The Frutarian - eat nothing but fruit for 6 years

[da_vinci]

jared leto would not be puling those dimes if he wasnt rich and famous. dudes nose is fucked up looking and he is a twink. could deifnitely pull plenty of 7's and 8's with a good personality, but the idea hes getting smokin hot chicks cuz of his looks is fuckiin wacked.

Well from quite a good amount of females I know (of various ages) I've heard that he's very good looking... I'll take that as a truth, as I can't really make an adequate evaluation of ther guys looks the way females can..
 I like some of his music and def. like him as an actor (I'd say he's still underestimated). Can pull off subtle roles quite well.

[aesthetics]

jared leto would not be puling those dimes if he wasnt rich and famous. dudes nose is fucked up looking and he is a twink. could deifnitely pull plenty of 7's and 8's with a good personality, but the idea hes getting smokin hot chicks cuz of his looks is fuckiin wacked.

uhm what? are you kidding? he looks amazing for his age, he looks better than 95% of the 20 year old americans you see on the street and pulling a 9-10s isn't that hard and doesn't require money just confidence and decent looks.

also women don't find muscular guys attractive, ask any of them and they will prefer a thin twink to a bloofy half balding bodybuilder with fucked up skin from too much aas.

[aesthetics]

u actually think one person living at the age of 40 disproves a theory? have you ever attended college? think about that statment, there are  people who eat glass and are 85 which proves glass enhances longevity.

yes, it sure does. maybe not conclusively but it does. secondly eating glass is irrelevant and comparing apples to oranges. if you were stating that eating glass is fatal as a fact then that would be a good comparison but as it stands it's a poor analogy.

jared leto hasn't aged in 20 years, he even looks younger than a lot of people in their 20's and it's all due to a high fructose, and glucose diet.

[flinstones1]

uhm what? are you kidding? he looks amazing for his age, he looks better than 95% of the 20 year old americans you see on the street and pulling a 9-10s isn't that hard and doesn't require money just confidence and decent looks.

also women don't find muscular guys attractive, ask any of them and they will prefer a thin twink to a bloofy half balding bodybuilder with fucked up skin from too much aas.

oh brother, here we go again. Put this build next to Leto and let's see who gets more chicks

[flinstones1]

jared leto would not be puling those dimes if he wasnt rich and famous. dudes nose is fucked up looking and he is a twink. could deifnitely pull plenty of 7's and 8's with a good personality, but the idea hes getting smokin hot chicks cuz of his looks is fuckiin wacked.

Jared Leto's nose is too small to be considered handsome which makes him an ugly fuck he looks like a girl. Look.. you can have the prettiest face in the world I have said it a million times, but you need a masculine nose or you will never get respect in this world. Which sucks for a guy like you who has otherwise perfect features, but was unfortunately born with an upturned nose of a 12 year old who hasn't hit puberty. Nothing wrong with it, you look like Matt Damon. But at the same time Matt Damon looks like a pretty boy pussy. Which works for 18 years old I suppose, but will he ever have that "character" of a Gunter? Fuck no!

btw No I dont mean a nose like Johnnynoname thats a ugly nose, I mean a nose like myself and  Gunter=STUDLY
big nose= high testosterone..it's universally attractive to every woman just like large jaws, thick eyebrows, broad shoulders, and big muscles.
gunter


bradley cooper


hugh jackman



Matarazzo




rest my case friend

[suckmymuscle]

i didnt gloss over the part, you are not interpreting what they said correctly, read
in what individuals was the effect found in? which group was the effect of fructose not found in? there is the answer right there, the paper is shit imo.

  I am not interpreting anything incorrectly. The paper clearly states that fructose regulates blood sugar in diabetics by increasing glucokinase activity. The effect was not found in non-diabetics because they have perfectly functional glucokinase. It's right there for you to read.

i have already posted several

  You haven't posted one, let alone several.

i can post new ones however, we were not arguing fruit that is moving the goalposts, different fruits as ive already outlined have numerous constituents which cloud the argument, no type of fruit is the same, i stated that fructose is a metabolic poison since in your opening post you claimed it was a healthy sugar with numerous benefits.

