luni, 6 decembrie 2010
marți, 30 noiembrie 2010
joi, 18 noiembrie 2010
miercuri, 10 noiembrie 2010
joi, 21 octombrie 2010
sâmbătă, 16 octombrie 2010
insulin
ultima parte dintr-o serie de articole interesante despre insulina aici
The bottom line is that insulin does not deserve the bad reputation that it has been given, and the “carbohydrates drive insulin which drives fat storage” mantra is wrong. To summarize:
Insulin suppresses appetite; it does not increase it
A high carbohydrate diet does not cause chronically high insulin levels
Protein is insulinemic, and in certain cases, can be just as insulinemic as carbohydrate
Contrary to popular belief, glucagon does not “cancel out” the suppression of lipolysis by insulin when protein is ingested
The insulinemic effects of protein are due to a direct stimulatory effect on the pancreas, and not because the protein is converted to glucose
The combination of protein and carbohydrate can produce greater insulin secretion than either one alone, yet high protein, moderate-to-high carbohydrate diets are very effective for weight loss
Very high carbohydrate diets have been demonstrated to produce weight loss when people are in an energy deficit
Dairy is extremely insulinemic, just as insulinemic as white bread, yet does not promote weight gain in the absence of an energy surplus. This is supported by a very large number of studies, including animal studies, observational studies, and randomized controlled trials.
Insulin is not required for fat storage
Insulin levels are not predictive of weight gain or weight loss in the majority of prospective studies
Exenatide restores rapid phase insulin release in diabetics, yet causes weight loss
The effects of insulin injection cannot be compared to normal physiological insulin release, since amylin is co-secreted with insulin from the pancreas
Insulin mainly functions as an inhibitory hormone rather than a storage hormone, acting as a brake on many important physiologic processes
A type I diabetic without insulin becomes hyperglycemic because of overproduction of glucose by the liver, not because insulin can’t get into cells
Insulin enhances the uptake of glucose into cells, but is not required for it
Insulin regulates blood sugar after a meal both by stopping the liver from producing glucose and enhancing glucose uptake into cells.
In a fasted state, insulin regulates blood sugar by controlling glucose production of the liver, not by affecting the uptake of glucose into cells
You cannot simply look at the temporary effects of insulin on lipolysis and glucose storage. You have to address what is happening over a 24-hour period; body fat will not increase if there is no overall energy surplus.
The bottom line is that insulin does not deserve the bad reputation that it has been given, and the “carbohydrates drive insulin which drives fat storage” mantra is wrong. To summarize:
Insulin suppresses appetite; it does not increase it
A high carbohydrate diet does not cause chronically high insulin levels
Protein is insulinemic, and in certain cases, can be just as insulinemic as carbohydrate
Contrary to popular belief, glucagon does not “cancel out” the suppression of lipolysis by insulin when protein is ingested
The insulinemic effects of protein are due to a direct stimulatory effect on the pancreas, and not because the protein is converted to glucose
The combination of protein and carbohydrate can produce greater insulin secretion than either one alone, yet high protein, moderate-to-high carbohydrate diets are very effective for weight loss
Very high carbohydrate diets have been demonstrated to produce weight loss when people are in an energy deficit
Dairy is extremely insulinemic, just as insulinemic as white bread, yet does not promote weight gain in the absence of an energy surplus. This is supported by a very large number of studies, including animal studies, observational studies, and randomized controlled trials.
Insulin is not required for fat storage
Insulin levels are not predictive of weight gain or weight loss in the majority of prospective studies
Exenatide restores rapid phase insulin release in diabetics, yet causes weight loss
The effects of insulin injection cannot be compared to normal physiological insulin release, since amylin is co-secreted with insulin from the pancreas
Insulin mainly functions as an inhibitory hormone rather than a storage hormone, acting as a brake on many important physiologic processes
A type I diabetic without insulin becomes hyperglycemic because of overproduction of glucose by the liver, not because insulin can’t get into cells
Insulin enhances the uptake of glucose into cells, but is not required for it
Insulin regulates blood sugar after a meal both by stopping the liver from producing glucose and enhancing glucose uptake into cells.
In a fasted state, insulin regulates blood sugar by controlling glucose production of the liver, not by affecting the uptake of glucose into cells
You cannot simply look at the temporary effects of insulin on lipolysis and glucose storage. You have to address what is happening over a 24-hour period; body fat will not increase if there is no overall energy surplus.
luni, 11 octombrie 2010
miercuri, 29 septembrie 2010
low carb diets study on mortality
Low-carbohydrate diets and all-cause and cause-specific mortality: two cohort studies.
Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu FB.
Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Comment in:
* Ann Intern Med. 2010 Sep 7;153(5):337-9.
Abstract
BACKGROUND: Data on the long-term association between low-carbohydrate diets and mortality are sparse.
OBJECTIVE: To examine the association of low-carbohydrate diets with mortality during 26 years of follow-up in women and 20 years in men.
DESIGN: Prospective cohort study of women and men who were followed from 1980 (women) or 1986 (men) until 2006. Low-carbohydrate diets, either animal-based (emphasizing animal sources of fat and protein) or vegetable-based (emphasizing vegetable sources of fat and protein), were computed from several validated food-frequency questionnaires assessed during follow-up.
SETTING: Nurses' Health Study and Health Professionals' Follow-up Study.
