Louis Nutrition research

[Weib]

For 2009 my professional goal is to research more into nutrition and diet planning.
I will list my findings here about different diets and supplementation.

[Jordon]

good luck.

[Weib]

Building Mass while keeping your abs.

That's the holy grail of bodybuilding, isn't it? Everyone wants to get huge but stay lean, but getting lean is damn hard work for most people.

For natural physique enthusiasts the old paradigm of bulking over the winter and leaning out for the summer can be a recipe for disaster as too much fat is laid down during the winter, often causing your muscular definition to suffer so you end up looking like a "fat guy with big forearms." Let me save you from that fate.

Summer's long gone, but that's no reason to lose the beach body.

Adopting a cyclic approach to your nutritional plan is a surefire way to keep you lean but get you big. When using a cyclic approach to dieting, the two most common variables that are manipulated are time of the cycle and nutrients being cycled.

In regards to carb cycling, the cycles are usually a couple of days long and carbohydrates and calories are cycled. When cycling your carbs/calories you usually intersperse higher carb days into your week based on when you train. These higher carb days are also higher calorie days.

I believe this cycling of carbohydrates in relation to your training is a good idea and should be structured into most of your nutritional plans. (I'll outline specific plans later.)


When To Cycle?

If you need to lose a lot of weight, then carb cycling isn't for you.

If you need to put on a large amount of muscle (>15-20 pounds), then carb cycling isn't for you.

Carb cycling is for someone who's lean already and who wants to pack on more muscle at a slow and steady pace. If you have a lot of weight to lose, then you're better off dieting down first. If you have a lot of muscle to pack on your frame, then focus on taking in lots of calories.

Focus solely on one as you'll get faster results than if you try to carb cycle your way to a massive (or lean) physique. Carb cycling should be thought of as fine-tuning.


Carb Cycling for Mathematicians

Now that we've laid out the basic structure and pin pointed the people that'll benefit the most, let's get into the details. This would normally be the part of the article in which I give you very specific gram/pound body weight recommendations for carbohydrates on the various low/moderate/high carb days...but I'm not going to.

This is Carb Cycling for Idiots, remember? Not Carb Cycling for Mathematicians. I deal with a lot of real world people: business professionals, college students, people with families, etc. These people don't have the time to figure out that on Monday they need to eat 0.5g of carbs per pound and on Tuesday they need to eat 0.75g of carbs per pound, etc. They don't have that kind of time.

Practicality trumps everything for these people. People need to be focused on results, not how much time they can spend making a meal plan to get those results. It's important to remember that counting calories and being very specific about which nutrients cross your lips doesn't make you advanced. Results are what matters.

The best way to elicit a desired nutritional result without having to worry about counting calories is to focus on food selections. In this case, I'm talking about starchy carbohydrates — rice, oatmeal, sweet potatoes, whole grain pasta, etc, etc. These foods are high in carbohydrates and calorically dense compared to their vegetable counterparts.

We're going to exploit this difference to allow you to keep your six-pack while you pile on so much beef onto your frame you'll need to turn sideways to walk though a doorway.

Here's the plan (and it is so simple you can start tomorrow). You're going to consume protein and fruits/vegetables every meal. Your fat intake is going to be inversely proportional to your starch intake, meaning if you eat lots of starches at a meal then your fat intake should lower. If you don't eat any starches then your fat intake is higher.

As I mentioned above, ability to cycle carbohydrate intake is going to be purely dependent on your starch intake. There are 4 types of days in this model

No Starch — This is obvious, you just don't eat any starches. Your carbohydrate intake will be entirely made up of fruits and vegetables.

Low Starch — You'll have starches during your workouts and in the first meal following your workout.

Moderate Starch — You'll have workout starches and starches at your first two meals following your workout.

High Starch — Breakfast starches, workout starches, and starches at your first two meal post workout.

Now if you use the "starch cycling" approach, your weekly nutrition plan will look like the following, depending on whether you're doing full body training or some kind of upper/lower split training:

Full Body Training

Sunday: Off — No Starches

Monday: Full Body — High Starch

Tuesday: Off — No Starches

Wednesday: Full Body — High Starch

Thursday: Off — No Starches

Friday: Full Body — High Starch

Upper/Lower Split Training*

Sunday: Off — No Starch

Monday: Upper Body — Moderate Starch

Tuesday: Lower Body — High Starch

Wednesday: Off — No Starch

Thursday: Upper Body — Moderate Starch

Friday: Lower Body — High Starch

Saturday: Off — No Starch

*The upper days are allocated moderate carbs, but if you want to focus on improving the muscles of your upper body then allocate the high carb days to your upper body workout days and moderate carb days to your lower body workout days.

If you're using body part splits, then use the Low Starch days for smaller muscle groups (e.g. arms). A shoulder day would warrant moderate starch while chest, back, or legs need to be on high starch.

http://www.t-nation.com/readArticle.do?id=1825995

[Weib]

My summary of the Gflux/Carb cycle orientation -

I've been playing with the idea of the gflux/carb cycling idea on gains in performance while retaining relative leanness.
I won't say its a concrete plan but I've roughly grasp the understanding on how it works.

I've did a low carb variant of the carb cycling which actually is more carbs on training days, less carbs on non-training day while adding the gflux element into it.

For training days, my meal consumption can soar extremely high meaning my caloric requires for that day has been bumped up by metabolic demands - i cannot help it even if i tried because the hunger pangs will kill me.
I liked it because my performance grew steadily, i was consuming more carbs than usual and i do not experience much crashes. The good deal was that i didn't bloat up and actually grew a little without putting on much fat.
as it is, i believe if i planned my meals properly, i can even excel in my performance and maybe size?

I did note that fat loss is possible however extremely slow unless you do a drastic flux out of energy on this two paradigms however it was good enough for me as my performance isn't lacking which what matters.
Too much flux you lose too much performance, too little and you'd get nothing. This as what many people say, it is not an efficient tool for fat loss just a way not to bloat up.

On the brighter side of performance -
I was able to recover alot faster, i fatigue less and i can get through grueling work outs without feeling too bummed out, I'd say its a good training tool in a training stand point rather than nutrition stand point.

What i could have done better -

Measured my caloric requirements to what I've ate for the day
Measured my carb intake and vary it to find the optimum intake
Ensure little variables with my m.nutrient intake

[Weib]

Insulin Resistance—A Lethal Link Between Metabolic Disease and Heart Attack
By William Davis, MD
Insulin Resistance—A Lethal Link BetweenMetabolic Disease and Heart Attack

Due to multimillion dollar advertising and marketing campaigns by the pharmaceutical industry, patients and physicians alike seem to associate heart attack and stroke risk only with cholesterol. Drugs that lower cholesterol (statins), have created a windfall of profit for pharmaceutical companies, with a single company’s statin drug often exceeding several billion dollars in annual sales. However, cardiovascular risk entails far more than just elevated cholesterol levels.