  Fructose has never been demonstrated to raise plasma triglycerides per se in humans. Ever. I want to see a double-blind, placebo controlled  study where, when controlled for calories, a person on a 100% fructose diet showing greater levels of plasma triglycerides and their metabolites than a person on a diet of 100% glucose, or 100% protein or 100% fat. This is the only way to know. Until then, you are shooting straws. And I think it's funny you consider caffeine, something that hasn't any nutritional qualities, a "food" but regard fructose as a poison.

Am J Clin Nutr. 2011 Aug;94(2):479-85. Epub 2011 Jun 15.
Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial.
Aeberli I, Gerber PA, Hochuli M, Kohler S, Haile SR, Gouni-Berthold I, Berthold HK, Spinas GA, Berneis K.
Source
Division of Endocrinology, Diabetes, and Clinical Nutrition, University Hospital Zurich, Zurich, Switzerland.
Abstract
Background: Sugar-sweetened beverages (SSBs) have unfavorable effects on glucose and lipid metabolism if consumed in high quantities by obese subjects, but the effect of lower doses in normal-weight subjects is less clear. OBJECTIVE: The aim was to investigate the effects of SSBs consumed in small to moderate quantities for 3 wk on LDL particle distribution and on other parameters of glucose and lipid metabolism as well as on inflammatory markers in healthy young men. Design: Twenty-nine subjects were studied in a prospective, randomized, controlled crossover trial. Six 3-wk interventions were assigned in random order as follows: 600 mL SSBs containing 1)40 g fructose/d [medium fructose (MF)], 2) 80 g fructose/d [high fructose (HF)], 3) 40 g glucose/d [medium glucose (MG)], 4) 80 g glucose/d [high glucose (HG)], 5) 80 g sucrose/d [high sucrose (HS)], or 6) dietary advice to consume low amounts of fructose. Outcome parameters were measured at baseline and after each intervention. Results: LDL particle size was reduced after HF by -0.51 nm (95% CI: -0.19, -0.82 nm) and after HS by -0.43 nm (95% CI: -0.12, -0.74; P < 0.05 for both). Similarly, a more atherogenic LDL subclass distribution was seen when fructose-containing SSBs were consumed (MF, HF, and HS: P < 0.05). Fasting glucose and high-sensitivity C-reactive protein (hs-CRP) increased significantly after all interventions (by 4-9% and 60-109%, respectively; P < 0.05); leptin increased during interventions with SSBs containing glucose only (MG and HG: P < 0.05). CONCLUSION: The present data show potentially harmful effects of low to moderate consumption of SSBs on markers of cardiovascular risk such as LDL particles, fasting glucose, and hs-CRP within just 3 wk in healthy young men, which is of particular significance for young consumers. This trial was registered at clinicaltrials.gov as NCT01021969

  This study was not controlled for calories, and there were still significant amounts of other monosaccharides on all control groups. Worthless.

here is a review

Lipids Health Dis. 2011 Jan 24;10:20.
Fructose impairs glucose-induced hepatic triglyceride synthesis.
Huang D, Dhawan T, Young S, Yong WH, Boros LG, Heaney AP.
Source
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Abstract
Obesity, type 2 diabetes and hyperlipidemia frequently coexist and are associated with significantly increased morbidity and mortality. Consumption of refined carbohydrate and particularly fructose has increased significantly in recent years and has paralled the increased incidence of obesity and diabetes. Human and animal studies have demonstrated that high dietary fructose intake positively correlates with increased dyslipidemia, insulin resistance, and hypertension. Metabolism of fructose occurs primarily in the liver and high fructose flux leads to enhanced hepatic triglyceride accumulation (hepatic steatosis). This results in impaired glucose and lipid metabolism and increased proinflammatory cytokine expression. Here we demonstrate that fructose alters glucose-stimulated expression of activated acetyl CoA carboxylase (ACC), pSer hormone sensitive lipase (pSerHSL) and adipose triglyceride lipase (ATGL) in hepatic HepG2 or primary hepatic cell cultures in vitro. This was associated with increased de novo triglyceride synthesis in vitro and hepatic steatosis in vivo in fructose- versus glucose-fed and standard-diet fed mice. These studies provide novel insight into the mechanisms involved in fructose-mediated hepatic hypertriglyceridemia and identify fructose-uptake as a new potential therapeutic target for lipid-associated diseases.