PARTICIPANTS: 85 168 women (aged 34 to 59 years at baseline) and 44 548 men (aged 40 to 75 years at baseline) without heart disease, cancer, or diabetes.
MEASUREMENTS: Investigators documented 12 555 deaths (2458 cardiovascular-related and 5780 cancer-related) in women and 8678 deaths (2746 cardiovascular-related and 2960 cancer-related) in men.
RESULTS: The overall low-carbohydrate score was associated with a modest increase in overall mortality in a pooled analysis (hazard ratio [HR] comparing extreme deciles, 1.12 [95% CI, 1.01 to 1.24]; P for trend = 0.136). The animal low-carbohydrate score was associated with higher all-cause mortality (pooled HR comparing extreme deciles, 1.23 [CI, 1.11 to 1.37]; P for trend = 0.051), cardiovascular mortality (corresponding HR, 1.14 [CI, 1.01 to 1.29]; P for trend = 0.029), and cancer mortality (corresponding HR, 1.28 [CI, 1.02 to 1.60]; P for trend = 0.089). In contrast, a higher vegetable low-carbohydrate score was associated with lower all-cause mortality (HR, 0.80 [CI, 0.75 to 0.85]; P for trend
LIMITATIONS: Diet and lifestyle characteristics were assessed with some degree of error. Sensitivity analyses indicated that results were probably not substantively affected by residual confounding or an unmeasured confounder. Participants were not a representative sample of the U.S. population.
CONCLUSION: A low-carbohydrate diet based on animal sources was associated with higher all-cause mortality in both men and women, whereas a vegetable-based low-carbohydrate diet was associated with lower all-cause and cardiovascular disease mortality rates.
Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu FB.
Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Comment in:
* Ann Intern Med. 2010 Sep 7;153(5):337-9.
Abstract
BACKGROUND: Data on the long-term association between low-carbohydrate diets and mortality are sparse.
OBJECTIVE: To examine the association of low-carbohydrate diets with mortality during 26 years of follow-up in women and 20 years in men.
DESIGN: Prospective cohort study of women and men who were followed from 1980 (women) or 1986 (men) until 2006. Low-carbohydrate diets, either animal-based (emphasizing animal sources of fat and protein) or vegetable-based (emphasizing vegetable sources of fat and protein), were computed from several validated food-frequency questionnaires assessed during follow-up.
SETTING: Nurses' Health Study and Health Professionals' Follow-up Study.
PARTICIPANTS: 85 168 women (aged 34 to 59 years at baseline) and 44 548 men (aged 40 to 75 years at baseline) without heart disease, cancer, or diabetes.
MEASUREMENTS: Investigators documented 12 555 deaths (2458 cardiovascular-related and 5780 cancer-related) in women and 8678 deaths (2746 cardiovascular-related and 2960 cancer-related) in men.
RESULTS: The overall low-carbohydrate score was associated with a modest increase in overall mortality in a pooled analysis (hazard ratio [HR] comparing extreme deciles, 1.12 [95% CI, 1.01 to 1.24]; P for trend = 0.136). The animal low-carbohydrate score was associated with higher all-cause mortality (pooled HR comparing extreme deciles, 1.23 [CI, 1.11 to 1.37]; P for trend = 0.051), cardiovascular mortality (corresponding HR, 1.14 [CI, 1.01 to 1.29]; P for trend = 0.029), and cancer mortality (corresponding HR, 1.28 [CI, 1.02 to 1.60]; P for trend = 0.089). In contrast, a higher vegetable low-carbohydrate score was associated with lower all-cause mortality (HR, 0.80 [CI, 0.75 to 0.85]; P for trend
LIMITATIONS: Diet and lifestyle characteristics were assessed with some degree of error. Sensitivity analyses indicated that results were probably not substantively affected by residual confounding or an unmeasured confounder. Participants were not a representative sample of the U.S. population.
CONCLUSION: A low-carbohydrate diet based on animal sources was associated with higher all-cause mortality in both men and women, whereas a vegetable-based low-carbohydrate diet was associated with lower all-cause and cardiovascular disease mortality rates.
joi, 16 septembrie 2010
marți, 14 septembrie 2010
luni, 6 septembrie 2010
marți, 10 august 2010
luni, 9 august 2010
duminică, 25 iulie 2010
joi, 22 iulie 2010
marți, 20 iulie 2010
indulcitorii cu valoare calorica redusa . . . sunt ok
Br J Nutr. 2010 Jul 12:1-6. [Epub ahead of print]
Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release.
Renwick AG, Molinary SV.
School of Medicine, University of Southampton, Southampton SO17 1BJ, UK.
Abstract
The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro, in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro, in situ or knockout studies in animals.
Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release.
Renwick AG, Molinary SV.
School of Medicine, University of Southampton, Southampton SO17 1BJ, UK.
