t nation marketing

selling bull crap

back pain

cancer again

oamenii astia chiar vor sa demonstreze ca reducerea carbohidratilor din dieta are un efect asupra tumorilor maligne

frecventa meselor

in ultimul timp mi-e lene sa scriu asa ca mai pun linkuri din cand in cand

un post interesant are o perspectiva noua privind frecventa meselor

intamplator sau nu, in ultimul timp mananc doar de doua ori pe zi...pe la doua si pe la noua, ca sa rimeze :-)

battle of the diets

ce am mancat la pranz

spanac cu doua oua ochiuri (oua de tara, facute in apa nu in ulei) - 10 lei

piept de pui cu orez, legume si sofran - 15 lei

salata de telina, mere, ananas, nuci - 12 lei

salata de fructe (struguri, kiwi, ananas, portocala si grapefruit) - 6 lei

toate de la Sana Gout...curat, sanatos si foarte bun

PS n-am nici un interes sa-i promovez

fish oil...not good news

un post interesant

raceala/gripa

un post interesant de la Dr. Ben Kim ... se pare ca nu e asa rau sa mai fii si racit din cand in cand

protein requirements

Curr Opin Clin Nutr Metab Care. 2009 Oct 16. [Epub ahead of print]

Evidence that protein requirements have been significantly underestimated.

Elango R, Humayun MA, Ball RO, Pencharz PB.

The Research Institute, The Hospital for Sick Children, Toronto, Canada, Department of Nutritional Sciences, Canada, Department of Paediatrics, University of Toronto, Ontario, Canada, Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada.

PURPOSE OF REVIEW: This review discusses recent evidence that suggests a significant underestimation of protein requirements in adult humans. RECENT FINDINGS: Traditionally, total protein requirements for humans have been determined using nitrogen balance. The recent Dietary Reference Intake recommendations for mean and population-safe intakes of 0.66 and 0.8 g/kg/day, respectively, of high-quality protein in adult humans are based on a meta-analysis of nitrogen balance studies using single linear regression analysis. We reanalyzed existing nitrogen balance studies using two-phase linear regression analysis and obtained mean and safe protein requirements of 0.91 and 0.99 g/kg/day, respectively. The two-phase linear regression analysis is considered more appropriate for biological analysis of dose-response curves. Considering the inherent problems associated with the nitrogen balance method, we developed an alternative method, the indicator amino acid oxidation technique, to determine protein requirements The mean and population-safe requirements in adult men were determined to be 0.93 and 1.2 g/kg/day and are 41 and 50%, respectively, higher than the current Dietary Reference Intakes recommendations. SUMMARY: The indicator amino acid oxidation-based requirement values of 0.93 and 1.2 g protein/kg/day and the reanalysis of existing nitrogen balance studies are significantly higher than current recommendations. Therefore, there is an urgent need to reassess recommendations for protein intake in adult humans.

cancer

am mai scris despre legatura dintre carbohidrati si cancer aici

am vazut azi ca a aparut un studiu interesant pe aceeasi tema

concluziile sunt urmatoarele:

We have shown that acetoacetate added to glucose medium causes variable but parallel reductions of ATP concentration and cell growth in seven human cancer cell lines. The effect lies along a continuum with control fibroblasts at one extreme in which neither cell growth is inhibited nor is ATP concentration reduced. The effect is consistent with an "inefficient" Randle cycle due to over-expression of uncoupling protein 2, seen only in the cancer lines, and is plausible in light of current models of a transformed cell's adaptive microscopic development and progression toward the cancer phenotype. More work must be done to prove metabolic inhibition by this mechanism. If proven, the results speak to the hypothesized potential for ketogenic diets as non-toxic therapeutic strategies, as adjuvants to standard therapies, and to multimodality therapies to improve the control of malignant disease.

clean eatin

date dintr-un studiu interesant privind consumul energetic al organismului uman

Organ or Tissue	Metabolic Rate (kcal/kg/day)		% Overall Resting Energy Expenditure	Weight in Kg	Weight in Lb	%Body Weight
Adipose	4.5		4	15	33	21.4%
Muscle	13		22	28.2	61.6	40
Other	12		16	23.2	10.5	33.1
Liver	200		21	1.8	3.96	2.6
Brain	240		22	1.4	3.08	2.0
Heart	400		9	0.3	0.66	0.5
Kidneys	400		8	0.3	0.66	0.5

recomandare

in ultimul timp am mancat foarte des de aici

mancarea este foarte gustoasa, portiile sunt asa cum trebuie, totul este gatit natural si curat. noodles-ul de legume, de exemplu, este genial

felicitari !

un studiu nou si interesant despre creatina

Clinical Journal of Sport Medicine
Issue: Volume 19(5), September 2009, pg. 399-404

Three Weeks of Creatine Monohydrate Supplementation Affects Dihydrotestosterone to Testosterone Ratio in College-Aged Rugby Players
van der Merwe, Johann MBChB; Brooks, Naomi E PhD; Myburgh, Kathryn H PhD
Author Information
From the Department of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa.
Submitted for publication February 1, 2009; accepted July 22, 2009.
Reprints: Kathryn H. Myburgh, PhD, Department of Physiological Sciences, Stellenbosch University, Private Bag XI, Matieland 7602, Stellenbosch, South Africa (e-mail:khm@sun.ac.za).

Abstract

Objective: This study investigated resting concentrations of selected androgens after 3 weeks of creatine supplementation in male rugby players. It was hypothesized that the ratio of dihydrotestosterone (DHT, a biologically more active androgen) to testosterone (T) would change with creatine supplementation.

Design: Double-blind placebo-controlled crossover study with a 6-week washout period.

Setting: Rugby Institute in South Africa.

Participants: College-aged rugby players (n = 20) volunteered for the study, which took place during the competitive season.

Interventions: Subjects loaded with creatine (25 g/day creatine with 25 g/day glucose) or placebo (50 g/day glucose) for 7 days followed by 14 days of maintenance (5 g/day creatine with 25 g/day glucose or 30 g/day glucose placebo).

Main Outcome Measures: Serum T and DHT were measured and ratio calculated at baseline and after 7 days and 21 days of creatine supplementation (or placebo). Body composition measurements were taken at each time point.

Results: After 7 days of creatine loading, or a further 14 days of creatine maintenance dose, serum T levels did not change. However, levels of DHT increased by 56% after 7 days of creatine loading and remained 40% above baseline after 14 days maintenance (P < 0.001). The ratio of DHT:T also increased by 36% after 7 days creatine supplementation and remained elevated by 22% after the maintenance dose (P < 0.01).

Conclusions: Creatine supplementation may, in part, act through an increased rate of conversion of T to DHT. Further investigation is warranted as a result of the high frequency of individuals using creatine supplementation and the long-term safety of alterations in circulating androgen composition.