J Am Soc Nephrol. 2010 Dec;21(12):2036-9. Epub 2010 Nov 29.
The effect of fructose on renal biology and disease.
Johnson RJ, Sanchez-Lozada LG, Nakagawa T.
Source
Division of Renal Diseases and Hypertension, University of Colorado, Aurora, Colorado 80045, USA. richard.johnson@ucdenver.edu
Abstract
Dietary fructose intake is increasing. It is increasing primarily from added sugars, including sucrose and high fructose corn syrup, and correlates epidemiologically with the rising prevalence of metabolic syndrome and hypertension worldwide. The administration of fructose to animals and humans increases BP and the development of metabolic syndrome. These changes occur independently of caloric intake because of the effect of fructose on ATP depletion and uric acid generation. Fructose ingestion may also be a risk factor for kidney disease that includes glomerular hypertension, renal inflammation, and tubulointerstitial injury in animals. We suggest excessive fructose intake should be considered an environmental toxin with major health implications.

  I am still waiting for a cause-and-effect link fructose where it is not combined with glucose and where the studies are controlled for calories. Suppose you put two guys on two different diets, one with 1,000 calories and the other with 3,000. On the first diet, the guy eats 100 grams of fructose and on the other diet, the guy eats 200 grams. Then you take blood samples that demonstrate that the guy on the second diet shows greater plasma triglycerides than on the first diet and you attribute it to the fructose. He is eating more fructose on diet 2 and has higher levels of plasma triglycerides, but he is also consuming a lot more of other monosaccharides, fatty acids and amino acids. How can you attribute it to the fructose? You can't. You need to control for not only monosaccharide type, but also for calories.

i still think fruit is good but fructose has nothing to do with it in the slightest.

  Fructose may or may not cause increased plasma glycerols than glucose, amino acids or fatty acids. I will agree when I see a study, controlled for calories and nutritional substrate, that demonstrates a cause-and-effect relationship between fructose being more liopenic than other nutritional substrates. However in small amounts fructose actually seems to decrease plasma glucose levels like the studies I posted proves.

SUCKMYMUSCLE

[Necrosis]

yes, it sure does. maybe not conclusively but it does. secondly eating glass is irrelevant and comparing apples to oranges. if you were stating that eating glass is fatal as a fact then that would be a good comparison but as it stands it's a poor analogy.

jared leto hasn't aged in 20 years, he even looks younger than a lot of people in their 20's and it's all due to a high fructose, and glucose diet.

what? maybe its his genetics, maybe he eats a calorie restricted diet, perhaps he takes mega doses of vitamins, perhaps he takes care of his skin with spa treatments and moisturizers, you have no idea if eating a vegan diet has an effect on looking younger. The reason being there are people who eat like jared but look terrible so we have two truths here if we attribute his looks solely to his diet, it makes people look good and then at the same time look terrible as there is ample examples of vegetarians that look like shit warmed over.

my analogy stands and you are making a clear logical fallacy.

[Necrosis]

 I am not interpreting anything incorrectly. The paper clearly states that fructose regulates blood sugar in diabetics by increasing glucokinase activity. The effect was not found in non-diabetics because they have perfectly functional glucokinase. It's right there for you to read.

  You haven't posted one, let alone several.

  Fructose has never been demonstrated to raise plasma triglycerides per se in humans. Ever. I want to see a double-blind, placebo controlled  study where, when controlled for calories, a person on a 100% fructose diet showing greater levels of plasma triglycerides and their metabolites than a person on a diet of 100% glucose, or 100% protein or 100% fat. This is the only way to know. Until then, you are shooting straws. And I think it's funny you consider caffeine, something that hasn't any nutritional qualities, a "food" but regard fructose as a poison.