Abstract
The present review explores the interactions between sweeteners and enteroendocrine cells, and consequences for glucose absorption and insulin release. A combination of in vitro, in situ, molecular biology and clinical studies has formed the basis of our knowledge about the taste receptor proteins in the glucose-sensing enteroendocrine cells and the secretion of incretins by these cells. Low-energy (intense) sweeteners have been used as tools to define the role of intestinal sweet-taste receptors in glucose absorption. Recent studies using animal and human cell lines and knockout mice have shown that low-energy sweeteners can stimulate intestinal enteroendocrine cells to release glucagon-like peptide-1 and glucose-dependent insulinotropic peptide. These studies have given rise to major speculations that the ingestion of food and beverages containing low-energy sweeteners may act via these intestinal mechanisms to increase obesity and the metabolic syndrome due to a loss of equilibrium between taste receptor activation, nutrient assimilation and appetite. However, data from numerous publications on the effects of low-energy sweeteners on appetite, insulin and glucose levels, food intake and body weight have shown that there is no consistent evidence that low-energy sweeteners increase appetite or subsequent food intake, cause insulin release or affect blood pressure in normal subjects. Thus, the data from extensive in vivo studies in human subjects show that low-energy sweeteners do not have any of the adverse effects predicted by in vitro, in situ or knockout studies in animals.
miercuri, 14 iulie 2010
Martin Berkhan Protein Muffins
Protein muffins. Check out the stats on these bastards.
411 kcal
69 g protein
8.8 g fat
19 g carbs
Lots of protein. Ain't bad considering they're supposed to be pretty tasty. By popular demand, here's the recipe:
One whole extra large egg
The egg white from two extra large eggs
250 g low fat cottage cheese
33 g casein protein powder. Chocolate flavored powder was used for these.
One teaspoon bicarbonate
One teaspoon flax seed
Cinnamon
Sweetener. 1/2 deciliter, aspartame (Hermesetas). Not the liquid variety. You'll have to play this by ear depending on what sweetener you're using and how sweet you want them to be.
Mix everything together, split it up those muffin-shaped forms, and put it in the oven for 25 minutes at 150 degrees. There you go. Hope I got it right because I can't bake for shit. That's probably a good thing. Otherwise I'd be making cheesecakes all day long.
411 kcal
69 g protein
8.8 g fat
19 g carbs
Lots of protein. Ain't bad considering they're supposed to be pretty tasty. By popular demand, here's the recipe:
One whole extra large egg
The egg white from two extra large eggs
250 g low fat cottage cheese
33 g casein protein powder. Chocolate flavored powder was used for these.
One teaspoon bicarbonate
One teaspoon flax seed
Cinnamon
Sweetener. 1/2 deciliter, aspartame (Hermesetas). Not the liquid variety. You'll have to play this by ear depending on what sweetener you're using and how sweet you want them to be.
Mix everything together, split it up those muffin-shaped forms, and put it in the oven for 25 minutes at 150 degrees. There you go. Hope I got it right because I can't bake for shit. That's probably a good thing. Otherwise I'd be making cheesecakes all day long.
luni, 12 iulie 2010
joi, 8 iulie 2010
miercuri, 7 iulie 2010
marți, 6 iulie 2010
luni, 5 iulie 2010
low carb metabolic advantage...not really
e interesanta schimbarea de pozitie a autorului unui studiu care afirma in 2006 existenta unui avantaj metabolic al dietelor low carb (chiar keto)...aici
"Thus, the primary reason why low-carbohydrate diets tend to show superior weight loss in the short-term has nothing to do with a metabolic advantage, or an effect on insulin, or some other magical unknown effect. It all has to do with appetite control. When people consume a low-carbohydrate, high-protein diet, they are getting a “double-whammy” in regards to appetite regulation. They’re getting the dramatic benefit of increasing protein, and an additional (although smaller) benefit of a ketogenic diet. The bottom line is that the people on these diets spontaneously eat less….A LOT less.
The bottom line is that there is no metabolic advantage to a low carbohydrate intake that is independent of a high protein intake. There is a metabolic advantage to a high protein diet, which will increase the calories you burn by 80-100 calories per day. There is also a dramatic satiety advantage to a high protein intake. A low carbohydrate intake (low enough to cause ketosis) can increase this satiety advantage, but individual responses will vary. The best dietary approach for you will depend upon a variety of factors."
"Thus, the primary reason why low-carbohydrate diets tend to show superior weight loss in the short-term has nothing to do with a metabolic advantage, or an effect on insulin, or some other magical unknown effect. It all has to do with appetite control. When people consume a low-carbohydrate, high-protein diet, they are getting a “double-whammy” in regards to appetite regulation. They’re getting the dramatic benefit of increasing protein, and an additional (although smaller) benefit of a ketogenic diet. The bottom line is that the people on these diets spontaneously eat less….A LOT less.
The bottom line is that there is no metabolic advantage to a low carbohydrate intake that is independent of a high protein intake. There is a metabolic advantage to a high protein diet, which will increase the calories you burn by 80-100 calories per day. There is also a dramatic satiety advantage to a high protein intake. A low carbohydrate intake (low enough to cause ketosis) can increase this satiety advantage, but individual responses will vary. The best dietary approach for you will depend upon a variety of factors."
miercuri, 30 iunie 2010
luni, 28 iunie 2010
one benefit of fasting
Autophagy. 2010 Aug 14;6(6).
Short-term fasting induces profound neuronal autophagy.
Alirezaei M, Kemball CC, Flynn CT, Wood MR, Whitton JL, Kiosses WB.
Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA, USA.