In fact, the phenomenon known as insulin resistance offers a direct link between metabolic disease and cardiovascular risk, and is an often overlooked culprit underlying diabetes and heart disease. Learn how and why these two common diseases are intimately related and how to untangle them from your life.

http://www.lef.org/magazine/mag2008/aug ... ack_01.htm

[Weib]

Summary

Most experts believe that we are seeing just the tip of the iceberg represented by melatonin’s versatile, system-wide effects. This formerly “niche” hormone, long thought to be responsible only for day-night cycling and important effects on sleep, is turning out to be the “dark horse” of biomedicine in the early 21st century. We’ve seen how melatonin’s intense antioxidant activities, remarkable ability to modulate the immune system, and capacity to manage inflammatory consequences of tissue injury throughout the body are leading to its use in just about every conceivable setting. From the tragic consequences of severe head trauma to the neurological deficits experienced by Alzheimer’s and stroke patients, to the deadly effects of advanced cancers, melatonin has shown that it has important wide-ranging applications for medical treatment.

http://www.lef.org/magazine/mag2008/aug ... nin_01.htm

[Weib]

Resveratrol: A Caloric-Restriction Mimetic

A 2003 study at Harvard University found that resveratrol mimics the effects of caloric restriction in yeast cells, boosting their life spans by as much as 70%.3 The following year the researchers went on to demonstrate that resveratrol slows aging in two standard laboratory animals, roundworms and fruit flies.4 That made resveratrol the first compound to show anti-aging effects in widely divergent species. Then in 2006, scientists in Pisa, Italy, showed that resveratrol’s magic could be applied to more advanced animals— large doses of resveratrol extended the life span by more than 50% in a species of fish, Nothobranchius furzeri, which typically lives just nine weeks.5
Resveratrol: A Caloric-Restriction Mimetic

In a study published in 2006 in the journal Cell, researchers in France found that resveratrol protects mice against diet-induced insulin resistance and obesity.6 Furthermore, mice given the resveratrol supplement demonstrated improved endurance levels during exercise. The researchers also studied the cell-signaling pathway in the mitochondria of these mice. Mitochondria are the power plants of cells, which are responsible for intracellular energy production. Resveratrol activated a protein in the sirtuin family (SIRT1), which then stimulated the activity of another protein involved in mitochondrial function. Other recent studies, including one conducted at the Joslin Diabetes Center, have found another member of the sirtuin family of cellular proteins that may play a major role in how fat is produced and stored, offering a new target for treatments to prevent obesity and reduce the risk of type 2 diabetes.7,8

The French researchers surmised that resveratrol helped control weight gain by enhancing energy expenditure.6 Since the study found a link between sirtuins and energy utilization, the researchers concluded that resveratrol may be helpful in the prevention and treatment of certain metabolic disorders, especially those related to mitochondrial dysfunction, such as Alzheimer’s and Parkinson’s disease—two neurodegenerative conditions that become more prevalent with aging.9

Resveratrol Produces Favorable Metabolic Changes

In a landmark mouse study published in the journal Nature, resveratrol countered some effects of a high-calorie diet, improving the health of the mice and increasing their life span, even though they did not lose any weight.32 These mice shared many of the problems of humans on an equivalent diet, including obesity, insulin resistance, and heart disease.

The study compared middle-aged mice fed a standard diet with those on a high-fat (60% of daily calories) diet, with and without high-dose resveratrol supplements. Over a two-year period, the resveratrol-fed mice on the high-fat diet lived as long as the ones on a standard diet and at least 15% longer than their untreated, obese peers. How much better off were the treated mice? The resveratrol-treated mice demonstrated improved insulin sensitivity compared with their obese counterparts who did not receive resveratrol, suggesting that resveratrol conferred important benefits for longevity and diabetes prevention.32 Additionally, the resveratrol-treated animals displayed greater numbers of liver mitochondria than animals who consumed a high-fat diet that did not contain resveratrol. The study further suggested that resveratrol might lead to better health and endurance than is usually seen in obese mice. Resveratrol’s exact working mechanism is not yet known with certainty, but the researchers believe it may be activating SIRT1, a sirtuin protein that is thought to be involved with longevity.

The mouse studies also hinted that resveratrol induces basic metabolic changes akin to those produced by caloric restriction.6,32 Gene-expression analysis in livers of these aged and overweight mice indicated that resveratrol favorably modified some of the known metabolic pathways that are also affected by caloric restriction.32 Perhaps the most intriguing result of the recent mouse studies was resveratrol’s ability to increase the number of mitochondria, the key cell components that serve as energy producers.6,32

Resveratrol’s ability to restore function to mitochondria is especially exciting because it seems that restored mitochondria are more efficient than the aging mitochondria they replace, are less prone to churn out free radicals, and are more efficient at ridding the body of damaged cells that induce chronic inflammatory reactions. Caloric restriction appears to do the same thing, but is much more difficult to implement and maintain in humans.

Resveratrol’s effect on mitochondria may be enough by itself to account for much of the compound’s demonstrable effects in the mouse studies. It may account for the enhanced running abilities observed in the overweight mice treated with resveratrol. What makes the findings of these recent mouse studies so potentially significant to researchers is that humans have genes similar to those linked to resveratrol intake in the mice.6,32

http://www.lef.org/magazine/mag2008/feb ... rol_01.htm

[Weib]

Other Recent Advances in Vitamin C Therapy

Nutritional researchers are constantly uncovering new health benefits for vitamin C. Recent findings include vitamin C’s role in the following applications:

Respiratory illnesses: The impact of vitamin C in staving off the common cold has been hotly debated for more than three decades. Large, well-designed studies continue to show, however, that regular vitamin C supplements reduce the frequency29 and duration of the common cold.30 More serious illnesses also benefit from the antioxidant effects of vitamin C, particularly asthma.31-33 Asthmatic children given an antioxidant supplement containing 250 mg vitamin C and 50 mg vitamin E had markedly decreased responses to environmental asthma triggers.4 And vitamin C supplements (1,000 mg/day) also reduced the amount of long-term inhaled corticosteroids needed by adults with asthma.34

Cancer: Exciting new work is showing that vitamin C supplementation may decrease the toxic effects of chemotherapy drugs (such as damage to heart tissue)35 and increase the anti-tumor activity of chemotherapy.36 Further, promising studies show that vitamin C may synergize with other antioxidant and anti-inflammatory nutraceuticals to help fight cancer.37,38 Chronic supplementation with vitamin C and other antioxidants might also serve a vital chemopreventive role, reducing the risk of actually developing cancer in the first place.5,39-41

Diabetes: Human studies have now demonstrated that vitamin C supplements may help lower blood glucose levels in diabetics, with additional beneficial reductions in low-density lipoprotein (LDL) and plasma free radicals.6,42

