How to Get Ripped to the Bone - Mind And Muscle

bodybuilder lifting heavy dummbellsby: Anssi Manninen, M.H.S.
How to Get Ripped to the Bone ?

If you’ve studied exercise physiology or nutrition, you have probably heard the old biochemical mantra “fats burn in a carbohydrate flame.” I also remember reading it in the exercise physiology textbook, but I later realized it was just another metabolic urban legend. A more accurate mantra would be that both muscle fats and carbs burn in an amino acid flame.

Probably the most ridiculous urban legend in the nutrition worlds is that low carb intake leads to progressive loss of muscle mass (muscle protein). Fortunately, the human body is way smarter than some nutrition “experts.” True, animals share the metabolic deficiency of the total (or almost total) inability to convert fatty acids to glucose (blood sugar). So, the primary source for a substrate for gluconeogenesis (the formation of glucose from non-carbohydrate molecules) is amino acid, a building block of protein, with some help from glycerol from fat tissue triglycerides (i.e., storage form of fat; contains one glyceride molecule plus three fatty acid molecules).

However, when the rate of mobilization of fatty acids from fat tissue is accelerated, as, for example, during a very-low-carb diet, the liver produces ketone bodies. The liver cannot utilize ketone bodies and thus, they flow from the liver to extra-hepatic (outside of the liver) tissues (e.g., brain, muscle) for use as a fuel. Simply stated, ketone body metabolism by the brain displaces glucose utilization and thus spares muscle mass. In other words, the brain derives energy from storage fat during a very-low-carb diet. This article examines the effects of the very-low-carb diets on fat loss and muscle mass preservation.

Very-Low-Carb Diets Burn Lard like there´s No Tomorrow

In general, strength-power athletes substantially decrease carb intake during the cutting phase (when they seek to “cut” fat before competition). The hormonal changes associated with a very-low-carb diet include a reduction in the circulating levels of insulin along with increased levels of glucagon (a hormone secreted in response to a fall in blood sugar levels). Insulin has many actions, the most well-known of which is stimulation of glucose and amino acid uptake from the blood to various tissues. This is coupled with stimulation of anabolic processes (or synthetic reactions) such as protein, glycogen and fat synthesis. (Glycogen refers to the storage form of carbs in human body).

Glucagon has opposing effects, causing the release of glucose from glycogen and stimulation of gluconeogenesis and fat mobilization. So, the net stimulus would seem to be for increasing muscle protein breakdown. However, well-controlled studies indicate that a very-low-carb diet results in body composition changes that favor loss of fat mass and preservation (or even increase) in lean body mass.

In 1971, Dr. C.M. Young and colleagues compared three diets containing the same amounts of calories (1,800 kcal/day) and protein (115 grams/day) but differing in carb content (30, 60 and 104 grams). After nine weeks on the 30-gram, 60-gram and 104-gram carb diets, weight loss was 16.2, 12.8 and 11.9 kilograms (26.2 pounds) and fat accounted for 95, 84, and 75 percent of the weight loss, respectively. Although these results should be interpreted cautiously given the low number of subjects, we must conclude that the very-low-carb group (30 grams/day) burned fat like there’s no tomorrow while maintaining muscle mass. This study was published in the well-respected American Journal of Clinical Nutrition, but was ignored by the high-carb-is-the-only-way-to-go camp.

More recently, Dr. Jeff Volek and his co-workers at the University of Connecticut examined the effects of a six-week very-low-carb diet on total and regional body composition and the relationship to fasting hormones. Twelve healthy normal-weight men switched from their habitual diet (48 percent carb) to a very-low-carb-diet (eight percent carb) for six weeks and eight men served as controls, consuming their normal diet. Subjects were encouraged to consume adequate dietary energy to maintain body mass during the intervention.

The results indicated that fat mass was significantly decreased (-3.4 kilograms or –7.5 pounds) and lean body mass significantly increased (+1.1 kilograms, or +2.4 pounds) at week six. However, there were no significant changes in composition in the control group. So, Dr. Volek concluded that a very-low-carb diet resulted in a significant reduction in fat mass and an accompanying increase in lean body mass in normal-weight men. In other words, the entire loss in bodyweight was from lard.

Not surprisingly, the results also indicated that the very-low-carb diet led to a significant decrease in insulin and that there was a significant correlation between the decrease in insulin and the decrease in body fat. Finally, there were no adverse responses in any of the biochemical variables studied. This well-controlled study was published in the prestigious scientific journal Metabolism, but the mainstream nutrition experts largely ignored it. (“What the heck is this Metabolism anyway? I only read the Journal of the American Dietetic Association”).

Lastly, Dr. KA Mecklin and colleagues at the University of Guelph in Canada examined the effects of a very-low-carb diet on weight loss and biochemical parameters in overweight women. Twenty women completed an eight-week trial that reduced their daily carb intake from 232 to 71 grams. The average weight loss was five kilograms (11 pounds), with a loss of 3.4 percent body fat (four kilograms, or 8.8 pounds) and a loss of one kilogram (2.2 pounds) of lean body mass (mostly water). Furthermore, systolic blood pressure decreased by an average of 9.0 mmHg and diastolic blood pressure decreased by 7 mmHg. Also, total cholesterol decreased significantly, all of which was accounted for by a decrease in LDL (“bad”) cholesterol with no change in HDL (“good”) cholesterol. Finally, triacylglycerols (harmful blood fats) decreased significantly.

