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DO NOT drink COKE or ANY FIZZY drinks!!!!!!

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and oh god, i just read youre a fan of john berardi.. hahahahha

me and john have quite a few arguments. feel free to send him this info and have him refute it. he's yet beena ble to. good guy, but king of voodoo nutrition. absolute king.

God, if you reference something from JB, I honestly think I'll have a heart attack from laughter

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If you don't mind me asking, blahblah....what exactly do you do for a living?

(PS: I thought I was the only one who said "kiddo" on this board!) bb_lol.gif

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i have a BS from UCLA in kinesiology as well as a lot of backround info human physiology, biochemistry, enorcrinology, nutrition, etc. as well as CSCS cert.

now? well i have no social life so i basically sit around and research. my income comes from working with people for positive physique changes, as well as writing articles from time to time. working on a book smile.gif

one of my biggest hobbies is putting to rest nutritional myths and bs. unfortunately due to the industry everybody has to appear cutting edge - thus berardi's food combining voodoo nutrition, etc. i don't blame them. i'm sure my poorness is attributed to my bland, straight forward, no bs advice/training style

the only reason i got agitated is ol evigrex had to 1) insult 2) BOLD EVERY WORD HE SAID AND PUT IT IN CAPS IN ATTEMPT TO MAKE HIS OPINION, ALBEIT WRONG, SEEM MORE CONVINCING

it's not a wise thing to insult ones intelligence without having proper knowledge of who you're insulting.

too bad, though, you being 26 and all and speaking so hastly without taking the time to think outside of the box. sorry i challenged mighty evigrex on an internet forum!

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btw, evigrex, if you can get them, see the following smile.gif

Cianflone, K et. al. Actylation stimulating protein (ASP), an adipocyte

autocrine: new direction. Cell and Developmental Biology (1999) 10: 31-41.

Londos, C. et. al. On the control of lipolysis in adipocytes. Ann NY

Academy of Sciences (1999) 892: 155-168.

Maslowska, M. et. al. Acylation Stimulating protein (ASP): Role in

adipose tissue. Chapter 8 in "Progress in Obesity Research: 8" Ed. Guy

Grand and Ailuaud (1999) 65-70.

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my income comes from working with people for positive physique changes, as well as writing articles from time to time. working on a book smile.gif

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i dont like being called a personal trainer (as the certs required are an absolute joke) but yes i work with people (ranging from d1-elite athletes, housewives, bodybuilders, powerlifters, aspiring SEALS, etc)

i want to just write books and live off of that. training/designing nutritional programs is a pain.

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But that's gotta feel good, no? Helping people get into shape and feel good about themselves?

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Okay. Your definition of insulin is wrong:

Here's the dictionary version.

5 entries found for insulin.

in·su·lin ( P ) Pronunciation Key (ns-ln)

n.

A polypeptide hormone secreted by the islets of Langerhans and functioning in the regulation of the metabolism of carbohydrates and fats, especially the conversion of glucose to glycogen, which lowers the blood glucose level.

Any of various pharmaceutical preparations containing this hormone that are derived from the pancreas of certain animals or produced through genetic engineering and are used in the medical treatment and management of diabetes mellitus (type I).

Here's a more in depth explanation:

Insulin is a hormone produced by the beta cells of the pancreas in response to raised blood glucose (sugar) levels. Its whole purpose (as the above definition demonstrates) is to regulate the metabolism of glucose and other nutrients.

When your body goes without food for a time you develop a sensation of hunger, which generally leads you to consume a carbohydrate (or any macro nutrient) meal. These carbohydrates become converted to sugars in the blood, which causes the release of insulin. The insulin allows sugars to leave the blood and enter the cells of the body; this leads to a change in brain chemistry and this change generates a feeling of satisfaction. Over the course of hours, the insulin-to-blood sugar ratio will once more change and brain chemistry will again cause a sensation of hunger.

This is necessary because cell membranes are made up of a fat matrix. Along this fat matrix are small door-like portals called ‘protein carrier molecules.’ Through these "doors" insulin carries the nutrients into cells in a process called ‘facilitated diffusion.’ With this basic knowledge we can now look at how diet affects blood glucose levels and learn how to use insulin to our advantage.

What have we established here? Insulin exists to dispose of blood glucose, and that glucose is in turn shuttled to fat cells, among other things. We will see below that hyperglycemia increases the risk of fat gain.