Statement of Clinical Relevance: Although creatine is a widely used ergogenic aid, the mechanisms of action are incompletely understood, particularly in relation to dihydrotestosterone, and therefore the long-term clinical safety cannot be guaranteed.

la 74 de ani

proteine

Nu e neaparat nevoie de un camion de proteine la o masa pentru stimularea cresterii musculare....

J Am Diet Assoc. 2009 Sep;109(9):1582-6.

A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects.

Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D.

Graduate Center for Gerontology, University of Kentucky, Lexington, USA.

Ingestion of sufficient dietary protein is a fundamental prerequisite for muscle protein synthesis and maintenance of muscle mass and function. Elderly people are often at increased risk for protein-energy malnutrition, sarcopenia, and a diminished quality of life. This study sought to compare changes in muscle protein synthesis and anabolic efficiency in response to a single moderate serving (113 g; 220 kcal; 30 g protein) or large serving (340 g; 660 kcal; 90 g protein) of 90% lean beef. Venous blood and vastus lateralis muscle biopsy samples were obtained during a primed, constant infusion (0.08 mumol/kg/min) of L-[ring-(13)C(6)] phenylalanine in healthy young (n=17; 34+/-3 years) and elderly (n=17; 68+/-2 years) individuals. Mixed muscle fractional synthesis rate was calculated during a 3-hour postabsorptive period and for 5 hours after meal ingestion. Data were analyzed using a two-way repeated measures analysis of variance with Tukey's pairwise comparisons. A 113-g serving of lean beef increased muscle protein synthesis by approximately 50% in both young and older volunteers. Despite a threefold increase in protein and energy content, there was no further increase in protein synthesis after ingestion of 340 g lean beef in either age group. Ingestion of more than 30 g protein in a single meal does not further enhance the stimulation of muscle protein synthesis in young and elderly.

Dan Duchaine

the guru

hohohohohohoh

roids movie

bar barians

berardi show

aici

mda, generalitati, banalitati, prostii de-a dreptul...auzi, proteinele accelereaza metabolismul...no shit

calorii

un articol interesant

lower-crossed syndrome

daca stai mare parte din zi pe scaun, la birou, mai mult ca sigur ai asa ceva

quote of the day

"Everybody has a plan until they get punched in the face." — Mike Tyson

bai baiatulee

un nene dimineata la radio ne explica el ca bauturile carbogazoase sunt dracu gol, ca strica orice dieta. sa mori tu? tre sa fie gazul ala...

low carb diet

un post excelent pe blogul lui Tom Venuto

ce bf level

nu e o injuratura...ce body fat level...ce procent de grasime corporala

subiect la moda, mai ales acum ca a venit vara

in general, intr-o forma sau alta, lumea mananca mai mult iarna (ca nu se vede) si tine regim vara, sa moara dusmanii de invidie :-)

pentru astia ca mine pasionati de fitness, nutritie si alte cacaturi, chestia asta poate deveni o obsesie, cu accente de boala psihica...mama, am pus 1 cm in talie, sunt futut...arat ca o balena :-)

ce prostie. 99% dintre oameni n-o sa observe 1 cm in plus sau in minus

ca sa revin la procentul de grasime corporala, probleme sunt urmatoarele:

1. cat sa fie

2. cum fac sa ajung acolo

3. cum fac sa-l mentin

O precizare....toate astea se refera la persoane care nu folosesc steroizi sau alte chimicale (clen, dnp, etc.). nu ca ar fi ceva rau in asta, mai ales ca daca faci bani din cum arati ca barbat nu ai cum sa nu folosesti asa ceva... doar ca substantele astea schimba radical datele problemei si sunt cam mult pentru cineva care vrea doar sa arate decent ...

A doua precizare...e vorba de barbati...femeile pot adauga cam 8 la cifrele astea

1. cat sa fie, cat sa fie...aici e pe dos, tre sa fie cat mai mic :-)

bine, cat de mic permite geneticul, fara sa arati ca un om bolnav. degeaba ai 5% bf (despre cum se masoara vezi posturi mai vechi) daca arati ca un schelet....bine, se poarta la modele dar nu prinde pe toata lumea lookul asta. si mai e o chestie...un procent prea mic are ceva de prost gust, ca un tricou DG accesorizat cu lantic de aur... e usor vulgar sa ti se vada toate, chiar toate venele daca nu esti pe scena la un show de culturism...

cred ca un 8-10% e ok...asta o sa te faca sa arati ca un sportiv (daca ai ceva muschi), nu ca un culturist...

plus ca un procent prea mic de grasime corporala (cam sub 8%) nu e sanatos pe termen lung

2. cum ajungi acolo...despre asta parca am mai scris cate ceva...cu suferinta si privatiuni :-))

3. cum il mentii...cam cum l-ai obtinut, doar ca fara atatea privatiuni...

ce recomand eu este nu va ingrasati prea mult iarna si sa ramaneti in jur de 10% tot anul...in felul asta privatiunile aproape ca nu mai exista...

bine, n-o sa moara nimeni de invidie ce abdomen aveti dar mai sunt si alte chestii mai importante in viata

good luck :-)

carbohidrati/cancer

din ce in ce mai multe studii confirma ca o dieta ketogenica este de preferat pentru cei bolnavi de cancer. o explicatie sumara mai jos...

"Unlike healthy cells, which generate energy by metabolizing sugar in their mitochondria, cancer cells appeared to fuel themselves exclusively through glycolysis, a less-efficient means of creating energy through the fermentation of sugar in the cytoplasm. The theory is simple: If most aggressive cancers rely on the fermentation of sugar for growing and dividing, then take away the sugar and they should stop spreading. Meanwhile, normal body and brain cells should be able to handle the sugar starvation; they can switch to generating energy from fatty molecules called ketone bodies — the body's main source of energy on a fat-rich diet — an ability that some or most fast-growing and invasive cancers seem to lack."