  This study was not controlled for calories, and there were still significant amounts of other monosaccharides on all control groups. Worthless.

here is a review


  I am still waiting for a cause-and-effect link fructose where it is not combined with glucose and where the studies are controlled for calories. Suppose you put two guys on two different diets, one with 1,000 calories and the other with 3,000. On the first diet, the guy eats 100 grams of fructose and on the other diet, the guy eats 200 grams. Then you take blood samples that demonstrate that the guy on the second diet shows greater plasma triglycerides than on the first diet and you attribute it to the fructose. He is eating more fructose on diet 2 and has higher levels of plasma triglycerides, but he is also consuming a lot more of other monosaccharides, fatty acids and amino acids. How can you attribute it to the fructose? You can't. You need to control for not only monosaccharide type, but also for calories.

  Fructose may or may not cause increased plasma glycerols than glucose, amino acids or fatty acids. I will agree when I see a study, controlled for calories and nutritional substrate, that demonstrates a cause-and-effect relationship between fructose being more liopenic than other nutritional substrates. However in small amounts fructose actually seems to decrease plasma glucose levels like the studies I posted proves.

SUCKMYMUSCLE

your first sentence indicates what im stating you claimed that fructose improves glucose utilization via increasing GK activity. However, the paper you posted doesn't state this, it clearly shows that only the people with already fucked up glucose utilization benefit from the primed GK activity, not healthy people, hence your argument makes no sense. Using an ill population to show the health benefits  of something is ridiculous, it would be like showing exogenous insulin improves quality of life when comparing type 1 diabetics to healthy controls, those extrapolations are meaningless.

dude are you even reading the studies?


"This study was not controlled for calories, and there were still significant amounts of other monosaccharides on all control groups. Worthless."

no theres not, read the study again.

  "Fructose has never been demonstrated to raise plasma triglycerides per se in humans. Ever. I want to see a double-blind, placebo controlled  study where, when controlled for calories, a person on a 100% fructose diet showing greater levels of plasma triglycerides and their metabolites than a person on a diet of 100% glucose, or 100% protein or 100% fat. This is the only way to know. Until then, you are shooting straws. And I think it's funny you consider caffeine, something that hasn't any nutritional qualities, a "food" but regard fructose as a poison."

this is ridiculous, nobody would survive on a 100% fructose diet, it doesnt occur so why would you request it to be studied? What makes way more sense and what has been done is have people follow normal diets but supplement with higher fructose to have the study obtain generalisability something your  design fails to do. that is not the only way to know, what you are suggesting would be wrought with confounding variables, the people would be deficient in nutrients, fatty acids, proteins etc, why would you chalk there plasma triglycerides up to the fructose and not the malnutrition? its silly.


"Fructose may or may not cause increased plasma glycerols than glucose, amino acids or fatty acids. I will agree when I see a study, controlled for calories and nutritional substrate, that demonstrates a cause-and-effect relationship between fructose being more liopenic than other nutritional substrates. However in small amounts fructose actually seems to decrease plasma glucose levels like the studies I posted proves."

the scientific community agrees with that review, im not sure what liopenic means so you will have to elaborate on that as i don't think its an actual term so im not sure what you are getting at. Your studies were in individuals that were sick with a disease that makes glucose regulation abnormal, hardly evidence that fructose lowers plasma glucose in healthy people, in fact it was shown not to via your own study.

[Necrosis]

i just went back and looked at the study you presented it was a review where they took data from studies on overweight and obese patients with various diets and extrapolated the results, it also contradicts the last study you posted if you actually read it. It doesnt even say what normal fructose intake is, they just claim it. i cant see the full paper so perhaps you could post the introduction which should have that info, and the methods and materials.

J Clin Invest. 2009 May;119(5):1322-34. doi: 10.1172/JCI37385. Epub 2009 Apr 20.
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ.
Source
Department of Molecular Biosciences, UCD, Davis, California 95616, USA.
Abstract
Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

this study is the exact same.