Let me present you with a few studies. These studies demonstrate that hyperglycemia (and subsequent hyperinsulinonemia) promotes fat storage, and also shows the effiacy of low carbohydrate diets in normal, insulin resistant and type 2 diabetic invididuals. Since those that are insulin resistant/diabetic do not respond to insulin properly - and you assert that insulin has nothing to do with fat gain - it would stand to reason that there would be no difference.

Summary:

Although weight loss can be achieved by any means of energy restriction, current dietary guidelines have not prevented weight regain or population-level increases in obesity and overweight. Many high-carbohydrate, low-fat diets may be counterproductive to weight control because they markedly increase postprandial hyperglycemia and hyperinsulinemia. Many high-carbohydrate foods common to Western diets produce a high glycemic response [high-glycemic-index (GI) foods], promoting postprandial carbohydrate oxidation at the expense of fat oxidation, thus altering fuel partitioning in a way that may be conducive to body fat gain. In contrast, diets based on low-fat foods that produce a low glycemic response (low-GI foods) may enhance weight control because they promote satiety, minimize postprandial insulin secretion, and maintain insulin sensitivity. This hypothesis is supported by several intervention studies in humans in which energy-restricted diets based on low-GI foods produced greater weight loss than did equivalent diets based on high-GI foods. Long-term studies in animal models have also shown that diets based on high-GI starches promote weight gain, visceral adiposity, and higher concentrations of lipogenic enzymes than do isoenergetic, macronutrientcontrolled, low-GI-starch diets. In a study of healthy pregnant women, a high-GI diet was associated with greater weight at term than was a nutrient-balanced, low-GI diet. In a study of diet and complications of type 1 diabetes, the GI of the overall diet was an independent predictor of waist circumference in men. These findings provide the scientific rationale to justify randomized, controlled, multicenter intervention studies comparing the effects of conventional and low-GI diets on weight control.

Brand-Miller, J.C., Holt, S.H., Pawlak, D.B., et al., "Glycemic Index and Obesity", American Journal of Clinical Nutrition, 76(1), 2002, pages 281S-285S.

Oh what do we have here, a study that directly contradicts your assertion that insulin and glycemic response to a meal has nothing to do with fat gain...interesting.

Effects of insulin-induced hypoglycaemia on energy intake and food choice at a subsequent test meal.

Dewan S, Gillett A, Mugarza JA, Dovey TM, Halford JC, Wilding JP.

Diabetes and Endocrinology Research Group, University Hospital Aintree, Liverpool, UK.

BACKGROUND AND AIMS: Hypoglycaemia is assumed to increase food intake, but there is little data on the magnitude or qualitative nature of this effect. We have therefore investigated the effects of insulin-induced hypoglycaemia on food intake at a test meal. METHODS: Sixteen healthy men (age 29.8 +/- 11 years; mean +/- SD) were studied; either insulin (0.05 units/kg) or saline was given intravenously in a double-blind crossover design. Blood glucose was monitored at regular intervals. Participants were given an ad libitum breakfast 20 min after injections and food intake and appetite scores were recorded. RESULTS: Blood glucose was unchanged following saline (4.3 +/- 0.4 to 4.4 +/- 0.3 mmol/L). There was a transient decline in blood glucose after insulin with a nadir at 20 min (4.31 +/- 0.34 to 2.41 +/- 0.45 mmol/L, p < 0.0001), which returned to baseline at 40 min. Total energy intake was 17% higher (1701.1 +/- 895.3 kcal vs 1427.7 +/- 815 kcal, p = 0.026) following insulin administration compared to that following saline. Macronutrient analysis revealed a significant increase in high-fat foods (muffins) (69.2 +/- 54.1 vs 29 +/- 42.3 g, p = 0.009) after insulin. Appetite scores were similar after saline and insulin despite these changes in food intake. CONCLUSIONS: Transient insulin-induced hypoglycaemia increases energy intake. Participants consumed more fat after insulin compared to that after saline. High-fat foods can lead to passive overconsumption and have a low glycaemic index, which may prolong hypoglycaemia. Both factors could ultimately promote weight gain in individuals with recurrent hypoglycaemia. Copyright 2004 John Wiley & Sons, Ltd.PMID: 15343587 [PubMed - in process

short version - Insulin causes hypoglycaemia, and ultimately promotes weight gain

Effects of dietary glycaemic index on adiposity, glucose homoeostasis, and plasma lipids in animals.

Pawlak DB, Kushner JA, Ludwig DS.