vegetable oils

antioxidanti

nu intotdeauna buni

harvard info

Putting the joie de vivre back into health, Part 1
Lately, health researchers are reporting that maybe we can have our health and enjoy ourselves, too. Studies have elevated coffee to health-drink status by linking it to a reduced risk of dementia and Parkinson’s disease. Dozens of findings have shown that alcohol and chocolate may have cardiac benefits. Here is a rundown of research showing how to enjoy and be healthy — in that order! Alcohol Drinking increases “good” HDL cholesterol, reduces factors in blood that make it more likely to clot, and may directly affect blood vessels, keeping the linings smooth and pliable and thus less vulnerable to atherosclerosis. European researchers reported interesting findings in 2008 that show a connection between alcohol intake and higher blood levels of omega-3 fats. Indeed, temperate tippling has been associated with everything from greater bone density to less risk for Alzheimer’s disease and vascular dementia, as well as protection against heart disease and stroke. Moderation is paramount when it comes to alcohol, because drinking too much is patently ruinous. Triglycerides and blood pressure go up. Binge drinking can lead to stroke. Moderation is flexibly defined, but the American Heart Association guidelines are often cited: for men, one to two drinks a day; for women, just one. A drink is defined as a 12-ounce beer, 4 ounces of wine, or 1.5 ounces of 80-proof liquor. Women do need to worry about alcohol increasing breast cancer risk. Alcohol may drive up estrogen levels, and estrogen seems to play an integral part in the development of many breast cancers. However, at moderate amounts (the drink-a-day level), the risk is small. Folic acid may help offset the breast cancer risk posed by alcohol, so women who drink are encouraged to get an extra 400 micrograms per day. Chocolate A steady stream of studies has shown chocolate improves blood flow through arteries that supply the heart and the brain. In 2008, Harvard researchers found that two weeks of enhanced chocolate intake quickened blood flow through the middle cerebral artery. And Italian researchers reported a possible connection between eating dark chocolate and low levels of C-reactive protein, a marker for inflammation. The chocolate-as-healthful dream does need a couple of reality checks. The most likely explanation for chocolate’s good effects is that cocoa beans contain substances called flavonols (specifically, catechin and epicatechin, which are also found in tea) that stimulate production of nitric oxide, a chemical that relaxes blood vessels. In the studies cited above, researchers have used “flavonol-rich” chocolate. Dark chocolate may have more flavonols than other types, but you can’t go just by darkness. Some companies have started to market products advertised as preserving the cocoa bean’s flavonol content. Another caveat: the sugar and fat content of chocolate candy translates into calories (over 200 in a 3.5-ounce bar of expensive dark chocolate). And some of the fat in many chocolate bars is the unhealthful saturated variety. Coffee For the health conscious, a cup of coffee was once a somewhat perilous pleasure. Early studies showed a connection between coffee and heart attack, a worry that seemed to be validated by coffee’s ability to quicken the pulse. Some other studies cast the gloomy shadow of cancer risk. But the cancer research was flawed or overturned by more definitive findings. Meanwhile, the coffee–cardiovascular disease research has done an about-face: now the gist is that coffee drinkers seem to be less likely to have heart attacks and strokes and develop diabetes than nondrinkers. Study results indicate that coffee drinking may tamp down the risk of developing Parkinson’s disease. No one is sure why, although it’s been suggested that caffeine affects receptors in the basal ganglia, the part of the brain most damaged in Parkinson’s. Other studies are brewing hopes that coffee may affect our brain cells in ways that diminish risk for dementia and Alzheimer’s disease. Coffee does still come with cautionary notes. Pregnant women are still advised to limit, if not avoid, caffeine intake. Another caution: unfiltered coffee — which includes coffee drinks made with espresso — may increase “bad” LDL levels because some harmful substances in the coffee don’t get filtered out. There’s nothing wrong with the occasional latte or cappuccino, but overdoing it may mean a return to the bad old days when coffee was cardiovascularly suspect. For more information on nutrition and health, order our Special Health Report, Healthy Eating: A guide to the new nutrition, at www.health.harvard.edu/HE.

despre culturism

un post misto

hydroxycut

forget about it

you sucker

DIY

un fraier

avantajul metabolic al dietelor ketogenice

lyle dixit

who wins?

urmatoarea carte a lui Lyle McDonald

Chapter 1: Your fat is your fault
Chapter 2: Why you are the source of all of your problems
Chapter 3: Eat right, exercise and die anyway
Chapter 4: Chicks don't dig abs, chicks dig cold hard fucking cash

go see this

milk

movnat

crossfit

impinsul culcat nu este tocmai sport pentru cineva anchilozat de stat pe scaun 12 ore pe zi

am devenit tot mai interesat de exercitii care sa contracareze sedentarismul asta excesiv si sa ma faca sa ma simt in forma

crossfit este un concept foarte interesant. aici gasiti cateva exercitii

cateva mituri facute praf

- e nevoie sa manci de 5-6 ori pe zi ca sa accelerezi metabolismul

- daca nu mananci din 3 in 3 ore sigur o sa te catabolizezi

- pentru un abdomen definit sunt necesare sute de abdomene

- pentru slabire trebuie sa eviti carbohidratii

- daca eviti carbohidratii poti sa mananci oricat ca slabesti

- fara suplimente nu se poate sa pui muschi sau sa slabesti

- ca sa arati bine trebuie sa stai 3 ore pe zi la sala

- cardio este necesar pentru slabire

- mancarea organica este net superioara celei normale

- alcoolul este nesanatos

- nu poti sa pui muschi fara sa pui si grasime

- mancarea negatita este mai sanatoasa

- colesterolul mare e nenorocire

- painea ingrasa

- laptele e doar pentru vitei

- muschii ard o gramada de calorii in plus

- mancat corect inseamna proteine+ carbohidrati sau proteine+ grasimi

- lactatele trebuie evitate intr-un regim de slabire

pangasius - mai bine NU

Qu'est ce qu'un Panga ?
Uploaded by sudotone

powerball pb

12.058

for the low carb fanatics - de pe un forum

Like most low carb fanatics who are ignorant of all but the most pop-physiology, you’re incorrect to think that fat balance is all about insulin. You need to understand that there are a multitude of enzymes that are involved in triacylglycerol synthesis and lipolysis. “Insulin” is not a pathway. It’s one of several hormones that have an effect on the enzymes that comprise the actual pathways. What enzymes am I talking about? For fatty acid uptake, there’s FAT/CD36, FATP-1 to -6, and FABPpm. For fatty acid synthesis, there’s fatty acid synthase. For glucose uptake, there’s Glut1 and Glut4. For esterfication, there’s GPAT, PAP1, and DGAT1 and DGAT2. For lipolysis, there’s HSL, perilipin, and Protein kinase A. What “regulates all this?” It’s definitely not just “insulin”. That’s an incredibly simplistic, insulinocentric view. You know what else has an effect on these lipogenic/lipolytic enzymes besides insulin? There’s angiotensin II, the adrenergic receptor (catacholamines), FoxC2, PTP1B, and last but not least ASP. ASP stimulates triacylglycerol synthesis more than any other known adipose tissue factor. It’s also a potent stimulator of glucose transport [PMID: 9130021]. It works independently of insulin, through a different signaling pathway. It effectively synthesizes triacylglycerol even in the absence of glucose and insulin [PMID: 8492712]. Finally, guess what the primary regulator of ASP production is? Dietary fat (packaged as chylomicrons) [PMID: 9694837]. Fat intake and ASP will lead to a positive fat balance just as much as carb intake and insulin will. Which is why it’s all about calories. Unfortunately, low carb nuts never look past insulin. They ignore (or are ignorant of) the fact that fat stores itself with tremendous efficiency without any insulin whatsoever. Take a look at the broader picture. Fatty acids are taken up into adipocytes via facilitated diffusion, mediated by fatty acid transporters like the ones I mentioned above. You don’t need insulin for this. Dietary FFAs will diffuse into adipocytes down the concentration gradient. There may even be passive diffusion. You then need a triacylglycerol backbone and the acylation (esterfication) steps that lead to the production of a triacylglycerol. ASP can stimulate both. After all, it’s called “acylation-stimulating protein.” This process works just fine with basal levels of insulin or glucose. And as explained before, ASP is produced in response to FAT INTAKE. Weight loss is all about negative calorie balance, not lowering of insulin. Research clearly shows that when isonitrogenous diets are compared, higher carb diets (with higher insulin levels) do JUST AS WELL as lower carb diets at reducing bodyfat. While low carb diets have lower insulin levels, they have higher ASP levels. And vice versa with a low fat diet. Why? Because carb intake (or type) and insulin levels are absolutely unable to account for fat loss. It’s all about energy balance.

