View Full Version : Random Reading....
mc4_a
04-24-2009, 08:09 PM
Very interesting stuff:
http://www.jci.org/articles/view/37385
"In general, insulin sensitivity and glucose tolerance were not affected by the consumption of glucose but were decreased during the consumption of fructose (Table 5). Fasting glucose concentrations decreased in subjects consuming glucose but increased in subjects consuming fructose. Fasting insulin concentrations were unchanged during glucose consumption but were increased during consumption of fructose beverages."
"...both total abdominal fat and VAT volume were significantly increased in subjects consuming fructose"
Worth the read.
willldabeast
05-02-2009, 01:13 PM
"fasting participants" is all i need to read
in10city
05-02-2009, 01:28 PM
Very interesting stuff:
http://www.jci.org/articles/view/37385
"In general, insulin sensitivity and glucose tolerance were not affected by the consumption of glucose but were decreased during the consumption of fructose (Table 5). Fasting glucose concentrations decreased in subjects consuming glucose but increased in subjects consuming fructose. Fasting insulin concentrations were unchanged during glucose consumption but were increased during consumption of fructose beverages."
"...both total abdominal fat and VAT volume were significantly increased in subjects consuming fructose"
Worth the read.
So is not taking the results out of context from the study.
There is nothing shocking about what would happen when you take obese subjects eating god knows how much and pump them full of an impractical amount of fructose - 25% of their caloric intake was fructose - about 150 grams worth.
mc4_a
05-02-2009, 03:35 PM
So is not taking the results out of context from the study.
There is nothing shocking about what would happen when you take obese subjects eating god knows how much and pump them full of an impractical amount of fructose - 25% of their caloric intake was fructose - about 150 grams worth.
Right, the interesting point here is that the reaction between fructose and glucose was different.
EmperorRyker
05-03-2009, 12:34 AM
"fasting participants" is all i need to read
What, where did you see that? I haven't read the whole thing, but from what I've gathered, only the blood tests were taken in a fasted state, which I think is a pretty common practice.
alan aragon
05-03-2009, 12:40 AM
Very interesting stuff:
http://www.jci.org/articles/view/37385
"In general, insulin sensitivity and glucose tolerance were not affected by the consumption of glucose but were decreased during the consumption of fructose (Table 5). Fasting glucose concentrations decreased in subjects consuming glucose but increased in subjects consuming fructose. Fasting insulin concentrations were unchanged during glucose consumption but were increased during consumption of fructose beverages."
"...both total abdominal fat and VAT volume were significantly increased in subjects consuming fructose"
Worth the read. Let's say some guy likes to play 3 games of basketball per week. Let's say some other guy likes to do a 60-minute nonstop succession of jumps off off his rooftop 3x per week... Which guy stands a greater chance of hurting himself?
mc4_a
05-04-2009, 11:40 AM
Let's say some guy likes to play 3 games of basketball per week. Let's say some other guy likes to do a 60-minute nonstop succession of jumps off off his rooftop 3x per week... Which guy stands a greater chance of hurting himself?
I'm not sure I understand your point, Yoda.
wobemaster
05-05-2009, 12:00 AM
Here's a far better and far more realistic study:
Dietary Fructose and Glucose Differentially Affect Lipid and Glucose Homeostasis.
Schaefer EJ, Gleason JA, Dansinger ML.
Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Cardiovascular Research Laboratory, Friedman School of Nutrition Science and Policy at Tufts University, Tufts University School of Medicine, Boston, MA 02111.
Absorbed glucose and fructose differ in that glucose largely escapes first-pass removal by the liver, whereas fructose does not, resulting in different metabolic effects of these 2 monosaccharides. In short-term controlled feeding studies, dietary fructose significantly increases postprandial triglyceride (TG) levels and has little effect on serum glucose concentrations, whereas dietary glucose has the opposite effects. When dietary glucose and fructose have been directly compared at approximately 20-25% of energy over a 4- to 6-wk period, dietary fructose caused significant increases in fasting TG and LDL cholesterol concentrations, whereas dietary glucose did not, but dietary glucose did increase serum glucose and insulin concentrations in the postprandial state whereas dietary fructose did not. When fructose at 30-60 g ( approximately 4-12% of energy) was added to the diet in the free-living state, there were no significant effects on lipid or glucose biomarkers. Sucrose and high-fructose corn syrup (HFCS) contain approximately equal amounts of fructose and glucose and no metabolic differences between them have been noted. Controlled feeding studies at more physiologic dietary intakes of fructose and glucose need to be conducted. In our view, to decrease the current high prevalence of obesity, dyslipidemia, insulin resistance, and diabetes, the focus should be on restricting the intake of excess energy, sucrose, HFCS, and animal and trans fats and increasing exercise and the intake of vegetables, vegetable oils, fish, fruit, whole grains, and fiber.
alan aragon
05-05-2009, 09:53 AM
I'm not sure I understand your point, Yoda.
Let's imagine a girl named Glucy beats her forehead against her bedroom wall for 3 hrs a day. Her friend Frucy beats her forehead against her concrete driveway for 3 hrs a day. Both aren't wearing protective gear.
Now the question: does the fact that Frucy is worse off than Glucy have any real-world application, or is it a laughably far-fetched scenario with no relevance to us?
Please answer this question to the best of your ability, thanks.
Ryanmcd
05-05-2009, 09:58 AM
Let's imagine a girl named Glucy beats her head against her forehead against her bedroom wall for 3 hrs a day. Her friend Frucy beats her forehead against her concrete driveway for 3 hrs a day. Both aren't wearing protective gear.
Now the question: does the fact that Frucy is worse off than Glucy have any real-world application, or is it a laughably far-fetched scenario with no relevance to us?
Please answer this question to the best of your ability, thanks.
My guess is Frucy is going to be much worse off because concrete is harder then a wall, that is unless she gets lucky and hits a stud. But ya I get the points in this here post ;)
P.S. Tuna eggs chicken all day everyday.
mc4_a
05-06-2009, 08:23 PM
Let's imagine a girl named Glucy beats her forehead against her bedroom wall for 3 hrs a day. Her friend Frucy beats her forehead against her concrete driveway for 3 hrs a day. Both aren't wearing protective gear.
Now the question: does the fact that Frucy is worse off than Glucy have any real-world application, or is it a laughably far-fetched scenario with no relevance to us?
Please answer this question to the best of your ability, thanks.
Condescending...is that necessary? Perhaps if you made yourself clear instead of trying to come up with colorful idioms you wouldn't have to repeat yourself.
I think it's is important for people that struggle with problem areas like belly fat. If fructose is a factor there, every little bit counts. Unless you're on a total low carb / no carb diet, it is a factor and may effect how you pick your carb sources. Considering how obsessive people get out G load and the GI index, I hardly see how interest in this study so distasteful to you. The regular caveats about sample size and the rest apply...
Own3r
05-07-2009, 04:32 AM
Oh damn it... so fruits are bad again?
*Runs to throw out his 10lb costco apple bag*
Feels gooood.
factotum
05-07-2009, 10:55 AM
Oh damn it... so fruits are bad again?
*Runs to throw out his 10lb costco apple bag*
Feels gooood.
Fruits are fine. While they do contain fructose it is in negligible amounts. Eating a piece of fruit preworkout is fine. Eating 40 per day may be a different story.
Own3r
05-07-2009, 11:13 AM
Fruits are fine. While they do contain fructose it is in negligible amounts. Eating a piece of fruit preworkout is fine. Eating 40 per day may be a different story.
Fruits cause teh fat gainz and the distruction of my ripped fibraz.
alan aragon
05-07-2009, 04:42 PM
Condescending...is that necessary? Perhaps if you made yourself clear instead of trying to come up with colorful idioms you wouldn't have to repeat yourself.
I think it's is important for people that struggle with problem areas like belly fat. If fructose is a factor there, every little bit counts. Unless you're on a total low carb / no carb diet, it is a factor and may effect how you pick your carb sources. Considering how obsessive people get out G load and the GI index, I hardly see how interest in this study so distasteful to you. The regular caveats about sample size and the rest apply...1) You failed to answer my question. I'm not being condescending, I'm teaching Socratically. Now, if you want to learn, you can follow my line of questioning, which was prompted by you calling me Yoda & claiming that you didn't understand my response.
2) If you feel that "every little bit counts" tell me how you would apply the findings of this study to your carb choices. Then, tie in your response to the original question I asked you.
wobemaster
05-08-2009, 01:18 AM
If fructose is a factor there, every little bit counts. Unless you're on a total low carb / no carb diet, it is a factor and may effect how you pick your carb sources
I think you missed the study i posted, so ill pick out the key bit for you:
"When fructose at 30-60 g ( approximately 4-12% of energy) was added to the diet in the free-living state, there were no significant effects on lipid or glucose biomarkers."
so when you eat sane amounts, it doesnt adversely effect anything
Emma-Leigh
09-12-2009, 02:18 AM
As above....^^
Simply a thread to post any links to articles of interest you feel like sharing.... :)
Emma-Leigh
09-12-2009, 02:26 AM
http://www.ncbi.nlm.nih.gov/pubmed/17356526
Int J Obes (Lond). 2007 Sep;31(9):1378-83. Epub 2007 Mar 13. Links
How adaptations of substrate utilization regulate body composition.
Hall KD, Bain HL, Chow CC.
Laboratory of Biological Modeling, National Institute of Diabetes & Digestive & Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. kevinh@niddk.nih.gov
OBJECTIVE: To elucidate the mathematical relationship between longitudinal changes of body composition and the adaptations of substrate utilization required to produce those changes. DESIGN: We developed a simple mathematical model of macronutrient balance. By using an empirical relationship describing lean body mass as a function of fat mass, we derived a mathematical expression for how substrate utilization adapts to changes of diet, energy expenditure and body fat such that energy imbalances produced the required changes of body composition. RESULTS: The general properties of our model implied that short-term changes of dietary fat alone had little impact on either fat or non-fat oxidation rates, in agreement with indirect calorimetry data. In contrast, changes of non-fat intake caused robust adaptations of both fat and non-fat oxidation rates. Without fitting any model parameters, the predicted body composition changes and oxidation rates agreed with experimental studies of overfeeding and underfeeding when the measured food intake, energy expenditure and initial body composition were used as model inputs. CONCLUSION: This is the first report to define the quantitative connection between longitudinal changes of body composition and the required relationship between substrate utilization, diet, energy expenditure and body fat mass. The mathematical model predictions are in good agreement with experimental data and provide the basis for future study of how changes of substrate utilization impact body composition regulation.
PMID: 17356526 [PubMed - indexed for MEDLINE]
Emma-Leigh
09-12-2009, 02:29 AM
http://www.ncbi.nlm.nih.gov/pubmed/19501861
Metabolism. 2009 Sep;58(9):1320-8. Epub 2009 Jun 18. Links
Individual responsiveness to exercise-induced fat loss is associated with change in resting substrate utilization.
Barwell ND, Malkova D, Leggate M, Gill JM.
Integrative and Systems Biology, Faculty of Biomedical and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, United Kingdom. j.gill@bio.gla.ac.uk
Fat loss in response to exercise training varies between individuals, even when differences in compliance to the exercise program are accounted for. The purpose of this study was to investigate whether individual variation in change in fasting respiratory quotient (RQ) after exercise training contributes to this interindividual variability. Fifty-five premenopausal women participated in a 7-week endurance-type exercise training program; and fitness, body composition, and resting substrate utilization and metabolic rate in the fasted state were assessed at baseline and postintervention. Total net energy expenditure of the exercise intervention (exEE) was determined from heart rate obtained in all exercise sessions and individualized calibration of the heart rate vs oxygen uptake relationship. Dietary intake and physical activity (by constant heart rate monitoring) were assessed at baseline and during the final week of the intervention. Mean change in fat mass for the group was -0.97 kg (range, +2.1 to -5.3 kg). The strongest correlate of change in fat mass was exEE (r = 0.60, P < .0005). Change in fasting RQ correlated significantly (r = -0.26, P = .05) with the residual for change in fat mass after adjusting for the effects of both exEE and change in energy intake, explaining 7% of the variance. In multiple regression analysis, exEE (P < .0005) and change in fasting RQ (P = .02) were the only statistically significant independent predictors of change in fat mass, together explaining 40.2% of the variance. Thus, fat loss in response to exercise training depends not only on exercise energy expenditure but also on exercise training-induced changes in RQ at rest. This suggests that development of strategies to maximize the change in resting fat oxidation in response to an exercise training program may help individuals to maximize exercise-induced fat loss.
PMID: 19501861 [PubMed - indexed for MEDLINE]
Emma-Leigh
09-12-2009, 02:31 AM
http://www.ncbi.nlm.nih.gov/pubmed/18840293
Dyn Med. 2008 Oct 7;7:16. Links
Modeling transitions in body composition: the approach to steady state for anthropometric measures and physiological functions in the Minnesota human starvation study.
Hargrove JL, Heinz G, Heinz O.
Department of Foods and Nutrition, University of Georgia, Dawson Hall, Athens, GA, USA 30602. jhargrov@fcs.uga.edu.
ABSTRACT: BACKGROUND: This study evaluated whether the changes in several anthropometric and functional measures during caloric restriction combined with walking and treadmill exercise would fit a simple model of approach to steady state (a plateau) that can be solved using spreadsheet software (Microsoft Excel(R)). We hypothesized that transitions in waist girth and several body compartments would fit a simple exponential model that approaches a stable steady-state. METHODS: The model (an equation) was applied to outcomes reported in the Minnesota starvation experiment using Microsoft Excel's Solver(R) function to derive rate parameters (k) and projected steady state values. However, data for most end-points were available only at t = 0, 12 and 24 weeks of caloric restriction. Therefore, we derived 2 new equations that enable model solutions to be calculated from 3 equally spaced data points. RESULTS: For the group of male subjects in the Minnesota study, body mass declined with a first order rate constant of about 0.079 wk-1. The fractional rate of loss of fat free mass, which includes components that remained almost constant during starvation, was 0.064 wk-1, compared to a rate of loss of fat mass of 0.103 wk-1. The rate of loss of abdominal fat, as exemplified by the change in the waist girth, was 0.213 wk-1.On average, 0.77 kg was lost per cm of waist girth. Other girths showed rates of loss between 0.085 and 0.131 wk-1. Resting energy expenditure (REE) declined at 0.131 wk-1. Changes in heart volume, hand strength, work capacity and N excretion showed rates of loss in the same range. The group of 32 subjects was close to steady state or had already reached steady state for the variables under consideration at the end of semi-starvation. CONCLUSION: When energy intake is changed to new, relatively constant levels, while physical activity is maintained, changes in several anthropometric and physiological measures can be modeled as an exponential approach to steady state using software that is widely available. The 3 point method for parameter estimation provides a criterion for testing whether change in a variable can be usefully modelled with exponential kinetics within the time range for which data are available.
PMID: 18840293 [PubMed - in process]
Emma-Leigh
09-12-2009, 02:32 AM
http://www.ncbi.nlm.nih.gov/pubmed/18369435
PLoS Comput Biol. 2008 Mar 28;4(3):e1000045. Links
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
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.
PMID: 18369435 [PubMed - indexed for MEDLINE]
Emma-Leigh
09-12-2009, 02:33 AM
http://www.ncbi.nlm.nih.gov/pubmed/19386028
Nutr Rev. 2009 May;67(5):249-54. Links
The energy balance equation: looking back and looking forward are two very different views.
Schoeller DA.
Department of Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA. dschoell@nutrisci.wisc.edu
The energy balance equation has served as an important tool for the study of bioenergetics. It is based on one of the most fundamental properties of thermodynamics and has been invaluable in understanding the interactions of energy intake, energy expenditure, and body composition. Recently, however, the obesity epidemic has extended the use of the equation to the creation of public health messages for preventing or even reversing secular trends in body mass index. This usage often fails to consider how changes in any one term of the equation can lead to accommodations in one or both of the other two terms. It is concluded that research and public health messages should not simply consider how interventions affect just energy expenditure or energy intake, but rather how they affect the balance or gap between energy intake and expenditure.
Emma-Leigh
09-12-2009, 02:33 AM
http://www.ncbi.nlm.nih.gov/pubmed/18842775
Am J Clin Nutr. 2008 Oct;88(4):906-12. Links
Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight.
Rosenbaum M, Hirsch J, Gallagher DA, Leibel RL.
Columbia University College of Physicians & Surgeons, New York Presbyterian Medical Center, New York, NY 10032, USA. mr475@columbia.edu
BACKGROUND: After weight loss, total energy expenditure -- in particular, energy expenditure at low levels of physical activity -- is lower than predicted by actual changes in body weight and composition. An important clinical issue is whether this reduction, which predisposes to weight regain, persists over time. OBJECTIVE: We aimed to determine whether this disproportionate reduction in energy expenditure persists in persons who have maintained a body-weight reduction of > or =10% for >1 y. DESIGN: Seven trios of sex- and weight-matched subjects were studied in an in-patient setting while receiving a weight-maintaining liquid formula diet of identical composition. Each trio consisted of a subject at usual weight (Wt(initial)), a subject maintaining a weight reduction of > or =10% after recent (5-8 wk) completion of weight loss (Wt(loss-recent)), and a subject who had maintained a documented reduction in body weight of >10% for >1 y (Wt(loss-sustained)). Twenty-four-hour total energy expenditure (TEE) was assessed by precise titration of fed calories of a liquid formula diet necessary to maintain body weight. Resting energy expenditure (REE) and the thermic effect of feeding (TEF) were measured by indirect calorimetry. Nonresting energy expenditure (NREE) was calculated as NREE = TEE - (REE +TEF). RESULTS: TEE, NREE, and (to a lesser extent) REE were significantly lower in the Wt(loss-sustained) and Wt(loss-recent) groups than in the Wt(initial) group. Differences from the Wt(initial) group in energy expenditure were qualitatively and quantitatively similar after recent and sustained weight loss. CONCLUSION: Declines in energy expenditure favoring the regain of lost weight persist well beyond the period of dynamic weight loss.
PMID: 18842775 [PubMed - indexed for MEDLINE]
Emma-Leigh
09-12-2009, 02:34 AM
http://www.ncbi.nlm.nih.gov/pubmed/19253879
Rev Prat. 2009 Jan 20;59(1):41-7.Links
[Energy expenditure. How can they be measured?]
[Article in French]
Rigaud D.