Department of Medicine, Children's Hospital, Boston, MA, USA. david.ludwig@childrens.harvard.edu

BACKGROUND: Clinical studies suggest a role for dietary glycaemic index (GI) in bodyweight regulation and diabetes risk. However, partly because manipulation of GI can produce changes in potentially confounding dietary factors such as fibre content, palatability, and energy density, its relevance to human health remains controversial. This study examined the independent effects of GI in animals. METHODS: Partially pancreatectomised male Sprague-Dawley rats were given diets with identical nutrients, except for the type of starch: high-GI (n=11) or low-GI (n=10). The animals were fed in a controlled way to maintain the same mean bodyweight in the two groups for 18 weeks. Further experiments examined the effects of GI in rats in a cross-over design and C57BL/6J mice in a parallel design. FINDINGS: Despite having similar mean bodyweight (547.9 [sE 13.4] vs 549.2 [15.2] g), rats given high-GI food had more body fat (97.8 [13.6] vs 57.3 [7.2] g; p=0.0152) and less lean body mass (450.1 [9.6] vs 491.9 [11.7] g; p=0.0120) than those given low-GI food. The high-GI group also had greater increases over time in the areas under the curve for blood glucose and plasma insulin after oral glucose, lower plasma adiponectin concentrations, higher plasma triglyceride concentrations, and severe disruption of islet-cell architecture. Mice on the high-GI diet had almost twice the body fat of those on the low-GI diet after 9 weeks. INTERPRETATION: These findings provide a mechanistic basis for interpretation of studies of GI in human beings. RELEVANCE TO PRACTICE: The term GI describes how a food, meal, or diet affects blood sugar during the postprandial period. GI as an independent factor can cause obesity and increase risks of diabetes and heart disease in animals. Use of low-GI diets in prevention and treatment of human disease merits thorough examination.

Wait....I thought the Glucose response to a meal didn't increase fat gain...right??

Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes.

Gannon MC, Nuttall FQ.

Metabolic Research Laboratory (111G), VA Medical Center, One Veterans Drive, Minneapolis, MN 55417. ganno004@umn.edu

There has been interest in the effect of various types and amounts of dietary carbohydrates and proteins on blood glucose. On the basis of our previous data, we designed a high-protein/low-carbohydrate, weight-maintaining, nonketogenic diet. Its effect on glucose control in people with untreated type 2 diabetes was determined. We refer to this as a low-biologically-available-glucose (LoBAG) diet. Eight men were studied using a randomized 5-week crossover design with a 5-week washout period. The carbohydrate:protein:fat ratio of the control diet was 55:15:30. The test diet ratio was 20:30:50. Plasma and urinary beta-hydroxybutyrate were similar on both diets. The mean 24-h integrated serum glucose at the end of the control and LoBAG diets was 198 and 126 mg/dl, respectively. The percentage of glycohemoglobin was 9.8 +/- 0.5 and 7.6 +/- 0.3, respectively. It was still decreasing at the end of the LoBAG diet. Thus, the final calculated glycohemoglobin was estimated to be approximately 6.3-5.4%. Serum insulin was decreased, and plasma glucagon was increased. Serum cholesterol was unchanged. Thus, a LoBAG diet ingested for 5 weeks dramatically reduced the circulating glucose concentration in people with untreated type 2 diabetes. Potentially, this could be a patient-empowering way to ameliorate hyperglycemia without pharmacological intervention. The long-term effects of such a diet remain to be determined.

PMID: 15331548 [PubMed - in process]

Two points here. You say that insulin has nothing to do with fat gain. Since diabetics don't respond properly to the insulin they produce, how is that the case? And why are they faring better with a low carbohydrate diet? Lets go on...

Beneficial effect of low carbohydrate in low calorie diets on visceral fat reduction in type 2 diabetic patients with obesity.

Miyashita Y, Koide N, Ohtsuka M, Ozaki H, Itoh Y, Oyama T, Uetake T, Ariga K, Shirai K.

Center of Diabetes, Endocrine and Metabolism, Sakura Hospital, School of Medicine, Toho University, 564-1 Shimoshizu, Sakura-City, Chiba 285-0841, Japan.