cardio

mult hulitul cardio e numit aiurea, neexistand se pare nici un beneficiu cardiovascular

cardio se traduce prin orice fel de miscare al carei scop este arderea de calorii. ca nu le mananci/bei sau le arzi facand cardio e acelasi lucru

in ultimul timp am facut cardio cam de 3-4 ori pe saptamana. din moment ce scopul este sa ard niste calorii, nu mi-am propus sa ating un numar de minute ci un numar de calorii, conform estimarii aparatului (chiar daca estimarea este in general prea optimista)

400 de calorii este un antrenament ok. prefer sa le ard mai repede si mai intens...ieri a durat cam 28 de minute pe o bicicleta eliptica. probabil ca daca alerg ard 400 de calorii in mai putin de 20 de minute

pulsul nu este un indicator foarte bun al intensitatii exercitiului. la persoanele neantrenate pulsul creste foarte tare chiar daca exercitiul nu este foarte dificil. oricum, un puls peste 120 este de preferat

berea e sanatoasa

in cantitate moderata, binenteles

Clin Nutr. 2009 Feb 25. [Epub ahead of print]Click here to read Links
Melatonin present in beer contributes to increase the levels of melatonin and antioxidant capacity of the human serum.
Maldonado MD, Moreno H, Calvo JR.

Department Medical Biochemistry and Molecular Biology, University of Seville Medical School, Avda. Sánchez Pizjuán 4, 41009 Seville, Spain.

BACKGROUND & AIM: Melatonin is a molecule with antioxidative properties including direct free radical scavenging and indirect stimulatory actions on a variety of antioxidative enzymes which further promote its ability to reduce the toxicity of radicals and their associated reactants. Beer is an integral element of the diet of numerous people and is rich in antioxidants. We analyzed if melatonin is present in beer and if so, at what concentration. It further determines whether the moderate consumption of beer has an effect on the total antioxidant status (TAS) of human serum. METHODS: We analyzed 18 brands of beer with different percentage of alcohol content in order to determine the concentration of melatonin. Serum samples were collected from 7 healthy volunteers. These samples were used to measure melatonin and TAS on basal conditions and after drinking beer. RESULTS: Showed that all the beer analyzed did indeed contain melatonin and the more they have got, the greater was its degree of alcohol. Both melatonin and TAS in human serum increased after drinking beer. CONCLUSIONS: Melatonin present in the beer does contribute to the total antioxidative capability of human serum and moderate beer consumption can protect organism from overall oxidative stress.

slabiti la McD

http://www.bowlingformorgan.com/

credit crisis

The Crisis of Credit Visualized from Jonathan Jarvis on Vimeo.

exuberant animal

Exuberant Animal's Frank Forencich gives hope to the modern man (and woman) from Lauren Muney on Vimeo.

(de) constructing computer guy

2 articole misto despre ce ar trebui sa faca la sala si in restul timpului cei care (ca mine) stau pe un  scaun toata ziua

aici si aici

i love dacia

i like ricky

in a non gay way :-)

asta

orthorexia nervosa

reprezinta obsesia de a manca doar alimente considerate sanatoase, "curate"

cu alte cuvinte, o boala psihica. nu exista alimente "curate" si alimente "murdare". lucrurile sunt mai complexe :-)

"Orthorexia begins, innocently enough, as a desire to overcome chronic illness or to improve general health. But because it requires considerable willpower to adopt a diet that differs radically from the food habits of childhood and the surrounding culture, few accomplish the change gracefully. Most must resort to an iron self-discipline bolstered by a hefty dose of superiority over those who eat junk food. Over time, what to eat, how much, and the consequences of dietary indiscretion come to occupy a greater and greater proportion of the orthorexic's day.

The act of eating pure food begins to carry pseudospiritual connotations. As orthorexia progresses, a day filled with sprouts, umeboshi plums, and amaranth biscuits comes to feel as holy as one spent serving the poor and homeless. When an orthorexic slips up (which may involve anything from devouring a single raisin to consuming a gallon of Haagen Dazs ice cream and a large pizza), he experiences a fall from grace and must perform numerous acts of penitence. These usually involve ever-stricter diets and fasts.

This "kitchen spirituality" eventually reaches a point where the sufferer spends most of his time planning, purchasing, and eating meals. The orthorexic's inner life becomes dominated by efforts to resist temptation, self-condemnation for lapses, self-praise for success at complying with the chosen regime, and feelings of superiority over others less pure in their dietary habits.

This transference of all of life's value into the act of eating makes orthorexia a true disorder. In this essential characteristic, orthorexia bears many similarities to the two well-known eating disorders anorexia and bulimia. Where the bulimic and anorexic focus on the quantity of food, the orthorexic fixates on its quality. All three give food an excessive place in the scheme of life."

ca sa combat boala asta, de care am suferit si eu o buna perioada (ani de zile...un exemplu de cretinism maxim: asta vara am fost in Italia si nu am mancat inghetata), azi la pranz am mancat o prajitura de la chocolat :-)

bine, pana maine dimineata nu mai mananc nimic, dar nu pentru ca ma simt vinovat sau ceva de genul asta...pur si simplu vreau sa mai slabesc un pic si asta fara deficit caloric nu se poate

experimentele continua...

gatit

un articol interesant despre rolul gatitului in evolutia omului

post

in ultimele 24 de ore n-am mancat nimic

a fost excelent. nu mi-a fost foame absolut deloc. am facut doua antrenamente foarte bune. m-am simtit grozav, probabil de la secretia de catecolamine

am de gand sa fac asta de 1-2 ori pe saptamana de acum incolo

powerball pb

akis, fa-mi loc in top

am facut 11.978...