Stomach Health: Supplementing with vitamin C can also protect against oxidative damage wrought by the bacterium Helicobacter pylori, a major cause of gastritis and stomach ulcers. Vitamin C supplements can also reduce the dose of antibiotics needed to eradicate the organism39,43 and may directly prevent the gastritis it causes.44 And there’s encouraging evidence that higher vitamin C levels are associated with lower long-term gastric cancer risk.45

http://www.lef.org/magazine/mag2008/apr ... n-C_01.htm

[Weib]

Green Tea and EGCG May Help Prevent Obesity, Diabetes

Because diabetes and cardiovascular disease share some of the same risk factors, particularly obesity, it is not surprising that green tea, by ameliorating these risk factors,17 can help protect against diabetes as well as against heart disease.6-8

“Subjects with long-term consumption of green tea are characterized by a lower percentage of total body fat, smaller waist circumference, and decreased waist-to-hip ratio,” Dr. Wolfram says. “In intervention studies, it was shown that consumption of green tea can reduce body weight and abdominal fat as well as increase fat oxidation and energy expenditure. Furthermore, green tea consumption may reduce the incidence of type 2 diabetes and improve glucose control and insulin sensitivity.”

The exact mechanism of how green tea helps control overweight and high blood sugar is not completely understood, and probably involves several different hormonal and metabolic mechanisms.8 However, Dr. Wolfram notes that EGCG regulates genes involved in fat oxidation and storage, as well as genes involved in insulin signaling and glucose metabolism.66-68

Amazingly, EGCG can even improve survival and function of insulin-secreting pancreatic islet cells grown in the laboratory, and could have future applications in enhancing the success of pancreatic islet cell transplantation.69 Furthermore, EGCG suppresses glucose production by liver cells.70 Drinking green tea was shown to improve glucose metabolism in healthy human volunteers,71 and in a population study, women who drank four or more cups of tea per day had a tendency toward lower diabetes risk, compared with women who drank no tea.72

Extensive studies by Dr. Babu’s group of the effects of green tea and its catechins in animal models of type 1 and type 2 diabetes.53,61,62,73 have shown that green tea helps optimize glucose utilization, thereby reducing blood glucose levels.

“Green tea administration significantly reduced elevated serum glucose level in [drug]-induced diabetic rats and increased glucose tolerance in normal rats,” Dr. Babu says. “Green tea also has been shown to lower blood glucose level both in [chemically induced] diabetic mice and a genetic model of type 2 diabetes.”

By lowering glucose production in liver cells and decreasing the activity of genes that enhance glucose production, “EGCG was reported to mimic insulin,” Dr. Babu explains. “Green tea also reduced accumulation of cholesterol, free fatty acids, and triglycerides in the heart of diabetic rats.”

The chronic, disabling complications of diabetes result from changes to the blood vessels in the limbs, eyes, kidneys, heart, and other organs. In the presence of high blood sugar levels, these complications arise when damaging byproducts of sugar metabolism, called advanced glycation end products (AGEs), interfere with cross-linking of collagen in connective tissue. Abnormal collagen fiber cross-linking contributes to fibrosis, in which the heart muscle and other tissues become increasingly dysfunctional as they stiffen and become rigid, much as pliable metal wires linked together can form an impenetrable coat of armor. Once again, green tea may intervene in this disease process.53,74

“Green tea extract administration reduced the accumulation of collagen, extent of glycation, formation of advanced glycation end products and cross-linking of collagen in [chemically induced] diabetic rats,”

Dr Babu says. “In our study, we proposed that green tea may have a therapeutic effect in the treatment of glycation-induced complications of diabetes.”

http://www.lef.org/magazine/mag2008/apr ... Tea_01.htm

[Weib]

Metabolic Syndrome and Diabetes

An alarming number of Americans suffer from diabetes and metabolic syndrome—conditions of aberrant blood sugar metabolism associated with a greatly increased risk of cardiovascular disease. In fact, estimates suggest that 7% of the population have diabetes and more than 20% are affected by metabolic syndrome.7,8 Studies strongly suggest that magnesium may offer important protection against both metabolic syndrome and diabetes.
Metabolic Syndrome and Diabetes

Metabolic syndrome is characterized by insulin resistance—the situation in which muscle, liver, or fat tissues cannot properly respond to insulin’s signal to bring glucose into cells. As a result, glucose and triglyceride levels rise in the blood, beneficial high-density lipoprotein (HDL) declines, and blood pressure rises. In a five-year-long epidemiological study of more than 1,000 healthy adults, scientists found that greater magnesium intake was linked with improved insulin sensitivity.9

In another compelling study, scientists prospectively examined the relationship between magnesium intake and the development of metabolic syndrome and its components in healthy young adults. Nearly 5,000 Americans aged 18-30 were monitored through 15 years of follow-up. After adjustment for possible confounding factors, those in the highest quartile of magnesium intake had a 31% decreased risk of metabolic syndrome. Greater magnesium intake was also linked with a lower plasma glucose and weight circumference and higher high-density lipoprotein (HDL). The authors concluded that higher magnesium intake may offer protection against the epidemic of metabolic syndrome.10

According to a research review from Northwestern University, magnesium could address several components of metabolic syndrome by increasing levels of HDL, decreasing triglycerides, and favorably impacting glucose homeostasis, insulin action, and insulin secretion.2 Increased magnesium intake has also been linked with protection against hypertension, another component of the metabolic syndrome.2,11

A magnesium-rich diet abundant in foods such as spinach, almonds, and whole-wheat bread can substantially reduce the risk of developing type 2 diabetes, according to a report from Harvard University investigators. Researchers followed 85,000 women and 42,000 men for 18 and 12 years respectively, during which time 5,400 participants developed type 2 diabetes. Even in those at increased risk for diabetes based on risk factors such as excess weight, increasing age, little physical activity, and smoking, those with the highest levels of dietary magnesium intake reduced their risk of developing type 2 diabetes by up to 34%.3

Magnesium deficiency has been linked with chronic diabetic complications such as retinopathy (eye disease), nephropathy (kidney disease), neuropathy (nerve disease), and foot ulcerations. These findings suggest that individuals with existing diabetes should pay very close attention to their magnesium status in order to avoid the long-term manifestations of the disease.12

http://www.lef.org/magazine/mag2008/may ... ces_01.htm

[Weib]

Silymarin Lowers Glucose, Lipid Levels in Diabetics

Silymarin, a milk thistle seed extract, helps lower elevated blood sugar and lipid levels in diabetics, according to new findings.1

Scientists administered 200 mg of silymarin three times daily for four months to 25 type II diabetes patients, while 26 diabetics received a placebo. Blood levels of fasting glucose, hemoglobin A1c (HbA1c, which reflects long-term glucose control), insulin, total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides were measured before the trial and at its conclusion.