The adequate composition of carbohydrate and fat in low calorie diets for type 2 diabetes mellitus patients with obesity is not fully established. The aim of this study was to investigate the effects of low carbohydrate diet on glucose and lipid metabolism, especially on visceral fat accumulation, and comparing that of a high carbohydrate diet. Obese subjects with type 2 diabetes mellitus were randomly assigned to take a low calorie and low carbohydrate diet ( [Formula: see text], 1000kcal per day, protein:carbohydrate: [Formula: see text] :40:35) or a low calorie and high carbohydrate diet ( [Formula: see text], 1000kcal per day, protein:carbohydrate: [Formula: see text] :65:10) for 4 weeks. Similar decreases in body weight and serum glucose levels were observed in both groups. Fasting serum insulin levels were reduced in the low carbohydrate diet group compared to the high carbohydrate diet group (-30% versus -10%, [Formula: see text] ). Total serum cholesterol and triglyceride levels decreased in both groups, but were not significantly different from each other. High-density lipoprotein-cholesterol (HDL-C) increased in the low carbohydrate diet group but not in the high carbohydrate diet group (+15% versus 0%, [Formula: see text] ). There was a larger decrease in visceral fat area measured by computed tomography in the low carbohydrate diet group compared to the high carbohydrate diet group (-40cm(2) versus -10cm(2), [Formula: see text] ). The ratio of visceral fat area to subcutaneous fat area did not change in the high carbohydrate diet group (from 0.70 to 0.68), but it decreased significantly in the low carbohydrate diet group (from 0.69 to 0.47, [Formula: see text] ). These results suggest that, when restrict diet was made isocaloric, a low calorie/low carbohydrate diet might be more effective treatment for a reduction of visceral fat, improved insulin sensitivity and increased in HDL-C levels than low calorie/high carbohydrate diet in obese subjects with type 2 diabetes mellitus.

Again, you say that insulin and GI has nothing to do with fat gain. Eh??

PMID: 15331203 [PubMed - in process]

Effects of a low-fat diet compared with those of a high-monounsaturated fat diet on body weight, plasma lipids and lipoproteins, and glycemic control in type 2 diabetes.

Gerhard GT, Ahmann A, Meeuws K, McMurry MP, Duell PB, Connor WE.

Division of Endocrinology, Diabetes and Clinical Nutrition, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098, USA.

BACKGROUND: An important therapeutic goal for patients with type 2 diabetes is weight loss, which improves metabolic abnormalities. Ad libitum low-fat diets cause weight loss in nondiabetic populations. Compared with diets higher in monounsaturated fat, however, eucaloric low-fat diets may increase plasma triacylglycerol concentrations and worsen glycemic control in persons with type 2 diabetes. OBJECTIVE: We investigated whether, in type 2 diabetes patients, an ad libitum low-fat diet would cause greater weight loss than would a high-monounsaturated fat diet and would do this without increasing plasma triacylglycerol concentrations or worsening glycemic control. DESIGN: Eleven patients with type 2 diabetes were randomly assigned to receive an ad libitum low-fat, high-carbohydrate diet or a high-monounsaturated fat diet, each for 6 wk. The diets offered contained 125% of the estimated energy requirement to allow self-selection of food quantity. The response variables were body weight; fasting plasma lipid, lipoprotein, glucose, glycated hemoglobin A(1c), and fructosamine concentrations; insulin sensitivity; and glucose disposal. RESULTS: Body weight decreased significantly (1.53 kg; P < 0.001) only with the low-fat diet. Plasma total, LDL-, and HDL-cholesterol concentrations tended to decrease during both diets. There were no interaction effects between diet and the lipid profile response over time. Plasma triacylglycerol concentrations, glycemic control, and insulin sensitivity did not differ significantly between the 2 diets. CONCLUSION: Contrary to expectations, the ad libitum, low-fat, high-fiber diet promoted weight loss in patients with type 2 diabetes without causing unfavorable alterations in plasma lipids or glycemic control.

PMID: 15321807 [PubMed - in process]

Once again. Should I repeat myself?

High prevalence of insulin resistance in postpubertal Asian Indian children is associated with adverse truncal body fat patterning, abdominal adiposity and excess body fat.

Misra A, Vikram NK, Arya S, Pandey RM, Dhingra V, Chatterjee A, Dwivedi M, Sharma R, Luthra K, Guleria R, Talwar KK.

1Department of Medicine, All India Institute of Medical Sciences, New Delhi, India.