Abstract
Disruption of autophagy-a key homeostatic process in which cytosolic components are degraded and recycled through lysosomes-can cause neurodegeneration in tissue culture and in vivo. Upregulation of this pathway may be neuroprotective, and much effort is being invested in developing drugs that cross the blood brain barrier and increase neuronal autophagy. One well-recognized way of inducing autophagy is by food restriction, which upregulates autophagy in many organs including the liver; but current dogma holds that the brain escapes this effect, perhaps because it is a metabolically-privileged site. Here, we have re-evaluated this tenet using a novel approach that allows us to detect, enumerate and characterize autophagosomes in vivo. We first validate the approach by showing that it allows the identification and characterization of autophagosomes in the livers of food-restricted mice. We use the method to identify constitutive autophagosomes in cortical neurons and Purkinje cells, and we show that short-term fasting leads to a dramatic upregulation in neuronal autophagy. The increased neuronal autophagy is revealed by changes in autophagosome abundance and characteristics, and by diminished neuronal mTOR activity in vivo, demonstrated by a reduction in levels of phosphorylated S6 ribosomal protein in Purkinje cells. The increased abundance of autophagosomes in Purkinje cells was confirmed using transmission electron microscopy. Our data lead us to speculate that sporadic fasting might represent a simple, safe and inexpensive means to promote this potentially therapeutic neuronal response.
PMID: 20534972 [PubMed - as supplied by publisher]
Short-term fasting induces profound neuronal autophagy.
Alirezaei M, Kemball CC, Flynn CT, Wood MR, Whitton JL, Kiosses WB.
Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA, USA.
Abstract
Disruption of autophagy-a key homeostatic process in which cytosolic components are degraded and recycled through lysosomes-can cause neurodegeneration in tissue culture and in vivo. Upregulation of this pathway may be neuroprotective, and much effort is being invested in developing drugs that cross the blood brain barrier and increase neuronal autophagy. One well-recognized way of inducing autophagy is by food restriction, which upregulates autophagy in many organs including the liver; but current dogma holds that the brain escapes this effect, perhaps because it is a metabolically-privileged site. Here, we have re-evaluated this tenet using a novel approach that allows us to detect, enumerate and characterize autophagosomes in vivo. We first validate the approach by showing that it allows the identification and characterization of autophagosomes in the livers of food-restricted mice. We use the method to identify constitutive autophagosomes in cortical neurons and Purkinje cells, and we show that short-term fasting leads to a dramatic upregulation in neuronal autophagy. The increased neuronal autophagy is revealed by changes in autophagosome abundance and characteristics, and by diminished neuronal mTOR activity in vivo, demonstrated by a reduction in levels of phosphorylated S6 ribosomal protein in Purkinje cells. The increased abundance of autophagosomes in Purkinje cells was confirmed using transmission electron microscopy. Our data lead us to speculate that sporadic fasting might represent a simple, safe and inexpensive means to promote this potentially therapeutic neuronal response.
PMID: 20534972 [PubMed - as supplied by publisher]
joi, 24 iunie 2010
miercuri, 23 iunie 2010
vineri, 18 iunie 2010
cel mai bun baton proteic ever
Detour Bar ... unul dintre cele mai bune lucruri pe care le-am mancat vreodata
Batoanele proteice au gust de medicament si consistenta de carton presat...asta face snickers de rusine la gust
si continutul e ok...pacat ca nu se gaseste la noi...Cristi?
marți, 15 iunie 2010
vineri, 11 iunie 2010
joi, 10 iunie 2010
luni, 7 iunie 2010
vineri, 4 iunie 2010
ce sa mananci/bei 2010
In 2008 scriam despre ceea ce cred eu ca e ok (sau mai putin) sa mananci/bei... m-am gandit ca n-ar strica sa fac o lista revizuita:
SUPER OK: legume (cu prioritate), fructe (orice fructe, de preferat in forma lor naturala, cu coaja daca e comestibila), carne (da, si porc), peste, fructe de mare, branza (de vaci, telemea, cas, urda, cascaval, etc.), iaurt (si sana, kefir etc.), unt, oua, ulei de peste, ulei de masline, ulei de cocos, otet, condimente (fara zahar), ceai verde, apa minerala sau plata
OK: nuci (inclusiv migdale, fistic, caju etc., toate de preferat crude), soia, paine, cereale, orez, paste, batoane proteice, concentrate proteice, lapte, sucuri 100% naturale (fara adaos de zahar, de preferat si cu ceva fibre), bauturi de tip cola zero (cu indulcitori), un pahar de vin rosu (o bere neagra) pe zi, cafea
DE PRFERAT FARA: margarina, mezeluri, dulciuri (prajituri, biscuiti, ciocolata, inghetata etc.), pateuri, croissante, pizza, fast food, orice "deep fried" (gogosi, snitzele etc.), popcorn, iaurturi cu fructe, cereale cu zahar, bauturi cu zahar
observatii:
- nu exista super alimente;
- contextul si cantitatea conteaza;
- atentie la aportul caloric, in special la alimentele dense caloric (nuci, uleiuri, unt, mancaruri grase) etc.