Lyle McDonald - hierarchy of nutrition

Focusing on the insulin response (or lack thereof) is missing the point. 

Your body comp will be determined primarily by your calorie surplus/deficit. Then, below that are issues with macronutrients (essentially, if you are eating enough protein). 

Then below that (MUCH below) are issues with nutrient timing (and being sure to eat carbs+protein around your workout is about all you can do to optimize this) and finally, issues with individual food sub-types (sweet potatos vs white potatos, peanut butter vs. almond butter etc.) are essentially meaningles.

radio misto

profm latino

colesterol

treaba nu e asa de simpla cum pare la prima vedere

it's all about calories in/calories out

un studiu publicat acum in New England Journal of Medicine confirma faptul ca se poate slabi la fel indiferent de compozitia dietei, atata timp cat exista deficit caloric

ABSTRACT

Background The possible advantage for weight loss of a diet that emphasizes protein, fat, or carbohydrates has not been established, and there are few studies that extend beyond 1 year.

Methods We randomly assigned 811 overweight adults to one of four diets; the targeted percentages of energy derived from fat, protein, and carbohydrates in the four diets were 20, 15, and 65%; 20, 25, and 55%; 40, 15, and 45%; and 40, 25, and 35%. The diets consisted of similar foods and met guidelines for cardiovascular health. The participants were offered group and individual instructional sessions for 2 years. The primary outcome was the change in body weight after 2 years in two-by-two factorial comparisons of low fat versus high fat and average protein versus high protein and in the comparison of highest and lowest carbohydrate content.

Results At 6 months, participants assigned to each diet had lost an average of 6 kg, which represented 7% of their initial weight; they began to regain weight after 12 months. By 2 years, weight loss remained similar in those who were assigned to a diet with 15% protein and those assigned to a diet with 25% protein (3.0 and 3.6 kg, respectively); in those assigned to a diet with 20% fat and those assigned to a diet with 40% fat (3.3 kg for both groups); and in those assigned to a diet with 65% carbohydrates and those assigned to a diet with 35% carbohydrates (2.9 and 3.4 kg, respectively) (P>0.20 for all comparisons).Among the 80% of participants who completed the trial, the average weight loss was 4 kg; 14 to 15% of the participants had a reduction of at least 10% of their initial body weight. Satiety, hunger, satisfaction with the diet, and attendance at group sessions were similar for all diets; attendance was strongly associated with weight loss (0.2 kg per session attended). The diets improved lipid-related risk factors and fasting insulin levels.

Conclusions Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize. (ClinicalTrials.gov number, NCT00072995[ClinicalTrials.gov] .)

statine

eu zic sa luati cat mai multe

colesterolul si bolile cardiovasculare

corelatia dintre colesterol si bolile cardiovasculare (foarte profitabila de exemplu pentru producatorii de statine) primeste inca o lovitura

studiul de mai jos (care acopera o perioada de 60 de ani) arata ca principalul factor care creste riscul unui infact de miocard nu este colesterolul ci resistenta insulinica. asta este cauzata de o alimentatie "sanatoasa" bazata pe carbohidrati rafinati care include si grasimi "sanatoase" ca margarina 

pe locul doi este hipertensiunea arteriala....

Eddy D, Schlessinger L, Kahn R, et al. Relationship of Insulin Resistance and Related Metabolic Variables to Coronary Artery Disease: A Mathematical Analysis. Diabetes Care 2009; 32 : 361-366 

Abstract

OBJECTIVE — People with diabetes have an increased risk of coronary artery disease (CAD). An unanswered question is what portion of CAD can be attributed to insulin resistance, related metabolic variables, and other known CAD risk factors. 

RESEARCH DESIGN AND METHODS — The Archimedes model was used to estimate the proportion of myocardial infarctions that would be prevented by maintaining insulin resistance and other risk factors at healthy levels. Person-specific data from the National Health and Nutrition Examination Survey 1998–2004 were used to create a simulated population representative of young adults in the U.S. This population was then entered into a series of simulated clinical trials designed to explore the effects of each risk factor. Each trial had a control arm (all risk factors were allowed to progress without interventions) and a treatment arm (a risk factor was held to its value in young healthy adults). The trials continued for 60 years. The effects of these hypothetical "cures" of each risk factor provide estimates of their impact on CAD. 

RESULTS — In young adults, preventing insulin resistance would prevent ~42% of myocardial infarctions. The next most important determinant of CAD is systolic hypertension, prevention of which would reduce myocardial infarctions by ~36%. Following systolic blood pressure, the most important determinants are HDL cholesterol (31%), BMI (21%), LDL cholesterol (16%), triglycerides (10%), fasting plasma glucose and smoking (both ~9%), and family history (4%). 

CONCLUSIONS — Insulin resistance is likely the most important single cause of CAD. A better understanding of its pathogenesis and how it might be prevented or cured could have a profound effect on CAD.

grasimile polinesaturate si cancerul

cu dedicatie pentru madam nutritionist care ieri ne explica ea ce sanatoase sunt grasimile polinesaturate

"The researches used the imaging and cell-counting tools to document that linoleic acid, which is predominant in polyunsaturated fats, caused increasing membrane phase separation, whereas oleic acid, found in monounsaturated fats, did not. Increased membrane phase separation could improve the opportunity of circulating tumor cells to adhere to blood vessel walls and escape to organs far from the original tumor site. The new findings support earlier evidence from other research that consuming high amounts of polyunsaturated fat may increase the risk of cancer spreading."

nutritionista cu acte in regula

cat de haotica e madam

in anul 2009 inca mai exista un nutritionist care spune ca untul este rau dar margarina e buna

care ne spune ca uleiul de floarea soarelui e bun, dar grasimea din carne si din lactate e rea

cica grasimile sunt principalii furnizori de energie

ba ne laaasi

taking questions

astept intrebari legate de nutritie si antrenament

daca tot am o pana de inspiratie poate intrebarile voastre sa ma trezeasca

Fedor the almighty

beavis and butthead

o parte dintr-un articol interesant din EJCN

Which are the greatest recent discoveries and the greatest future challenges in nutrition?

Discoveries

The discovery that folic acid prevents birth defects was judged to be the greatest discovery in nutrition science since 1976. It was a discovery in which neither the speakers nor the audience had been actively involved. In fact, the discovery that periconceptional supplementation with folic acid prevents most cases of spina bifida and anencephaly was not made by nutrition scientists, but by British doctors working on the prevention of birth defects (Smithells et al., 1976; MRC Vitamin Study Research Group, 1991). The story of this discovery spans 50 years (Willett, 1998). A synthesis of data from clinical observations, biochemistry, epidemiology, genetics and randomized clinical trials was required to establish that periconceptional folic acid prevents birth defects. The discovery also overturned the dogma that an apparently balanced diet provides enough of all nutrients. The subsequent addition of folic acid to staple foods in North America clearly reduced the incidence of this most common of the major congenital abnormalities (Persad et al., 2002).