OBJECTIVE:: The objectives were to study the relationships of insulin resistance with generalized and abdominal obesity, and body fat patterning in urban postpubertal Asian Indian children. DESIGN:: Cross-sectional, population-based epidemiological study. SUBJECTS:: In all, 250 (155 males and 95 females) healthy urban postpubertal children. MEASUREMENTS:: Anthropometric profile, percentage of body fat (%BF), fasting serum insulin, and lipoprotein profile. RESULTS:: Fasting insulin correlated significantly with body mass index (BMI), %BF, waist circumference (WC), central and peripheral skinfold thicknesses and sum of four skinfold thicknesses ( summation operator 4SF) in both sexes, and with systolic blood pressure and waist-to hip circumference ratio (W-HR) in males only. Consistent increase in fasting insulin was noted with increasing values of central skinfold thickness at each tertile of peripheral skinfold thickness, WC, and %BF. Central skinfold thickness correlated with fasting insulin even after adjusting for WC, W-HR, and %BF. The odds ratios (OR) (95% CI) of hyperinsulinemia (fasting insulin concentrations in the highest quartile) were 4.7 (2.4-9.4) in overweight subjects, 8 (4.1-15.5) with high %BF, 6.4 (3.2-12.9) with high WC, 3.7 (1.9-7.3) with high W-HR, 6.8 (3.3-13.9) with high triceps skinfold thickness, 8 (4.1-15.7) with high subscapular skinfold thickness, and 10.1 (5-20.5) with high summation operator 4SF. In step-wise multiple logistic regression analysis, %BF [OR (95% CI): 3.2 (1.4-7.8)] and ?4SF [OR (95% CI): 4.5 (1.8-11.3)] were independent predictors of hyperinsulinemia, similar to insulin resistance assessed by HOMA (homeostatic model of assessment) in the study. CONCLUSION:: A high prevalence of insulin resistance in postpubertal urban Asian Indian children was associated with excess body fat, abdominal adiposity, and excess truncal subcutaneous fat. Primary prevention strategies for coronary heart disease and diabetes mellitus in Asian Indians should focus on the abnormal body composition profile in childhood.International Journal of Obesity advance online publication, 17 August 2004; doi:10.1038/sj.ijo.0802704

PMID: 15314636 [PubMed - as supplied by publisher]

Oh yeah, I forgot..insulin has nothing to do with gaining fat...so why would insulin resistance be a factor in gaining weight?

The role of diet and whether a CALORIE IS A CALORIE

So, definitionally, a calorie is certainly a calorie, just like a degree Celsius is a degree Celsius. However, when someone asks the question "Is a calorie a calorie?", they require more information. What they mean to ask is, "When I consume a calorie of protein, does my physiology respond the same way as when I consume a calorie of fat or carbohydrate?" The answer in this situation is a resounding no!

I could write volumes about this in support of my contention that functionally, a calorie is not a calorie, but don't worry, today I'll spare you. Instead let me address just a few points and give a few examples of why a calorie isn't a calorie.

Let's start out with a simple comparison that sounds a bit extreme but will illustrate my point. If I agreed with the idea that a calorie is a calorie, then I'd have to believe that my body would behave the same way if I ate 3000 calories a day from celery (yes, that's a lot of celery) as it would if I ate 3000 calories a day from butter. Is a calorie just a calorie, or might some of the fibrous content in the celery fail to be absorbed, decreasing the amount of calories actually reaching the cells?

Since some of the fibrous calories will indeed fail to be absorbed, we can see that during the first step of physiological food processing (digestion), the inherent caloric value of food is already altered and fewer of the ingested calories reach the cells. So, 3000 calories of celery are certainly different from 3000 calories of butter. If you're eating only celery and 3000 calories constitutes deficit eating for you, then you'll get far less calories than you'd hoped.

In the end, my point here is that reading food labels doesn't give a good indication of the exact amount of calories that'll actually reach the cells for energy provision or storage. Functionally, a calorie is not a calorie.

The next main reason that people ask, "Is a calorie a calorie?" is because they want to try to manipulate their caloric intake so that it'll be below, match, or exceed calorie needs. This is so they can lose, maintain, or gain weight. But the problem with thinking that a calorie is a calorie is that the very act of eating different foodstuffs can change metabolic rate. A good example of this is the thermic effect of food.

The digestion and metabolism of food actually increases the metabolic rate after a meal. Since protein foods have double the thermic effect of food verses carbohydrates or fats, it should be obvious that the metabolic rate will be higher when more protein is consumed. Again, functionally, a calorie is not a calorie!

When on a hypocaloric diet, protein needs are increased. In studies comparing groups on hypocaloric diets that are low in protein and those that are high in protein (calories are the same in both groups), the diets high in protein lead to increased metabolic rates, increased weight loss, and better preservation of lean mass. Clearly, a calorie is not a calorie in this case either.

While the previous paragraphs discussed different macronutrients, even different varieties of the same macronutrients have different physiological effects. When low glycemic carb diets are compared to high glycemic carb diets, it's clear that the groups of individuals eating mostly high glycemic carbs have higher body fat percentages, higher fasting glucose and insulin levels, and have higher risks for cardiovascular disease. Functionally, a carbohydrate isn't even a carbohydrate, let alone a calorie a calorie!