- daca vrei sa slabesti trebuie sa consumi mai mult decat mananci; nu exista vreun aliment cu aport caloric negativ deci la regim nu adaugi alimente ca sa slabesti;
- cu cat mai putin procesat e un aliment cu atat mai bine;
- orice combinatie este ok, atata timp cat o tolerezi;
- nu e nici o problema sa mananci seara;
- nu e nici o problema sa nu mananci dimineata;
- nu ai nici un avantaj daca mananci din 3 in 3 ore; mancatul normal de 3 ori pe zi e ok;
- daca mergi la sala si faci exercitii cu greutati, e bine ca majoritatea aportului caloric din ziua respectiva sa fie dupa sala;
- daca faci cardio, macar 3-4 ore inainte nu manca nimic;
- mancarea nu trebuie sa devina o obsesie; daca mananci curat de obicei ajunge, nu trebuie sa fie totul perfect intotdeauna !
SUPER OK: legume (cu prioritate), fructe (orice fructe, de preferat in forma lor naturala, cu coaja daca e comestibila), carne (da, si porc), peste, fructe de mare, branza (de vaci, telemea, cas, urda, cascaval, etc.), iaurt (si sana, kefir etc.), unt, oua, ulei de peste, ulei de masline, ulei de cocos, otet, condimente (fara zahar), ceai verde, apa minerala sau plata
OK: nuci (inclusiv migdale, fistic, caju etc., toate de preferat crude), soia, paine, cereale, orez, paste, batoane proteice, concentrate proteice, lapte, sucuri 100% naturale (fara adaos de zahar, de preferat si cu ceva fibre), bauturi de tip cola zero (cu indulcitori), un pahar de vin rosu (o bere neagra) pe zi, cafea
DE PRFERAT FARA: margarina, mezeluri, dulciuri (prajituri, biscuiti, ciocolata, inghetata etc.), pateuri, croissante, pizza, fast food, orice "deep fried" (gogosi, snitzele etc.), popcorn, iaurturi cu fructe, cereale cu zahar, bauturi cu zahar
observatii:
- nu exista super alimente;
- contextul si cantitatea conteaza;
- atentie la aportul caloric, in special la alimentele dense caloric (nuci, uleiuri, unt, mancaruri grase) etc.
- daca vrei sa slabesti trebuie sa consumi mai mult decat mananci; nu exista vreun aliment cu aport caloric negativ deci la regim nu adaugi alimente ca sa slabesti;
- cu cat mai putin procesat e un aliment cu atat mai bine;
- orice combinatie este ok, atata timp cat o tolerezi;
- nu e nici o problema sa mananci seara;
- nu e nici o problema sa nu mananci dimineata;
- nu ai nici un avantaj daca mananci din 3 in 3 ore; mancatul normal de 3 ori pe zi e ok;
- daca mergi la sala si faci exercitii cu greutati, e bine ca majoritatea aportului caloric din ziua respectiva sa fie dupa sala;
- daca faci cardio, macar 3-4 ore inainte nu manca nimic;
- mancarea nu trebuie sa devina o obsesie; daca mananci curat de obicei ajunge, nu trebuie sa fie totul perfect intotdeauna !
joi, 3 iunie 2010
Women Power by TC from T-Mag
Whether she's the live-at-home daughter of a pig farmer, a cashier at the Kwik-E-Mart, or an underwear model, most beautiful women discovered power at an early age, power in the form of sexual attractiveness, and power in the rather sad but overwhelming desire men have for their approval.
Put these two factors together, and a beautiful woman is, to most men, the most intimidating creature in the world; sort of like Freddie Krueger--same sculpted nails but with an awesome rack and a hellacious ass.
You get the sexual flip side to this when women are in the presence of a rich, powerful man. Suddenly, they're put in the same psychosexual tight wire act that men face when they're interacting with a beautiful woman.
Sure, put an ordinary woman in a room with Donald Trump and suddenly she knows how most men feel in her presence, only instead of the Donald merely firing her, men face the considerably more bleak prospect of not getting any primo ass.
Of course, if you pit a beautiful woman against a powerful man, then the power grab is nullified and they'll hook up and their spawn will wreck the remake of The Karate Kid.
For me, the intimidation comes not from the inherent power of beautiful women, but the fear of losing out on something wonderful. The nervousness I feel when I only get a few moments to lure a wünder babe into my man lair is like the nervousness a bass fisherman might feel when he's trying to land a record-setting fish, only instead of fearing you might not get your pic on the cover of Bass Master magazine, you might not get to stick your penis inside a world class hoo-hah and slide it back and forth, which, if successful, could possibly earn you the cover of Ass Master magazine.
I supposed the only way to combat this nervousness and the associated high cortisol is to, whenever in the presence of a beautiful woman, remind yourself of your inestimable talents and your self-worth. Most women can sense confidence and they're attracted to it. You have to admit, it sure beats splattering her suede pumps with urine from your nervous bladder.
If, on the other hand you don't have any talents or self-worth, you might possibly adopt a c'est la vie attitude and realize there's no reason to be nervous because there are plenty of other fish in the oil-coated sea that are already plenty drunk enough to overlook your multiple shortcomings.
Put these two factors together, and a beautiful woman is, to most men, the most intimidating creature in the world; sort of like Freddie Krueger--same sculpted nails but with an awesome rack and a hellacious ass.
You get the sexual flip side to this when women are in the presence of a rich, powerful man. Suddenly, they're put in the same psychosexual tight wire act that men face when they're interacting with a beautiful woman.