CHU Dijon, h?pital du Bocage, service endocrinologie-nutrition, 21079 Dijon Cedex, France. daniel.rigaud@chu-dijon.fr
Body weight is dependent on the mass of the body and on the fat-free mass. In order to accomplish its mechanical and biochemical functions, the Krebs cycle is activated and generates ATP formation. From ATP, ADP is generated, releasing energy. Total energy expenditure (EE) includes: resting EE, diet-induced thermogenesis, activity-based EE and EE from thermoregulation. They represent 65%, 15%, 20% and 2% of total EE in sedentary human being. The subjects who will being overweight have, as a mean, decreased REE, DIT, PAEE and EETR. At the opposite, the thin subjects have elevated REE, DIT, PAEE and may be EETR. When an obese people is slimming, REE, DIT, PAEE and EETR decrease. When a thin people is gaining weight, REE, DIT, PAEE and EETR increase. This adaptative phenomenon explains why change in body weight and body masses are not linear.
Emma-Leigh
09-12-2009, 02:36 AM
http://www.ncbi.nlm.nih.gov/pubmed/12199298
Nutr Rev. 2002 Aug;60(8):223-33. Links
The thermic effect of food and obesity: discrepant results and methodological variations.
Granata GP, Brandon LJ.
Department of Human Performance and Health Promotion, University of New Orleans, LA 70148, USA.
Studies have yielded discrepant results concerning whether the thermic effect of food (TEF) is reduced in obesity. Methodological variations among published studies make understanding the discrepant results very difficult. Although methodological differences are often noted as contributing to the discrepant results, little work has been done to address these differences and standardize experimental protocols. This paper reviews 50 studies that have investigated TEF in obesity and focuses on factors related to experimental protocol and subject control that reportedly affect measurements of resting energy expenditure, postprandial energy expenditure, and the calculation of TEF.
PMID: 12199298 [PubMed - indexed for MEDLINE]
Emma-Leigh
09-12-2009, 02:37 AM
http://www.ncbi.nlm.nih.gov/pubmed/16166564
Arterioscler Thromb Vasc Biol. 2005 Dec;25(12):2451-62. Epub 2005 Sep 15. Links
Fast food, central nervous system insulin resistance, and obesity.
Isganaitis E, Lustig RH.
Department of Pediatrics, University of California, San Francisco, CA 94143-0434, USA.
Rates of obesity and insulin resistance have climbed sharply over the past 30 years. These epidemics are temporally related to a dramatic rise in consumption of fast food; until recently, it was not known whether the fast food was driving the obesity, or vice versa. We review the unique properties of fast food that make it the ideal obesigenic foodstuff, and elucidate the mechanisms by which fast food intake contributes to obesity, emphasizing its effects on energy metabolism and on the central regulation of appetite. After examining the epidemiology of fast food consumption, obesity, and insulin resistance, we review insulin's role in the central nervous system's (CNS) regulation of energy balance, and demonstrate the role of CNS insulin resistance as a cause of leptin resistance and in the promotion of the pleasurable or "hedonic" responses to food. Finally, we analyze the characteristics of fast food, including high-energy density, high fat, high fructose, low fiber, and low dairy intake, which favor the development of CNS insulin resistance and obesity.
Emma-Leigh
09-12-2009, 02:38 AM
http://www.ncbi.nlm.nih.gov/pubmed/17451048
Ideggyogy Sz. 2007 Mar 30;60(3-4):97-108.Links
Brain insulin signalling in the regulation of energy balance and peripheral metabolism.
Diamant M.
Department of Endocrinology, VU University Medical Center, PO BOX 7057, 1007 MB Amsterdam, The Netherlands. m.diamant@vumc.nl
The unparalleled global rates of obesity and type 2 diabetes, together with the associated cardiovascular morbidity and mortality, are referred to as the "diabesity pandemic". Changes in lifestyle occurring worldwide, including the increased consumption of high-caloric foods and reduced exercise, are regarded as the main causal factors. Central obesity and insulin resistance have emerged as important linking components. Understanding the aetiology of the cluster of pathologies that leads to the increased risk is instrumental in the development of preventive and therapeutic strategies. Historically, skeletal muscle, adipose tissue and liver were regarded as key insulin target organs involved in insulin-mediated regulation of peripheral carbohydrate, lipid and protein metabolism. The consequences of impaired insulin action in these organs were deemed to explain the functional and structural abnormalities associated with insulin resistance. The discovery of insulin receptors in the central nervous system, the detection of insulin in the cerebrospinal fluid after peripheral insulin administration and the well-documented effects of intracerebroventricularly injected insulin on energy homeostasis, have identified the brain as an important target for insulin action. In addition to its critical role as a peripheral signal integrating the complex network of hypothalamic neuropeptides and neurotransmitters that influence parameters of energy balance, central nervous insulin signalling is also implicated in the regulation of peripheral glucose metabolism. This review summarizes the evidence of insulin action in the brain as part of the multifaceted circuit involved in the central regulation of energy and glucose homeostasis, and discuss the role of impaired central nervous insulin signalling as a pathogenic factor in the obesity and type 2 diabetes epidemic.
PMID: 17451048 [PubMed - indexed for MEDLINE]
dimasso69
09-12-2009, 05:09 AM
Effects of severe protein restriction with ketoanalogues in advanced renal failure.Malvy D, Maingourd C, Pengloan J, Bagros P, Nivet H.
Centre Ren? Labusqui?re and INSERM U.330, Universit? Victor Segalen Bordeaux 2, France.
OBJECTIVE: To compare a severe protein restriction diet supplemented with ketoanalogues to a moderate protein restriction diet in order to limit glomerular filtration rate (GFR) decrease in an advanced renal insufficiency stage. DESIGN: Prospective randomised study conducted to compare a severe protein restriction diet (0.30 g/kg/day) supplemented with a preparation of ketoanalogues, hydroxyanalogues of aminoacids and aminoacids (Group A) to a moderate protein restriction diet (0.65 g/kg/day) (Group B). PATIENTS: 50 uremic patients included (25 in each group) with GFR is <20 mL/min/1.73m2. RESULTS: There were no statistically significant differences between the two dietary regimens for the renal survival. But uremia decreased significantly in Group A (22.7+/-5.2 to 18.5+/-6.7 mmol/L) and increased in Group B (26.8+/-9.0 to 34.9+/-9.9 mmol/L). Calcemia increased in Group A from 2.28+/-0.18 to 2.42+/-0.17 mmol/L, p<0.01 with a stable phosphoremia while calcemia decreased in Group B (2.33+/-0.18 to 2.25+/-0.17 mmol/L, p<0.05). At the end of the study, Group A was different from Group B for calcemia (2.42+/-0.17 vs. 2.25+/-0.17 mmol/L, p<0.01), phosphoremia (1.39+/-0.30 vs. 1.80+/-0.65 mmol/L, p<0.02), alkaline phosphatase (61.42+/-22.93 vs. 78.8+/-27.0, p<0.05) and parathormone plasma levels (2.71+/-1.55 vs. 5.91+/-1.41 ng/mL, p<0.001). COMMENTS: Compared to a moderate protein restriction (0.65 g/kg/day), a severe protein restriction (0.3 g/kg/day) supplemented by ketoanologues does not limit GFR decrease when GFR is below 20 mL/min/1.73m2, but improves phosphocalcic plasma parameters.
http://www.ncbi.nlm.nih.gov/pubmed/10511331?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Plasma urea appearance rate is lower when children with kwashiorkor and infection are fed egg white-tryptophan rather than milk protein.Manary MJ, Yarasheski KE, Hart CA, Broadhead RL.
Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, USA.
In kwashiorkor, there is less endogenous proteolysis in response to acute infection than in a well-nourished state. Thus the amino acid composition of dietary protein may be more important in facilitating the acute phase response in kwashiorkor. This study tested the hypothesis that during the treatment of kwashiorkor with infection, there is a lower rate of urea appearance when the dietary intake of amino acids more closely resembles the amino acid composition of acute phase proteins. Thirty children in Malawi with kwashiorkor and acute infection were fed isoenergetic, isonitrogenous meals containing either egg white-tryptophan or milk as a protein source. After 24 h, the rates of urea appearance and whole-body protein breakdown and synthesis were measured with the use of 1-13C-leucine and 15N2-urea tracers. Plasma concentrations of seven acute phase proteins, interleukin 6 and tumor necrosis factor-alpha were measured on admission, and at 24 and 48 h. The 16 children who received egg white-tryptophan had lower rates of urea appearance than those who received milk [57+/-30 vs. 87+/-36 micromol/(kg x h), mean +/- SD, P<0.02]. No significant differences were found in the rates of whole-body protein turnover or in the concentration of any of the acute phase proteins or cytokines. The concentration of interleukin 6 was consistent with an appropriate proinflammatory response and correlated directly with the concentrations of C-reactive protein (r = 0.67, P<0.01) and alpha1-antitrypsin (r = 0.40, P<0.05). The findings suggest that egg white-tryptophan is associated with less amino acid oxidation in kwashiorkor and acute infection than is milk.
http://www.ncbi.nlm.nih.gov/pubmed/10720167?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Emma-Leigh
09-12-2009, 06:26 PM
http://www.ncbi.nlm.nih.gov/pubmed/12436270
Eur J Appl Physiol. 2002 Nov;88(1-2):50-60. Epub 2002 Aug 15. Links
Muscular adaptations in response to three different resistance-training regimens: specificity of repetition maximum training zones.
Campos GE, Luecke TJ, Wendeln HK, Toma K, Hagerman FC, Murray TF, Ragg KE, Ratamess NA, Kraemer WJ, Staron RS.
Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Irvine Hall, rm 430, Athens, OH 45701, USA.
Thirty-two untrained men [mean (SD) age 22.5 (5.8) years, height 178.3 (7.2) cm, body mass 77.8 (11.9) kg] participated in an 8-week progressive resistance-training program to investigate the "strength-endurance continuum". Subjects were divided into four groups: a low repetition group (Low Rep, n = 9) performing 3-5 repetitions maximum (RM) for four sets of each exercise with 3 min rest between sets and exercises, an intermediate repetition group (Int Rep, n = 11) performing 9-11 RM for three sets with 2 min rest, a high repetition group (High Rep, n = 7) performing 20-28 RM for two sets with 1 min rest, and a non-exercising control group (Con, n = 5). Three exercises (leg press, squat, and knee extension) were performed 2 days/week for the first 4 weeks and 3 days/week for the final 4 weeks. Maximal strength [one repetition maximum, 1RM), local muscular endurance (maximal number of repetitions performed with 60% of 1RM), and various cardiorespiratory parameters (e.g., maximum oxygen consumption, pulmonary ventilation, maximal aerobic power, time to exhaustion) were assessed at the beginning and end of the study. In addition, pre- and post-training muscle biopsy samples were analyzed for fiber-type composition, cross-sectional area, myosin heavy chain (MHC) content, and capillarization. Maximal strength improved significantly more for the Low Rep group compared to the other training groups, and the maximal number of repetitions at 60% 1RM improved the most for the High Rep group. In addition, maximal aerobic power and time to exhaustion significantly increased at the end of the study for only the High Rep group. All three major fiber types (types I, IIA, and IIB) hypertrophied for the Low Rep and Int Rep groups, whereas no significant increases were demonstrated for either the High Rep or Con groups. However, the percentage of type IIB fibers decreased, with a concomitant increase in IIAB fibers for all three resistance-trained groups. These fiber-type conversions were supported by a significant decrease in MHCIIb accompanied by a significant increase in MHCIIa. No significant changes in fiber-type composition were found in the control samples. Although all three training regimens resulted in similar fiber-type transformations (IIB to IIA), the low to intermediate repetition resistance-training programs induced a greater hypertrophic effect compared to the high repetition regimen. The High Rep group, however, appeared better adapted for submaximal, prolonged contractions, with significant increases after training in aerobic power and time to exhaustion. Thus, low and intermediate RM training appears to induce similar muscular adaptations, at least after short-term training in previously untrained subjects. Overall, however, these data demonstrate that both physical performance and the associated physiological adaptations are linked to the intensity and number of repetitions performed, and thus lend support to the "strength-endurance continuum".
PMID: 12436270 [PubMed - indexed for MEDLINE]
fodosho
09-12-2009, 08:01 PM
Here is something I think everyone who is getting serious about their diet should read
http://www.jissn.com/content/5/1/17
Emma-Leigh
09-14-2009, 02:41 AM
http://www.ncbi.nlm.nih.gov/pubmed/17413101
Am J Clin Nutr. 2007 Apr;85(4):1023-30. Links
Comment in:
Am J Clin Nutr. 2007 Oct;86(4):1249-50; author reply 1250.
Long-term effects of 2 energy-restricted diets differing in glycemic load on dietary adherence, body composition, and metabolism in CALERIE: a 1-y randomized controlled trial.
Das SK, Gilhooly CH, Golden JK, Pittas AG, Fuss PJ, Cheatham RA, Tyler S, Tsay M, McCrory MA, Lichtenstein AH, Dallal GE, Dutta C, Bhapkar MV, Delany JP, Saltzman E, Roberts SB.
Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA.
BACKGROUND: There remains no consensus about the optimal dietary composition for sustained weight loss. OBJECTIVE: The objective was to examine the effects of 2 dietary macronutrient patterns with different glycemic loads on adherence to a prescribed regimen of calorie restriction (CR), weight and fat loss, and related variables. DESIGN: A randomized controlled trial (RCT) of diets with a high glycemic load (HG) or a low glycemic load (LG) at 30% CR was conducted in 34 healthy overweight adults with a mean (+/-SD) age of 35 +/- 6 y and body mass index (kg/m(2)) of 27.6 +/- 1.4. All food was provided for 6 mo in diets controlled for confounding variables, and subjects self-administered the plans for 6 additional months. Primary and secondary outcomes included energy intake measured by doubly labeled water, body weight and fatness, hunger, satiety, and resting metabolic rate. RESULTS: All groups consumed significantly less energy during CR than at baseline (P < 0.01), but changes in energy intake, body weight, body fat, and resting metabolic rate did not differ significantly between groups. Both groups ate more energy than provided (eg, 21% and 28% CR at 3 mo and 16% and 17% CR at 6 mo with HG and LG, respectively). Percentage weight change at 12 mo was -8.04 +/- 4.1% in the HG group and -7.81 +/- 5.0% in the LG group. There was no effect of dietary composition on changes in hunger, satiety, or satisfaction with the amount and type of provided food during CR. CONCLUSIONS: These findings provide more detailed evidence to suggest that diets differing substantially in glycemic load induce comparable long-term weight loss.
Emma-Leigh
09-18-2009, 05:46 PM
some readings behind why anorexia requires >>> energy intake than what would be predicted...
http://www.ajcn.org/cgi/content/abstract/80/6/1469
American Journal of Clinical Nutrition, Vol. 80, No. 6, 1469-1477, December 2004
? 2004 American Society for Clinical Nutrition
ORIGINAL RESEARCH COMMUNICATION
Factors associated with the increase in resting energy expenditure during refeeding in malnourished anorexia nervosa patients1,2,3
Virginie Van Wymelbeke, Laurent Brondel, Jean Marcel Brun and Daniel Rigaud
1 From the Centre Europ?en des Sciences du Go?t, Medical Research Unit-National Center of Scientific Research 5170, Dijon, France (VVW, LB, and DR), and the Service d'Endocrinologie, Le Bocage University Hospital, Dijon, France (DR and JMB)
Background: In malnourished anorexia nervosa (AN) patients, body-weight gain during refeeding is slowed by an increase in resting energy expenditure (REE).
Objective: The objective of the study was to identify factors associated with the increase in REE during refeeding.
Design: Before and 8, 30, and 45 d after the beginning of refeeding, REE was studied by indirect calorimetry in 87 female AN patients [ ? SD age: 23.4 ? 7.9 y; body mass index (in kg/m2) 13.2 ? 1.3]. Energy intake, body composition (by bioelectrical impedance analysis), physical activity, smoking behavior, abdominal pain, anxiety, depressive mood, serum thyrotropin and thyroid hormone, and urinary catecholamines were measured. REE was also evaluated in 18 patients after 1 y of recovery.
Results: By day 8, REE increased from 3.84 ? 0.6 to 4.36 ? 0.59 MJ/d (P < 0.01). This increase (13.4%) was significantly (P < 0.01) greater than that expected on the basis of the increase in fat-free mass (FFM; 1.6%). Thereafter, the ratio of REE to FFM remained high and, in multivariate analysis, was significantly related to 4 factors: energy intake (P < 0.01), anxiety (P < 0.01), abdominal pain (P < 0.05), and depressive mood (P < 0.05). The ratio also increased significantly with physical activity (P < 0.01) and cigarette smoking (P < 0.02). This rise in REE leveled off after recovery from AN.
Conclusion: In AN patients, the rise in REE observed during refeeding was independently linked to anxiety level, abdominal pain, physical activity, and cigarette smoking, and it contributed to resistance to weight gain.
http://jcem.endojournals.org/cgi/content/abstract/92/5/1623
The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 5 1623-1629
Copyright ? 2007 by The Endocrine Society
Hormonal and Psychological Factors Linked to the Increased Thermic Effect of Food in Malnourished Fasting Anorexia Nervosa
Daniel Rigaud, Bruno Verges, Nicole Colas-Linhart, Anne Petiet, Myriam Moukkaddem, Virginie Van Wymelbeke and Laurent Brondel
Centre Europ?en des Sciences du Go?t (D.R., V.V.W., L.B.), Unit? Mixte de Recherche-Centre National de la Recherche Scientifique 5170, 21000 Dijon, France; Centre Hospitalier Universitaire Le Bocage (B.V., M.M.), 21079 Dijon, France; and Faculty of Medicine X. Bichat (N.C.-L., A.P.), 75018 Paris, France
Address all correspondence and requests for reprints to: Prof. Daniel Rigaud, Service d?Endocrinologie et Nutrition, H?pital Centre Hospitalier Universitaire Le Bocage, 21079 Dijon Cedex, France. E-mail: daniel.rigaud@chu-dijon.fr.
Objectives: In patients with anorexia nervosa (AN), weight gain is lower than that expected from the energy content of the meals. Thus we investigated the thermic effect of food (TEF) in relation to subjective feelings and plasma hormone levels in a group of AN patients.