Br J Nutr. 2008 Nov;100(5):947-52.
Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women.
Swarbrick MM, Stanhope KL, Elliott SS, Graham JL, Krauss RM, Christiansen MP, Griffen SC, Keim NL, Havel PJ.
Source
Department of Nutrition, University of California, Davis, CA 95616, USA.
Abstract
Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19 % (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.

thats like 10 studies ive posted that have shown a negative effect, compared to your cohort study and one with people that already have mucked up glucose utilization.

[suckmymuscle]

your first sentence indicates what im stating you claimed that fructose improves glucose utilization via increasing GK activity. However, the paper you posted doesn't state this, it clearly shows that only the people with already fucked up glucose utilization benefit from the primed GK activity, not healthy people, hence your argument makes no sense. Using an ill population to show the health benefits  of something is ridiculous, it would be like showing exogenous insulin improves quality of life when comparing type 1 diabetics to healthy controls, those extrapolations are meaningless.

dude are you even reading the studies?

  My point stands: fructose in small amounts improves glucose utilization, even if only in diabetic patients. Is there evidence that it induces insulin resistence per se to a greater degree than glucose or other nutritional substrates? No.

no theres not, read the study again.

  80% fructose still means that 20% of calories come from other sources.

this is ridiculous, nobody would survive on a 100% fructose diet, it doesnt occur so why would you request it to be studied? What makes way more sense and what has been done is have people follow normal diets but supplement with higher fructose to have the study obtain generalisability something your  design fails to do. that is not the only way to know, what you are suggesting would be wrought with confounding variables, the people would be deficient in nutrients, fatty acids, proteins etc, why would you chalk there plasma triglycerides up to the fructose and not the malnutrition? its silly.

  Because it is the only way to determine if fructose per se increases plasma triglycerides and induces insulin resistence. This is called the scientific method, where you control for extrinsic variables to establish a cause-and-effect link between cause A and effect B. I was never suggesting a 100% fructose diet. Get real, dude.

the scientific community agrees with that review, im not sure what liopenic means so you will have to elaborate on that as i don't think its an actual term so im not sure what you are getting at. Your studies were in individuals that were sick with a disease that makes glucose regulation abnormal, hardly evidence that fructose lowers plasma glucose in healthy people, in fact it was shown not to via your own study.

  Lipogenic = fat forming. Anyways, fructose doesen't regulate glucokinase in healthy individuals because it doesen't need to. Does it seem likely that a substrate that causes increased insulin resistence and diabetes would ameliorate hyperglycemia in diabetics? Can't you see your flawed logic?

SUCKMYMUSCLE

[aesthetics]

what? maybe its his genetics, maybe he eats a calorie restricted diet, perhaps he takes mega doses of vitamins, perhaps he takes care of his skin with spa treatments and moisturizers, you have no idea if eating a vegan diet has an effect on looking younger. The reason being there are people who eat like jared but look terrible so we have two truths here if we attribute his looks solely to his diet, it makes people look good and then at the same time look terrible as there is ample examples of vegetarians that look like shit warmed over.

my analogy stands and you are making a clear logical fallacy.

its merely conjecture which is about as much conclusive evidence you have proving that eating fruit and fructose will age the body. if that is a logical fallacy then so is everything you've posted.

truthfully though, it really was a terrible and extraneous analogy

[maxkane69]

oh brother, here we go again. Put this build next to Leto and let's see who gets more chicks

Sadly Leto would get more pussy than Arnold in his prime!
I hope this help!

[flinstones1]

Sadly Leto would get more pussy than Arnold in his prime!
I hope this help!

 Arnold was a fucken god

[maxkane69]

Arnold was a fucken god

That doesen't change the fact that Arnold would get a fraction of the pussy of Leto!

[booty]

Arnold was a fucken god

X 2 

[Nomad]

That doesen't change the fact that Arnold would get a fraction of the pussy of Leto!

Someone post a story of how Arnold would pick up chicks to shut this fool up.

[maxkane69]

Someone post a story of how Arnold would pick up chicks to shut this fool up.

There is no need to post a story of how Arnold would pick up chicks when you have pics as a proof!