Sure, put an ordinary woman in a room with Donald Trump and suddenly she knows how most men feel in her presence, only instead of the Donald merely firing her, men face the considerably more bleak prospect of not getting any primo ass.
Of course, if you pit a beautiful woman against a powerful man, then the power grab is nullified and they'll hook up and their spawn will wreck the remake of The Karate Kid.
For me, the intimidation comes not from the inherent power of beautiful women, but the fear of losing out on something wonderful. The nervousness I feel when I only get a few moments to lure a wünder babe into my man lair is like the nervousness a bass fisherman might feel when he's trying to land a record-setting fish, only instead of fearing you might not get your pic on the cover of Bass Master magazine, you might not get to stick your penis inside a world class hoo-hah and slide it back and forth, which, if successful, could possibly earn you the cover of Ass Master magazine.
I supposed the only way to combat this nervousness and the associated high cortisol is to, whenever in the presence of a beautiful woman, remind yourself of your inestimable talents and your self-worth. Most women can sense confidence and they're attracted to it. You have to admit, it sure beats splattering her suede pumps with urine from your nervous bladder.
If, on the other hand you don't have any talents or self-worth, you might possibly adopt a c'est la vie attitude and realize there's no reason to be nervous because there are plenty of other fish in the oil-coated sea that are already plenty drunk enough to overlook your multiple shortcomings.
joi, 27 mai 2010
miercuri, 26 mai 2010
mai mare nu e neaparat mai atractiv
GI Joe or Average Joe? The impact of average-size and muscular male fashion models on men's and women's body image and advertisement effectiveness
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Received 8 December 2009;
revised 11 March 2010;
accepted 31 March 2010.
Available online 21 May 2010.
Abstract
Increasing body size and shape diversity in media imagery may promote positive body image. While research has largely focused on female models and women's body image, men may also be affected by unrealistic images. We examined the impact of average-size and muscular male fashion models on men's and women's body image and perceived advertisement effectiveness. A sample of 330 men and 289 women viewed one of four advertisement conditions: no models, muscular, average-slim or average-large models. Men and women rated average-size models as equally effective in advertisements as muscular models. For men, exposure to average-size models was associated with more positive body image in comparison to viewing no models, but no difference was found in comparison to muscular models. Similar results were found for women. Internalisation of beauty ideals did not moderate these effects. These findings suggest that average-size male models can promote positive body image and appeal to consumers.
marți, 25 mai 2010
miercuri, 19 mai 2010
claims of weight loss supplements
Claims on dietary and herbal supplements attribute weight loss to several mechanisms including the following:
* Increase of energy expenditure: ephedra, caffeine, guarana, bitter orange, yerba maté
* Increase in satiety: soluble fibers such as guar gum, glucomannan, psyllium
* Increase of fat oxidation: hydroxycitric acid (HCA), green tea, conjugated linoleic acid (CLA), fish oil, capsaicin, carnitine
* Blocking of dietary fat absorption: chitosan
* Modulation of carbohydrate metabolism: chromium
* Increase of fat excretion: calcium
* Increased water elimination: dandelion, cascara
* Enhancement of mood: St. John's wort
* Increase of energy expenditure: ephedra, caffeine, guarana, bitter orange, yerba maté
* Increase in satiety: soluble fibers such as guar gum, glucomannan, psyllium
* Increase of fat oxidation: hydroxycitric acid (HCA), green tea, conjugated linoleic acid (CLA), fish oil, capsaicin, carnitine
* Blocking of dietary fat absorption: chitosan
* Modulation of carbohydrate metabolism: chromium
* Increase of fat excretion: calcium
* Increased water elimination: dandelion, cascara
* Enhancement of mood: St. John's wort
marți, 18 mai 2010
luni, 17 mai 2010
vineri, 30 aprilie 2010
joi, 29 aprilie 2010
marți, 27 aprilie 2010
luni, 26 aprilie 2010
Intermittent fasting - Martin Berkhan style
Leangains Guide
cam asta fac si eu:
Two pre-workout meals
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)
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
scrie un articol misto despre slabire aici
un citat elocvent:
"There’s no food that, once you eat it, flips on a metabolic switch that completely shuts down fat burning and weight loss if you’re maintaining a daily caloric deficit. It’s a question of quantity, moderation and context."
vineri, 16 aprilie 2010
eat less / exercise more
Nutr Rev. 2010 Mar;68(3):148-54.
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.
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
Abstract from the recent Cardiovascular Disease Epidemiology and Prevention Conference, not been cleared for publication yet.
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.
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
N Z Med J. 2010 Mar 19;123(1311):53-7.
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.
