD among specific subgroups of the population can not be excluded. Current evidence shows high egg consumption may increase both risk of CVD/CHD and risk of all-cause mortality among subjects with type 2 diabetes (b).

References:
a) Weggemans RM. Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis. Am J Clin Nutr. 2001 May;73(5):885-91. http://www.ajcn.org/cgi/content/full/73/5/885
b) Hoenselaar R. Eggs and mortality from all causes. Canceranddiet.nl June 28. 2010. http://canceranddiet.nl/survival-mortality/eggs.html

Source: Hoenselaar R. Eggs and Cardiovascular disease. 30 juni 2010. Canceranddiet.nl. http://canceranddiet.nl/cardiovascul...ease/eggs.html

[thegymbum]

The abstract...

Background
Alfa-Hydroxy-isocaproic acid (HICA) is an end product of leucine metabolism in human tissues such as muscle and connective tissue. According to the clinical and experimental studies, HICA can be considered as an anti-catabolic substance. The present study investigated the effects of HICA supplementation on body composition, delayed onset of muscle soreness (DOMS) and physical performance of athletes during a training period.

Methods
Fifteen healthy male soccer players (age 22.1+/-3.9 yr) volunteered for the 4-week double-blind study during an intensive training period. The subjects in the group HICA (n = 8) received 583 mg of sodium salt of HICA (corresponding 500 mg of HICA) mixed with liquid three times a day for 4 weeks, and those in the group PLACEBO (n = 7) received 650 mg of maltodextrin mixed with liquid three times a day for the same period. According to a weekly training schedule, they practiced soccer 3 - 4 times a week, had strength training 1 - 2 times a week, and had one soccer game during the study. The subjects were required to keep diaries on training, nutrition, and symptoms of DOMS. Body composition was evaluated with a dual-energy X-ray absorptiometry (DXA) before and after the 4-week period. Muscle strength and running velocity were measured with field tests.

Results
As compared to placebo, the HICA supplementation increased significantly body weight (p < 0.005) and whole lean body mass (p < 0.05) while fat mass remained constant. The lean body mass of lower extremities increased by 400 g in HICA but decreased by 150 g in PLACEBO during the study. This difference between the groups was significant (p < 0.01). The HICA supplementation decreased the whole body DOMS symptoms in the 4th week of the treatment (p < 0.05) when compared to placebo. Muscle strength and running velocity did not differ between the groups.

Conclusion
Already a 4-week HICA supplementation of 1.5 g a day leads to small increases in muscle mass during an intensive training period in soccer athletes.

Wonder if this stuff will become commercially available? Sounds like it might not be bad stuff for bulking

[coals]

The abstract...


Wonder if this stuff will become commercially available? Sounds like it might not be bad stuff for bulking

The question is how does this compare with Normal Leucine / BCAA Supplementation? Would supplementing with the end product change anything vs supplementing with the raw materials? If the answer is no i can't see this being useful.