Methods: TEF, feelings (14 items), and plasma release of ?-endorphin, ACTH, cortisol, dopamine, and catecholamines were evaluated in 15 AN patients (body mass index, 13.6 ? 1.2 kg?m?2) and in 15 healthy women after three gastric loads (0, 300, 700 kcal) infused by a nasogastric tube in a blind design.
Results: In AN, the blind loads induced an energy-dependent increase in TEF (P < 0.001), which was higher than that observed in healthy women (P < 0.001). Only in AN, a load-dependent decline in the high basal plasma level of ?-endorphin (P < 0.01), an increase in plasma ACTH (P < 0.02) after the two caloric loads, and an increase in cortisol, norepinephrine, and dopamine levels after the 700-kcal load only (P < 0.05) were noted. A calorie-dependent (P < 0.001) increase in nausea, abdominal discomfort, and fear of being fat ratings and a decrease in liking to eat (P < 0.001) and body image were observed in AN patients (P < 0.05). TEF correlated with ratings on satiation, nausea, uncomfortable abdominal swelling, body image, and fear of being fat (for all, P < 0.01).
Conclusion: In AN women, blindly infused loads induced a dose-dependent increase in TEF, which correlated with the increase in plasma cortisol, ACTH, and catecholamines as in unpleasant sensations, fear of being fat, and anxiety as well as a decline in elevated basal ?-endorphin. These results could explain the difficulty for AN patients in gaining weight.
elmariachii
10-29-2009, 02:29 AM
Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men
Moore DR, Robinson MJ, Fry JL, Tang JE, Glover EI, Wilkinson SB, Prior T, Tarnopolsky MA, Phillips SM.
Am J Clin Nutr. 2009 Jan;89(1):161-8. Epub 2008 Dec 3.
http://www.ncbi.nlm.nih.gov/pubmed/19056590
BACKGROUND: The anabolic effect of resistance exercise is enhanced by the provision of dietary protein. OBJECTIVES: We aimed to determine the ingested protein dose response of muscle (MPS) and albumin protein synthesis (APS) after resistance exercise. In addition, we measured the phosphorylation of candidate signaling proteins thought to regulate acute changes in MPS. DESIGN: Six healthy young men reported to the laboratory on 5 separate occasions to perform an intense bout of leg-based resistance exercise. After exercise, participants consumed, in a randomized order, drinks containing 0, 5, 10, 20, or 40 g whole egg protein. Protein synthesis and whole-body leucine oxidation were measured over 4 h after exercise by a primed constant infusion of [1-(13)C]leucine. RESULTS: MPS displayed a dose response to dietary protein ingestion and was maximally stimulated at 20 g. The phosphorylation of ribosomal protein S6 kinase (Thr(389)), ribosomal protein S6 (Ser(240/244)), and the epsilon-subunit of eukaryotic initiation factor 2B (Ser(539)) were unaffected by protein ingestion. APS increased in a dose-dependent manner and also reached a plateau at 20 g ingested protein. Leucine oxidation was significantly increased after 20 and 40 g protein were ingested. CONCLUSIONS: Ingestion of 20 g intact protein is sufficient to maximally stimulate MPS and APS after resistance exercise. Phosphorylation of candidate signaling proteins was not enhanced with any dose of protein ingested, which suggested that the stimulation of MPS after resistance exercise may be related to amino acid availability. Finally, dietary protein consumed after exercise in excess of the rate at which it can be incorporated into tissue protein stimulates irreversible oxidation.
elmariachii
10-29-2009, 02:30 AM
Hepatoprotective effects of whey protein on D-galactosamine-induced hepatitis and liver fibrosis in rats.
Biosci Biotechnol Biochem. 2006 May;70(5):1281-5.
Kume H, Okazaki K, Sasaki H.
http://www.ncbi.nlm.nih.gov/pubmed/16717438?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed _ResultsPanel.Pubmed_RVDocSum&ordinalpos=8
The hepatoprotective effects of whey protein on two injections of D-galactosamine (300 mg/kg, i.p.) were investigated in rats fed a modified AIN-93M diet formulated with a protein source of casein or whey for 16 d. The whey protein-containing diet clearly suppressed an increase in plasma alanine and aspartate aminotransferase activity, lactate dehydrogenase and bilirubin, which are hepatitis markers, and also hyaluronic acid, a fibrosis marker. In addition, it suppressed histopathological signs of portal fibrosis, bile duct proliferation, and perivenular sclerosis. These results suggest that supplementation with whey protein can help prevent the development of hepatitis and portal fibrosis.
dustinlima
10-29-2009, 03:53 PM
Mary G. Enig, lipid biology PhD
http://www.westonaprice.org/knowyourfats/index.html
Consider it
Emma-Leigh
10-29-2009, 07:27 PM
Mary G. Enig, lipid biology PhD
http://www.westonaprice.org/knowyourfats/index.html
KNOW THEM!
^ appreciate your input but a somewhat dodgy source. :o
A little misinformation mixed up with the truth in many of those articles.
dustinlima
10-29-2009, 11:17 PM
Mmk I edited the "KNOW THEM" to "Consider it" :)
At least consider the articles with multiple references (like 15+)
xAlphax
10-30-2009, 12:56 AM
Mmk I edited the "KNOW THEM" to "Consider it" :z
At least consider the articles with multiple references (like 15+)
No one's going to consider anything. Also, I've read that link way back, it looks pretty simple.
blumnblam
11-11-2009, 04:08 PM
Pre- and Post-prandial Appetite Hormone Levels in Normal Weight and Severely Obese Women
Joseph J. Carlson; Amy A. Turpin; Gail Wiebke; Steven C. Hunt; Ted D. Adams
Published: 10/14/2009
Abstract
Background: Appetite is affected by many factors including the hormones leptin, ghrelin and adiponectin. Ghrelin stimulates hunger, leptin promotes satiety, and adiponectin affects insulin response. This study was designed to test whether the pre- and postprandial response of key appetite hormones differs in normal weight (NW) and severely obese (SO) women.
Methods: Twenty three women ages 25-50 were recruited for this study including 10 NW (BMI = 23.1 ? 1.3 kg/m2) and 13 SO (BMI = 44.5 ? 7.1 kg/m2). The study was conducted in a hospital-based clinical research centre. Following a 12-hour fast, participants had a baseline blood draw, consumed a moderately high carbohydrate meal (60% carbohydrate, 20% protein, 20% fat) based on body weight. Postprandially, participants had six blood samples drawn at 0, 15, 30, 60, 90, and 120 minutes. Primary measures included pre- and post-prandial total ghrelin, leptin, adiponectin and insulin. A repeated measures general linear model was used to evaluate the hormone changes by group and time (significance p ≤ 0.05).
Results: There were significant differences between the NW and the SO for all hormones in the preprandial fasting state. The postprandial responses between the SO versus NW revealed: higher leptin (p < 0.0001), lower adiponectin (p = 0.04), trend for lower ghrelin (p = 0.06) and insulin was not different (p = 0.26). Postprandial responses over time between the SO versus NW: higher leptin (p < 0.001), lower ghrelin and adiponectin (p = 0.004, p = 0.015, respectively), and trend for higher insulin (p = 0.06).
Conclusion: This study indicates that significant differences in both pre- and selected post- prandial levels of leptin, ghrelin, adiponectin and insulin exist between NW and SO women. Improving our understanding of the biochemical mechanisms accounting for these differences in appetite hormones among individuals with varying body size and adiposity should aid in the development of future therapies to prevent and treat obesity.
More interesting stuff on leptin, adiponectin, insulin connection.
Question: Have any pharmaceuticals/supplement companies done anything to try and increase expression of adiponectin?
snorkelman
01-12-2010, 09:51 AM
In a recent study (published in the January 2010 issue of the Journal of the American Dietetic Association), researchers from Tufts University found that some restaurant and frozen foods contained more calories than indicated in nutritional labeling.
The Accuracy of Stated Energy Contents of Reduced-Energy, Commercially Prepared Foods Journal of the American Dietetic Association, Volume 110, Issue 1, Pages 116-123 L. Urban, et. al.
Can anyone attach to this thread the full text?
Emma-Leigh
01-12-2010, 11:16 PM
In a recent study (published in the January 2010 issue of the Journal of the American Dietetic Association), researchers from Tufts University found that some restaurant and frozen foods contained more calories than indicated in nutritional labeling.
The Accuracy of Stated Energy Contents of Reduced-Energy, Commercially Prepared Foods Journal of the American Dietetic Association, Volume 110, Issue 1, Pages 116-123 L. Urban, et. al.
Can anyone attach to this thread the full text?
I have the full paper - but due to copyright issues can't post it here for all to see...
However - abstract:
Abstract
The accuracy of stated energy contents of reduced-energy restaurant foods and frozen meals purchased from supermarkets was evaluated. Measured energy values of 29 quick-serve and sit-down restaurant foods averaged 18% more than stated values, and measured energy values of 10 frozen meals purchased from supermarkets averaged 8% more than originally stated. These differences substantially exceeded laboratory measurement error but did not achieve statistical significance due to considerable variability in the degree of underreporting. Some individual restaurant items contained up to 200% of stated values and, in addition, free side dishes increased provided energy to an average of 245% of stated values for the entrees they accompanied. These findings suggest that stated energy contents of reduced-energy meals obtained from restaurants and supermarkets are not consistently accurate, and in this study averaged more than measured values, especially when free side dishes were taken into account. If widespread, this phenomenon could hamper efforts to self-monitor energy intake to control weight, and could also reduce the potential benefit of recent policy initiatives to disseminate information on food energy content at the point of purchase.
And Conclusions:
Mean measured energy contents of reduced-energy restaurant and supermarket meals in this pilot study exceeded vendor-stated amounts by substantially more than could be accounted for by laboratory measurement error. Although the discrepancies were within acceptable limits based on federal regulations for most packaged and restaurant foods (which are not subject to these federal regulations) some restaurant foods did have measured energy contents that were double those stated by the restaurant, and free side dishes contained more energy on average than the entrees they accompanied. On an individual level, discrepancies of this magnitude, if widespread, are likely to substantially hamper efforts to control weight by individuals self-monitoring their energy intake. On a public scale, the emerging policy initiatives on requiring energy information at the point of purchase may not translate into improved dietary intake if foods typically contain more energy than stated. Based on these findings, registered dietitians can advise consumers about the wide variability in accuracy of stated energy contents for prepared reduced-energy foods. Approaches to improving the accuracy of stated energy information may include increased attention to quality control in food preparation. Additional measures may also be needed such as improved federal and state regulations and a monitoring system to ensure compliance.
snorkelman
01-13-2010, 04:40 AM
I figured that y'all would find this interesting
Blueberries make their mark on cardiovascular and diabetes risks, U-M animal study finds
Research shows blueberry intake reduced abdominal fat and lowered risk for cardiovascular disease and metabolic syndrome in obese lab rats
Blueberries make their mark on cardiovascular and diabetes risks, U-M animal study finds
Meet the expert:
Steven Bolling, M.D.
ANN ARBOR, Mich. — Could eating blueberries help get rid of belly fat? And could a blueberry-enriched diet stem the conditions that lead to diabetes? A new University of Michigan Cardiovascular Center study suggests so.
The new research, presented Sunday at the Experimental Biology convention in New Orleans, gives tantalizing clues to the potential of blueberries in reducing risk factors for cardiovascular disease and metabolic syndrome. The effect is thought to be due to the high level of phytochemicals - naturally occurring antioxidants - that blueberries contain.
The study was performed in laboratory rats. While the animal findings suggest blueberries may be protective against two health conditions that affect millions of Americans, more research should be done.
The researchers studied the effect of blueberries (freeze dried blueberries crushed into a powder) that were mixed into the rat diet, as part of either a low- or high-fat diet. They performed many comparisons between the rats consuming the test diets and the control rats receiving no blueberry powder. All the rats were from a research breed that is prone to being severely overweight.
In all, after 90 days, the rats that received the blueberry-enriched powder, measured as 2 percent of their diet, had less abdominal fat, lower triglycerides, lower cholesterol, and improved fasting glucose and insulin sensitivity, which are measures of how well the body processes glucose for energy.
While regular blueberry intake reduced these risks for cardiovascular disease and metabolic syndrome, the health benefits were even better when combined with a low-fat diet.
In addition to all the other health benefits, the group that consumed a low-fat diet had lower body weight, lower total fat mass and reduced liver mass, than those who ate a high fat diet. An enlarged liver is linked to obesity and insulin resistance, a hallmark of diabetes.
The rats in the study were similar to Americans who suffer fatty liver disease and metabolic syndrome as a result of high-fat diets and obesity. Metabolic syndrome is a group of health problems that include too much fat around the waist, elevated blood pressure, elevated blood sugar, high triglycerides, and together these conditions increase the risk of heart attacks, strokes and diabetes.
But were the health benefits seen in rats a result of losing abdominal fat, or something else?
"Some measurements were changed by blueberry even if the rats were on a high fat diet," says E. Mitchell Seymour, M.S., lead researcher and manager of the U-M Cardioprotection Research Laboratory. "We found by looking at fat muscle tissue, that blueberry intake affected genes related to fat-burning and storage. Looking at muscle tissue, we saw altered genes related to glucose uptake."
Steven Bolling, M.D., a U-M heart surgeon and head of the Cardioprotection Laboratory, says: "The benefits of eating fruits and vegetables has been well-researched, but our findings in regard to blueberries shows the naturally occurring chemicals they contain, such as anthocyanins, show promise in mitigating these health conditions."
Although the current study was supported by the U.S. Highbush Blueberry Council, which also supplied the blueberry powder, the council did not play a role in the study’s conduct, analysis or the preparation of the poster presentation.
Experimental Biology 2009 convention, where the study results were presented, includes the annual meetings of six societies and brings together scientists from throughout the United States and the world, representing dozens of scientific areas, from laboratory to translational to clinical research.
For more information on the U-M Cardioprotection Research Laboratory, visit http://sitemaker.umich.edu/cardiac.phytomed/research
Antioxidant activity of blueberry fruit is impaired by association with milk.
Serafini M, Testa MF, Villaño D, Pecorari M, van Wieren K, Azzini E, Brambilla A, Maiani G.
Antioxidant Research Laboratory, Unit of Human Nutrition, Istituto Nazionale di Ricerca per gli Alimenti e la Nutrizione, 00178 Rome, Italy. serafini_mauro@yahoo.it
The antioxidant properties of dietary phenolics are believed to be reduced in vivo because of their affinity for proteins. In this study we assessed the bioavailability of phenolics and the in vivo plasma antioxidant capacity after the consumption of blueberries (Vaccinium corymbosum L.) with and without milk. In a crossover design, 11 healthy human volunteers consumed either (a) 200 g of blueberries plus 200 ml of water or (b) 200 g of blueberries plus 200 ml of whole milk. Venous samples were collected at baseline and at 1, 2, and 5 h postconsumption. Ingestion of blueberries increased plasma levels of reducing and chain-breaking potential (+6.1%, p<0.001; +11.1%, p<0.05) and enhanced plasma concentrations of caffeic and ferulic acid. When blueberries and milk were ingested there was no increase in plasma antioxidant capacity. There was a reduction in the peak plasma concentrations of caffeic and ferulic acid (-49.7%, p<0.001, and -19.8%, p<0.05, respectively) as well as the overall absorption (AUC) of caffeic acid (p<0.001). The ingestion of blueberries in association with milk, thus, impairs the in vivo antioxidant properties of blueberries and reduces the absorption of caffeic acid.
Emma-Leigh
01-17-2010, 01:30 AM
See - exercise makes your brain big too... :p
Journal Of Science And Medicine In Sport / Sports Medicine Australia [J Sci Med Sport] 2009 Nov; Vol. 12 (6), pp. 688-90. Date of Electronic Publication: 2009 Jan 14.
Can exercise shape your brain? Cortical differences associated with judo practice.
Jacini WF; Cannonieri GC; Fernandes PT; Bonilha L; Cendes F; Li LM
Laboratory of Neuroimaging, Faculty of Medical Sciences of State University of Campinas (UNICAMP), Brazil.
Abstract:
Experimental animal studies have shown that physical exercise, associated with planning and execution of complex movements, are related to changes in brain structure. In humans, changes in cortical tissue density in relation to physical activity are yet to be fully determined and quantified. We investigated differences on gray matter volume in judo players by using voxel-based morphometry. Comparison between a group of eight internationally competitive judo players and a group of 18 healthy controls showed a significantly higher gray matter tissue density in brain areas of judo players.
PMID: 19147406
Emma-Leigh
01-22-2010, 12:37 AM
Diabetes Care September 2005 vol. 28 no. 9 2123-212
Influence of Glycemic Index/Load on Glycemic Response, Appetite, and Food Intake in Healthy Humans
Rita C.G. Alfenas, PHD1 and Richard D. Mattes, PHD2
+ Author Affiliations
1Departamento de Nutrição e Saúde, Universidade Federal de Viçosa, Viçosa, Brazil
2Department of Foods and Nutrition, Purdue University, West Lafayette, Indiana
Address correspondence and reprint requests to Richard D. Mattes, PhD, Department of Foods and Nutrition, Purdue University, Stone Hall, Rm. 212, 700 W. State St., West Lafayette, Indiana. E-mail: mattes@purdue.edu
Next Section
Abstract
OBJECTIVE—High glycemic index (GI)/load (GL) diets reportedly enhance appetite and promote positive energy balance. Support for this hypothesis stems largely from acute feeding trials and longer-term studies lacking control over the macronutrient composition and palatability of test foods. This study evaluated the effects of consuming high- and low-GI/GL meals, matched on macronutrient composition and palatability, plasma glucose and insulin, appetite, and food intake.
RESEARCH DESIGN AND METHODS—Thirty-nine healthy adults consumed only low- or only high-GI foods ad libitum in the laboratory for 8 days in either high (three foods per meal)- or low (one food per meal)-variety conditions. Glucose and insulin concentrations as well as appetitive sensations were determined before and for 2 h following breakfast and lunch on days 1 and 8. Energy intake was monitored daily.
RESULTS—There were no significant differences in plasma glucose or insulin responses, appetitive ratings, or food intake between treatments.
CONCLUSIONS—These data indicate that the differential glycemic response of foods tested in isolation under fixed time are not preserved under conditions of chronic ad libitum consumption of mixed meals.
Emma-Leigh
01-24-2010, 11:17 AM
...