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.
vineri, 2 aprilie 2010
miercuri, 31 martie 2010
Princeton fructose stupidity
un articol interesant despre concluziile aberante sau cel putin pripite ale cercetatorilor de la Princeton privind efectele consumului de fructoza
vineri, 26 martie 2010
Lyle - How we get fat
un articol foarte bun
citatul cheie: "Fat is directly stored and carbs and protein cause you to store the fat you’re eating by decreasing fat oxidation."
marți, 9 martie 2010
duminică, 7 martie 2010
intermittent fasting in action
din cand in cand nu mananc de seara pana a doua zi la pranz sau chiar seara
14-24 de ore fara nimic caloric..doar cafea, apa, ceai
ce e interesant, si am citit ca si altii au simtit asta, este ca devin mult mai productiv, mai concentrat
plus ca imi permite sa fiu mai flexibil cu dieta in rest
2000 de kcal la o masa, la regim, da :-)
PS ma enerveaza grasutu ala de la dimineata cu razvan si dani care ne explica procesul de productie al rebuturilor de soia din "lapte de soia" dupa un proces la fel ca cel din laptele de vaca...sa mulgi tu soia pufosule
miercuri, 3 martie 2010
fish oil court claim
marți, 23 februarie 2010
MSG is safe
sa nu ne panicam aiurea
monosodium glutamat aka MSG e ok
Independent expert panel confirms safety of Monosodium Glutamate (MSG) |
An international team of experts has met to consider new evidence on the safety of the food additive, monosodium glutamate (MSG), which is used to enhance flavour in Chinese food and some processed food and beverage products. The resulting consensus was intended to replace a similar exercise published in 1997.
Experts addressed common concerns about MSG and considered relevant literature. These concerns included the likelihood of glutamate crossing the placental or blood-brain barriers, whether MSG has adverse effects on immune function or lung health, and the risks of certain consumers being sensitive to MSG.
Total intake of glutamate from food in European countries was found to be stable at between 5 to 12 g/day. New evidence on immune function was scarce. In one study, 109 people with asthma were tested after consumption of oriental food or oral glutamate to establish tolerance. No adverse reactions were noted. Two studies investigating the impact of glutamate on lung function found no effect. There was no new evidence to support the idea that specific individuals experience sensitivity to glutamate.
Turning to concerns about the metabolic fate of glutamate, the expert panel spent some time considering whether the blood brain barrier (which restricts passage of substances from the bloodstream to the brain) was vulnerable to high intakes of MSG. It was agreed that, provided the blood brain barrier was intact, passive influx of glutamate into the brain was likely to be insignificant. However, several diseases are known to impair the blood brain barrier and it can’t be ruled out that a single high dose of glutamate may have adverse effects in such cases. At present, there is no data to suggest that raised blood levels of glutamate would translate into high brain glutamate concentrations.
Data from animal studies indicate that very high concentrations of glutamate in maternal blood do not find their way across the placenta. This suggests that maternal consumption of MSG would have minimal implications for foetal development. Interestingly, breast milk in Western countries has been found to contain measurable amounts of free glutamate, increasing the likelihood that infants have a higher intake of free glutamate than they do later in life. No ill-effects of this were noted.
The expert panel regarded a dose of 16,000 mg/kg body weight (or 16 g/kg body weight) to be a safe maximum intake of MSG for adults. It was concluded that current use of glutamate salts (monosodium-L-glutamate and others) as food additives was “harmless for the whole population” and, at low doses, could help to improve appetite in the elderly.
For more information, see Beyreuther K et al (2007). Consensus meeting: monosodium glutamate – an update. European Journal of Clinical Nutrition, vol 61: pp 304-313.
luni, 22 februarie 2010
hardcore
acum vreo 8-9 ani citeam pe testosterone.net (devenit ulterior t-nation, t-muscle, t-bullshit) ca daca nu vrei sa mergi degeaba la sala trebuie sa faci genuflexiuni cu bara in spate si indreptari
ani de zile am facut asta...genuflexiuni cu 130 de kg in spate, indreptari cu 160 de kg. rezultatul? o minunata hernie de disc, ani de zile de dureri, rmn-uri, medicamente si probabil, in final o operatie
un sfat: daca nu esti halterofil sau culturist de performanta, lasa dracu prostiile si fa niste exercitii mai sigure
duminică, 21 februarie 2010
joi, 18 februarie 2010
marți, 16 februarie 2010
luni, 15 februarie 2010
miercuri, 10 februarie 2010
miercuri, 3 februarie 2010
luni, 1 februarie 2010
duminică, 31 ianuarie 2010
joi, 28 ianuarie 2010
no fuckin difference...low fat slightly healthier
Diabetes. 2009 Dec;58(12):2741-8. Epub 2009 Aug 31.
Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial.
Bradley U, Spence M, Courtney CH, McKinley MC, Ennis CN, McCance DR, McEneny J, Bell PM, Young IS, Hunter SJ.
Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Belfast, U.K.
OBJECTIVE: Low-fat hypocaloric diets reduce insulin resistance and prevent type 2 diabetes in those at risk. Low-carbohydrate, high-fat diets are advocated as an alternative, but reciprocal increases in dietary fat may have detrimental effects on insulin resistance and offset the benefits of weight reduction. RESEARCH DESIGN AND METHODS: We investigated a low-fat (20% fat, 60% carbohydrate) versus a low-carbohydrate (60% fat, 20% carbohydrate) weight reduction diet in 24 overweight/obese subjects ([mean +/- SD] BMI 33.6 +/- 3.7 kg/m(2), aged 39 +/- 10 years) in an 8-week randomized controlled trial. All food was weighed and distributed, and intake was calculated to produce a 500 kcal/day energy deficit. Insulin action was assessed by the euglycemic clamp and insulin secretion by meal tolerance test. Body composition, adipokine levels, and vascular compliance by pulse-wave analysis were also measured. RESULTS: Significant weight loss occurred in both groups (P < p =" 0.40)." p =" 0.28)," p =" 0.71)." p =" 0.04);">, with no difference between groups (P = 0.40). Peripheral glucose uptake increased, but there was no difference between groups (P = 0.28), and suppression of endogenous glucose production was also similar between groups. Meal tolerance-related insulin secretion decreased with weight loss with no difference between groups (P = 0.71). The change in overall systemic arterial stiffness was, however, significantly different between diets (P = 0.04); this reflected a significant decrease in augmentation index following the low-fat diet, compared with a nonsignificant increase within the low-carbohydrate group. CONCLUSIONS: This study demonstrates comparable effects on insulin resistance of low-fat and low-carbohydrate diets independent of macronutrient content. The difference in augmentation index may imply a negative effect of low-carbohydrate diets on vascular risk.