Subjects who received silymarin experienced significant reductions in fasting blood glucose, HbA1c, total cholesterol, LDL, and triglycerides, while fasting blood glucose, total cholesterol, triglycerides, and HbA1c increased in the placebo group.

By decreasing glucose and lipid levels, silymarin may thus play an important role in the management of type II diabetes.

—Dayna Dye

http://www.lef.org/magazine/mag2007/jan2007_itn_01.htm

[Weib]

DHA Suppresses Production of Fat Cells

New research shows that docosahexaenoic acid (DHA), an omega-3 fatty acid in fish oil, may fight excess body weight by thwarting the development of fat cells.9

Working with cultured pre-adipocytes (immature fat cells), scientists showed that levels of DHA obtainable through the diet may help avert obesity by preventing new fat cells from forming and encouraging existing fat cells to undergo programmed cell death (apoptosis). DHA also encouraged adipose cells to release their stores of fatty acids, a process popularly referred to as “burning fat.”

Previous research has shown that dietary omega-3 fatty acids decrease body fat and fat accumulation in rodents,10,11 but the present study helps explain precisely how DHA may work to reduce obesity.

—Dale Kiefer

European Doctors Advise Fish Oil After Heart Attacks

Although heart-attack survivors in Europe are routinely prescribed fish oil, this practice is rarely followed in the United States, according to a recent report in the New York Times.20

In numerous studies, fish oil rich in omega-3 fatty acids has been shown to improve survival after heart attacks and to reduce fatal heart rhythms. In the US, however, heart attack victims are rarely given omega-3 fatty acids, though they are routinely prescribed more expensive and invasive treatments, such as cholesterol-lowering drugs and implantable defibrillators.

Dr. Terry Jacobson, a preventive cardiologist at Emory University in Atlanta, told the Times, “Most cardiologists here are not giving omega-3s, even though the data support it—there’s a real disconnect. They have been very slow to incorporate the therapy.”

Wide variations in cardiac care around the world underscore the decisive role that drug companies play in disseminating medical information, according to the Times report. Because prescription fish oil is not licensed to prevent heart disease in the US, drug companies may not legally promote it for that purpose, and doctors routinely fail to recommend it to their patients.

According to a recent study published in the Journal of the American Board of Family Medicine, only 17% of family doctors were likely to prescribe fish oil to their patients, including those who had suffered a heart attack. The authors concluded that there was a great need to “improve awareness of this important advice.”

In a landmark study of fish oil conducted more than a decade ago, Italian researchers from the GISSI Group gave 11,000 patients 1 gram of prescription fish oil a day after they had suffered a heart attack. After three years, the number of deaths was reduced by 20% and the number of sudden deaths by 40% compared to a control group. By 2004, medical regulatory authorities in almost all European countries, including Spain, France and Britain, had approved prescription fish oil for use in heart attack patients. The American College of Cardiology now advises patients with coronary artery disease to increase their consumption of omega-3 acids to 1 gram a day.

Dr. Maria Franzosi, a researcher at the Mario Negri Institute in Milan, told the Times that the use of fish oil “is very popular here in Italy, I think partly because so many cardiologists in this country participated in the studies and were aware of the results. In other countries, uptake may be harder because doctors think of it as just a dietary intervention.”

Research on fish oil continues to gain momentum in Europe. Researchers from the GISSI Group are now conducting two major trials to examine fish oil’s effects in patients with abnormal heart rhythms and in patients with heart failure.

—Matt Sizing

http://www.lef.org/magazine/mag2007/feb2007_itn_01.htm

[Yxy]

good stuff...I take a couple of NOW foods magnesium citrate before sleeping...cheaper than ZMA

Metabolic Syndrome and Diabetes

In another compelling study, scientists prospectively examined the relationship between magnesium intake and the development of metabolic syndrome and its components in healthy young adults. Nearly 5,000 Americans aged 18-30 were monitored through 15 years of follow-up. After adjustment for possible confounding factors, those in the highest quartile of magnesium intake had a 31% decreased risk of metabolic syndrome. Greater magnesium intake was also linked with a lower plasma glucose and weight circumference and higher high-density lipoprotein (HDL). The authors concluded that higher magnesium intake may offer protection against the epidemic of metabolic syndrome.10

According to a research review from Northwestern University, magnesium could address several components of metabolic syndrome by increasing levels of HDL, decreasing triglycerides, and favorably impacting glucose homeostasis, insulin action, and insulin secretion.2 Increased magnesium intake has also been linked with protection against hypertension, another component of the metabolic syndrome.2,11

A magnesium-rich diet abundant in foods such as spinach, almonds, and whole-wheat bread can substantially reduce the risk of developing type 2 diabetes, according to a report from Harvard University investigators. Researchers followed 85,000 women and 42,000 men for 18 and 12 years respectively, during which time 5,400 participants developed type 2 diabetes. Even in those at increased risk for diabetes based on risk factors such as excess weight, increasing age, little physical activity, and smoking, those with the highest levels of dietary magnesium intake reduced their risk of developing type 2 diabetes by up to 34%.3

Magnesium deficiency has been linked with chronic diabetic complications such as retinopathy (eye disease), nephropathy (kidney disease), neuropathy (nerve disease), and foot ulcerations. These findings suggest that individuals with existing diabetes should pay very close attention to their magnesium status in order to avoid the long-term manifestations of the disease.12

http://www.lef.org/magazine/mag2008/may ... ces_01.htm

[Weib]

Mega dosing Fish oil -

So i had 2 weeks to load up myself for 20 grams of fish oil average.
I had stop supplementation of any kind for at least 1 month prior for this experiment.

Within that 1 month, i have had flaky dry skin on the side of my head and my eyebrow which could pass off as dandruff.
After 2 weeks of mega dosing, my skin conditioning is getting better...actually its gone heh.

Recovery wise, i'm doing better than before. Little problems with doms, occasionally get it but thats not really causing me to be crippled.
Will see how it goes.

Adding two more supplements this week - yohimbe and DHEA and will monitor the effects.

[Weib]

Ostojic SM Yohimbine: the effects on body composition and exercise performance in soccer players. Res Sports Med. 2006 Oct-Dec;14(4):289-99.

The main aim of this study was to determine the effects of yohimbine supplementation on body composition and exercise performance in professional soccer players. The athletes (20 top-level male soccer players) were allocated to two randomly assigned trials. Subjects in the yohimbine group orally ingested tablets that contains yohimbine at a dose of 20 milligrams per day in two equal doses for 21 days. Subjects in the placebo group ingested an equal number of identical-looking pills that contained cellulose. There were no statistically significant changes in body mass and muscle mass within or between trials (p > 0.05) after the supplementation protocol. Percentage of body fat significantly decreased in the yohimbine group after the supplementation protocol (9.3 +/- 1.1 vs. 7.1 +/- 2.2%; p < 0.05). Furthermore, fat mass was significantly lower in the yohimbine versus placebo trial at postsupplementation assessment (7.1 +/- 2.2 vs. 9.2 +/- 1.9%; p < 0.05). There were no changes in exercise performance indicators (bench and leg press, vertical jump, dribble and power test results, shuttle run) within or between. trials (p > 0.05). No subject reported any side effects from yohimbine. The results of the current study indicate that supplementation with yohimbine combined with resistance training does not significantly alter the body mass, muscle mass, or performance indicators in professional soccer players. Nonetheless, yohimbine supplementation appears to be suitable as a fat loss strategy in elite athletes.