Horm Metab Res. 2010 Jan 21. [Epub ahead of print]
Effect of Carbohydrate- and Protein-rich Meals on Exercise-induced Activation of Lipolysis in Obese Subjects.
Erdmann J, Tholl S, Schusdziarra V.
Else-Kröner-Fresenius Center of Nutritional Medicine, Klinikum rechts der Isar,Technical University of Munich, Munich, Germany.
Exercise is an important part of obesity treatment concepts to support fat mobilisation from adipose tissue and also fat oxidation nolich is impaired in obese subjects. In normal weight subjects it is well known that stimulation of plasma insulin levels by a carbohydrate meal can inhibit lipolysis and subsequent fat oxidation. Since obese subjects frequently have elevated basal and postprandial insulin levels the effect of carbohydrate- and protein-rich test meals on exercise-induced activation of lipolysis is of special interest. Twenty obese subjects performed bicycle exercise for 30 min in the fasted state, 30 min after a carbohydrate-or a protein-rich meal, and 120 min after the carbohydrate meal (n=12), respectively, at low intensity. Activation of lipolysis was assessed by plasma glycerol levels. In addition, plasma insulin, glucose, and lactate concentrations were determined. In comparison to the fasted state, the carbohydrate meal suppressed activation of lipolysis. Following the protein meal, exercise led to an attenuated but significant increase of glycerol levels. A similar rise was observed when the carbohydrate meal was ingested 2 h prior to the exercise bout. To improve exercise-induced lipolysis and subsequent fat oxidation during low-intensity exercise obese subjects should not ingest carbohydrates immediately before exercise. Hunger sensations should be satisfied with protein-rich food. When carbohydrates are consumed 2 h prior to exercise its lipolytic effect is comparable to the protein meal. These data are useful in every day dietary counselling and might help to improve weight loss during obesity treatment. © Georg Thieme Verlag KG Stuttgart · New York.
determined4000
01-24-2010, 12:06 PM
...
Slightly confused. 1st it says the protein-rich meal improved conditions. Then it says that a similar effect was observed when carbohydrates were ingested 2hrs prior. And then says carbohydrates should not be ingested prior. What am I misunderstanding?
EmperorRyker
01-24-2010, 12:46 PM
Slightly confused. 1st it says the protein-rich meal improved conditions. Then it says that a similar effect was observed when carbohydrates were ingested 2hrs prior. And then says carbohydrates should not be ingested prior. What am I misunderstanding?
The study says the carbs should not be ingested 30 min prior to LISS, while it's supposedly alright if you eat them 120 mins prior to.
in10city
01-24-2010, 01:48 PM
Slightly confused. 1st it says the protein-rich meal improved conditions. Then it says that a similar effect was observed when carbohydrates were ingested 2hrs prior. And then says carbohydrates should not be ingested prior. What am I misunderstanding?
All of the test meals reduced exercise induced lipolysis. Unfortunately they didn't do any metabolic - RER, and other ventilatory measurements like actually quantify the significance of the change. Lipolysis is one thing - oxidation is another.
In another recent study that evaluated that latter difference, it was tiny when you look further away in time from the acute effects.
http://www.ncbi.nlm.nih.gov/pubmed/17111004
determined4000
01-24-2010, 02:31 PM
The study says the carbs should not be ingested 30 min prior to LISS, while it's supposedly alright if you eat them 120 mins prior to.
Ok thats what I gathered. IF your goal is not fat loss, would it still be optimal to ingest earlier?
Insight
01-26-2010, 06:18 PM
A caveat: I have not thoroughly read this study, I don't have the time right now. The abstract alone indicates that there are serious problems with the way this study was conducted. Despite that, it provides some interesting food for thought about the way many "treat" foods and tend to overgeneralize them as "good" vs "bad."
There are a lot of problems with this study. But the fact that someone even thought to study this at all demonstrates a lateral and critical thinking pattern that serious researchers in a field often display, which many people never develop. Most laypeople assume that even though we like high-GI foods, they are "bad" -- assuming an positive correlation between the pleasure of a stimulus and its maladaptive potential. Many nutrition experts, on the other hand, treat the glycemic index as an antiquated relic that is of little practical usefulness.
These researchers were brilliant in questioning this and assuming otherwise. What is even more brilliant IMO is their lateral thinking to consider that perhaps "enjoying" a high-GI carb might actually be represented as an increase in serotonin, which is a physical and concrete biological marker. Then they considered that this might presumably lead to other tangible, positive health effects (in this case the decrease of premenstrual symptoms).
Just pointing out how the real "experts" in a field of study tend to think. Nothing is taken for granted, and everything has a concrete explanation. This is what separates the intellectual bourgeoisie from the proletariat: the ability to "demystify" a certain topic (like that people tend to enjoy eating high-GI carbohydrates) and consider what the real concrete and scientific explanation for this might be, and then use that as the basis for a further train of thought.
Here is the link:
http://www.nutritionjrnl.com/article/S0899-9007%2808%2900085-3/abstract
And here's the abstract:
Objectives
High glycemic index (GI) carbohydrates may increase brain serotonin, which in turn acts to alleviate premenstrual symptoms, because, although the main determinant of brain serotonin concentration is a high plasma ratio of tryptophan to other large neutral amino acids, a high-GI diet has been shown to increase this ratio. In this observational cross-sectional study, we investigated associations between dietary GI and other dietary carbohydrates and premenstrual symptoms.
Methods
Subjects were 640 female Japanese dietetic students 18?22 y of age. Dietary carbohydrates were assessed using a validated, self-administered, comprehensive diet history questionnaire. Menstrual cycle symptoms were assessed using the retrospective version of the Moos Menstrual Distress Questionnaire (MDQ). Independent associations of dietary GI and glycemic load and intake of available carbohydrate and dietary fiber with the MDQ total score and subscale scores (pain, concentration, behavioral change, autonomic reactions, water retention, and negative affect) in the premenstrual phase (expressed as percentages relative to those in the intermenstrual phase) were examined.
Results
Dietary GI was independently inversely associated with total MDQ score in the premenstrual phase (P for trend = 0.02). Dietary GI also showed independent and inverse associations with several MDQ subscale scores in the premenstrual phase, including concentration, autonomic reactions, and water retention (P for trend < 0.05). Conversely, dietary glycemic load and intake of available carbohydrate and dietary fiber were not associated with any of the MDQ scores in the premenstrual phase.
Conclusion
Dietary GI was independently associated with decreased premenstrual symptoms in a group of young Japanese women.
Some interesting parts were bolded. While from this abstract this seems like far from the most conclusive study on the matter (diet history questionnaire? lol), there is an interesting concept here that I would like to see studied further.
The last bolded sentence, that dietary glycemic load is not also associated with this sane trend, is what really makes this interesting for me -- this would generally indicate that it doesn't matter how much of the high-GI food is being eaten, but that it is being eaten that counts (with some caveats, such as foods that are extremely high GI and extremely low GL). AKA, the results were different between someone who ate ice cream and an equivalent-GL serving of oatmeal.
This increase in serotonin could be due to that in general high-GI foods are "sweeter", and that the pleasure felt from eating sweet foods itself IS represented as an increase in serotonin. Or it could be that allowing oneself to eat foods that one likes leads to a more positive state of mind, represented in general as an increase in serotonin. Or it could simply be due to some physiological property of high-GI foods (though I doubt it).
Either way, this study subtly hints at something I have believed for a long time now - that incorporating some "pleasure foods" into ones diet can lead to improved psychological health - represented in the body via certain neurological markers - which can lead to improved physical health as well.
Emma-Leigh
01-29-2010, 09:44 PM
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 – 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
01-29-2010, 09:46 PM
Journal of the American College of Nutrition, Vol. 23, No. 5, 373-385 (2004)
Published by the American College of Nutrition
The Effects of High Protein Diets on Thermogenesis, Satiety and Weight Loss: A Critical Review
Thomas L. Halton and Frank B. Hu, MD, PhD
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts
Address reprint requests to: Dr. Frank Hu, Dept. of Nutrition, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115. E-mail: frank.hu@channing.harvard.edu
For years, proponents of some fad diets have claimed that higher amounts of protein facilitate weight loss. Only in recent years have studies begun to examine the effects of high protein diets on energy expenditure, subsequent energy intake and weight loss as compared to lower protein diets. In this study, we conducted a systematic review of randomized investigations on the effects of high protein diets on dietary thermogenesis, satiety, body weight and fat loss. There is convincing evidence that a higher protein intake increases thermogenesis and satiety compared to diets of lower protein content. The weight of evidence also suggests that high protein meals lead to a reduced subsequent energy intake. Some evidence suggests that diets higher in protein result in an increased weight loss and fat loss as compared to diets lower in protein, but findings have not been consistent. In dietary practice, it may be beneficial to partially replace refined carbohydrate with protein sources that are low in saturated fat. Although recent evidence supports potential benefit, rigorous longer-term studies are needed to investigate the effects of high protein diets on weight loss and weight maintenance.
Key words: high protein diets, thermogenesis, satiety, body weight, fat loss
Key teaching points:
? Although authors of some fad diets have advocated increasing dietary protein for weight loss, not until recently have studies begun to investigate the effects of high protein diets on weight loss.
? Convincing evidence exists that protein exerts an increased thermic effect when compared to fat and carbohydrate. Evidence is also convincing that higher protein diets increase satiety when compared to lower protein diets.
? Higher protein diets may facilitate weight loss when compared to a lower protein diet in the short term (within 6 months). But long-term data are limited.
? Exchange protein for carbohydrates has been shown to improve blood lipids, and in epidemiologic studies, higher protein diets have been associated with lower blood pressure and reduced risk of coronary heart disease.
? Although the optimal amount and sources of protein cannot be determined at this time, the weight of evidence suggests that in dietary practice, it may be beneficial to partially replace refined carbohydrate with protein sources that are low in saturated fat.
Emma-Leigh
01-29-2010, 09:55 PM
International Journal of Obesity & Related Metabolic Disorders; Jul1997, Vol. 21 Issue 7, p608, 6p
Effect of food palatability on early (cephalic) phase of diet-induced thermogenesis in nonobese and obese man.
Authors: Hashkes, Philip J, Gartside, Peter S, Blondheim, S H
OBJECTIVE: To study the effect on the early (cephalic) phase of diet-induced thermogenesis (EDT) of palatable vs unpalatable food, in nonobese and obese man. SUBJECTS: Twenty-four nonobese volunteers and 19 obese clinic patients. DESIGN AND MEASUREMENTS: A palatable, liquid formula meal of Ensure (1048 KJ, 450 ml), and of Ensure made unpalatable by addition of aqueous KCI, were sipped on nonconsecutive mornings. O[sub 2] consumption (ml/min) was measured before, and starting 30, 60 and 90 min after beginning the test meal, from which EDT was calculated as KJ/min. RESULTS: Palatability of the test meal significantly increased EDT (palatability effect, P=0.004) but obesity status per se, did not affect EDT. Nevertheless, the effect of palatability on EDT was dependent on obesity status, being seen only in the nonobese. EDT was significantly greater in the nonobese after the palatable than the unpalatable meal: (mean?s.e.m.) 2.45?0.14 vs 1.83?0.14; P<0.0001, but not in the obese: 1.93?0.28 vs 1.73?0.20; P<0.21. Therefore only after the palatable meal was EDT less in the obese compared with the nonobese: P<0.05. The threshold for the unpleasant taste of added KCI was 31% higher in the obese than the nonobese: 4.2?0.4 vs 3.2?0.2 [g KCI]; P < 0.025. CONCLUSIONS: The early (cephalic) phase of dietary thermogenesis (EDT) is significantly increased in the nonobese by palatability, but not in the obese, so that only after a palatable meal is EDT less, or 'deficient,' in the obese compared with the nonobese. Also, the obese have a higher threshold for the unpleasant taste of KCI (in Ensure) than the nonobese. [ABSTRACT FROM AUTHOR]
ISSN: 03070565
Emma-Leigh
01-29-2010, 09:57 PM
International Journal of Eating Disorders; Jul96, Vol. 20 Issue 1, p33-41, 9p
Resting metabolic rate and diet-induced thermogenesis in restrained and unrestrained eaters.
Authors: Platte, Petra1, Wurmser, Harald1, Wade, Stephen E.1, Mecheril, Anita1, Pirke, Karl M.2
Abstract:
The hypothesis was studied whether restrained eaters had reduced resting metabolic rate (RMR) and diet-induced thermogenesis (DIT) and whether the effect was caused by weight cycling. Restrained eaters had significantly lower RMR than unrestrained eaters. No difference in DIT was found. Weight cycling and no weight cycling restrained eaters did not differ with regard to RMR and DIT. These data indicate that restrained eating but not weight cycling significantly reduces RMR. [ABSTRACT FROM AUTHOR]
determined4000
01-29-2010, 10:00 PM
American Journal of Clinical Nutrition, (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)
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.
It makes sense the EE would be higher when protein is exchanged for carbohydrates,
but how is it that the overall diet was so much higher given the much higher fat intake (and supposed Thermic effect of fat compared to carbohydrates)
Emma-Leigh
01-29-2010, 10:06 PM
Nutrition Bulletin (NUTR BULL), 2007 Mar; 32: Suppl 1: 22-31 (75 ref)
Sustained protein intake for bodyweight management.
Westerterp-Plantenga MS; Smeets A; Nieuwenhuizen A
Department of Human Biology, Maastricht University, Maastricht, The Netherlands
Abstract:
Recent findings suggest that an elevated protein intake plays a key role in bodyweight management, through increased satiety (related to increased diet-induced thermogenesis), and its effect on thermogenesis, body composition and decreased energy efficiency. These factors are related to protein metabolism. Supported by these mechanisms, larger weight loss and subsequent improved bodyweight maintenance have been observed after high-protein diets. Increased insulin sensitivity may occur, but it is unclear whether this is owing to weight loss or type of diet. Under conditions of slight bodyweight regain (while aiming for weight maintenance), a high-protein diet shows a reduced energy efficiency related to the composition of the bodyweight regained. A high-protein diet during negative energy balance and during weight maintenance thereafter preserves, or increases, fat-free mass and reduces fat mass, thus improving the metabolic profile. As protein intake is studied at different energy intakes, absolute and relative protein intakes need to be discriminated. In absolute terms (grams per day), a normal-protein diet becomes a relatively high-protein diet if combined with negative energy balance and at weight maintenance. Therefore, 'high protein, negative energy balance diets' aim to keep the amount (grams) of protein ingested at the same level as consumed at energy balance, despite lower energy intakes.
^
lots of interesting stuff in this article...
Emma-Leigh
01-29-2010, 10:07 PM
International Journal of Obesity; Dec2006 Supplement 3, Vol. 30, pS16-S23, 8p
Dietary protein, metabolism, and body-weight regulation: dose?response effects.
Authors: Westerterp-Plantenga, M. S.1,2 M.Westerterp@hb.unimaas.nl
Luscombe-Marsh, N.1,2
Lejeune, M. P. G. M.1,2
Diepvens, K.1
Nieuwenhuizen, A.1,2
Engelen, M. P. K. J.2,3
Deutz, N. E. P.2,3
Azzout-Marniche, D.4
Tome, D.4
Westerterp, K. R.1,2
Abstract:
Body-weight management requires a multifactorial approach. Recent findings suggest that an elevated protein intake seems to play a key role herein, through (i) increased satiety related to increased diet-induced thermogenesis; (ii) its effect on thermogenesis; (iii) body composition; and (iv) decreased energy-efficiency, all of which are related to protein metabolism. Supported by these mechanisms, relatively larger weight loss and subsequent stronger body-weight maintenance have been observed. Increased insulin sensitivity may appear, but it is unclear whether this is due to weight loss or type of diet. The phenomenon of increased satiety is utilized in reduced energy-intake diets, mainly in the ad libitum condition, whereby sustained satiety is achieved with sustained absolute protein intake in grams, despite lower energy intake. Elevated thermogenesis and glucagon-like peptide-1 (GLP-1) appear to play a role in high-protein induced satiety. Under conditions of weight maintenance, a high-protein diet shows a reduced energy efficiency related to the body composition of the body weight regained, that is, in favor of fat-free mass. Indeed, during body-weight loss, as well as during weight regain, a high-protein diet preserves or increases fat-free mass and reduces fat mass and improves the metabolic profile. In the short-term this may be supported by a positive protein and a negative fat balance, through increased fat oxidation. As protein intake is studied under various states of energy balance, absolute and relative protein intake needs to be discriminated. In absolute grams, a normal protein diet becomes a relatively high-protein diet in negative energy balance and at weight maintenance. Therefore, ?high protein negative energy balance diets? aim to keep the grams of proteins ingested at the same level as consumed at energy balance, despite lower energy intakes.International Journal of Obesity (2006) 30, S16?S23. doi:10.1038/sj.ijo.0803487 [ABSTRACT FROM AUTHOR]
Emma-Leigh
01-29-2010, 10:14 PM
yummmmyyy.... fungus.......
Nutrition Bulletin (NUTR BULL), 2008 Dec; 33(4): 298-310 (50 ref)
Mycoprotein and health.
Denny A; Aisbitt B; Lunn J
Abstract:
Mycoprotein is a high protein, high fibre, low fat food ingredient derived from fermentation of the filamentous fungus Fusarium venenatum. Interest in the putative role of mycoprotein in lowering blood cholesterol concentrations, reducing energy intakes and controlling blood sugar levels has generated a small number of human studies investigating the effects of mycoprotein on cholesterol reduction, satiety and insulinaemia/glycaemia. In today's 'obesogenic' environment, in which there is an abundance of foods high in fat and/or sugar available to consumers, there is growing interest in foods that are both nutritious and satiating, but that are of low-energy density, and are low in saturates, salt and sugar. Mycoprotein has a favourable fatty acid profile (being relatively low in saturates), a fibre content that is comparable with other vegetarian protein sources, and a naturally low sodium content. Mycoprotein is a good source of zinc and selenium but the levels of iron and vitamin B12 in mycoprotein are low in comparison to red meat. A small number of studies investigating the cholesterol-lowering effects of mycoprotein have been carried out among normo- and hypercholesterolaemic adults. The published studies to date have a number of limitations (including small sample sizes and short study durations), but overall the studies report statistically significant reductions in total cholesterol amongst hypercholesterolaemic subjects (in the order of 4-14%). These results look promising in terms of the ability of mycoprotein to contribute modest but meaningful effects on blood cholesterol concentrations, as part of a varied and balanced diet. However, the exact amount of mycoprotein that would need to be consumed in free-living populations to have meaningful effects on cholesterol is a candidate for further confirmatory research. A number of studies have investigated the effects of mycoprotein in comparison with other protein sources on satiety. Several studies suggest that the effects of mycoprotein on satiety are greater than an equivalent amount of chicken but it is unclear what mechanism underlies this. The studies conducted so far are relatively small, and carried out under controlled conditions, so it is difficult to extrapolate the results to larger free-living populations. The promotion of mycoprotein could potentially be useful, alongside other strategies, in the management of obesity and type 2 diabetes, as it appears to show beneficial effects on glycaemia and insulinaemia in the small number of studies where this has been investigated. More research is needed to better understand the mechanism of action whereby mycoprotein influences glycaemia and insulinaemia, and whether there is any dose-dependent effect. This paper reviews the published evidence for mycoprotein and the topics above, draws interim conclusions about the role of mycoprotein in human health and identifies areas for future research.