Studies done in rats have shown that when they eat diets of identical calorie levels, their body compositions are dramatically altered by the composition of fat in the diet. When omega-3 fatty acids make up a large percentage of the diet, the rats are lean and muscular. When omega-6 fatty acids make up a large percentage of the diet, the rats are obese. A fat isn't even a fat, let alone a calorie a calorie!

Here's a cool study that illustrates my point quite well. This study was done to compare the effects of twelve weeks of a moderate hypocaloric (high protein) diet and resistance training in male police officers. In this study, there were three total groups - a control group that didn't exercise, and two groups that did. In the two exercise groups, two different protein supplements were used to increase protein intake. Several very telling things emerged from this study:

1) Before the study began, the subjects' diets were analyzed. It turned out that subjects had actually been consuming a hypocaloric diet that was approximately 10 to 20% below their calculated calorie needs (15% protein, 60% carbohydrate, 25% fat). Despite the calorie deficit, they were all between 22 and 35% body fat and had been gaining weight over the previous five years! So if a calorie were really just a calorie, they should've been leaner and losing fat, right? But no, they were gaining fat!

2) In the control group that didn't exercise, the macronutrient composition of the diet remained the same as before the study (15% protein, 60% carbohydrate, 25% fat) but subjects made smarter food choices. They simply consumed fewer simple carbohydrates and ate more complex carbohydrates.

In addition, these subjects ate less food before sleep and more during the active hours of their days. If a calorie were a calorie, we wouldn't expect to see any changes in their body compositions. However, these simple changes led to an average 5.5 pound weight loss and an average 2.5% decrease in body fat. If a calorie were just a calorie, then there shouldn't have been a change in weight or body fat percentage!

3) That's already plenty of evidence to make the next person that says "a calorie is a calorie" eat his words, but let's go ahead and kick him while he's down, shall we? Let's discuss the interesting changes between the two exercise/high protein groups.

These subjects consumed the exact same number of calories as they did before the study. In addition, the two groups consumed the same exact percentage of the different macronutrients as each other (26% protein, 52% carbohydrate, 20% fat) and did the same exercise routine. Interestingly, the subjects consuming one type of protein (a casein and milk protein product) lost almost 6.5 pounds more fat and gained nearly 4.5 pounds more muscle than those consuming another type of protein (whey).

Not only was body composition altered, but the subjects in the casein/milk protein group had a 31% improvement over the whey-only group in muscle strength. If a calorie is a calorie, the two groups should've had the same results. Clearly they didn't, so, yet again, a calorie is not a calorie!

I could go on all day but I'll stop here. From this discussion, I hope it's clear that the old notion that a calorie is a calorie is a dying idea. Anyone who continues to make this assertion is completely wrong due to either a lack of current information or due to a closed mind. Whatever the reason, neither type of person has any place giving out nutritional advice.


before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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LOL, and you did EXACTLY what I said you'd do laugh.giflaugh.giflaugh.gif

you even referenced the cop study, which to anybody respectable in the field is an absolute joke/flawed study.

now, give me time and i'll educate you on what a real researcher does. he analyzes and understands full texts, and then critiques them. the above have already been discussed and beaten to death by myself and colleagues however i'll go over them. like i did for you, give me time as typing is not my forte smile.gif

but, evigrex, please.. in your OWN words, with your OWN brain, tell me how this is wrong, this is based on CURRENT literature:

1. It takes only tiny amounts of insulin to affect fat cell metabolism.

2. Protein more than sufficiently raises insulin this much so protein + fat works just as well to both inhibit fat cell mobilization and stimulate storage of nutrients.

3. Insulin is important to increase LPL activity. Lpl was thought to be rate limiting for fat storage but this is not the case. All LPL does is release fatty acids from chylomicrons.

4. Acylation stimulation protein (ASP) is the real player in triglyceride synthesis in the fat cell. It is stimulated by the mere presence of chylomicrons in the bloodstream and is insulin independent.

and please tell me, in your own words, whats wrong with this study like i'll tell you whats wrong with yours:

Curr Opin Lipidol. 2000 Jun;11(3):291-6. Related Articles, Links

Of mice and men (and women) and the acylation-stimulating protein pathway.

Sniderman AD, Maslowska M, Cianflone K.

Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Centre, Royal Victoria Hospital, Montreal, Quebec, Canada. allan.sniderman@muhc.mcgill.ca

The storage and release of energy by adipocytes is of fundamental biologic importance. Not surprisingly, therefore, the rate at which these processes occur can be modulated by a variety of physiologic molecules. A newly recognized participant is produced by adipocytes themselves: acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidence regarding how the ASP pathway may influence energy storage and release. In brief, the rate at which triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) is determined by lipoprotein lipase and insulin, which is the principal hormone that regulates lipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to triglycerides by adipocytes. Under certain circumstances, however, reduction of activity of the ASP pathway may negatively impact on the first step of the process. ASP also influences the rate at which fatty acids are released by adipocytes, and it is clear that insulin and ASP interact in a variety of ways that involve energy storage and release. Accordingly, to understand the impact of any intervention on energy storage and release by adipocytes, the effects of both insulin and ASP must be taken into account.

Note "By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to TG in adipocytes."

all insulin does is activate LPL (which ASP also does) which mobilized FA from the chylos. ASP is the key player in fat storage. It also increases glucose uptake, stimulates insulin release, etc, etc

stop looking at outdated models!

ps: i di dnot define insulin

give me 30-45 smile.gif

but, i will make this clear. from me to you, you are not "in your league" - you are posting misguided studies which actually, in full texts, dont even support your point. it doesnt appear that you have any educational backround in this, nor experience in actual interpretation of text.

by the way, even JB agrees now that overall caloric balance is the primary role in +/-'s, email him and ask.

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and as for the comment that i shouldnt be giving nutirtional advice.. lol.. i've worked with elite athletes (olympic inc.) and have ACTUAL EXPERIENCE in the REAL WORLD as well as a great trackrecord.. you have..? acne.org messageboards?? laugh.giflaugh.gif

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*sigh* I tried to lighten the mood, folks....I truly did. smile.gif

you have..? acne.org messageboards??

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LOL, and you did EXACTLY what I said you'd do  laugh.gif  laugh.gif  laugh.gif

you even referenced the cop study, which to anybody respectable in the field is an absolute joke/flawed study.

now, give me time and i'll educate you on what a real researcher does. he analyzes and understands full texts, and then critiques them. the above have already been discussed and beaten to death by myself and colleagues however i'll go over them. like i did for you, give me time as typing is not my forte smile.gif

but, evigrex, please.. in your OWN words, with your OWN brain, tell me how this is wrong, this is based on CURRENT literature:

1. It takes only tiny amounts of insulin to affect fat cell metabolism.

2. Protein more than sufficiently raises insulin this much so protein + fat works just as well to both inhibit fat cell mobilization and stimulate storage of nutrients.

3. Insulin is important to increase LPL activity. Lpl was thought to be rate limiting for fat storage but this is not the case. All LPL does is release fatty acids from chylomicrons.

4. Acylation stimulation protein (ASP) is the real player in triglyceride synthesis in the fat cell. It is stimulated by the mere presence of chylomicrons in the bloodstream and is insulin independent.

and please tell me, in your own words, whats wrong with this study like i'll tell you whats wrong with yours:

Curr Opin Lipidol. 2000 Jun;11(3):291-6. Related Articles, Links

Of mice and men (and women) and the acylation-stimulating protein pathway.

Sniderman AD, Maslowska M, Cianflone K.

Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Centre, Royal Victoria Hospital, Montreal, Quebec, Canada. allan.sniderman@muhc.mcgill.ca

The storage and release of energy by adipocytes is of fundamental biologic importance. Not surprisingly, therefore, the rate at which these processes occur can be modulated by a variety of physiologic molecules. A newly recognized participant is produced by adipocytes themselves: acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidence regarding how the ASP pathway may influence energy storage and release. In brief, the rate at which triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) is determined by lipoprotein lipase and insulin, which is the principal hormone that regulates lipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to triglycerides by adipocytes. Under certain circumstances, however, reduction of activity of the ASP pathway may negatively impact on the first step of the process. ASP also influences the rate at which fatty acids are released by adipocytes, and it is clear that insulin and ASP interact in a variety of ways that involve energy storage and release. Accordingly, to understand the impact of any intervention on energy storage and release by adipocytes, the effects of both insulin and ASP must be taken into account.

Note "By contrast, the ASP pathway modulates the rate at which fatty acids are taken up and converted to TG in adipocytes."

all insulin does is activate LPL (which ASP also does) which mobilized FA from the chylos. ASP is the key player in fat storage. It also increases glucose uptake, stimulates insulin release, etc, etc

stop looking at outdated models!

ps: i di dnot define insulin

give me 30-45 smile.gif

but, i will make this clear. from me to you, you are not "in your league" - you are posting misguided studies which actually, in full texts, dont even support your point. it doesnt appear that you have any educational backround in this, nor experience in actual interpretation of text. 

by the way, even JB agrees now that overall caloric balance is the primary role in +/-'s, email him and ask.


before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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i am almost positive that excessive amounts of sugar break me out, POSITIVE

now this is what i'm talking about,you don't need science to tell us otherwise when we have people like me and you SAYING that sugar is a problem for them.