My comments: Yohimbe has been around for many years, first popularized by Dan Duchaine in his seminal work "Bodyopus: Militant Weight Loss and Body Recomposition" where he proposed its use for the loss of stubborn bodyfat. Myself, Elzi Volk and others have written about its use and a forthcoming book (to be written after I finish the protein book) on Stubborn Bodyfat and how to get rid of it will tell you all you ever wanted to know about it for the same purpose.

Falsely thought to raise testosterone (because it gives men erections and has been used to treat erectile dysfunction), yohimbe is an alpha-2 receptor antagonist. This means that it blocks the effects of the alpha-2 receptors.

By means of background, the body has two general categories of receptors for the catecholamine (adrenaline/noradrenaline) hormones. They are beta and alpha receptors. Beta receptors have at least 3 variants (although beta-1 and 2 are the ones found most in humans) and alpha recpeptors have two primary variants (alpha-1 and alpha-2).

Without getting into too much complexity, you can think of beta receptors as accelerators. When they are activated, they tend to increase heart rate, blood pressure, muscle force output and of interest here, fat breakdown and mobilizatoin. You can think of the alpha receptors as brakes, when activated they tend to slow things down. Of interest here, activation of alpha-2 receptors on fat cells inhibits fat breakdown.

Of even more interest, stubborn bodyfat (especially women's lower bodyfat) has been found to contain significantly more alpha-2 receptors than beta receptors. This is part of why losing lower bodyfat is so difficult. Men's abdominal and love handle fat is at least similar.

Previous studies have suggested a role for yohimbe for fat loss but none have used athletes, hence this study. Recruiting male soccer players, the subjects received either 20 mg of yohimbine per day (in two divided doses) or a placebo and were placed on the same periodized training program (not described in the paper, unfortunately). Diet was uncontrolled which is one major limitation of the study. A number of fitness tests (bench and leg press, vertical jump, dribble and power test results, shuttle run) were done in addition to bodyfat as measured by 7 site skinfold. The fitness tests were run because of the (false in my opinion) belief that yohimbe is anabolic or improves training. The study lasted 21 days.

The subjects weighed 81 kg and started at approximately 9% bodyfat for both groups, other aspects of the subjects were also nearly identical between groups. This means that the yohimbine dose was slightly higher than the typically used/recommended .2 mg/kg dose (typically a 81 kg subject would take 16 mg/day).

Over that time period, there were no significant differences in changes in the fitness status of the subjects; all improved about equally. However, there was a difference in fat mass with the yohimbine supplemented subjects dropping from 9.3 to 7.2% bodyfat (the placebo group went from 8.9 to 9.2% but this wasn't statistically significant). And while bodymass did go up slightly in the yohimbe group, this is probably due to yohimbe's tendency to cause water retention more than anything else. No side effects were reported.

Frankly, that's a pretty major fat loss for such a short period of time with no (apparent) change in diet. As above, since diet was uncontrolled, it's impossible to know if the yohimbine group did change their diet. There is some evidence that yohimbe may affect satiety and food intake so it's possible that the supplement group reduced their food intake; coupled with the training program this could explain the fat loss.

However, the point still stands, whether the yohimbe worked by inhibiting alpha-2 receptors and mobilizing stubborn bodyfat or causing a spontaneous reduction in food intake, the fat loss still occurred.

I should mention that a lack of side-effects is not a universal report, this is especially true if yohimbe bark (as opposed to pure yohimbine HCL) is used. The various alkaloids in herbal yohimbe can cause a myriad number of side effects including chills, nausea, tremors and panic. High dose yohimbe is also used to induce anxiety attacks and people prone to such should probably stay the hell away from it. Given that its fairly easy to obtain pure yohimbine HCL, the herbal should be unnecessary in the first place. I used to use the old Twinalb Yohimbe fuel and the side effects were there. Pure yohimbine HCL (I've used the Primaforce brand) doesn't generate nearly the same issues. Note that yohimbine HCL can only be sold in amounts of 2.5 mg per pill so you end up having to take a bunch of them at once.

Starting with a half dose to assess tolerance is still probably the best approach. I also dont feel that splitting the dose across the day is the best way to use it; I prefer a combination of yohimbe and caffeine 30-60 minutes before aerobic training. The yohimbe/caffeine mobilized fatty acids which are then burned off during the cardio. You'll have to wait for my stubborn bodyfat book for more details than that.

pull it off some forum, apparently its from lyle's newsletter.

[Weib]

A little horse sense

One of the biggest logical flaws of the “don’t mix carbs with fat” philosophy is that it’s extremely rare for individuals consuming more than one or two meals per day to be in a truly fasted state aside from waking in the morning. For most of us, there’s a constant meal absorption overlap that keeps insulin, glucose, amino acids, and lipids in the blood above fasting levels. Since we spend most of our waking hours in the ‘fed state’, it’s flat-out silly to think we can avoid this overlap by simply separating our carb and fat intake by a few hours. So, is this mixture of substrates in circulation a bad thing for fat loss in the first place? Buckle up, here comes the cold, hard data.

http://avidityfitness.net/2008/09/24/ca ... after-all/

[Weib]

Looking at the body of evidence as a whole, fish oil (or increased fish consumption) has great potential for improving cardiovascular health. But for reducing body fat, the effects are minor to nonexistent. Let’s not forget that fish oil isn’t some magical negative-calorie food. It still contains 9 calories per gram, and no matter how much of those calories are used in its processing within the body, it’s still a net gain in calories after consumption. To sum everything up, fish oil has health benefits, as well as potential risks. It’s certainly not a matter of more-is-better. It might have minor fat loss effects in the obese and overweight population, but their fat loss effect in general is far from conclusively established. Get a variety of fats in your diet, and get them from whole foods whenever possible. Fish oil is merely one of many agents that can contribute to optimal health within the context of well-balanced nutrition. Keep it in perspective, and keep your eye on the facts.

http://alanaragon.com/fish-oil.html

[Weib]

Conclusions (For Now)

GI is gives us clues to the behavior of certain foods, but that's exactly the main point of this article. Clues; mere hints are all we get from our current knowledge of GI. Successful application of GI is most consistent when we use higher GI sources to enhance the speed of postworkout glycogenesis, and that's about it. Carb foods are better judged on the basis of degree processing, refinement, or alteration/removal of micronutrition -- NOT on the basis of GI, or even GL. This is as good a time as any to crush the folly of what I call "food discrimination". A prime example of this is cutting out potatoes on the basis of GI. This happens all the time, & the dieter takes pride in thinking he/she is being prudent. Well, the critical thing to realize here is that all food species in nature have unique nutrient profiles. Therefore, unique nutritional benefit can be derived from each species. The natural matrix of plant &/or animal tissue cannot be duplicated in the lab, & hence there are many unidentified beneficial agents in, say, the humble potato. As a matter of trivia, it surpasses bananas in potassium & vitamin C concentration. Not to mention, it provides default hydration, and of course is a great whole-food source of starch. The list goes on & on.