:p
Emma-Leigh
02-09-2010, 01:42 AM
'Starving' Fat Suppresses Appetite
Randy Seeley, PhD (Credit: Image courtesy of University of Cincinnati Academic Health Center)
ScienceDaily (Feb. 8, 2010)
Peptides that target blood vessels in fat and cause them to go into programmed cell death (termed apoptosis) could become a model for future weight-loss therapies, say University of Cincinnati (UC) researchers.
A research team led by Randy Seeley, PhD, of UC's Metabolic Diseases Institute, has found that obese animal models treated with proapoptotic peptide experienced decreased food intake and significant fat loss.
The study was published online ahead of print Jan. 26, 2010, in Diabetes, the official journal of the American Diabetes Association.
White adipose (fat) tissue is vascularized, much like a tumor, and growth of fat tissue is highly dependent on the tissue's ability to build new blood vessels -- a phenomenon called angiogenesis.
Inhibiting adipose angiogenesis -- essentially "starving" fat tissue -- can reverse the effects of a high-fat diet in mice and rats, says Seeley.
"The body is extremely efficient at controlling energy balance," says Seeley, a professor in UC's internal medicine department and recipient of the 2009 Outstanding Scientific Achievement Award from the American Diabetes Association.
"Think of fat tissue like a bathtub," he says. "To keep the amount of water the same, you have to make sure that the speed of the water coming in and the water going out match. If the water is coming in faster than the water is going out, eventually you have to build a bigger bathtub.
"Obesity is the same. People who eat more calories than they burn have to build a bigger fat tissue 'bathtub,' and building new blood vessels is crucial to building this bigger bathtub. For each additional pound of fat tissue, you need to build a mile of blood vessels.
"What we found is that if we can target these fat tissue blood vessels, animals eat less and lose weight as their 'bathtubs' get smaller."
Seeley and his team treated lean and obese mice and rats with the proapoptotic peptide for periods of four or 27 days. They measured energy intake and expenditure daily in all animals -- some on low-fat diets, others on high-fat diets. The team found that the peptide completely reversed high-fat-diet-induced obesity in already obese mice and also reduced body weight in the mice and rats placed on high-fat diets. No changes were recorded in animals on low-fat diets.
Seeley's team found that fat loss was occurring without major changes to energy expenditure, but with reduced food intake. The authors noted that there were no signs of illness with this treatment and results were independent of the actions of the appetite-controlling hormone leptin.
"These experiments indicate that there is a novel system that informs our brains about the size of our fat tissue 'bathtubs' and can influence how much we eat," says Seeley. "The findings highlight the ability to provide new therapeutic strategies for obesity based on these dynamics of blood vessels in our fat tissue." The next step, Seeley says, is to out the important signals that come from fat that cause the weight loss.
This study was supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases. Co-authors include Dong-Hoon Kim, PhD, and Stephen Woods, PhD, both of the University of Cincinnati.
Web address: http://www.sciencedaily.com/releases/2010/02/100201113756.htm
determined4000
03-07-2010, 08:21 PM
http://sun2.science.wayne.edu/~pkhosla/EJLST.pdf
I recently read the above article.
I had always avoided palm oil because of its SF content but this seems to contradict its harmfulness. I also wasn't sure if it made a difference that it was a vegetable source of SF rather than animal.
Emma-Leigh
03-23-2010, 01:06 AM
Effects of body weight and alcohol consumption on insulin sensitivity
Qiwei X Paulson , Jina Hong , Valerie B Holcomb and Nomeli P Nunez
Nutrition Journal 2010, 9:14doi:10.1186/1475-2891-9-14
Published: 22 March 2010
Abstract (provisional)
Background
Obesity is a risk factor for the development of insulin resistance, which can eventually lead to type-2 diabetes. Alcohol consumption is a protective factor against insulin resistance. The mechanism by which alcohol protects against the development of type-2 diabetes is not well known. To determine the mechanism by which alcohol improves insulin sensitivity, we fed water or alcohol to lean, overweight, and obese mice. The aim of this study was to determine whether alcohol consumption and body weights affect overlapping metabolic pathways and to identify specific target genes that are regulated in these pathways.
Method
Adipose tissue dysfunction has been associated with development of type-2 diabetes. We assessed possible gene expression alterations in epididymal white adipose tissue (WAT). We obtained WAT from mice fed a calorie restricted (CR), low fat (LF Control) or high fat (HF) diets and either water or 20% ethanol in the drinking water. We screened the expression of genes related to the regulation of energy homeostasis and insulin regulation using a gene array composed of 384 genes.
Results
Results indicated that alcohol consumption improved insulin sensitivity. The insulin resistance in obese mice was associated with the expression of inflammatory markers Cd68, Il-6 and Il-1alpha; in contrast, most of these genes were down-regulated in CR mice. Moreover, anti-inflammatory factors such as Il-10 and adrenergic beta receptor kinase 1 (Adrbk1) were decreased in obese mice and increased in CR and alcohol-consuming LF mice. For the first time, we report a direct correlation between body weight and the expression of the following genes: Kcnj11 (potassium inwardly-rectifying channel, subfamily J, member 11), Lpin2 (lipin2), and Dusp9 (dual-specificity MAP kinase phosphatase 9).
Conclusion
Our data provide evidence that alcohol consumption increased insulin sensitivity for all three body weights. We showed that alterations in insulin sensitivity induced by body weight were associated with alterations in inflammatory genes. We provide evidence that alcohol may improve insulin sensitivity through up-regulation of anti-inflammatory genes. Moreover, we have indentified potential gene targets in energy metabolic pathways and signal transducers that may contribute to obesity-related insulin resistance as well as calorie restriction and alcohol-induced insulin sensitivity.
Emma-Leigh
04-04-2010, 01:57 AM
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
04-04-2010, 03:20 AM
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
04-09-2010, 02:45 AM
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
04-09-2010, 02:54 AM
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
04-09-2010, 04:21 AM
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
04-09-2010, 10:13 AM
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
04-10-2010, 02:19 PM
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
04-14-2010, 04:10 PM
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.
Insight
04-17-2010, 03:31 PM
http://www.ncbi.nlm.nih.gov/pubmed/15831796
J Appl Physiol. 2005 Aug;99(2):707-14. Epub 2005 Apr 14.
Ingestion of a high-glycemic index meal increases muscle glycogen storage at rest but augments its utilization during subsequent exercise.
Wee SL, Williams C, Tsintzas K, Boobis L.
School of Sport and Exercise Sciences, Loughborough University, Loughborough, Leicestershire LE11 3TU, UK.
Abstract
The aim of this study was to compare the effect of preexercise breakfast containing high- and low-glycemic index (GI) carbohydrate (CHO) (2.5g CHO/kg body mass) on muscle glycogen metabolism. On two occasions, 14 days apart, seven trained men ran at 71% maximal oxygen uptake for 30 min on a treadmill. Three hours before exercise, in a randomized order, subjects consumed either isoenergetic high- (HGI) or low-GI (LGI) CHO breakfasts that provided (per 70 kg body mass) 3.43 MJ energy, 175 g CHO, 21 g protein, and 4 g fat. The incremental areas under the 3-h plasma glucose and serum insulin response curves after the HGI meal were 3.9- (P < 0.05) and 1.4-fold greater (P < 0.001), respectively, than those after the LGI meal. During the 3-h postprandial period, muscle glycogen concentration increased by 15% (P < 0.05) after the HGI meal but remained unchanged after the LGI meal. Muscle glycogen utilization during exercise was greater in the HGI (129.1 +/- 16.1 mmol/kg dry mass) compared with the LGI (87.9 +/- 15.1 mmol/kg dry mass; P < 0.01) trial. Although the LGI meal contributed less CHO to muscle glycogen synthesis in the 3-h postprandial period compared with the HGI meal, a sparing of muscle glycogen utilization during subsequent exercise was observed in the LGI trial, most likely as a result of better maintained fat oxidation.
Emma-Leigh
04-18-2010, 02:40 AM
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
04-27-2010, 12:03 PM
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...
Insight
05-03-2010, 05:07 PM
Effects of body weight and alcohol consumption on insulin sensitivity
Qiwei X Paulson , Jina Hong , Valerie B Holcomb and Nomeli P Nunez
Nutrition Journal 2010, 9:14doi:10.1186/1475-2891-9-14
Published: 22 March 2010
Abstract (provisional)
Background
Obesity is a risk factor for the development of insulin resistance, which can eventually lead to type-2 diabetes. Alcohol consumption is a protective factor against insulin resistance. The mechanism by which alcohol protects against the development of type-2 diabetes is not well known. To determine the mechanism by which alcohol improves insulin sensitivity, we fed water or alcohol to lean, overweight, and obese mice. The aim of this study was to determine whether alcohol consumption and body weights affect overlapping metabolic pathways and to identify specific target genes that are regulated in these pathways.
Method
Adipose tissue dysfunction has been associated with development of type-2 diabetes. We assessed possible gene expression alterations in epididymal white adipose tissue (WAT). We obtained WAT from mice fed a calorie restricted (CR), low fat (LF Control) or high fat (HF) diets and either water or 20% ethanol in the drinking water. We screened the expression of genes related to the regulation of energy homeostasis and insulin regulation using a gene array composed of 384 genes.
Results
Results indicated that alcohol consumption improved insulin sensitivity. The insulin resistance in obese mice was associated with the expression of inflammatory markers Cd68, Il-6 and Il-1alpha; in contrast, most of these genes were down-regulated in CR mice. Moreover, anti-inflammatory factors such as Il-10 and adrenergic beta receptor kinase 1 (Adrbk1) were decreased in obese mice and increased in CR and alcohol-consuming LF mice. For the first time, we report a direct correlation between body weight and the expression of the following genes: Kcnj11 (potassium inwardly-rectifying channel, subfamily J, member 11), Lpin2 (lipin2), and Dusp9 (dual-specificity MAP kinase phosphatase 9).
Conclusion
Our data provide evidence that alcohol consumption increased insulin sensitivity for all three body weights. We showed that alterations in insulin sensitivity induced by body weight were associated with alterations in inflammatory genes. We provide evidence that alcohol may improve insulin sensitivity through up-regulation of anti-inflammatory genes. Moreover, we have indentified potential gene targets in energy metabolic pathways and signal transducers that may contribute to obesity-related insulin resistance as well as calorie restriction and alcohol-induced insulin sensitivity.
Wow. Didn't see that one coming
blumnblam
05-07-2010, 12:23 PM
http://www.sciencenews.org/view/generic/id/58972/title/Taste_of_power_goes_to_the_head%2C_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
05-07-2010, 10:55 PM
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
05-13-2010, 08:20 PM
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 Somali 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
05-30-2010, 03:35 AM
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
05-31-2010, 05:39 AM
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
05-31-2010, 09:40 PM
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
05-31-2010, 09:42 PM
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
06-08-2010, 02:24 AM
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]
Insight
06-08-2010, 09:14 AM
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]
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.
Emma-Leigh
06-08-2010, 12:00 PM
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. :o
http://lib.bioinfo.pl/pmid:20503441
^
although a few have some good info in them....
tubalard
06-08-2010, 04:10 PM
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
06-11-2010, 10:35 PM
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.....!! :rolleyes:
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)
Hmm, this is most interesting.
[quote]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
06-13-2010, 07:55 PM
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
06-17-2010, 12:06 PM
"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
06-17-2010, 12:14 PM
interesting debate on IGF-1 and requirement for muscle growth:
http://jap.physiology.org/cgi/pdf_extract/108/6/1825
Emma-Leigh
06-17-2010, 12:21 PM
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
06-19-2010, 06:45 PM
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
06-19-2010, 06:45 PM
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
06-30-2010, 03:50 PM
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/cardiovascular_disease/eggs.html
thegymbum
07-04-2010, 12:08 PM
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
07-04-2010, 08:35 PM
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.
thegymbum
07-11-2010, 03:33 PM
Just came across an article that I found rather interesting. It's a little older, but interesting nonetheless. From Journal of Applied Physiology.
Skeletal muscle adaptation: training twice every second day vs. training once daily
Abstract...
"Low muscle glycogen content has been demonstrated to enhance transcription of a number of genes involved in training adaptation. These results made us speculate that training at a low muscle glycogen content would enhance training adaptation. We therefore performed a study in which seven healthy untrained men performed knee extensor exercise with one leg trained in a low-glycogen (Low) protocol and the other leg trained at a high-glycogen (High) protocol. Both legs were trained equally regarding workload and training amount. On day 1, both legs (Low and High) were trained for 1 h followed by 2 h of rest at a fasting state, after which one leg (Low) was trained for an additional 1 h. On day 2, only one leg (High) trained for 1 h. Days 1 and 2 were repeated for 10 wk. As an effect of training, the increase in maximal workload was identical for the two legs. However, time until exhaustion at 90% was markedly more increased in the Low leg compared with the High leg. Resting muscle glycogen and the activity of the mitochondrial enzyme 3-hydroxyacyl-CoA dehydrogenase increased with training, but only significantly so in Low, whereas citrate synthase activity increased in both Low and High. There was a more pronounced increase in citrate synthase activity when Low was compared with High. In conclusion, the present study suggests that training twice every second day may be superior to daily training."
Interesting. What are everyone's thoughts? I wonder what the trade off is between having the extra glycogen available to power you through your workout vs. the training adaptation benefits of being in a more depleted state?
xAlphax
08-12-2010, 07:22 AM
...
The influence of the type of dietary fat on postprandial fat oxidation rates: monounsaturated (olive oil) vs. saturated fat (cream).
OBJECTIVE: To compare postprandial whole-body fat oxidation rates in humans, following high-fat (43% of total energy) mixed breakfast meals, of fixed energy and macronutrient composition, rich in either monounsaturated fat (MUFA) from extra virgin olive oil or saturated fat (SFA) from cream. DESIGN: Paired comparison of resting metabolic rate (RMR), thermic effect of a meal and substrate oxidation rates following consumption of isocaloric breakfast meals, differing only in the type of fat, administered in random order 1-2 weeks apart. SUBJECTS: Fourteen male volunteers, body mass index (BMI) in the range 20-32 kg/m(2), aged 24-49 y and resident in Melbourne, Australia, were recruited by advertisement in the local media or by personal contact. MEASUREMENTS: Body size and composition was determined by anthropometry and dual energy X-ray absorptiometry (DEXA). Indirect calorimetry was used to measure RMR, thermic effect of a meal, post-meal total energy expenditure and substrate oxidation rate. Blood pressure and pulse rates were measured with an automated oscillometric system. Fasting and 2 h postprandial glucose and insulin concentrations and the fasting lipid profile were also determined. RESULTS: In the 5 h following the MUFA breakfast, there was a significantly greater postprandial fat oxidation rate (3.08+/-4.58 g/5 h, P=0.017), and lower postprandial carbohydrate oxidation rate (P=0.025), than after the SFA breakfast. Thermic effect of a meal was significantly higher (55 kJ/5 h, P=0.034) after the MUFA breakfast, in subjects with a high waist circumference (HWC > or = 99 cm) than those with a low waist circumference (LWC<99 cm). This difference was not detected following the SFA breakfast (P=0.910). CONCLUSION: If postprandial fat oxidation rates are higher after high MUFA, rather than SFA meals, then a simple change to the type of dietary fat consumed might have beneficial effects in curbing weight gain in men consuming a relatively high-fat diet. This may be particularly evident in men with a large waist circumference.
Int. Journal of Obesity
Emma-Leigh
10-28-2010, 02:39 AM
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.
PMID: 17848938 [PubMed - indexed for MEDLINE]PMCID: PMC2376744
Free PMC Article
Emma-Leigh
10-29-2010, 08:58 PM
Dietary fat: assessing the evidence in support of a moderate-fat diet; the benchmark based on lipoprotein metabolism
P M Kris-Etherton, A E Binkoski, G Zhao, S M Coval, et al.
The Proceedings of the Nutrition Society. Cambridge: May 2002. Vol. 61, Iss. 2; pg. 287, 12 pgs
Abstract (Summary)
There is a growing database that has evaluated the effects of varying amounts of total fat on risk factors for cardiovascular disease, diabetes and overweight and obesity. The evidence clearly suggests that extremes in dietary fat should be avoided, and instead a diet moderate in total fat (25-35 % energy) is preferable for the majority of individuals. Moreover, we now appreciate the importance of individualizing dietary fat recommendations within this range of total fat. With respect to cardiovascular disease, a diet higher in total fat (30-35 % energy) affects the lipid and lipoprotein risk profile more favourably than a lower-fat diet; this is also the case for individuals with diabetes, with the added benefit of better glycaemic control. Dietary fibre ([>, double =]25g/d) attenuates and even prevents the potentially adverse lipid and lipoprotein effects of a lower-fat diet. With respect to weight control, a moderate-fat diet can be as, or even more, effective than a lower-fat diet, because of advantages with long-term adherence and potentially favourable effects on lipids and lipoproteins. Thus, there is now a convincing scientific basis to advocate a diet moderate in total fat for the majority of individuals. Implicit to this position is that unsaturated fat has numerous beneficial health effects. However, because fat is energy dense, moderation in fat intake is essential for weight control. Consequently, a simple message to convey is to avoid diets that are very low and very high in fat. Moreover, within the range of a moderate-fat diet it is still important to individualize the total fat prescription. Nonetheless, the guiding principle is that moderation in total fat is the defining benchmark for a contemporary diet that reduces risk of chronic disease. [PUBLICATION ABSTRACT]
hankst
11-21-2010, 12:50 PM
http://www.ncbi.nlm.nih.gov/pubmed/19833807
J Appl Physiol. 2009 Dec;107(6):1847-56. Epub 2009 Oct 15.
