vineri, 30 aprilie 2010
joi, 29 aprilie 2010
marți, 27 aprilie 2010
luni, 26 aprilie 2010
Intermittent fasting - Martin Berkhan style
This is the usual protocol for people with normal working hours.
Sample setup
12-1 PM or around lunch/noon: Meal one. Approximately 20-25% of daily total calorie intake. (in jur de 500 kcal pentru mine)
4-5 PM: Pre-workout meal. Roughly equal to the first meal. (tot cam 500 kcal)
8-9 PM: Post-workout meal (largest meal). (cam 1.000 kcal)
duminică, 25 aprilie 2010
mancati branza
Dietary vitamin K intake in relation to cancer incidence and mortality: results from the Heidelberg cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC-Heidelberg)1,2,3
1 From the Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany (KN, SR, RK, and JL); the Department of Nutrition, Harvard School of Public Health, Boston, MA (KN); and the Institute of Epidemiology, Helmholtz Zentrum München, Neuherberg, Germany (JL).
2 Supported by ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5:"Food Quality and Safety" (contract no 513943).
3 Address correspondence to J Linseisen, Institute of Epidemiology, Helmholtz Zentrum München, German Research Centre for Environmental Health, Ingolstädter Landstr. 1, D-85746 Neuherberg, Germany. E-mail: j.linseisen@helmholtz-muenchen.de.
Background: Anticarcinogenic activities of vitamin K have been observed in animal and cell studies.
Objective: On the basis of the growth inhibitory effects of vitamin K as observed in a variety of cancer cell lines, we hypothesized that dietary intake of phylloquinone (vitamin K1) and menaquinones (vitamin K2) may be associated with overall cancer incidence and mortality.
Design: In the prospective EPIC-Heidelberg (European Prospective Investigation into Cancer and Nutrition–Heidelberg) cohort study, 24,340 participants aged 35–64 y and free of cancer at enrollment (1994–1998) were actively followed up for cancer incidence and mortality through 2008. Dietary vitamin K intake was estimated from food-frequency questionnaires completed at baseline by using HPLC-based food-composition data. Multivariate-adjusted hazard ratios (HRs) and 95% CIs were estimated by using Cox proportional hazards models.
Results: During a median follow-up time of >10 y, 1755 incident cancer cases occurred, of which 458 were fatal. Dietary intake of menaquinones was nonsignificantly inversely associated with overall cancer incidence (HR for the highest compared with the lowest quartile: 0.86; 95% CI: 0.73, 1.01; P for trend = 0.08), and the association was stronger for cancer mortality (HR: 0.72; 95% CI: 0.53, 0.98; P for trend = 0.03). Cancer risk reduction with increasing intake of menaquinones was more pronounced in men than in women, mainly driven by significant inverse associations with prostate (P for trend = 0.03) and lung (P for trend = 0.002) cancer. We found no association with phylloquinone intake.
Conclusion: These findings suggest that dietary intake of menaquinones, which is highly determined by the consumption of cheese, is associated with a reduced risk of incident and fatal cancer.
miercuri, 21 aprilie 2010
luni, 19 aprilie 2010
Martin Berkham
vineri, 16 aprilie 2010
eat less / exercise more
Physical activity, food intake, and body weight regulation: insights from doubly labeled water studies.
Westerterp KR.
Department of Human Biology, Maastricht University, Maastricht, the Netherlands. k.westerterp@hb.unimaas.nl
Abstract
Body weight and energy balance can be maintained by adapting energy intake to changes in energy expenditure and vice versa, whereas short-term changes in energy expenditure are mainly caused by physical activity. This review investigates whether physical activity is affected by over- and undereating, whether intake is affected by an increase or a decrease in physical activity, and whether being overweight affects physical activity. The available evidence is based largely on studies that quantified physical activity with doubly labeled water. Overeating does not affect physical activity, while undereating decreases habitual or voluntary physical activity. Thus, it is easier to gain weight than to lose weight. An exercise-induced increase in energy requirement is typically compensated by increased energy intake, while a change to a more sedentary routine does not induce an equivalent reduction of intake and generally results in weight gain. Overweight and obese subjects tend to have similar activity energy expenditures to lean people despite being more sedentary. There are two ways in which the general population trend towards increasing body weight can be reversed: reduce intake or increase physical activity. The results of the present literature review indicate that eating less is the most effective method for preventing weight gain, despite the potential for a negative effect on physical activity when a negative energy balance is reached.
marți, 13 aprilie 2010
luni, 12 aprilie 2010
un studiu nou despre satietate - mesele scurte si dese NU controleaza mai bine foamea
Obesity (Silver Spring). 2010 Mar 25. [Epub ahead of print]
The Influence of Higher Protein Intake and Greater Eating Frequency on Appetite Control in Overweight and Obese Men.
Leidy HJ, Armstrong CL, Tang M, Mattes RD, Campbell WW.
[1] Department of Dietetics & Nutrition, University of Kansas Medical Center, Kansas City, Kansas, USA [2] Department of Foods & Nutrition, Ingestive Behavior Research Center, Purdue University, West Lafayette, Indiana, USA.