Satiety, micronutrient density, insulin response, & surrounding factors altering glucose kinetics are all much like a roll of the dice in terms of bottom-line certainty & reliability of GI. Like all things in science - especially the deep bubbly cauldron that is applied nutritional science - it ain't all that simple. All avenues in this area are winding & complex.

http://alanaragon.com/elements-challeng ... index.html

[Weib]

http://www.thelivinlowcarbshow.com/podp ... donald.mp3

Pretty much without fail, every decade seems to see the resurgence of the idea that extremely low-carbohydrate diets have a ‘metabolic advantage’ over carb-based diets; that is the claim is made that the very low-carbohydrate diet will generate more weight or fat loss at the same (or sometimes even a higher calorie level).

http://www.bodyrecomposition.com/resear ... eview.html

[Weib]

Elements Challenging the Concept, Principle, & Strict Application of Glycemic Index
PREFACE

The fact is that many bodybuilding, health, & fitness enthusiasts stake their entire moral judgment of carbohydrate foods based on their glycemic index (GI) without realizing that a considerable set of confounders challenges its validity. Becoming blindly enamored with something that may enhance our physiques &/or health is natural, and something we've all been guilty of. But alas, the GI data is neither perfect nor consistent, nor is it free of bugs. Consider the following facts, and re-think your obsession with GI & what you think you know about GI.

A POSSIBLE DEFINITION SHIFT

The current general definition of GI is a food's ability to raise blood sugar, which almost automatically is regarded in terms of glucose entry into the blood. However, recent eye-opening research by Schenk & colleagues clearly showed that the rate of disappearance of glucose from systemic circulation is an important determinant of GI - not just glucose's rate of entry into circulation [1]. They found that the lower GI of bran cereal was due to a quicker/sooner surge of insulin sweeping glucose out of circulation - not a slower appearance/entrance of glucose as once assumed. Although strictly speculative at this point, this phenomenon may have possible performance detriment implications (ie, rebound hypoglycemia) in sensitive individuals if meals of this nature are mistimed relative to training.

DETERMINATION VS. APPLICABILITY

GI values are determined in an overnight-fasted state using isolated foods. This is not a reflection of real life, where the digestion/absorption of previous meals, as well as the context of the carbohydrate food can drastically alter GI.

AFFECTING FACTORS

The interplay of many variables can either raise or lower GI, and are often difficult to control. Increased acidity, the presence of fiber, fat, and certain protein foods can lower glycemic response. Reduced particle size, greater ripeness, and heat in cooking can raise glycemic response.

GLYCEMIC LOAD DISPARITY

Glycemic load (GL), which is the amount of carbohydrate per serving or unit of volume, is not always directly proportional to GI. For example, watermelon has a GI of 72, which is considered high. Low-GI advocates have vilified watermelon without realizing the fact that it has a relatively low glycemic load, approximately 6g carbohydrate per 4oz serving. The same disparity of GI & GL applies to carrots, potatoes, and even sports drinks such as Gatorade.

SATIETY INDEX DISPARITY

Lower-GI foods have been associated with greater satiety, but most of this data comes from single-meal experimental designs. Longer-term studies on GI & satiety are conflicting, and not always controlled for energy intake and energy density of the test meal [2]. In the longest study to date on GI & satiety is an ad libitium 30d crossover design where Kiens & Richter observe no difference in amount of consumption [3]. In this metabolic study, a LOWER resistance to insulin was seen in the high-GI group at the end of the trial. GI does not reliably correspond with satiety index (SI). White rice, wheat bread, and potatoes all have high GIs, but rank among the top of the list for delaying the onset of hunger. In fact, Holt's team found that potatoes had by far the highest SI of all the foods tested [4].

INSULIN ISSUES

As a classic example of chaos physics, the typical rules that predict GI do not necessarily help in predicting insulin response. Unfortunately for GI-conscious people, insulin is usually what they are trying to control. Despite having a very low GI of 15-36, milk and yogurt have a high insulin index equivalent to that of the high-GI white bread [5]. Baked beans, another low-GI food, have a very high insulin index of 120. Cheese, beef, and fish have II's that are comparable to many carbohydrate foods.

Coingestion of fat with carbohydrate slows gastric emptying and thus the release of glucose into the blood, ultimately lowering GI. While this is usually true for GI, the degree of insulin response evoked by this combination is determined by the degree of the fat's saturation. For example, Collier & others observed that butter coingested with potato not only fails to lower postprandial insulinemia, it actually causes a synergistically heightened insulin response, even in healthy subjects [6,7].

Foods that should have a low GI due to their high fat content do not always have a low GI. Examples are fries, cookies, croissants, and doughnuts. Incidentally, these foods also have a high insulin index, presumably because their fat is mostly saturated. As of this writing, full-fat ice cream (low GI of appx 37) has not been tested for II, but it's safe to assume that it probably has disparate GI & II values.

Rasmussen & colleagues observed no increased insulin response with the addition of 40g or 80g olive oil, but saw a significant increase with 50g & 100g butter [8]. Joannic's team observed a coingestion of carbohydrate with fats of increasing degree of unsaturation having a corresponding decrease in insulin response [9]. A more recent study by Robertson & colleagues compared the effect of MUFA, PUFA, & SFA coingestion with carbohydrate and observed SFA's superior ability to raise postprandial insulin levels [10].

Coingestion of protein with carbohydrate is often recommended to lower GI, but it doesn't necessarily lower insulin response. Gannon & Nutall's research on type-2 diabetics showed that coingested cottage cheese & glucose raised insulin levels beyond either food separately, indicating a synergistic effect [11]. Van Loon & colleagues saw a similar phenomenon when comparing the insulin effect of various carb-protein/amino acid and carb-only solutions [12]. Those containing free leucine, phenylalanine, & arginine, and the drinks with free leucine, phenylalanine, & wheat protein hydrolysate were followed by the largest insulin response (101% and 103% greater, respectively, than with the carb-only solution).