When energy balance is maintained, exercise does not induce negative fat balance in lean sedentary, obese sedentary, or lean endurance-trained individuals.
Melanson EL, Gozansky WS, Barry DW, Maclean PS, Grunwald GK, Hill JO.
Division of Endocrinology, Metabolism, and Diabetes, Center for Human Nutrition, University of Colorado Denver, School of Medicine, Denver, Colorado 80045, USA. Ed.melanson@ucdenver.edu
Abstract
Fat oxidation during exercise is increased by endurance training, and evidence suggests that fat oxidation during exercise is impaired in obesity. Thus the primary aim of this study was to compare the acute effects of exercise on 24-h fat oxidation and fat balance in lean sedentary [LS, n = 10, body mass index (BMI) = 22.5 +/- 6.5 kg/m(2)], lean endurance-trained (LT, n = 10, BMI = 21.2 +/- 1.2 kg/m(2)), and obese sedentary (OS, n = 7, BMI = 35.5 +/- 4.4 kg/m(2)) men and women. Twenty-four-hour energy expenditure and substrate oxidation were measured under sedentary (control; CON) and exercise (EX) conditions while maintaining energy balance. During EX, subjects performed 1 h of stationary cycling at 55% of aerobic capacity. Twenty-four-hour fat oxidation did not differ on the CON or EX day in LS (43 +/- 9 vs. 29 +/- 7 g/day, respectively), LT (53 +/- 8 vs. 42 +/- 5 g/day), or OS (58 +/- 7 vs. 80 +/- 9 g/day). However, 24-h fat balance was significantly more positive on EX compared with CON (P < 0.01). Twenty-four-hour glucose, insulin, and free fatty acid (FFA) profiles were similar on the EX and CON days, but after consumption of the first meal, FFA concentrations remained below fasting levels for the remainder of the day. These data suggest that when exercise is performed with energy replacement (i.e., energy balance is maintained), 24-h fat oxidation does not increase and in fact, may be slightly decreased. It appears that the state of energy balance is an underappreciated factor determining the impact of exercise on fat oxidation.
PMID: 19833807 [PubMed - indexed for MEDLINE]
---------------
"No ****, Sherlock!"
But it's good to have this one handy when someone preaches to you how oh so very possible it is to lose fat by doing cardio while eating at maintenance.
spoch
12-30-2010, 09:24 AM
So is it still considered bad to go w/ fructose post workout?
stancel
12-30-2010, 10:10 AM
Very interesting stuff:
http://www.jci.org/articles/view/37385
"In general, insulin sensitivity and glucose tolerance were not affected by the consumption of glucose but were decreased during the consumption of fructose (Table 5). Fasting glucose concentrations decreased in subjects consuming glucose but increased in subjects consuming fructose. Fasting insulin concentrations were unchanged during glucose consumption but were increased during consumption of fructose beverages."
"...both total abdominal fat and VAT volume were significantly increased in subjects consuming fructose"
Worth the read.
lol, what bullsh*t, fructose beverages (HFCS?), of course they got fat. They're drinking sugar water with tons of sugar. Make them get their fructose in its moderately low natural state with water and fiber in fruit and veggies and then show us what happens.
Emma-Leigh
01-17-2011, 09:06 PM
See - nutritionists aren't right - eating breakfast is bad for you.... :p
Nutrition Journal 2011, 10:5doi:10.1186/1475-2891-10-5
Published: 17 January 2011
Abstract (provisional)
Impact of breakfast on daily energy intake - an analysis of absolute versus relative breakfast calories
Volker Schusdziarra , Margit Hausmann , Claudia Wittke , Johanna Mittermeier , Marietta Kellner , Aline Naumann , Stefan Wagenpfeil and Johannes Erdmann
Objective
The role of breakfast energy in total daily energy intake is a matter of debate. Acute feeding experiments demonstrated that high breakfast energy leads to greater overall intake supported by cross-sectional data of a free-living population. On the other hand, a large intraindividual analysis has indicated that a high proportion of breakfast to overall intake is associated with lower daily energy intake. To evaluate these apparently contradictory results in greater detail both ways of analysis were applied to the same data set of dietary records.
Methods
On an intraindividual basis total daily energy intake was related to the absolute values of breakfast energy intake or to the ratio of breakfast to overall intake, respectively. Food intake of 280 obese and 100 normal weight subjects was analyzed who recorded over 10 (obese) or 14 (normal weight) consecutive days, respectively.
Results
Increasing breakfast energy was associated with greater overall intake in normal weight and obese subjects. The increasing ratio of breakfast to total daily energy intake was associated with a significant reduction of overall intake on days where post-breakfast energy was significantly reduced. Correlational and multiple regression analysis support the concept that absolute breakfast calories have the strongest influence on daily energy intake.
Conclusion
Reduced breakfast energy intake is associated with lower total daily intake. The influence of the ratio of breakfast to overall energy intake largely depends on the post-breakfast rather than breakfast intake pattern. Therefore, overweight and obese subjects should consider the reduction of breakfast calories as a simple option to improve their daily energy balance.
Emma-Leigh
01-17-2011, 09:16 PM
J Nutr Sci Vitaminol (Tokyo). 2009 Jun;55(3):201-7.
Is glycemic index of food a feasible predictor of appetite, hunger, and satiety?
Niwano Y, Adachi T, Kashimura J, Sakata T, Sasaki H, Sekine K, Yamamoto S, Yonekubo A, Kimura S.
Carbohydrate Task Force, International Life Sciences Institute Japan, Tokyo. y.niwano@sunnyhealth.co.jp
Abstract
This review assesses the feasibility of using glycemic index (GI) as a predictor of appetite, hunger and satiety by surveying published human intervention studies. We also discuss the relationship between GI and two appetite/satiety control hormones, leptin and ghrelin. Ingestion of high-GI food increased hunger and lowered satiety in short-term human intervention studies. This effect may be attributed to the rapid decline in blood glucose level following a hyperinsulinemic response caused by a sharp and transient increase in blood glucose level that occurs after the ingestion of high-GI food, which is defined as the glucostatic theory. However, appetite, hunger and satiety after the ingestion of foods with varying GI were inconsistent among long-term human intervention studies. From the few relevant long-term studies available, we selected two recent well-designed examples for analysis, but they failed to elicit clear differences in glycemic and insulinemic responses between high- and low-GI meals (consisting of a combination of different foods or key carbohydrate-rich foods incorporated into habitual diets). One of the reasons that these studies could not predict glycemic response to mixed meals is presumably that the GI of each particular food was not reflected in that of the mixed meals as a whole. Thus, it is difficult to conclude that the GI values of foods or mixed meals are a valid long-term predictor for appetite, hunger and satiety. Both insulin and insulin-mediated glucose uptake and metabolism in adipose tissue affect blood leptin concentration and its diurnal pattern. Circulating ghrelin level is suppressed by carbohydrate-rich meals, presumably via glycemia and insulinemia. Accordingly, low-GI foods may not necessarily increase satiety or suppress appetite and/or hunger because of the lack of insulin-mediated leptin stimulation and ghrelin suppression. However, insulin-mediated leptin stimulation and ghrelin suppression per se is not consistent among studies; thus we were not able to identify a clear relationship among GI, satietogenic leptin, and appetitic ghrelin.
PMID: 19602827 [PubMed - indexed for MEDLINE]Free Article
synthetic
01-22-2011, 09:32 AM
educate yourself on fats: 3 pages..
http://www.scientificpsychic.com/fitness/fattyacids.html
coals
02-01-2011, 06:48 AM
One of the most interesting articles I've ever been fortunate enough to read:
Title: Does the difference between physically active and couch potato lie in the dopamine system?
Obesity and other inactivity related diseases are increasing at an alarming rate especially in Western societies. Because of this, it is important to understand the regulating mechanisms involved in physical activity behavior. Much research has been done in regard to the psychological determinants of physical activity behavior; however, little is known about the underlying genetic and biological factors that may contribute to regulation of this complex trait. It is true that a significant portion of any trait is regulated by genetic and biological factors. In the case of voluntary physical activity behavior, these regulating mechanisms appear to be concentrated in the central nervous system. In particular, the dopamine system has been shown to regulate motor movement, as well as motivation and reward behavior. The pattern of regulation of voluntary physical activity by the dopamine system is yet to be fully elucidated. This review will summarize what is known about the dopamine system and regulation of physical activity, and will present a hypothesis of how this signaling pathway is mechanistically involved in regulating voluntary physical activity behavior. Future research in this area will aid in developing personalized strategies to prevent inactivity related diseases.
Keywords: Physical activity, behavior, dopamine, dopamine receptors, dopamine signaling, wheel running, motivation
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836544/
Emma-Leigh
02-01-2011, 12:37 PM
One of the most interesting articles I've ever been fortunate enough to read:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836544/
T'is a good one, isn't it. ;)
ps - did you ever get that other one I emailed you? :confused:
coals
02-01-2011, 03:14 PM
T'is a good one, isn't it. ;)
ps - did you ever get that other one I emailed you? :confused:
No! I thought you were ignoring me cause I occasionally (rarely really) troll people when they ask dumb questions lol
When I finished reading the dopamine article I put it down, blankly stared into space then raised my hands to the sky and called out "Oh god, the beauty that is this paper is too much for my mortal eyes!" And then cried tears of joy
When I get out of undergrad, this type of neuro-regulation of the various factors that contribute to obesity is EXACTLY what I want to research/study.
Brb Curing obesity... Serious.
reverse79
02-02-2011, 08:36 PM
Interesting study
http://www.ncbi.nlm.nih.gov/pubmed/21084649
robin91
02-03-2011, 12:14 PM
So effectively this article supports the theories behind IF, depending on your dietary approach. Good to hear! :D
coals
03-15-2011, 10:27 AM
So effectively this article supports the theories behind IF, depending on your dietary approach. Good to hear! :D
D'oh, imagine that. Providing a stimulus before the nutrients favorably redirects the nutrients ;)
Here we go:
Interesting article regarding protein retention and intake values looking at various groups (including a paragraph on bodybuilders). Also looks protein retention vs synthesis, good stuff. I've attached the full study.
Dietary protein for athletes: from requirements to metabolic advantage
Stuart M. Phillips
Abstract: The Dietary Reference Intakes (DRI) specify that the requirement for dietary protein for all individuals aged
19 y and older is 0.8 g protein kg–1 d–1.This Recommended Dietary Allowance (RDA) is cited as adequate for all persons .This amount of protein would be considered by many athletes as the amount to be consumed in a single meal, particularly for strength-training athletes. There does exist, however, published data to suggest that individuals habitually performing
resistance and (or) endurance exercise require more protein than their sedentary counterparts. The RDA values for protein are clearly set at ‘‘. . .the level of protein judged to be adequate... to meet the known nutrient needs for practically all healthy people. . .’’. The RDA covers protein losses with margins for inter-individual variability and protein quality; the notion of consumption of excess protein above these levels to cover increased needs owing to physical activity is not, however, given any credence. Notwithstanding, diet programs (i.e., energy restriction) espousing the virtue of high protein enjoy continued popularity. A number of well-controlled studies are now published in which ‘‘higher’’ protein diets have been shown to be effective in promoting weight reduction, particularly fat loss. The term ‘‘higher’’ refers to a diet that has people consuming more than the general populations’ average intake of ~15% of energy from protein, e.g., as much as
30%–35%, which is within an Acceptable Macronutrient Distribution Range (AMDR) as laid out in the DRIs. Of relevance to athletes and those in clinical practice is the fact that higher protein diets have quite consistently been shown to result in greater weight loss, greater fat loss, and preservation of lean mass as compared with ‘‘lower’’ protein diets. A framework for understanding dietary protein intake within the context of weight loss and athletic performance is laid out.
I'd also like to mention the first paragraph on mechanisms I found very interesting. Will probably pursue that next.
Would also like to highlight
. Even in the face of consumption of protein above requirement levels during energy deficit, excess amino acids, once deaminated, produce carbon skeletons that would be oxidized, but that are ultimately very poor lipogenic substrates; in fact, only leucine and lysine as purely ketogenic amino acids (i.e., yielding acetoacetyl CoA) could likely support significant lipogenesis. Simply put, it is very metabolically difficult to turn excess protein into fat
coals
03-19-2011, 01:13 PM
Just cause I've been re-evaluating protein requirements. And wondering why on earth so many people take in >250g's a day (especially the smaller kids)
This one is another Stuart Phillip's production (I think I'm developing a nerd-crush on this guy).
A Critical Examination of Dietary Protein Requirements, Benefits, and Excesses in Athletes
Authors: Stuart M. Phillips, Daniel R. Moore, Jason E. Tang
There is likely no other dietary component that inspires as much debate, insofar as athletes are concerned, as protein. How much dietary protein is required, optimal, or excessive? Dietary guidelines from a variety of sources have settled on an adequate dietary protein intake for those over the age of 19 of ~0.8–0.9 g protein·kg body weight–1·d–1. According to U.S. and Canadian dietary reference intakes (33), the recommended allowance for protein of 0.8 g protein·kg–1·d–1 is "the average daily intake level that is sufficient to meet the nutrient requirement of nearly all [~98%] . . . healthy individuals" (p. 22). The panel also stated, "in view of the lack of compelling evidence to the contrary, no additional dietary protein is suggested for healthy adults undertaking resistance or endurance exercise" (33, p. 661). Currently, no group or groups of scientists involved in establishing dietary guidelines see a need for any statement that athletes or people engaging in regular physical activity require more protein than their sedentary counterparts. Popular magazines, numerous Web sites, trainers, and many athletes decry protein intakes even close to those recommended. Even joint position stands from policy-setting groups state that "protein recommendations for endurance athletes are 1.2 to 1.4 g/kg body weight per day, whereas those for resistance and strength-trained athletes may be as high as 1.6 to 1.7 g/kg body weight per day" (1, p. 1544). The divide between those setting dietary protein requirements and those who might be making practical recommendations for athletes appears substantial, but ultimately, most athletes indicate that they consume protein at levels beyond even the highest recommendations. Thus, one might conclude that any debate on protein "requirements" for athletes is inconsequential; however, a critical analysis of existing and new data reveals novel ideas and concepts that may represent some common ground between these apparently conflicted groups. The goal of this review was to provide a critical and thorough analysis of current data on protein requirements in an attempt to provide some guidance to athletes, trainers, coaches, and sport dietitians on athletes' protein intake. In addition, an effort was made to clearly distinguish between "required" dietary protein, "optimal" intakes, and intakes that are likely "excessive," perhaps not from the standpoint of health, but certainly from the standpoint of potentially compromised performance.
Overall a very good review, Theres some things I'd like to highlight.
If we define an optimal level as being a protein intake that would 1.) support an athlete's ability to repair and replace any damaged proteins (resulting potentially from oxidative stress or mechanical disruption); 2.)adaptively "remodel" proteins in structures such as muscle, bone, tendon, and ligaments to better withstand the stress and strain imposed by training and competition; 3.) maintain optimal function of all metabolic pathways in which amino acids are participatory intermediates (which includes being oxidative fuels); 4.) support increments in lean mass, if desired; 5.) support an optimally functioning immune system; and 6.) support the optimal rate of production of all plasma proteins required for optimally physiological function, would the previous estimates of protein intake represent an optimal level?
Feel like no one really pays any attention to 3-6, all of which are important. A pretty good definition for optimal intake I'd say.
The results obtained with resistance exercise (30,58) may be markedly different from those seen with endurance exercise because resistance exercise is fundamentally anabolic and stimulates protein synthesis, such that loss of amino acids in the fasted state is reduced for up to 48h
Digression, but point scored for IF, come at me bros who say we catabolize all teh jack3d fibraz during the fast.
...Such a calculation relies, however, on a number of very tenuous assumptions that are not tested in most experimental paradigms, so increased leucine oxidation during endurance exercise may mean an increased need for dietary leucine and not necessarily an increased need for dietary protein.
Not to digress from the point of the paper, but this would be an interesting point to start looking at BCAA supplementation for resistance training. Could there be a similar mechanism behind resistance exercises that could prove beneficial (especiailly fasted if we're oxidizing leucine instead of glucose floating around from earlier meals/glycogen). Even more interesting, could supplementation with bcaa's, especially leucine, then lead to reduced requirement (by that I mean optimal levels) of overall intake /Do we need an entire caseinate protein (for example) if the body is really just after the leucine amino? Interesting idea to pursue, perhaps later. This bears substantial additional weight when considering fasted training, as higher protein oxidation is likely to be observed.
PM if you want it (it's a great read). Can't attach this one, dont' want to get in trouble :)
Emma-Leigh
03-30-2011, 11:51 PM
This one is interesting and reflects a few other studies / things I have researched in the past....
The Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2010-2944
Submitted on December 16, 2010, Accepted on March 14, 2011, Published online on March 30, 2011
Higher Energy Expenditure in Humans Predicts Natural Mortality
Reiner Jumpertz, Robert L. Hanson, Maurice L. Sievers, Peter H. Bennett, Robert G. Nelson and Jonathan Krakoff
Context: Higher metabolic rates increase free radical formation, which may accelerate aging and lead to early mortality.
Objective: Our objective was to determine whether higher metabolic rates measured by two different methods predict early natural mortality in humans.
Design: Nondiabetic healthy Pima Indian volunteers (n = 652) were admitted to an inpatient unit for approximately 7 d as part of a longitudinal study of obesity and diabetes risk factors. Vital status of study participants was determined through December 31, 2006. Twenty-four-hour energy expenditure (24EE) was measured in 508 individuals, resting metabolic rate (RMR) was measured in 384 individuals, and 240 underwent both measurements on separate days. Data for 24EE were collected in a respiratory chamber between 1985 and 2006 with a mean (SD) follow-up time of 11.1 (6.5) yr and for RMR using an open-circuit respiratory hood system between 1982 and 2006 with a mean follow-up time of 15.4 (6.3) yr. Cox regression models were used to test the effect of EE on natural mortality, controlled for age, sex, and body weight.