PMID: 19720791 [PubMed - indexed for MEDLINE]
miercuri, 27 ianuarie 2010
marți, 26 ianuarie 2010
margarina
In ultimele zile m-a surprins agresivitatea campaniei de promovare a Rama. Este de inteles, informatia ca margarina este nociva a ajuns pana si in cel mai indepartat sat din Romania. Si ce s-au gandit, cea mai buna aparare e atacul. Rama nu ca nu e nociva, e chiar sanatoasa. Ne jucam cu niste cuvinte mari, amintim de omega 3 si 6 (mama ce sanatos suna), aducem niste vedete si gata...daca spune Nadia ca e buna, ii da si lu ala micu, pfffff, 3 cutii de Rama va rog...
Am intrat si eu, disperat de campania lor, pe desprerama punct ro. Ma asteptam sa citesc ceva despre ingrediente, un profil nutritional (daca nu stii ce e aia intra de exemplu pe nutritiondata.com), informatii despre modul in care este produsa. De unde. Numai informatii penibile, aruncate la gramada sa dea o aparenta de stiinta solida in spatele produsului, cu alte cuvinte bull shit.
In concluzie, ramane cum am stabilit, margarina nu, UNT da !
luni, 25 ianuarie 2010
carbohidratii sunt raaaai....aha
Eur J Appl Physiol. 2009 Dec 20. [Epub ahead of print]
Influence of dietary carbohydrate intake on the free testosterone: cortisol ratio responses to short-term intensive exercise training.
Lane AR, Duke JW, Hackney AC.
Endocrine Section, Applied Physiology Laboratory, Department of Exercise and Sport Science, University of North Carolina, CB # 8700, Fetzer Building, Chapel Hill, NC, 27599, USA.
This study examined the effect of dietary carbohydrate (CHO) consumption on the free testosterone to cortisol (fTC) ratio during a short-term intense micro-cycle of exercise training. The fTC ratio is a proposed biomarker for overreaching-overtraining (i.e., training stress or imbalance) in athletes. The ratio was studied in two groups, control-CHO (~60% of daily intake, n = 12) and low-CHO (~30% of daily intake, n = 8), of male subjects who performed three consecutive days of intensive training (~70-75% maximal oxygen consumption, 60 min per day) with a dietary intervention (on the day before and during training). Resting, pre-exercise blood samples were collected under standardized-controlled conditions before each day of training (Pre 1, 2, 3) and on a fourth day after the micro-cycle (Rest). Bloods were analyzed for free testosterone and cortisol via radioimmunoassay procedures. Subjects performed no additional physical activity other than prescribed training. Statistical analysis (ANCOVA) revealed the fTC ratio decreased significantly (p <> 0.05) in the control-CHO group (-3%). Findings suggest if the fTC ratio is utilized as a marker of training stress or imbalance it is necessary for a moderately high diet of CHO to be consumed to maintain validity of any observed changes in the ratio value.
Influence of dietary carbohydrate intake on the free testosterone: cortisol ratio responses to short-term intensive exercise training.
Lane AR, Duke JW, Hackney AC.
Endocrine Section, Applied Physiology Laboratory, Department of Exercise and Sport Science, University of North Carolina, CB # 8700, Fetzer Building, Chapel Hill, NC, 27599, USA.
This study examined the effect of dietary carbohydrate (CHO) consumption on the free testosterone to cortisol (fTC) ratio during a short-term intense micro-cycle of exercise training. The fTC ratio is a proposed biomarker for overreaching-overtraining (i.e., training stress or imbalance) in athletes. The ratio was studied in two groups, control-CHO (~60% of daily intake, n = 12) and low-CHO (~30% of daily intake, n = 8), of male subjects who performed three consecutive days of intensive training (~70-75% maximal oxygen consumption, 60 min per day) with a dietary intervention (on the day before and during training). Resting, pre-exercise blood samples were collected under standardized-controlled conditions before each day of training (Pre 1, 2, 3) and on a fourth day after the micro-cycle (Rest). Bloods were analyzed for free testosterone and cortisol via radioimmunoassay procedures. Subjects performed no additional physical activity other than prescribed training. Statistical analysis (ANCOVA) revealed the fTC ratio decreased significantly (p <> 0.05) in the control-CHO group (-3%). Findings suggest if the fTC ratio is utilized as a marker of training stress or imbalance it is necessary for a moderately high diet of CHO to be consumed to maintain validity of any observed changes in the ratio value.
vineri, 22 ianuarie 2010
joi, 21 ianuarie 2010
miercuri, 13 ianuarie 2010
joi, 7 ianuarie 2010
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