GI & OBESITY - SLIM CHANCE FOR CORRELATION

a systematic review of human intervention studies comparing the effects of high and low-GI foods or diets arrived at the following results [13]:
---- in a total of 31 short-term studies, low-GI foods were associated with greater satiety or reduced hunger in 15 studies, whereas reduced satiety or no differences were seen in 16 other studies.
---- low-GI foods reduced ad libitum food intake in 7 studies, but not in 8 other studies. In 20 longer-term studies (<6 months), weight loss on a low-GI diet was seen in 4 and on a high-GI diet in 2, with no difference recorded in 14 studies.
---- an exhaustive assessment of these human intervention trials found no significant difference in the average weight loss between low & high GI diets. in conclusion, the current body of research evidence does not indicate that low-GI foods are superior to high-GI foods in regard to treating obesity.

SO, WHAT?!

Don't get it twisted, GI is a definitely useful tool that gives us clues to the behavior of certain foods, but that's exactly the main point of this article. Clues; mere hints are all we get from our current knowledge of GI. Successful application of GI is most consistent when we use higher GI sources to enhance the speed of postworkout glycogenesis, and lower-GI starch foods tend to be more micronutrient dense than their higher-GI counterparts, but that's really about the extent of it. Satiety, insulin response, & surrounding factors altering glucose kinetics are all much like a roll of the dice in terms of bottom-line certainty & reliability. Like all things in science - especially the deep bubbly cauldron that is applied nutritional science - it ain't all that simple. All avenues in this area are winding & complex.


References for you research nerds:

1) Schenk S, et al. Different glycemic indexes of breakfast cereals are not due to glucose entry into blood but to glucose removal by tissue. Am J Clin Nutr 2003;78(4):742-8.
2) Pi-Sunyer FX. Glycemic index and disease. Am J Clin Nutr 2002 Jul;76(1):290S-8S.
3) Kiens B, Richter EA. Types of carbohydrate in an ordinary diet affect insulin action and muscle substrates in humans. Am J Clin Nutr 1996;63:47-53.
4) Holt SH, Miller JC. A satiety index of common foods. Eur J Clin Nutr 1995 Sep;49(9):675-90.
5) Ostman EM, et al. Inconsistency between glycemic and insulinemic responses to regular and fermented milk products. Am J Clin Nutr 2001; 74(1):96-100.
6) Collier G, et al. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr 1983;37(6):941-4.
7) Collier G, et al. The acute effect of fat on insulin secretion. J Clin Endocrinol Metab 1988;66(2):323-6.
Rasmussen O, et al. Differential effects of saturated and monounsaturated fat on blood glucose and insulin responses in subjects with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1996 Feb;63(2):249-53.
9) Joannic JL, et al. How the degree of unsaturation of dietary fatty acids influences the glucose and insulin responses to different carbohydrates in mixed meals. Am J Clin Nutr 1997 May;65(5):1427-33.
10) Robertson MD, et al. Acute effects of meal fatty acid composition on insulin sensitivity in healthy post-menopausal women. Br J Nutr 2002;88(6):635-40.
11) Gannon MC, et al. Metabolic response to cottage cheese or egg white protein, with or without glucose, in type II diabetic subjects. Metabolism 1992;41(10):1137-45.
12) van Loon LJ, et al. Plasma insulin responses after ingestion of different amino acid or protein mixtures with carbohydrate. Am J Clin Nutr 2000;72(1):96-105.
13) Raben A. Should obese patients be counselled to follow a low-glycaemic index diet? No. Obes Rev. 2002 Nov;3(4):245-56.

http://forum.bodybuilding.com/showthrea ... did=283787

[Weib]

INTRO

GOAL CLARIFICATION & THE NATURE OF OPTIMA

pre, during, & postworkout nutrition is different for different sports. most of the data on this subject pertains to endurance athletes, and doesn't necessarily apply to bodybuilders. this is the classic conflict of arguments when different goals aren't clarified. what i'm gonna discuss is nutrition for bodybuilding resistance training, so let's get that straight before we dive in. another important concept to bear in mind is the fact that nutrient timing is of secondary importance to total amounts of each nutrient. i also want to make it clear that we're nitpicking over what's OPTIMAL. for example, total amount of carbohydrate is in fact more important than its glycemic index. it's important to note that there are quite a bit of confounding (validity-challenging) variables related to GI, which i covered in depth here. keep in mind that it's the general theory and format that you should focus on, because there's no way that i can provide a comprehensive list of example meals without boring myself to death, and everyone has their personal taste.

INDIVIDUAL DIFFERENCES

variations in total amounts will be determined by your general body mass & individual phyz, you'll just have to trial & error it out as with all plans. littler guys will do fine at the lower ranges, mega-mooses will do well at the higher ranges, and average joes will find the middle of the ranges to be good starting points from which to monitor progress. i'd like to make it perfectly clear that this article is an attempt to cater to the majority of trainees who may read it. as with all advice from ornery oracles, you MUST adapt it to your individual response & measure it against your progress, or lack thereof, and adjust accordingly. i highly recommend that you feel free to go "outside of the lines" of what i've written if/when necessary, and find out what works for you as an individual. the concept of trial & error being the ultimate judge - despite sound theoretical starting points - is not emphasized nearly enough in tutorials.

without further ado...


PRE-PREWORKOUT: THE GLYCOGEN FACTOR

glycogen is the limiting fuel for exercise in the glycolytic range of the energy substrate continuum. this means that even though bodybuilders aren't gonna be running marathon or growing impotent from sitting their asses on a hard bike seat doing the tour de france, glycogen is still important for muscular work in the rep ranges that primarily cause hypertrophy. many bodybuilders i know are on a "permanent precontest" phase, and keep their carbs low no matter what, and are really frustrated with their gains. actual amount of total carbs daily is another discussion, but suffice it to say that it's really tough to gain muscle - no matter how much protein you're chuggin' - when you're constantly averaging below 2/3 of your bodyweight a day in carb grams. this may be warranted on a cyclical basis for some folks during a precontest cut, but for general purposes & gaining muscle, you're better off averaging somewhere above this amount -- unless you've either been pathologically afraid of, or metabolically challenged by carbohydrate for a long enough duration for your body to adapt & get by on amounts chronically lower than this.


PREWORKOUT

OBJECTIVE

the objective here is to promote sustained carbohydrate & amino acid availability, minimize muscle catabolism, and spare glygogen as much as possible. it's important to note here that research is quite conflicting on the issue of GI & exercise performance. much of the latest studies show no real difference. the actual amount & physical nature of the meal depends on how soon your schedule allows you to eat or drink before training. there are at least 2 acceptable scenarios..