Results: In both groups, 27 natural deaths occurred during the study period. For each 100-kcal/24 h increase in EE, the risk of natural mortality increased by 1.29 (95% confidence interval = 1.00–1.66; P < 0.05) in the 24EE group and by 1.25 (95% confidence interval = 1.01–1.55; P < 0.05) in the RMR group, after adjustment for age, sex, and body weight in proportional hazard analyses.
Conclusions: Higher metabolic rates as reflected by 24EE or RMR predict early natural mortality, indicating that higher energy turnover may accelerate aging in humans.
What is that saying? Live hard/fast.... die young....
Emma-Leigh
03-31-2011, 12:10 AM
The answer to HTN - drink MORE coffee. ;)
First published March 30, 2011, doi: 10.3945/ajcn.110.004044
Am J Clin Nutr March 2011 ajcn.004044
Habitual coffee consumption and risk of hypertension: a systematic review and meta-analysis of prospective observational studies1,2,3
Zhenzhen Zhang, Gang Hu, Benjamin Caballero, Lawrence Appel, and Liwei Chen
+ Author Affiliations
Abstract
Background: In 2 meta-analyses of randomized controlled trials, increased coffee intake was associated with slightly higher blood pressure. However, these trials were short in duration (<85 d).
Objective: We conducted a systematic review and meta-analyses of long-term prospective studies that examined the association of habitual coffee consumption with risk of hypertension.
Design: We searched electronic databases (MEDLINE, EMBASE, Agricola, and Cochrane Library) through August 2009 with the use of a standardized protocol. Eligible studies were prospective cohort trials that examined the association of coffee consumption with incident hypertension or blood pressure.
Results: From 6 prospective cohort studies, a total of 172,567 participants and 37,135 incident hypertension cases were included. Mean follow-up ranged from 6.4 to 33.0 y. Compared with the lowest consumption [<1 cup (≈237 mL)/d], the pooled relative risks (RRs) for hypertension were 1.09 (95% CI: 1.01, 1.18) for the next higher category (1–3 cups/d), 1.07 (95% CI: 0.96, 1.20) for the second highest category (3–5 cups/d), and 1.08 (95% CI: 0.96, 1.21) for the highest category (>5 cups/d). A dose-response meta-analysis showed an inverse “J-shaped” curve (P for quadratic term < 0.001) with hypertension risk increasing up to 3 cups/d (RR for comparison of 3 with 0 cups/d: 1.07; 95% CI: 0.97, 1.20) and decreasing with higher intakes (RR for comparison of 6 with 0 cups/d: 0.99; 95% CI: 0.89, 1.10).
Conclusion: The results suggest that habitual coffee consumption of >3 cups/d was not associated with an increased risk of hypertension compared with <1 cup/d; however, a slightly elevated risk appeared to be associated with light-to-moderate consumption of 1 to 3 cups/d.
coals
04-09-2011, 11:02 AM
Intermittent fasting may potentially improve testosterone/estrogen ratio?
Abstract:
Gonadal transcriptome alterations in response to dietary energy intake: sensing the reproductive environment.
Martin B, Pearson M, Brenneman R, Golden E, Wood W, Prabhu V, Becker KG, Mattson MP, Maudsley S.
Laboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland, United States of America.
Abstract
Reproductive capacity and nutritional input are tightly linked and animals' specific responses to alterations in their physical environment and food availability are crucial to ensuring sustainability of that species. We have assessed how alterations in dietary energy intake (both reductions and excess), as well as in food availability, via intermittent fasting (IF), affect the gonadal transcriptome of both male and female rats. Starting at four months of age, male and female rats were subjected to a 20% or 40% caloric restriction (CR) dietary regime, every other day feeding (IF) or a high fat-high glucose (HFG) diet for six months. The transcriptional activity of the gonadal response to these variations in dietary energy intake was assessed at the individual gene level as well as at the parametric functional level. At the individual gene level, the females showed a higher degree of coherency in gonadal gene alterations to CR than the males. The gonadal transcriptional and hormonal response to IF was also significantly different between the male and female rats. The number of genes significantly regulated by IF in male animals was almost 5 times greater than in the females. These IF males also showed the highest testosterone to estrogen ratio in their plasma. Our data show that at the level of gonadal gene responses, the male rats on the IF regime adapt to their environment in a manner that is expected to increase the probability of eventual fertilization of females that the males predict are likely to be sub-fertile due to their perception of a food deficient environment.
Emma-Leigh
04-09-2011, 02:33 PM
Intermittent fasting may potentially improve testosterone/estrogen ratio?
Abstract:
Is there an echo in here?
:p
;)
coals
04-10-2011, 03:14 AM
lol what got you so interested in cannaboids all of a sudden :p , gonna pull post-contest arnold?
http://californiapotblog.com/wp-content/uploads/2010/04/arnold-schwarzenegger-smoking-marijuana-weed.jpg
Can you pm me those texts if you have them?
toolslave462@gmail.com
04-20-2011, 07:39 PM
http://en.m.wikipedia.org/wiki/Minnesota_Starvation_Experiment
In 1944 U of M did a 12 month study on a caloric deficit diet in warlike conditions. Which means basically they consumed bread potatoes and what not for the majority of their diet. Study results showed they lost 2.5lbs per week.
I was curious if there any scientific studies done similar to this except with a balanced diet?
HealthResearch
04-21-2011, 12:37 PM
http://en.m.wikipedia.org/wiki/Minnesota_Starvation_Experiment
In 1944 U of M did a 12 month study on a caloric deficit diet in warlike conditions. Which means basically they consumed bread potatoes and what not for the majority of their diet. Study results showed they lost 2.5lbs per week.
I was curious if there any scientific studies done similar to this except with a balanced diet?
Not to the extent the Minnesota study was done. That would probably be illegal now.
TheLadiesMan
05-06-2011, 07:19 PM
http :// health. usnews. co m/health-news/diet-fitness/diet/articles/2011/05/05/obese-teens-lack-vitamin-d-study-finds
Good read here, but whether raising levels would mitigate risks of being overweight remains unclear. Vitamin D is very underrated in my opinion, it has many great benefits including the prevention of osteomalacia. Osteomalacia causes weakness of the muscular system and brittle bones, and is most prevalent among adults with vitamin d deficiency.
WEDNESDAY, May 4 (HealthDay News) -- Low levels of vitamin D are common in obese adolescents, a new study finds.
Researchers screened 68 obese adolescents and found low vitamin D levels in all of the girls (72 percent were deemed deficient and 28 percent insufficient) and in 91 percent of the boys (69 percent deficient and 22 percent insufficient).
After treatment, 43 of the youths had their vitamin D levels measured again and, although levels generally increased, normal levels were achieved in just 28 percent of the participants. In the others, repeated bouts of vitamin D treatment did not bring the teens' vitamin D levels to normal, which the researchers described as "concerning."
The adolescents' lack of response to treatment may be due to the fact that vitamin D is sequestered in body fat, the researchers said.
"The prevalence of low vitamin D status among obese adolescents in this study is greater than previously reported for this age group," Dr. Zeev Harel, a pediatrician specializing in adolescent medicine at Hasbro Children's Hospital in Providence, R.I., and the study's lead author, said in a hospital news release.
The study was published in the May issue of the Journal of Adolescent Health.
Vitamin D is produced by the skin in response to exposure to sunlight. It is also found in certain foods, including eggs, fish and fortified foods such as dairy products and breakfast cereals.
"It is possible that the association between obesity and low vitamin D status is indirect, arising from obese individuals having fewer outdoor activities than lean individuals and, therefore, less exposure to sun," the researchers wrote. "Likewise, it is also possible that obese individuals do not consume enough foods that contain vitamin D."
They called for closer monitoring of vitamin D levels in obese adolescents and for more research to determine if restoring normal vitamin D levels could help reduce the health risks associated with obesity.
Obesity -- now estimated to affect 16.4 percent of kids and teens between 10 and 17 -- can increase the risk of high blood pressure, heart disease, and type 2 diabetes, as well as some types of cancer, the researchers noted.
Emma-Leigh
05-19-2011, 02:01 AM
This is an interesting one:
Int J Sport Nutr Exerc Metab. 2011 Apr;21(2):97-104.
Effect of two different weight-loss rates on body composition and strength and power-related performance in elite athletes.
Garthe I, Raastad T, Refsnes PE, Koivisto A, Sundgot-Borgen J.
Abstract
When weight loss (WL) is necessary, athletes are advised to accomplish it gradually, at a rate of 0.5-1 kg/wk. However, it is possible that losing 0.5 kg/wk is better than 1 kg/wk in terms of preserving lean body mass (LBM) and performance. The aim of this study was to compare changes in body composition, strength, and power during a weekly body-weight (BW) loss of 0.7% slow reduction (SR) vs. 1.4% fast reduction (FR). We hypothesized that the faster WL regimen would result in more detrimental effects on both LBM and strength-related performance. Twenty-four athletes were randomized to SR (n = 13, 24 ± 3 yr, 71.9 ± 12.7 kg) or FR (n = 11, 22 ± 5 yr, 74.8 ± 11.7 kg). They followed energy-restricted diets promoting the predetermined weekly WL. All athletes included 4 resistance-training sessions/wk in their usual training regimen. The mean times spent in intervention for SR and FR were 8.5 ± 2.2 and 5.3 ± 0.9 wk, respectively (p < .001). BW, body composition (DEXA), 1-repetition-maximum (1RM) tests, 40-m sprint, and countermovement jump were measured before and after intervention. Energy intake was reduced by 19% ± 2% and 30% ± 4% in SR and FR, respectively (p = .003). BW and fat mass decreased in both SR and FR by 5.6% ± 0.8% and 5.5% ± 0.7% (0.7% ± 0.8% vs. 1.0% ± 0.4%/wk) and 31% ± 3% and 21 ± 4%, respectively. LBM increased in SR by 2.1% ± 0.4% (p < .001), whereas it was unchanged in FR (-0.2% ± 0.7%), with significant differences between groups (p < .01). In conclusion, data from this study suggest that athletes who want to gain LBM and increase 1RM strength during a WL period combined with strength training should aim for a weekly BW loss of 0.7%.
shffl
05-29-2011, 11:51 AM
This one caught my eyes today. Not too much information yet but it does raise curiosity.
Background
Obesity and metabolic syndrome are important public concerns, and there is increasing demand for effective therapeutic strategies. Flavonoids are expected to improve the risk factors associated with metabolic syndrome. Anthocyanidins are a kind of flavonoids; well known for their anti-oxidative, anti-inflammatory and anti-tumor properties. However, their effects on adipocytes and molecular systems are not well defined. In this study, we examined the effects of anthocyanidins-enriched bilberry extracts on adipocyte differentiation.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063807/
Emma-Leigh
07-16-2011, 08:25 PM
More support as to why I use carbs at night:
Obesity , (7 April 2011) | doi:10.1038/oby.2011.48
Greater Weight Loss and Hormonal Changes After 6 Months Diet With Carbohydrates Eaten Mostly at Dinner
Sigal Sofer, Abraham Eliraz, Sara Kaplan, Hillary Voet, Gershon Fink, Tzadok Kima and Zecharia Madar
Abstract
This study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. Seventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were collected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMAIR), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were observed in comparison to controls. The experimental diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individuals suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes, and achieves improved metabolic response, compared to a more conventional dietary approach.
determined4000
07-16-2011, 10:26 PM
I lol'd at the participants all being obese police officers
Not exactly breaking any stereotypes there
No truth to the rumor the carbs they consumed were all donuts, danish and muffins
Emma-Leigh
08-15-2011, 01:18 AM
As posted in the meal frequency thread:
Am J Clin Nutr. 2011 Jul 27. [Epub ahead of print]Rapid aminoacidemia enhances myofibrillar protein synthesis and anabolic intramuscular signaling responses after resistance exercise.West DW, Burd NA, Coffey VG, Baker SK, Burke LM, Hawley JA, Moore DR, Stellingwerff T, Phillips SM.SourceExercise Metabolism Research Group, Departments of Kinesiology and Neurology, McMaster University, Hamilton, Canada.AbstractBACKGROUND:Ingestion of whey or casein yields divergent patterns of aminoacidemia that influence whole-body and skeletal muscle myofibrillar protein synthesis (MPS) after exercise. Direct comparisons of the effects of contrasting absorption rates exhibited by these proteins are confounded by their differing amino acid contents.
OBJECTIVE:Our objective was to determine the effect of divergent aminoacidemia by manipulating ingestion patterns of whey protein alone on MPS and anabolic signaling after resistance exercise.
DESIGN:In separate trials, 8 healthy men consumed whey protein either as a single bolus (BOLUS; 25-g dose) or as repeated, small, "pulsed" drinks (PULSE; ten 2.5-g drinks every 20 min) to mimic a more slowly digested protein. MPS and phosphorylation of signaling proteins involved in protein synthesis were measured at rest and after resistance exercise.
RESULTS:BOLUS increased blood essential amino acid (EAA) concentrations above those of PULSE (162% compared with 53%, P < 0.001) 60 min postexercise, whereas PULSE resulted in a smaller but sustained increase in aminoacidemia that remained elevated above BOLUS amounts later (180-220 min postexercise, P < 0.05). Despite an identical net area under the EAA curve, MPS was elevated to a greater extent after BOLUS than after PULSE early (1-3 h: 95% compared with 42%) and later (3-5 h: 193% compared with 121%) (both P < 0.05). There were greater changes in the phosphorylation of the Akt-mammalian target of rapamycin pathway after BOLUS than after PULSE.
CONCLUSIONS:Rapid aminoacidemia in the postexercise period enhances MPS and anabolic signaling to a greater extent than an identical amount of protein fed in small pulses that mimic a more slowly digested protein. A pronounced peak aminoacidemia postexercise enhances protein synthesis. This trial was registered at clinicaltrials.gov as NCT01319513.
Emma-Leigh
08-16-2011, 02:58 AM
Another Win for Incidental Exercise:
Int J Behav Nutr Phys Act. 2011 Jun 27;8:69.
Energy expenditure of interruptions to sedentary behavior.
Swartz AM, Squires L, Strath SJ.SourcePhysical Activity and Health Research Laboratory, Department of Human Movement Sciences, University of Wisconsin-Milwaukee, Enderis Hall Room 453, P,O, Box 413, Milwaukee, WI 53201-0413, USA. aswartz@uwm.edu.Abstra
ABSTRACT:
BACKGROUND: Advances in technology, social influences and environmental attributes have resulted in substan-tial portions of the day spent in sedentary pursuits. Sedentary behavior may be a cause of many chronic diseases including obesity, insulin resistance, type 2 diabetes and the metabolic syndrome. Research demonstrated that breaking up sedentary time was beneficially associated with markers of body composition, cardiovascular health and type 2 diabetes. Therefore, the purpose of this study was to quantify the total energy expenditure of three different durations of physical activity within a 30-minute sedentary period and to examine the potential benefits of interrupting sedentary behavior with physical activity for weight control.
METHODS: Participants completed four consecutive 30-minute bouts of sedentary behavior (reading, working on the computer, or doing other desk activities) with and without interruptions of walking at a self-selected pace. Bout one contained no walking interruptions. Bout two contained a 1-minute walking period. Bout three contained a 2-minute walking period. Bout four contained a 5-minute walking period. Body composition and resting metabolic rate were assessed.
RESULT: Twenty males and females (18-39 years) completed this study. Results of the repeated measures analysis of variance with post-hoc testing showed that significantly more energy was expended during each 30 minute sedentary bout with a walking break than in the 30 minute sedentary bout (p < 0.05 for all comparisons). On average, participants expended an additional 3.0, 7.4, and 16.5 additional net or activity kilocalories during bouts 2, 3, and 4, respectively compared with bout 1. When extrapolated for a full eight-hour working day, this data shows that an individual would theoretically expend an additional 24, 59 or 132 kilocalories per day, if they stood up and walked at a normal, self selected pace for one, two or five minutes every hour, respectively, compared with sitting for the 8-hour period.
CONCLUSIONS: This study demonstrated that making small changes, such as taking a five minute walking break every hour could yield beneficial weight control or weight loss results. Therefore, taking breaks from sedentary time is a potential outlet to prevent obesity and the rise of obesity in developed countries.
Emma-Leigh
09-03-2011, 09:42 PM
this one is interesting:
Nutrition. 2011 Aug 26. [Epub ahead of print]
Vegetarianism produces subclinical malnutrition, hyperhomocysteinemia and atherogenesis.
Ingenbleek Y, McCully KS.
Source
Laboratory of Nutrition, Faculty of Pharmacy, University Louis Pasteur, Strasbourg, France.
Abstract
OBJECTIVE:
To explain why vegetarian subjects develop morbidity and mortality from cardiovascular diseases unrelated to vitamin B status and Framingham criteria.
METHODS:
A study of 24 rural male subjects 18 to 30 y old and 15 urban male controls was conducted in the Sahel region of Chad. Food consumption was determined from a dietary questionnaire, and overall health status was assessed by body weight, body mass index, serum albumin, plasma transthyretin, urinary nitrogen, and creatinine. Plasma lipids, vitamins B6, B9 and B12, homocysteine, and related sulfur amino acids were measured as selected cardiovascular disease risk factors.
RESULTS:
Body weight, body mass index, blood, and urinary markers of protein status were significantly lower, with an estimated 10% decrease of lean body mass in the study group compared with urban controls. Neither lipid fractions nor plasma levels of vitamins B6, B9, and B12 were significantly different between the two groups. Although the mean consumption of sulfur amino acids (10.4 mg·kg(-1)·d(-1)) by rural subjects was significantly below the recommended dietary allowances (13 mg·kg(-1)·d(-1)), plasma methionine values were similar in the two groups. In contrast, homocysteine concentration was significantly increased (18.6 μmol/L, P < 0.001), and the levels of cysteine and glutathione were significantly decreased in the study group, demonstrating inhibition of the trans-sulfuration pathway. The strong negative correlation (r = -0.71) between transthyretin and homocysteine implicated lean body mass as a critical determinant of hyperhomocysteinemia.
CONCLUSION:
The low dietary intake of protein and sulfur amino acids by a plant-eating population leads to subclinical protein malnutrition, explaining the origin of hyperhomocysteinemia and the increased vulnerability of these vegetarian subjects to cardiovascular diseases.
Copyright © 2011 Elsevier Inc. All rights reserved.