Abstract
The purpose of this study was to determine the effects of dietary protein intake and eating frequency on perceived appetite, satiety, and hormonal responses in overweight/obese men. Thirteen men (age 51 +/- 4 years; BMI 31.3 +/- 0.8 kg/m(2)) consumed eucaloric diets containing normal protein (79 +/- 2 g protein/day; 14% of energy intake as protein) or higher protein (138 +/- 3 g protein/day; 25% of energy intake as protein) equally divided among three eating occasions (3-EO; every 4 h) or six eating occasions (6-EO; every 2 h) on four separate days in randomized order. Hunger, fullness, plasma glucose, and hormonal responses were assessed throughout 11 h. No protein x eating frequency interactions were observed for any of the outcomes. Independent of eating frequency, higher protein led to greater daily fullness (P <>Collectively, these data suggest that higher protein intake promotes satiety and challenge the concept that increasing the number of eating occasions enhances satiety in overweight and obese men.
duminică, 11 aprilie 2010
vineri, 9 aprilie 2010
cancer
Cancer as a metabolic disease
Thomas N Seyfried 
and Laura M Shelton 
Biology Department, Boston College, Chestnut Hill, MA 02467, USA
author email
corresponding author email
Nutrition & Metabolism 2010, 7:7doi:10.1186/1743-7075-7-7
The electronic version of this article is the complete one and can be found online at:http://www.nutritionandmetabolism.com/content/7/1/7
| Received: | 15 November 2009 |
| Accepted: | 27 January 2010 |
| Published: | 27 January 2010 |
© 2010 Seyfried and Shelton; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Emerging evidence indicates that impaired cellular energy metabolism is the defining characteristic of nearly all cancers regardless of cellular or tissue origin. In contrast to normal cells, which derive most of their usable energy from oxidative phosphorylation, most cancer cells become heavily dependent on substrate level phosphorylation to meet energy demands. Evidence is reviewed supporting a general hypothesis that genomic instability and essentially all hallmarks of cancer, including aerobic glycolysis (Warburg effect), can be linked to impaired mitochondrial function and energy metabolism. A view of cancer as primarily a metabolic disease will impact approaches to cancer management and prevention.
Conclusions
Evidence is reviewed supporting a general hypothesis that cancer is primarily a disease of energy metabolism. All of the major hallmarks of the disease can be linked to impaired mitochondrial function. In order to maintain viability, tumor cells gradually transition to substrate level phosphorylation using glucose and glutamine as energy substrates. While cancer causing germline mutations are rare, the abundance of somatic genomic abnormalities found in the majority of cancers can arise as a secondary consequence of mitochondrial dysfunction. Once established, somatic genomic instability can contribute to further mitochondrial defects and to the metabolic inflexibility of the tumor cells. Systemic metastasis is the predicted outcome following protracted mitochondrial damage to cells of myeloid origin. Tumor cells of myeloid origin would naturally embody the capacity to exit and enter tissues. Two major conclusions emerge from the hypothesis; first that many cancers can regress if energy intake is restricted and, second, that many cancers can be prevented if energy intake is restricted. Consequently, energy restricted diets combined with drugs targeting glucose and glutamine can provide a rational strategy for the longer-term management and prevention of most cancers.
nutrigenomics - low carb vs. low fat
Genetic Phenotypes Predict Weight Loss Success: The Right Diet Does Matter
Mindy Dopler Nelson, Stanford Univ, Palo Alto, CA; Prakash Prabhakar, Venkateswarlu Kondragunta, Interleukin Genetics, Waltham, MA; Kenneth S Kornman, Interleukin Genetics, Waltham, CA; Christopher Gardner, Stanford Univ, Palo Alto, CA
Background/Introduction: Recent evidence demonstrates there is no one weight loss diet that is most effective for everyone. Genetic heterogeneity may offer a partial explanation to differential responses to different diets. Genotype patterns of single nucleotide polymorphisms (SNPs) associated with obesity and weight loss have been identified. Objective: To determine whether genotype patterns associated with macronutrient metabolism will predict weight loss success in response to low-carbohydrate vs. low-fat diets. Design: This is a secondary analysis of data from 101 Caucasian women in the A TO Z weight loss study who provided DNA from buccal cells. The analysis included diet assignments, weight loss results, and anthropometric and lipid panel values. Functional SNPs relevant to weight loss and responsive to macronutrient composition in the diet were analyzed. Women in the original A TO Z study were randomly assigned to either Atkins (very low carbohydrate), Zone (low-carbohydrate/high protein), LEARN (low-fat) or Ornish (very low fat). The subset of women was classified into 3 genotype groups; low carbohydrate diet responsive genotype (LCG, n=61) and low fat diet responsive genotype (LFG, n=35), and a balanced diet responsive genotype (BDG, n=5). Results: Participants in the appropriate dietary groups for their genotype showed 2-3 fold greater 12-month weight loss compared to participants in inappropriate dietary groups for their genotype (p=0.02) with parallel findings for reduced waist circumference (p=0.01), decreased triglycerides (p=0.007), and increased high density lipoprotein (p= 0.01). Conclusion: These findings suggest a simple DNA test of buccal cells from a cheek swab could help predict whether someone is more likely to be successful with weight loss on a low carbohydrate vs. a low fat diet.
miercuri, 7 aprilie 2010
luni, 5 aprilie 2010
aspartam - safe
Aspartame--facts and fiction.
Magnuson B.
Senior Scientific and Regulatory Consultant, Cantox Health Sciences International, 2233 Argentia Road, Suite 308, Mississaunga, ON, Canada L5N 2X7. bmagnuson@cantox.com.
A team of nine independent internationally esteemed toxicologists, reviewed hundreds of studies on aspartame safety. The key findings of the review with respect to aspartame safety were: Aspartame is completely broken down in the intestine to components found in other foods. Aspartame consumption (even at levels much higher than consumed by the highest users) has virtually no impact on blood levels of amino acids, methanol or glucose. Aspartame safety is clearly documented and well established through extensive laboratory testing, animal experiments, human clinical trials and epidemiological (population) studies. There is no evidence from numerous well conducted studies that consumption of aspartame at levels found in the human diet are associated with conditions of nervous system, behaviour, or other illness. Aspartame does not cause mutations, and there is no credible evidence that it causes cancer.