COMPOSITION

scenario one: a solid, full-sized balanced meal finished 60-90 minutes preworkout consisting of 30-60g protein (0.2-0.25g/lb target BW) + 40-80g carb (0.33g/lb target BW). there are endless examples of how this can be constructed, & heres just one:
---- 5-8oz of any type of land or sea animal flesh
---- 1-2 cups of whole grain product or starchy vegetable or legume /or/ fistsize sweet potato, etc. Have your preference, focus on total amount rather than food subtype.
---- 1 or more cups fibrous vegetable like salad greens, broccoli, cauliflower, asparagus, spinach, kale, cabbage, onions, even carrots, etc, etc

[or]

scenario two: a liquid meal or shake finished 30-0 min preworkout:
---- 20-50g protein (0.15-0.2g/lb target BW). Whey is preferred for its BCAA content & gastric tolerability for most.
---- 40-80g (0.33g/lb target BW). Any fruit works well here, so does old fashioned oats. a solid case can be built for a combination of both. whether you include water/milk is a matter of digestive tolerance. milk just gets the anabolic/anticatabolic cascades rolling for those in a severe hurry to gain muscle. adding fat to this shake can slow the release of nutrients & benefit those who train for significantly more than 90 min, offering extra protection against energy dips - especially if you don't consume a dilute carb solution during your workout. note that most people will do fine without the fat.

to reiterate the factor of individual differences, don't be afraid to go outside of the listed guidelines & exceed the upper limit of listed carb intake as needed to power you through your training. conversely, don't be afraid to dip below it given your gastrointestinal tolerance for exogenous substrate during or pretraining.


DURING WORKOUT

OBJECTIVE

the same objectives as the preworkout meal apply here (to promote sustained carbohydrate availability & to a lesser degree amino acid availability, minimize muscle catabolism, and spare glygogen) - with the added objective of maximizing water availability & minimizing gastrointestinal upset.

COMPOSITION

again, be aware that we are talking bodybuilding workouts and not triathalon training. i am an advocate of keeping it simple and watering yourself down thoughout the workout with.. you guessed it, pure water. if you did your homework with the right construction & timing of the preworkout meal (& of course if you're sipping your preworkout shake during training which is fine too), there's little need for the bodybuilder to take in much else. now granted, if you were a boxer, triathlete, soccer player, basketball player, or marathoner trudging away for far past 90 minutes continuously in an endurance event, definitely sip the gatorade-type 4-8% carb solution throughout the workout, and shoot for 40-60g carbs/hr. Adding a scoop of whey (20g) to this solution will optimize it for the purposes of preserving muscle protein balance.

POSTWORKOUT

OBJECTIVE

The goal for postworkout nutrition is to maintain the elevated blood levels of glucose, amino acids, and insulin caused by the preworkout meal. The postworkout meal is mistakenly viewed as the most important meal of the day, which is BS. why? because if you're not properly fueled prior to this point, you might compromise your training performance, and you won't achieve the same level of protein synthesis & antiproteolysis. Thus, it's equally important in the large scheme of things

COMPOSITION

i'm not biased towards a shake-only postworkout philosophy, as long as either type contains a liquid component. 2 equally effective scenarios are:

scenario one: as soon as possible postworkout - or even at the tail end of the workout, say, 10-20 minutes before it's over. i start chugging my postworkout shake 60 minutes into my workout, regardless of how long my workout takes.
---- 30-60g protein (0.25g/lb target BW). whey again is pretty cheap & works great here. research shows that postworkout protein doesn't inhibit glycogen synthesis, and can improve protein synthesis. this means that you can hedge your anabolic & anticatabolic bets by taking in a sizable amount of protein postworkout. whey happens to be a highly insulinogenic protein, so this is ideal at this point.
---- 60-120g (0.5g/lb target BW). dextrose & maltodextrin have traditionally been emphasized as ideal for postworkout because of their high-GI. however, i have issues with going pure dex for postworkout for a couple of reasons - and they have nothing to do with the threat of insulin resistance, because that whole scenario applies to a completely different population. first off, you can get some default dex within fruit or milk. secondly, pure dex has no micronutrition; basically it's empty calories with little to no value for overall health. adding fruit to your postworkout mix of carbs can potentially benefit folks who train with a high volume & do a lot of cardio (ie, precontest). the protection of liver glycogen status under such conditions can maintain the centrally neurologic signaling of the "fed state" and hence prevent lean tissue catabolism -- especially during hypocaloric balance.

okay, so to be practical, simple examples are: 1.5 cups dry oats (OR) 1 cup dry oats + 1 banana (or pick any other fruit you like). these are just 2 examples out of many possibilities.

milk considerations: whether or not you add milk to your postworkout shake depends upon personal preference and tolerance. the cons of milk are that many folks have some degree of lactose intolerance or milk allergy, and therefore are excluded from the possibility.

scenario two: ASAP postworkout - a solid-food meal consisting of:
---- 30-60g protein (0.25g/lb target BW) in the form of lean flesh, all types are fine, 5-8oz suffices.
---- 60-120g starchy carbs (0.5g/lb target BW), good examples are white or brown rice, and all types of potatoes & breads. my bias and preference here is to include a serving of fruit.
---- water or milk, pick your poison.

now.. can you exceed the limits I listed postworkout? of course! your training program, body mass, & physiology may actually scream for it. this is merely a point of reference for the masses to digest, absorb, & process accordingly (gotta love corny nutrition puns).

The protocol I recommend currently is strikingly similar to the original, with a few VERY insignificant tweaks. Note that TBW = target bodyweight:

60-90 minutes preworkout, have a solid, balanced meal:

Protein = 0.25g/lb TBW
Carbs = 0.25g/lb TBW
Adding fat at this point is fine, use your discretion as long as it fits into your macro goals. Note that this meal is skipped if you train 1st thing in the morning.

[OR]

30-0 minutes preworkout - (and/or sipped throughout the workout), have a liquid or easily digested meal:

Protein = 0.25g/lb TBW
Carbs = 0.25g/lb TBW
If you were going to train for close to or more than 2 hours continuously, it would definitely benefit you to have this extra preworkout meal either immediately prior to, or sipped during training. Keep the fats here incidental & not added if you're prone to gastric distress during training.

Within 30 minutes postworkout, have either a liquid or solid meal:

Protein = 0.25g/lb TBW
Carbs = 0.25-0.5g/lb TBW, depending on how carb-restricted your diet is.
Amount of fat here doesn't matter as long as your daily target is hit.

Post-postworkout is simply your next sheduled meal, whether it's 1, 2, or 3 hrs later simply doesn't matter - especially if your immediate postworkout meal was designed as above.

NOTE: The small differences are mainly geared toward simplifying the guidelines. The rest of the recommendations about food types are pretty much the same. Also note that I no longer give a damn about GI, it doesn't really make a difference one way or another. If you want high GI carbs pre and/or during training, go for it. As time has passed, GI has proven itself to be a worthless, irrelevant index. Insulinogenesis is a separate issue, and slight elevations during & postworkout is a great idea. This accomplished by both food type & food amount, the latter being more important. To boot, the necessary insulin elevations for maximal net gains in protein balance are easily met without specific attempts at spiking it up. There's obviously a lot more to this, but that's the important basics. The rest is fringe.

http://forum.bodybuilding.com/showthread.php?t=272067