Emma-Leigh
09-03-2011, 09:46 PM
yes, rats...
Nutrition. 2011 Aug 25. [Epub ahead of print]
Dietary intake of medium- and long-chain triacylglycerols ameliorates insulin resistance in rats fed a high-fat diet.
Terada S, Yamamoto S, Sekine S, Aoyama T.
Source
Central Research Laboratory, The Nisshin OilliO Group, Ltd., Yokosuka City, Kanagawa Prefecture, Japan.
Abstract
OBJECTIVE:
Excessive accumulation of visceral fat is strongly associated with insulin resistance. The present investigation examined the effects of dietary intake of medium- and long-chain triacylglycerols (MLCTs), which have been shown to induce significantly lower visceral fat accumulation in rats and humans, on high-fat diet-induced obesity and insulin resistance in rats. These effects were then compared with those observed in long-chain triacylglycerol (LCT)-fed rats.
METHODS:
After an 8-wk feeding of a high-fat diet, which induced severe whole-body insulin resistance, male Sprague-Dawley rats were fed a standard diet containing LCTs or MLCTs for 6 wk. After the dietary treatment, an oral glucose tolerance test was performed.
RESULTS:
Although body weight and total intra-abdominal fat mass did not differ between the two groups, mesenteric fat weight in the MLCT-fed group was significantly lower than that in the LCT group (P < 0.05). The increase in plasma insulin concentrations, but not in glucose, after glucose administration (area under the curve) was significantly smaller in the MLCT group than in the LCT group (P < 0.01) and was significantly associated with mesenteric fat weight (P < 0.05). MLCT-fed rats had significantly higher plasma adiponectin concentrations compared with LCT rats (P < 0.05). Adiponectin concentrations were negatively correlated with the area under the curve for plasma insulin (P < 0.05) and tended to be inversely related to mesenteric fat weight (P = 0.08).
CONCLUSION:
These results suggest that dietary intake of MLCTs may improve insulin resistance in rats fed a high-fat diet, at least in part through increased adiponectin concentrations caused by a lower mesenteric fat mass.
Copyright © 2011 Elsevier Inc. All rights reserved.
PMID: 21872431 [PubMed - as supplied by publisher]
tina722
09-16-2011, 02:18 PM
I don't have access to this paper, but the abstract looks interesting.
Is sprint exercise a leptin signaling mimetic in human skeletal muscle?
Borja Guerra1, Hugo Olmedillas1, Amelia Guadalupe-Grau1, Jesús G. Ponce-González1, David Morales-Alamo1, Teresa Fuentes1, Esther Chapinal4,5, Leandro Fernández-Pérez2, Pedro De Pablos-Velasco3, Alfredo Santana1,4,5, and Jose A. L. Calbet1
+ Author Affiliations
Departments of 1Physical Education and
2Clinical Sciences, Molecular and Translational Endocrinology Group, University of Las Palmas de Gran Canaria;
3Endocrinology Service, Doctor Negrín Hospital, Las Palmas de Gran Canaria;
4Genetic Unit, Childhood Hospital-Materno Infantil de Las Palmas; and
5Research Unit, Hospital de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain
Address for reprint requests and other correspondence: J. A. L. Calbet, Departamento de Educación Física, Campus Universitario de Tafira, 35017 Las Palmas de Gran Canaria, Canary Island, Spain (e-mail: lopezcalbet@gmail.com).
Submitted 19 July 2010. Accepted 7 June 2011.
Abstract
This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.
snorkelman
09-21-2011, 08:40 AM
Can J Public Health. 2011 Jul-Aug;102(4):313-6.
Trans and saturated fat on food labels in Canada: fact or fiction?
Pantazopoulos P, Kwong K, Lillycrop W, Wong L, Gao Y, Chalouh S, Samadhin M, Ratnayake WM, Krenosky S, Dumais L, L'Abbe MR.
Source
Food Laboratory Division, Ontario Region, Regions and Programs Branch, Health Canada, Scarborough, ON. peter.pantazopoulos@hc-sc.gc.ca
Abstract
OBJECTIVE:
Food labels are the number one source for nutrition information for Canadians, but are food labels accurate? This study aims to provide an assessment of the accuracy of the reported trans fatty acid and saturated fatty acid values on food labels in selected foods.
METHODS:
Over 380 samples of cookies, crackers, granola bars, breakfast bars and a variety of frozen foods were collected between 2005 and 2008 in the Greater Toronto Area, Ottawa and Vancouver, as part of Health Canada's Trans Fat Monitoring Program. The food categories chosen were based on earlier studies indicating that they were significant sources of trans fatty acids and the individual samples were chosen based on market share data. The trans fatty acid and saturated fatty acid contents of the samples were determined by gas chromatography and the laboratory results were compared to the values reported in the Nutrition Facts tables.
CONCLUSIONS:
Statistical analysis indicated no significant difference between laboratory and food label values for cookies, crackers, granola bars, breakfast bars and frozen foods for trans fat or saturated fat. The results demonstrate that Canadians can rely on food labels for making informed dietary choices with respect to trans fat and saturated fat content.
PMID:
21913591
Full text for free:
http://www.thefreelibrary.com/_/print/PrintArticle.aspx?id=264481483
Emma-Leigh
09-28-2011, 11:20 PM
Thought this was just a good read from Jamie Hale - goes over a few different types of descriptive research methods (good to know when you're looking at articles):
http://psychcentral.com/blog/archives/2011/09/27/the-3-basic-types-of-descriptive-research-methods/
Emma-Leigh
10-09-2011, 03:26 AM
Why bland diets work better in those who don't strictly monitor calorie intake:
Eur J Clin Nutr. 2001 Jan;55(1):19-28.
Effect of altering the variety of sensorially distinct foods, of the same macronutrient content, on food intake and body weight in men.
Stubbs RJ, Johnstone AM, Mazlan N, Mbaiwa SE, Ferris S.
Source
The Rowett Research Institute, Bucksburn, Aberdeen, UK. j.stubbs@rri.sari.ac.uk
Abstract
OBJECTIVE:
To examine the effect of increasing the variety of sensorially distinct but nutritionally identical foods on appetite, food intake and body weight, over 7 days, in men.
DESIGN:
Six younger, lean men (mean (s.d.) age 27.0 (2.9) y; weight 74.7 (3.9) kg; height 1.78 (0.03) m; body mass index (BMI) 23.6 (1.1) kg/m2) and six older, overweight men (mean (s.d.) age 39.7 (2.9) y; weight 89.2 (4.4) kg; height 1.78 (0.04) m; BMI 28.1 (0.5) kg/m2) were each studied three times during a 9 day protocol, whilst resident in the Human Nutrition Unit. On days 1-2, subjects consumed a medium fat (MF) maintenance diet (40% fat, 13% protein and 47% carbohydrate by energy) calculated at 1.6 x resting metabolic rate (RMR). On days 3-9 subjects had ad libitum access to MF foods (550 kJ/100 g) with every item the same macronutrient composition and energy density. Subjects had continuous ad libitum access to 5, 10 or 15 food items per day on the low-variety (LV), medium-variety (MV) and high-variety (HV) treatments, respectively. The order of treatments was randomized across subjects. Subjective hunger was tracked hourly during waking hours using visual analogue scales (VAS). Body weight (as a proxy of changes in energy balance) was measured before eating and after voiding, each morning.
RESULTS:
Food and energy intake of the 12 men increased as the variety of foods increased, giving mean energy intakes of 10.13, 11.00 and 11.89 MJ/day on the LV, MV and HV treatments, respectively (F(2,20) = 10.32; P < 0.001). This effect was ascribable almost entirely to the lean men. Energy intake amounted to 1.57, 1.76 and 1.97 x RMR in the lean men and 1.33, 1.40 and 1.45 x RMR, for the overweight men on the LV, MV and HV diets, respectively. Weight changes amounted to -0.16, -0.28 and + 0.43 kg (lean) -1.03 and -1.52 kg and -0.66 kg (overweight), on the LV, MV and HV diets, respectively. The overweight men may have constrained their energy intake relative to expected requirements. This may have been due to a congnitive effect or an age effect. There was no significant group or diet effect on subjectively rated hunger.
CONCLUSIONS:
These data suggest that increasing the variety of sensorially distinct foods that are virtually identical in composition can increase food and energy intake and in the short to medium term can alter energy balance.
Emma-Leigh
10-29-2011, 08:46 PM
J Nutr. 2011 Oct 26. [Epub ahead of print]
Changes in Atherogenic Dyslipidemia Induced by Carbohydrate Restriction in Men Are Dependent on Dietary Protein Source.
Mangravite LM, Chiu S, Wojnoonski K, Rawlings RS, Bergeron N, Krauss RM.
Abstract
Previous studies have shown that multiple features of atherogenic dyslipidemia are improved by replacement of dietary carbohydrate with mixed sources of protein and that these lipid and lipoprotein changes are independent of dietary saturated fat content. Because epidemiological evidence suggests that red meat intake may adversely affect cardiovascular disease risk, we tested the effects of replacing dietary carbohydrate with beef protein in the context of high- vs. low-saturated fat intake in 40 healthy men. After a 3-wk baseline diet [50% daily energy (E) as carbohydrate, 13% E as protein, 15% E as saturated fat], participants consumed for 3 wk each in a randomized crossover design two high-beef diets in which protein replaced carbohydrate (31% E as carbohydrate, 31% E as protein, with 10% E as beef protein). The high-beef diets differed in saturated fat content (8% E vs. 15% E with exchange of saturated for monounsaturated fat). Two-week washout periods were included following the baseline diet period and between the randomized diets periods. Plasma TG concentrations were reduced after the 2 lower carbohydrate dietary periods relative to after the baseline diet period and these reductions were independent of saturated fat intake. Plasma total, LDL, and non-HDL cholesterol as well as apoB concentrations were lower after the low-carbohydrate, low-saturated fat diet period than after the low-carbohydrate, high-saturated fat diet period. Given our previous observations with mixed protein diets, the present findings raise the possibility that dietary protein source may modify the effects of saturated fat on atherogenic lipoproteins.
Emma-Leigh
10-29-2011, 08:50 PM
Am J Physiol Endocrinol Metab. 2011 Oct 25. [Epub ahead of print]
Catecholamine and insulin control of lipolysis in subcutaneous adipose tissue during long-term diet-induced weight loss in obese women.
Koppo K, Siklova-Vitkova M, Klimcakova E, Polak J, Marques MA, Berlan M, Van De Voorde J, Bülow J, Langin D, de Glisezinski I, Stich V Phd Md.
Abstract
The aim of this study was to investigate the evolution of the adrenergic regulation of lipolysis during different phases of a 6-months dietary intervention. Eight obese women underwent a 6-months dietary intervention consisting of 1 month very low calorie diet (VLCD), followed by 2 months low calorie diet (LCD) and 3 months weight maintenance diet (WM). At each phase of the dietary intervention, microdialysis of subcutaneous adipose tissue (SCAT) was performed at rest and during a 3-h hyperinsulinemic euglycemic clamp. Responses of dialysate glycerol concentration (DGC) were determined at baseline and during local perfusions with adrenaline or adrenaline and phentolamine, before and during the last 30 min of the clamp. Dietary intervention induced a body weight reduction and an improved insulin sensitivity. DGC progressively decreased during the clamp and this decrease was similar during the different phases of the diet. The adrenaline-induced increase in DGC was higher at VLCD and LCD compared with baseline condition, and returned to pre-diet levels at WM. In the probe with adrenaline and phentolamine, the increase of DGC was higher than that in the adrenaline probe at baseline and WM but it was not different at VLCD and LCD. The results suggest that the responsiveness of SCAT to adrenaline-stimulated lipolysis increases during the calorie-restricted phases due to a reduction of the α2-adrenoceptor mediated antilipolytic action of adrenaline. At WM, adrenaline-stimulated lipolysis returned to the pre-diet levels. Furthermore, no direct relationship between insulin and the diet-induced changes in the regulation of lipolysis was found.
t12jm
01-22-2012, 01:04 PM
For all my future atherosclerotic bros - http://www.ncbi.nlm.nih.gov/pubmed/21658928
Alpha-linolenic acid increases cholesterol efflux in macrophage-derived foam cells by decreasing stearoyl CoA desaturase 1 expression: evidence for a farnesoid-X-receptor mechanism of action.
Zhang J, Kris-Etherton PM, Thompson JT, Hannon DB, Gillies PJ, Vanden Heuvel JP.
Source
Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 16802, USA; Center of Excellence in Nutrigenomics, The Pennsylvania State University, University Park, PA 16802, USA.
Abstract
Increased cholesterol efflux from macrophage-derived foam cells (MDFCs) is an important protective mechanism to decrease lipid load in the atherosclerotic plaque. Dietary alpha-linolenic acid (ALA), an omega-3 polyunsaturated fatty acid (PUFA), decreases circulating cholesterol, but its role in cholesterol efflux has not been extensively studied. Stearoyl CoA desaturase 1 (SCD1) is the rate-limiting enzyme in the synthesis of monounsaturated fatty acids (MUFAs). Endogenous MUFAs are preferentially incorporated into triglycerides, phospholipids and cholesteryl ester, which are abundant in atherosclerotic plaque. This study investigated the mechanisms by which ALA regulated SCD1 and subsequent effect on cholesterol storage and transport in MDFCs. Small interfering RNA (siRNA) also was applied to modify SCD1 expression in foam cells. Alpha-linolenic acid treatment and SCD1 siRNA significantly decreased SCD1 expression in MDFCs. The reduction of SCD1 was accompanied with increased cholesterol efflux and decreased intracellular cholesterol storage within these cells. Alpha-linolenic acid activated the nuclear receptor farnesoid-X-receptor, which in turn increased its target gene small heterodimer partner (SHP) expression, and decreased liver-X-receptor dependent sterol regulatory element binding protein 1c transcription, ultimately resulting in repressed SCD1 expression. In conclusion, repression of SCD1 by ALA favorably increased cholesterol efflux and decreased cholesterol accumulation in foam cells. This may be one mechanism by which dietary omega-3 PUFAs promote atherosclerosis regression.
t12jm
01-22-2012, 02:59 PM
nothing that we didn't already know, but here's actual data.
T. Anabolic and catabolic hormones and energy balance of the male bodybuilders during the preparation for the competition. J Strength Cond Res 24(4): 1074-1081, 2010-The purpose of the study was to investigate simultaneous effects of energy balance, caloric intake, and the hormonal anabolic-catabolic balance in bodybuilders prior to competition. Fourteen male bodybuilders took part in an 11-week energy-restricted period to reduce body fat. The subjects were divided into the energy-restricted group (ERG) (n = 7), who were preparing for the competition, or the control group (CG) (n = 7) who continued to train regularly and did not change their dietary or training pattern. Participants were tested at 11 weeks (T1), 5 weeks (T2), and 3 days (T3) before competition for diet, body composition, and fasting hormonal assessment. Body mass and body fat percentage of ERG were significantly (p < 0.05) decreased during the study period. In ERG, insulinlike growth factor-1 (IGF-1) and insulin decreased significantly during the 11-week weight-reduction period (p < 0.05). Testosterone was decreased only from week 11 to week 5 (from 20.3 ± 6.0 to 18.0 ± 6.8 nmol/L). Changes in IGF-I concentration were significantly related to changes in insulin (r = 0.741), fat mass (r = 0.705), lean body mass (r = 0.696), and body mass (r = 0.652). Changes in insulin concentrations were significantly related to changes in fat mass (r = 0.630) and lean body mass (r = 0.725). These data indicate that severe energy restriction to extremely low body energy reserves decreases significantly the concentrations of 3 anabolic pathways despite high protein intake. Monitoring of insulin and IGF-1 concentration is suggested to prevent losses in muscle mass in energy-restricted conditions. Other nutritional strategies might be needed to prevent possible catabolic effect during preparation of bodybuilders to competition.
full text attached4069171
thegymbum
01-29-2012, 02:11 AM
In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.
Very interesting, thank you for sharing! It's interesting to think that, perhaps, this stimulation of leptin pathways plays a role in the appetite suppression that is sometimes observed in response to exercise. Hope someone follows up with that!
njman
03-19-2012, 03:09 PM
Fruit polyphenols, immunity and inflammation (Review)
They talk about exercise induced inflammation last.
"In summary, despite the well-established in vitro antioxidant and anti-inflammatory potential of flavonoids, inconsistent or null effects of human interventions do not tend to support a role of flavonoid supplementation as a countermeasure to exercise-induced immune and inflammatory changes."
http://search.proquest.com/docview/759548690
Bonuman
02-27-2013, 05:22 AM
Less nutrition, more physiological:
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-i
and subsequent parts:
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-ii
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-iii
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-iv
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-v
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-vi
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-vii
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-viii
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-ix
http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-x (this one's not published yet)
It explains a whole lot about cholesterol, it's use in the body, how it's transported throughout the body, how it's metabolized, how it's measured, what's relevant about it etc etc etc.
It's a long read, but it's VERY interesting and you'll learn a whole lot which is applicable in real life. Other articles on his site are very interesting as well.
Another great read: http://weightology.net/weightologyweekly/?page_id=319
An article series which debunks the "demonizing" of insulin as an obesity-causing hormone.
tina722
02-27-2013, 05:39 AM
Murine study, but really fascinating, with a huge amount of work.
http://www.sciencedirect.com/science/article/pii/S1550413112001891
Time-Restricted Feeding without Reducing Caloric Intake Prevents Metabolic Diseases in Mice Fed a High-Fat Diet
Hatori et al. June 2012. Cell Metabolism
While diet-induced obesity has been exclusively attributed to increased caloric intake from fat, animals fed a high-fat diet (HFD) ad libitum (ad lib) eat frequently throughout day and night, disrupting the normal feeding cycle. To test whether obesity and metabolic diseases result from HFD or disruption of metabolic cycles, we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day. Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination. The tRF regimen improved CREB, mTOR, and AMPK pathway function and oscillations of the circadian clock and their target genes' expression. These changes in catabolic and anabolic pathways altered liver metabolome and improved nutrient utilization and energy expenditure. We demonstrate in mice that tRF regimen is a nonpharmacological strategy against obesity and associated diseases.
In short: mice on a 60% fat diet (20weeks) do not gain weight or show any signs of metabolic syndrome when allowed to eat for only 8 hours a day. Food intake was similar between all groups.