Exibit number 1


Exibit number 2

[aesthetics]

Someone post a story of how Arnold would pick up chicks to shut this fool up.

also how he was a gay boy toy for joe weider and co. for a few years 

[suckmymuscle]

  I wonder from where "Necrosis" thinks we should get our energy to fuel our physiological processes then. Carbohydrates and especially monosaccharides are the most efficient energy source there is by far. Glucose is the only fuel for the brain under ordinary circumstances and it is the only fuel that can be used instantly by all cells of the body to release energy in a one-step reaction. The only other fuel for the body besides glucose are ketones. So from where should we get our primary fuel from according to "Necrosis"? There are only three options here:

  - We get glucose directly from food via carbohydrates.

  - We get glucose indirectly by converting protein or fat into glucose by gluconeogenesis in the liver.

  - We get ketones by breaking down fat in the liver via ketogenesis.

  These are the only three options. There are no other. So since "Necrosis" claims that monosaccharides are poisons, then is he suggesting we should live in a state of constant gluconeogenesis, which puts enormous stress in the liver and generates enormous amounts of ammonia and uric acid, both of which are toxic, as byproducts? Should we cut carbs completely and live on ketones which are even more toxic than ammonia and far less efficient as an energy source than glucose? I would like an honest answer to these questions.

SUCKMYMUSCLE

[booty]

There is no need to post a story of how Arnold would pick up chicks when you have pics as a proof!



Exibit number 2

HAHA...  

[notsureifsrs]

oh brother, here we go again. Put this build next to Leto and let's see who gets more chicks

More chicks what? to look at him?

[jprc10]

 I wonder from where "Necrosis" thinks we should get our energy to fuel our physiological processes then. Carbohydrates and especially monosaccharides are the most efficient energy source there is by far. Glucose is the only fuel for the brain under ordinary circumstances and it is the only fuel that can be used instantly by all cells of the body to release energy in a one-step reaction. The only other fuel for the body besides glucose are ketones. So from where should we get our primary fuel from according to "Necrosis"? There are only three options here:

  - We get glucose directly from food via carbohydrates.

  - We get glucose indirectly by converting protein or fat into glucose by gluconeogenesis in the liver.

  - We get ketones by breaking down fat in the liver via ketogenesis.

  These are the only three options. There are no other. So since "Necrosis" claims that monosaccharides are poisons, then is he suggesting we should live in a state of constant gluconeogenesis, which puts enormous stress in the liver and generates enormous amounts of ammonia and uric acid, both of which are toxic, as byproducts? Should we cut carbs completely and live on ketones which are even more toxic than ammonia and far less efficient as an energy source than glucose? I would like an honest answer to these questions.

SUCKMYMUSCLE

Great post.

Really, when you aren't posting things about gorillas or about how you are "in love" with a celebrity, you post plenty of excellent information regarding different topics like the one in this thread.

I don't think "necrosis" will respond to this though.

[greeneyes]

[Necrosis]

 My point stands: fructose in small amounts improves glucose utilization, even if only in diabetic patients. Is there evidence that it induces insulin resistence per se to a greater degree than glucose or other nutritional substrates? No.

no it doesn't.
well only in ten type 2 diabetics with no other controls for food, which is one of your issues apparently yet you do not claim this as a flaw in your study. Also, you made no claims about type 2 diabetes, you claimed that fructose lowers hyperglycemic events via GK priming, which is not true as this effect is only seen in type 2 diabetics, of which the study was small and poor. nor does the study prove your claim that fructose dramatically lowers blood glucose levels, in every study in healthy individuals it worsens it, you have yet to show it in healthy people, while i have.

  Because it is the only way to determine if fructose per se increases plasma triglycerides and induces insulin resistence. This is called the scientific method, where you control for extrinsic variables to establish a cause-and-effect link between cause A and effect B. I was never suggesting a 100% fructose diet. Get real, dude.

 

i understand the scientific method, what are you proposing then? there have been double blind placebo controlled cross over trials, im not sure what your issue is with them. You claimed that you wanted to see a study with 100% fructose diet, i took you literally, didnt realize you were using hyperbole.