The discovery ranked no. 2 was the health effects of trans fatty acids. Three of the five speakers had been involved in this discovery (Mensink and Katan, 1990;Willett et al., 1993), so there may be bias here. But the discovery of the adverse effects of trans fatty acids on blood lipoproteins and incidence of heart disease continues to affect both nutritional guidelines and food composition worldwide. Throughout the twentieth century, the partial hardening of oils with the concomitant production of trans fatty acids had been a pillar of the food industry, with huge investments in research and factories (Korver and Katan, 2006). All that is being phased out now, and the replacement of partially hydrogenated by unprocessed oils is likely to prevent many myocardial infarctions.

No. 3 was the nutritional regulation of gene transcription. Examples of this are the way dietary fatty acids regulate hepatic fatty acid synthesis and breakdown via nuclear receptors (Shulman and Mangelsdorf, 2005), but the discoveries go beyond that. Molecular biology is opening up the black box of the regulation of intermediary metabolism (Desvergne et al., 2006), and this has consequences for our understanding of vitamin, protein, lipid and carbohydrate metabolism, and of disease development.

Arguably, this discovery might have been combined with no. 6, the LDL receptor and its regulation by diet. The regulation of the activity of the LDL receptor by dietary cholesterol was elaborated by Brown and Goldstein around 1976 in a model of brilliant simplicity and predictive power (Kovanen et al., 1981). Unfortunately, we still lack a similar insightful explanation of why the structure of dietary fatty acids affects blood lipid levels. Why do saturated and trans-unsaturated fatty acids raise and cis-unsaturated fatty acids lower LDL cholesterol? Many mechanisms have been proposed, but none entirely satisfactory (Spritz et al., 1965; Spritz and Mishkel, 1969; Beynen and Katan, 1985; Fox et al., 1987; Lin et al., 2005).

Discovery nos. 4 and 5 both represent gains made in obesity research. Essential to discovery no. 4, progress in measuring energy intake, was the doubly labeled water technique for estimating energy expenditure and intake. Application of this technique to humans (Schoeller and van Santen, 1982) showed that traditional dietary history and recall methods underestimated energy intake, and that this bias increases with increasing body fatness. The paradox that the more obese a person is, the less they appeared to eat had puzzled scientists, but it took many doubly labeled water measurements plus years of heated debate before it was accepted that obese people eat more than lean people, at least in populations with limited variation in physical activity. The issue was sensitive because the results of the doubly labeled water studies seemed to put the blame on obese subjects, and in addition, they appeared to discredit the recall techniques so widely used in nutrition and dietetics.

Discovery no 5, fat tissue as an endocrine organ, was heralded by the discovery of leptin and its absence in a genetic model of rodent obesity (Zhang et al., 1994). Leptin was followed by tumor-necrosis factor-, adiponectin, resistin and other hormones. These have drastically changed our view of adipose tissue metabolism and have given important insights into the mechanisms linking obesity with type II diabetes, atherosclerosis and other diseases (Rosen and Spiegelman, 2006; Trujillo and Scherer, 2006).

No. 7, obesity is a normal response to an abnormal environment, represents a step forward in a different area of the obesity issue, namely the role of the environment. Until recently, the search for causes of weight gain focused on genetic or metabolic abnormalities of obese people. Also, obese individuals were considered to lack the willpower to eat less or exercise more (Prentice and Jebb, 1995). But from a public health point of view, obesity can be also be viewed as a normal reaction to an abnormal environment (Egger and Swinburn, 1997) instead of a disorder. Attempts to improve individual diet and exercise habits may not be enough to curb the obesity epidemic; we may also need to create healthier school environments, transportation systems and town planning.

No. 8, alcohol causes breast cancer (Williams and Horm, 1977), and no. 9, body fatness is the second most avoidable cause of cancer (Lew and Garfinkel, 1979), together represent the major known dietary causes of cancer. Implicitly, they also illustrate the problems and frustrations of the diet and cancer field. Early in our 30-year time frame, observations on carotenes and on dietary fat seemed to offer hope of reducing the incidence of cancer through changes in nutrient intake (Petoet al., 1981), but new research has shown that the prospects for reducing cancer through a change of nutrient intake are more limited (WCRF, 2007). There remains a real possibility that we have not investigated the critical periods in life. Effects of diet during childhood and early adult life on later risk of cancer remain to be explored, as are effects of various foods and nutrients. But such research will not come easily. As it is, reductions in alcohol intake and in obesity could already have a marked impact on the incidence of cancer of the breast and other organs. Both doctors and the general public are little aware of the alcohol–cancer link.

No. 10, plant stanols/sterols and lipid metabolism, was not a discovery of the period 1976–2006 proper, as the effect of plant sterols on cholesterol was already known in the 1950s (Wilkinson et al., 1955). But it took until the 1990s before large amounts of plant stanols could be incorporated into margarine in a way that conserves or even enhances their cholesterol-lowering potency. The effect of such margarines on cholesterol equals that of the rest of the diet combined (Miettinen et al., 1995; Jenkins et al., 2003). Products with sterols and stanols became the paradigm for branded foods with health claims, and they remain one of the few 'functional foods' with proven efficacy in reducing a biomarker for a disease. But they have to compete with a class of drugs with an unbeatable record for clinical effectiveness and safety, that is, the statins. Sterols/stanols owe their market position more to the fact that they are perceived as a food than to superior efficacy in preventing heart disease. There is also some concern that absorption of sterols may promote the very disease that they aim to prevent. The prototype of such an effect of absorbed sterols on atherosclerosis is phytosterolemia or sitosterolemia (Bhattacharyya and Connor, 1974). Patients with homozygous phytosterolemia overabsorb plant sterols, and they develop massive xanthomas and atherosclerosis.

No. 11, diabetes can be prevented by diet and lifestyle, builds on another observation made before 1976, namely that obesity causes type II diabetes. But in spite of the huge impact of obesity on diabetes risk seen in observational studies, the efficacy of lifestyle changes in trials still came as a surprise. A non-randomized study of modest levels of exercise and weight reduction from Sweden found a remission rate in diabetics of over 50% (Eriksson and Lindgarde, 1991), and in a Chinese study, the number of patients progressing from impaired glucose tolerance to frank diabetes was reduced by 36% (Pan et al., 1997). The first large randomized trial was done in Finland (Tuomilehto et al., 2001), closely followed by one in the United States, (Knowler et al., 2002) and both found that fairly small changes in diet, activity and weight reduced diabetes incidence by 58%. Diet and weight loss were clearly more efficacious than the standard drug treatment, metformin. (Knowler et al., 2002) How can 20 to 30 min of moderate exercise per day plus a 3- to 6-kg weight loss reduce the incidence of type II diabetes by more than half? We do not know. But an even more urgent question is how we can change our world so that more patients receive and comply with this most powerful of diabetes treatments.