Now maybe sugar itself isn't directly to blame?,but the side effect associated with large ammount of the stuff?.

im thinking this too dude. THe last 3-4 days ive cut out my sugar intake almost completely, i at least try to keep to to under 30 grams a day. Before i would drink 4 cans of pop in one day and large amounts of candy and i would break out sooo bad. But there were some days when I would just eat a little sugar and not break out at all (which is what made me think that sugar wasnt causing my breakouts) I went camping last week completely clear, ate an entire bag of campfired marshmellows and the next day my face looks like SHIT. Since i stopped eating large amounts of sugar I havent broken out once. Sugar is the only thing that has constantly been in my diet every day that i have had acne (i love candy and never thought twice about eating it) and I have narrowed that down to the cause of my acne. For the next couple months I will continue my cleansing routine but stop eating sugar and see how much my skin clears up

sleeping late, masturbation ,sex etc doesnt cause acne

but consuming too much sugar does, your body isnt supposed to consume large amounts of sugar contained in pop/candy so when you do the impurities come out through your face. I was my face and feel every inch of it every night before i go to bed, there have been days when i ate alot of sugar, went to sleep with a perfectly clean face, and woke up with a HUGE zit where there was NOTHING before, not even a sign of there being a pimple. Some pimples take days to develop, these may be indirectly related to sugar consumption or not, but i notice that most my pimples form overnight


give a man a key he cannot not open the door, give him something free and he'll resell it to the poor (c'est la vie)


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What you posted earlier:

sorry but fat storage has nothing to do with insulin or the amount of insulin present. fat storage is dependant on a positive energy balance not on gi. controlling GI for dieting purposes serves to simply keep blood sugar stable (-> less hunger) and thats about it.

Fat storage has nothing to do with insulin: So please tell me, what is disposing glucose in all those fat cells? Disregarding ATP, lipoprotein lipase and all that other crap that you spout about, are you saying that something OTHER than insulin is depositing glucose in those fat cells? And is it mere coincidence that folks on high carbohydrate diets gain weight more rapidly than others, even at the same levels of caloric intake.

Thats not even going into type 2 diabetics - many of whom cannot lose weight on a normal diet regardless of caloric intake.

Oh..your second statement: Tell that to the majority of dieters and diabetics that use it to manipulate their blood glucose/insulin levels, to achieve maximal fat loss.


before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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and as for the comment that i shouldnt be giving nutirtional advice.. lol.. i've worked with elite athletes (olympic inc.) and have ACTUAL EXPERIENCE in the REAL WORLD as well as a great trackrecord.. you have..? acne.org messageboards??  laugh.gif  laugh.gif

before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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*sigh*  I tried to lighten the mood, folks....I truly did.   smile.gif

you have..? acne.org messageboards??

PS: Hey!! That's hitting a little too close to home there, pal. bb_eusa_naughty.gif

I love this board!! bb_razz.gif


before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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by the way, even JB agrees now that overall caloric balance is the primary role in +/-'s, email him and ask.

before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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I'm sure he wouldn't mind sharing his name with us since he's the trainer of olympians and is given such high credibility by those in his field.

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i dont like being called a personal trainer (as the certs required are an absolute joke) but yes i work with people (ranging from d1-elite athletes, housewives, bodybuilders, powerlifters, aspiring SEALS, etc)

i want to just write books and live off of that. training/designing nutritional programs is a pain.


before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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i dont like being called a personal trainer (as the certs required are an absolute joke) but yes i work with people (ranging from d1-elite athletes, housewives, bodybuilders, powerlifters, aspiring SEALS, etc)

i want to just write books and live off of that. training/designing nutritional programs is a pain.


Please only PM me if it's something that cannot be talked about on the thread or is highly personal. This way, everyone benefits.


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The silence...is deafening. I don't expect him to post again here...his credibility is gone.


before you judge me take a look at you

can't you find something better to do

point the finger, slow to understand

arrogance and ignorance go hand in hand

- Metallica, "holier than thou"


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The silence...is deafening. I don't expect him to post again here...his credibility is gone.

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The silence...is deafening.  I don't expect him to post again here...his credibility is gone.

I'm certain he's just "researching".


Life is all about living!


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