 

 Lipogenic = fat forming. Anyways, fructose doesen't regulate glucokinase in healthy individuals because it doesen't need to. Does it seem likely that a substrate that causes increased insulin resistence and diabetes would ameliorate hyperglycemia in diabetics? Can't you see your flawed logic?

SUCKMYMUSCLE

i know what lipogenic means, you said liopenic hence my confusion.  Intuition is likely to get you no where in medicine, does it seem likely that an autoimmune condition could be treated by things that shut the immune function down (glucocorticoids) yet induce autoimmune issues in others? fructose doesn't improve glucose disposal, all the studies in healthy people show this, all of them, even your study showed it did not improve glucose disposal in healthy subjects. Since when did this argument become about one population of disease, and why would i care if i dont have type 2 diabetes? fructose is a metabolic poison.

i dont know why i have to post study after study to prove my point only to have to argue it again, its right here, its in all the studies ive posted fructose is shit for humans. People with osteoarthritis should avoid solane containing foods, normal people have no problem with them, lactose intolerant people have issues with lactose, other without it do not. If i claimed that lactose causes diarhhea and is bad for health would you accept a study on only lactose intolerant people? no you would not, and that is what you have done while i have posted studies in both populations, studies actually contradict your study and have more statistical power, that study is shit all around.

Br J Nutr. 2008 Nov;100(5):947-52.
Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women.
Swarbrick MM, Stanhope KL, Elliott SS, Graham JL, Krauss RM, Christiansen MP, Griffen SC, Keim NL, Havel PJ.
Source
Department of Nutrition, University of California, Davis, CA 95616, USA.
Abstract
Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19 % (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.

HERES MOAR

Ann N Y Acad Sci. 2010 Mar;1190:15-24.
Fructose consumption: recent results and their potential implications.
Stanhope KL, Havel PJ.
Source
Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
Abstract
In addition to acquiring a better understanding of foods that may have intrinsic health benefits, increasing our knowledge of dietary components that may adversely impact health and wellness, and the levels of consumption at which these adverse effects may occur, should also be an important priority for the Foods for Health initiative. This review discusses the evidence that additional research is needed to determine the adverse effects of consuming added sugars containing fructose. Current guidelines recommend limiting sugar consumption in order to prevent weight gain and promote nutritional adequacy. However, recent data suggest that fructose consumption in human results in increased visceral adiposity, lipid dysregulation, and decreased insulin sensitivity, all of which have been associated with increased risk for cardiovascular disease and type 2 diabetes. A proposed model for the differential effects of fructose and glucose is presented. The only published study to directly compare the effects of fructose with those of commonly consumed dietary sweeteners, high fructose corn syrup and sucrose, indicates that high fructose corn syrup and sucrose increase postprandial triglycerides comparably to pure fructose. Dose-response studies investigating the metabolic effects of prolonged consumption of fructose by itself, and in combination with glucose, on lipid metabolism and insulin sensitivity in both normal weight and overweight/obese subjects are needed.


MOAR ON THIS SHIT AFFECTING THE LIVER, it not only induces NAFLD but progresses it if you already have it.

Hepatology. 2010 Jun;51(6):1961-71.
Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease.
Abdelmalek MF, Suzuki A, Guy C, Unalp-Arida A, Colvin R, Johnson RJ, Diehl AM; Nonalcoholic Steatohepatitis Clinical Research Network.
Collaborators (111)