Discovery no. 12 was interaction of carbohydrate/glycemic load with insulin resistance. There is controversy over diets with a low glycemic index for the treatment of diabetes. However, the effect of glycemic index on postprandial blood glucose levels in diabetics is incontrovertible (Jenkins et al., 1983). New research is extending the concept of glycemic index beyond the treatment of diabetics to prevention of diabetes (Salmeron et al., 1997), but the data are still incomplete and therefore controversial.

Discovery no. 13 deals with the finding that something does not work: after high hopes for antioxidants, large randomized trials showed that vitamin E does not reduce cardiovascular disease, at least not in patients who have the disease or are at high risk for it. (The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group, 1994) It still remains possible that vitamin E has a role in the primary prevention of cardiovascular disease, but the issue is unlikely to be settled by clinical trial evidence.

No. 14, the effect of fish oil fatty acids to reduce mortality in coronary heart disease patients, has been a topic of interest ever since the initial observation that Eskimos (Inuit) have a high fat intake but low rates of coronary heart disease. (Bang et al., 1971) It received support from Nobel prize-winning research on fatty acids and prostaglandins, was strengthened by observational findings in Zutphen (Kromhout et al., 1985) and many subsequent epidemiological studies, and was initially upheld by clinical trials. Recent trial data have, however, been less consistent (Brouwer et al., 2006). More trials are in the pipeline.

No. 15, the multisystemic role of vitamin D, is still at an early stage. Reported effects of vitamin D on cancer, diabetes and muscle function are intriguing but not yet established beyond doubt (Garland et al., 1985; Martinez et al., 1996;Holick, 2006).

Challenges

The speakers and the audience together nominated 17 challenges. As some of these were similar, we collated them into the 14 challenges.

According to the audience, controlling obesity and insulin resistance through activity and diet, was the greatest challenge for nutrition research in the coming 30 years; it received 48 of the 128 votes. But is it a challenge for nutrition science or for society as a whole? After all, the causes of obesity are clear: too many dietary calories and too little energy expenditure. Still, the debate is raging whether some foods or nutrients exacerbate the problem, and other foods help to limit caloric intake. These questions seem simple, but the record of the past 30 years shows they are not, as witnessed by the long-standing controversy over the role of dietary fat in obesity (Connor and Connor, 1997; Katan et al., 1997;Astrup et al., 2000). We obviously need more thorough tests of proposed remedies. Such testing should involve large, well-controlled trials that last several years, and, even more demanding, the studies should ideally be double-blind, because food intake is highly sensitive to suggestion. That will be hard to achieve with most foodstuffs: what is the placebo for an apple?

Three other challenges also drew over 10% of the votes.

The first of these, and no. 2 in the overall ranking, was Can diet delay cognitive decline? Its election may have been helped by the recent completion in Wageningen of the FACIT trial, which showed that folic acid reduced the decline in memory in elderly volunteers (Durga et al., 2007). Further studies in this direction are obviously worthwhile, because the effect of B-vitamins on cognitive decline is far from settled. The effect of n-3 fatty acids from fish on cognitive decline also deserves further exploration (Beydoun et al., 2007; van Gelder et al., 2007).

Challenge no. 3 was restore the balance between private and public control of nutrition research. This had nothing to do with any specific line of research, but it reflected widespread concern that nutrition research has become overly market-oriented and sensitive to commercial interests (Katan, 2007). Over the past 20 years, there has been a strong preference for market forces to take care of research priorities, but some correction may be imminent. For example, the European Research Council is beginning to award research grants based exclusively on scientific excellence; this new program no longer requires the commercial applicability that is a prerequisite for much of the other research funded by the European Union. Although collaboration with industry can yield valuable research results, as testified by the FACIT (Durga et al., 2007) and SOFA (Brouwer et al., 2006) trials, industry-sponsored research will probably not lead to the long-term scientific breakthroughs that we need.

Challenge no. 4 was the reductionistic approach versus the food pattern approach. This sounds philosophical but it is a concrete issue that has been around for many years: should we do research and give dietary recommendations in terms of molecules and their actions, or of foods and diets? The popularity of the 'Mediterranean diet' (800 PubMed hits as of 17 May 2007), shows that the holistic approach is gaining territory among scientists. But when is a diet Mediterranean? That is hard to decide without assigning a number for 'Mediterranean-ness'. On the other hand, the benefits of certain foods are hard to summarize in terms of the molecules in them: the effect of low-fat, high-carbohydrate diet (Schaefer et al., 1995) on weight loss may be due more to their taste and structure than to a particular content of any macro- or micronutrient. Similarly, there is more to corn and pellagra than the low niacin content of corn. Foods are complex and our knowledge is limited, so nutrition and health is unlikely to be reduced entirely to molecular interactions.

Another 10 challenges each gathered a few percentage of the votes. Some referred to practical problems that have been with us for a while, such asimplementing diet in clinical practice and reduction of salt in foods, some were of a more general nature, such as diet and low-grade systemic inflammation, from genetics to epigenetics and the use of substances from plants to prevent disease. Some were methodological, for example, How can we prove that lifestyle interventions work? and How can we measure energy balance in free living people?

Finally, two represent work in progress in the diet-heart field. One is the role of B-vitamins and homocysteine lowering in the prevention of cardiovascular disease.Up till now the results of clinical trials of homocysteine lowering have been disappointing, but the largest trials will only report in the next few years (B-Vitamin Treatment Trialists' Collaboration, 2006). Trials may not provide the final answer, because short-term application of high doses in patients with existing disease may not be equivalent to long-term intake of modest amounts by healthy people. But a trial of the primary prevention of heart disease with B-vitamins in healthy subjects is unlikely to happen because the size and cost would be prohibitive.

Another work in progress is the role of -linolenic acid in prevention of coronary heart disease mortality. This might be solved by the ongoing Alpha Omega Trial (http://clinicaltrials.gov/ct/show/NCT00139464), which is due to report in 2010. Or it might not: certainty does not come easy in nutrition research, but fortunately, 2036 is still a long way off.

powerball

mi-am luat un powerball. foarte misto chestie :-)

informatii aici

deocamdata am facut 10302 de puncte

mancare libaneza misto

mezze

foarte buna mancarea

pe vremea asta livrarea acasa/la serviciu face toti banii

Romanian cities

Afumaţi - Neversober
Urlaţi – Gimme Some Noise
Constanţa - The Steadiness
Slobozia - A Very Wrong Local Tradition
Călăraşi - Silly-dressed Folks on Horses
Piteşti - Youdohide
Oneşti - The Sincere
Huşi - Shoo
Buhuşi - Boo
Satu-Mare - The Rather Roomy Rural Community
Slatina - Slut Tina
Târgu Frumos - The Aesthetically Pleasing Bazaar
Buzău - Really Fat Lip
Năvodari - Networkers
Dor Mărunt - Miniature Melancholy
Baia Mare – Big Bathroom

Voluntari - Town of Unpaid Assistants

repost

tii regim si nu ai rezultate? ia mai uita-te o data la asta 

marele secret al slabitului este ca nu exista nici un secret. cine iti spune altceva are ceva de vandut...

why are we fucked?

despre criza

for the love of house

aici gasiti niste radio-uri online

foame

Lyle McDonald scrie aici despre 9 modalitati de a combate foamea intr-un regim de slabire (proteine, fructe, fibre, grasimi, sport, post intermitent, suplimente care reduc apetitul, flexibilitate si vointa). pe langa astea cred ca se mai poate combate foamea mancand des si putin (cam din 3 in 3 ore) sau band apa/cola light

subiectul este extrem de important, controlul foamei fiind cheia oricarui regim de slabire

multivitamine

conform unui studiu recent pe 161.808 femei intr-o perioada de 8 ani, folosirea multivitaminelor nu a redus in nici un fel risul de cancer, boli cardiovasculare sau mortalitatea

bukres

un site misto

la sala de balet

paine

ne place sau nu suntem obisnuiti sa mancam cu paine. binenteles ca ne putem dezobisnui dar nu cred ca merita efortul. se poate manca foarte sanatos si se poate slabi foarte bine mancand paine

si in cazul asta "the dose makes the poison". una e sa mananci o franzela alba la o masa (sau chiar mai mult, cum imi aduc aminte ca faceam prin liceu) si alta e sa mananci o felie de paine integrala

1-2 felii de paine integrala la o masa sunt ok. in general doua felii de paine integrala au cam 100 de grame, respectiv 250 kcal. daca intr-o zi ai o limita de 1500 kcal si mananci de 4 ori, evident ca nu e ideal sa mananci paine de 1000 kcal

cum arata o paine buna. pai in primul rand nu are faina alba, zahar, coloranti, conservanti, uleiuri vegetale. are minim 5-6 g de fibre la 100 g. daca are si seminte e perfect

imi place o paine fara drojdie de la Greenland si painea de secara de la Natura Land

t mobile

T-Mobile Dance
Încărcat de Delichild

tattoo

organic vs. conventional

desi suna foarte bine, alimentele organice nu sunt intotdeauna de preferat celor obtinute in mod conventional

o analiza interesanta aici

diferentele sunt de fapt foarte mici. sunt plusuri si minusuri pentru ambele categorii de alimente. daca ai bani de mancare organica poti sa-ti cumperi dar nu e necasar sa mananci alimente organice ca sa mananci sanatos

vitamina D

o prezentare interesanta aici

un film frumos

fasting

de doua zile m-am apucat de post intermitent, leangains style

practic mananc doar intre ora 14 si ora 22. orice. oricat

sa vedem ce iese

dupa Martin Berkhan avantajele postului intermitent sunt urmatoarele:

* Increased insulin sensitivity, possibly resulting in superior nutrient partitioning as compared to traditional meal patterns; especially when combined with weightlifting. There are also several other health benefits, including improved blood lipids (scientifically proven).

* Possible to reduce bodyfat and increase lean mass through a cyclic calorie intake.

* No more obsessive thinking about food and worrying about eating every second hour.

* Very liberal approach to calorie intake in the eating window (8 hrs) and post-workout window; you can eat to your hearts content and still lose bodyfat.

* Increased mental focus, energy and productivity during the fast.

* Increased metabolism during the fast. Ironically, most people think it´s the other way around.

* Appetite suppression during the fast. This is particularily beneficial if your main priority is to lose bodyfat.

Lyle despre cofeina

aici

studiu romanesc in Nutrition Journal

publica si romanasii nostri ceva in Nutrition Journal

pe langa faptul ca e un studiu subtireanu rau (studiu e mult spus, un fel de rezumat), la concluzii sunt doua dezacorduri

asta e nivelul

pentru cei care evita grasimea dupa antrenament

P+C eaters, take this:


J Appl Physiol 97: 11–16, 2004.

Adding fat calories to meals after exercise does not alter glucose tolerance.
Amanda K. Fox, Amy E. Kaufman, and Jeffrey F. Horowitz
Division of Kinesiology, The University of Michigan, Ann Arbor, Michigan 48109
Submitted 26 December 2003; accepted in final form 16 February 2004

A single session of exercise increases insulin sensitivity for hours and even days, and dietary carbohydrate ingested after exercise alters the magnitude and duration of this effect. Although increasing systemic fatty acid availability
is associated with insulin resistance, it is uncertain whether increasing dietary fat availability after exercise alters the exercise induced increase in insulin sensitivity. The purpose of this study was to determine whether adding fat calories to meals after exercise alters glucose tolerance the next day. Seven healthy men cycled 90 min at 66 +/- 2% peak oxygen uptake followed by a maximum of five high-intensity intervals. During the hours after exercise, subjects ingested three meals containing either low-fat (5% energy from fat) or high-fat (45% energy from fat) foods (Low-Fat and High-Fat groups, respectively). Each diet contained the same amount of carbohydrate and protein. An oral glucose tolerance test was performed the next morning. Muscle glycogen and intramuscular triglyceride (IMTG) concentrations were measured in muscle biopsy samples obtained immediately before exercise and the next morning. The day after exercise, muscle glycogen concentration was identical in High-Fat and Low-Fat (393 +/-70 and 379 +/- 38 mmol/kg dry wt). At the same time, IMTG concentration was 20% greater during High-Fat compared with Low-Fat (42.5 +/- 3.4 and 36.3 +/- 3.3 mmol/kg dry wt; P 0.05). Despite the addition of 165 g of fat to meals after exercise (1,500 kcal) and a resultant elevation in IMTG concentration, glucose tolerance was identical in High-Fat and Low-Fat (compositeindex: 8.7 +/-
1.0 and 8.4 +/- 1.0). In summary, as long as meals ingested in the hours after exercise contain the same carbohydrate content, the addition of 1,500 kcal from fat to these meals did not alter muscle glycogen resynthesis or glucose tolerance the next day.