Source
Division of Gastroenterology, Duke University, Durham, NC 27710, USA. manal.abdelmalek@duke.edu
Abstract
The rising incidence of obesity and diabetes coincides with a marked increase in fructose consumption. Fructose consumption is higher in individuals with nonalcoholic fatty liver disease (NAFLD) than in age-matched and body mass index (BMI)-matched controls. Because fructose elicits metabolic perturbations that may be hepatotoxic, we investigated the relationship between fructose consumption and disease severity in NAFLD. We studied 427 adults enrolled in the NASH Clinical Research Network for whom Block food questionnaire data were collected within 3 months of a liver biopsy. Fructose consumption was estimated based on reporting (frequency x amount) of Kool-aid, fruit juices, and nondietary soda intake, expressed as servings per week, and classified into none, minimum to moderate (<7 servings/week), and daily (> or =7 servings/week). The association of fructose intake with metabolic and histological features of NAFLD was analyzed using multiple linear and ordinal logistic regression analyses with and without controlling for other confounding factors. Increased fructose consumption was univariately associated with decreased age (P < 0.0001), male sex (P < 0.0001), hypertriglyceridemia (P < 0.04), low high-density lipoprotein (HDL) cholesterol (<0.0001), decreased serum glucose (P < 0.001), increased calorie intake (P < 0.0001), and hyperuricemia (P < 0.0001). After controlling for age, sex, BMI, and total calorie intake, daily fructose consumption was associated with lower steatosis grade and higher fibrosis stage (P < 0.05 for each). In older adults (age > or = 48 years), daily fructose consumption was associated with increased hepatic inflammation (P < 0.05) and hepatocyte ballooning (P = 0.05). CONCLUSION: In patients with NAFLD, daily fructose ingestion is associated with reduced hepatic steatosis but increased fibrosis. These results identify a readily modifiable environmental risk factor that may ameliorate disease progression in patients with NAFLD.

Another in HEALHTY INDIVIDUALS

Int J Obes (Lond). 2010 Mar;34(3):454-61. Epub 2009 Dec 22.
Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response.
Perez-Pozo SE, Schold J, Nakagawa T, Sánchez-Lozada LG, Johnson RJ, Lillo JL.
Source
Renal Unit, Son Llatzer Hospital-Palm of Majorca, Balearic Islands, Spain. santose.perez@hsll.es
Abstract
BACKGROUND:
Excessive fructose intake causes metabolic syndrome in animals and can be partially prevented by lowering the uric acid level. We tested the hypothesis that fructose might induce features of metabolic syndrome in adult men and whether this is protected by allopurinol.

METHODS:
A randomized, controlled trial of 74 adult men who were administered 200 g fructose daily for 2 weeks with or without allopurinol. Primary measures included changes in ambulatory blood pressure (BP), fasting lipids, glucose and insulin, homeostatic model assessment (HOMA) index, body mass index and criteria for metabolic syndrome.

RESULTS:
The ingestion of fructose resulted in an increase in ambulatory BP (7+/-2 and 5+/-2 mm Hg for systolic (SBP) and diastolic BP (DBP), P<0.004 and P<0.007, respectively). Mean fasting triglycerides increased by 0.62+/-0.23 mmol l(-1) (55+/-20 mg per 100 ml), whereas high-density lipoprotein cholesterol decreased by 0.06+/-0.02 mmol l(-1) (2.5+/-0.7 mg per 100 ml), P<0.002 and P<0.001, respectively. Fasting insulin and HOMA indices increased significantly, whereas plasma glucose level did not change. All liver function tests showed an increase in values. The metabolic syndrome increased by 25-33% depending on the criteria. Allopurinol lowered the serum uric acid level (P<0.0001) and prevented the increase in 24-h ambulatory DBP and daytime SBP and DBP. Allopurinol treatment did not reduce HOMA or fasting plasma triglyceride levels, but lowered low-density lipoprotein cholesterol relative to control (P<0.02) and also prevented the increase in newly diagnosed metabolic syndrome (0-2%, P=0.009).

CONCLUSIONS:
High doses of fructose raise the BP and cause the features of metabolic syndrome. Lowering the uric acid level prevents the increase in mean arterial blood pressure. Excessive intake of fructose may have a role in the current epidemics of obesity and diabete



I MEAN I REST MY CASE.

[Necrosis]

Great post.

Really, when you aren't posting things about gorillas or about how you are "in love" with a celebrity, you post plenty of excellent information regarding different topics like the one in this thread.

I don't think "necrosis" will respond to this though.

ARE YOU A GIMMICK LMAO!!!!!!!!!!!!!