So, the authors concluded, “Carbohydrate restriction to 70 grams or less with concomitant energy restriction, without changes in protein or fat consumption, promotes weight loss and improvements in body composition, blood pressure and blood lipids [fats] without compromising glucose tolerance in moderately overweight women.”

How is Preservation of Muscle Mass Brought About?

There are at least three possible mechanisms:

1. Adrenergic stimulation (adrenergic refers to liberated or activated by adrenaline or a substance like adrenaline). The increase in blood adrenaline may be involved. Low blood sugar is a potent stimulus to adrenaline secretion and it’s now clear that skeletal muscle protein mass is also regulated by adrenergic influences. A study by Dr. T. Kadowaki and co-workers demonstrated that adrenaline directly inhibits breakdown of skeletal muscle.Further studies have demonstrated that when beta-2-adrenoceptor agonists (e.g., clenbuterol) are given in high doses, extended use produces significant increases in muscle mass in mice, rats and cattle. On the other hand, the adrenergic systems are important in stimulation of fat storage breakdown.2. Ketone bodies. As noted above, the liver produces ketone bodies during very low carbohydrate intake and they flow from the liver to extra-hepatic tissues (e.g., brain, muscle) for use as a fuel. In addition, ketone bodies exert a restraining influence on muscle protein breakdown. If the muscle is plentifully supplied with other substrates for burning (such as fatty acids and ketone bodies, in this case), then the burning of muscle protein-derived amino acids is suppressed.Dr. KS Nair and co-workers reported that beta-hydroxybutyrate (beta-OHB, a major ketone body) decreases leucine (an amino acid) burning and promotes protein synthesis in humans. Although blood concentrations of beta-OHB in their subjects during the infusion (the introduction of a solution especially into a vein) of beta-OHB were much lower than concentrations observed in humans during fasting; leucine incorporation into skeletal muscle showed a significant increase (five to 17 percent). In other words, beta-OHB stimulated muscle protein synthesis.

3. Growth hormone (GH) has a major role in regulating growth and development. GH is a protein anabolic hormone and it stimulates muscle protein synthesis. As low blood sugar increases GH secretions, we can assume the very-low-carbohydrate diet increases GH level.

Thyroid Involvement?

It has also been suggested that thyroid hormones may be involved. The principal hormones secreted by the thyroid are thyroxine (T4) and triiodothyronine (T3). T3 is also formed in the peripheral tissues by deiodination of T4. Small amounts of reverse triiodothyronine (RT3) and other compounds are also found in thyroid venous blood. T3 is more active than T4, whereas RT3 is inactive.

Thyroid hormones stimulate diverse metabolic activities in most tissues, leading to an increase in basal metabolic rate (i.e., resting energy expenditure). Not surprisingly, the onset of total starvation is marked by a decrease in the level of the active thyroid hormone triiodothyronine (T3) in the blood. There is also a shift toward production of inactive RT3, at the expense of active T3. Obviously, the effect of the fall in T3 concentration is to reduce overall metabolic rate and to reduce the rate of breakdown in muscle.

However, Dr. Volek and colleagues reported that a very-low-carb diet caused an increase in total thyroxine (T4) and the free T4 index. (A free T4 index can be calculated by measuring total T4 and multiplying it by the percentage of labeled T4 taken up by certain chemicals that bind free [biologically active] T4 in the blood). Also, they noted a non-significant change in T3 suggesting that T3 and T4 binding proteins were not affected by carb restriction. So, Dr. Volek suggested the significant increase in total T4 may represent an increase in the biologically active hormone available to cells.

Twelve obese women were studied by Dr. R.A. Mathienson and co-workers to determine the effects of the combination of an aerobic exercise program with either a high-carb, very-low-calorie diet or a low-carb, very-low-calorie diet on resting metabolic rate and blood thyroid hormones. Following a maintenance period, subjects consumed one of the two very-low-calorie diets for 28 days. In addition, all subjects participated in sub-maximal exercise sessions at 60 percent of maximal aerobic capacity three times per week.

Results indicated that bodyweight decreased significantly more for low-carb dieters than for high-carb dieters. Blood T4 was not significantly affected during the very-low-calorie diets. Although blood T3 decreased during the very-low-calorie diets for both groups, the decrease occurred faster and to a greater magnitude in low-carb than high-carb dieters. However, blood T3 of both groups returned to baseline concentrations following one week of the 1,000-calorie diet. Furthermore, both groups exhibited similar progressive decreases in resting metabolic rate during treatment (12.4 percent for low-carb and 20.8 percent for high-carb). In summary, it appears the old mantra “eat enough carbs to boost thyroid hormones” is another nutritional urban legend.

Ripped-to-the-Bone Program

    • This program is targeted to those who wish to maximize fat loss while maintaining muscle mass.
    • Follow a high-protein, low-carb, moderate-fat diet. Good protein sources include fish, eggs, lean meats and chicken. Also, include some non-fat dairy products in your diet because inadequate calcium intake blunts fat loss.
    • Choose only low-glycemic, high-fiber carb sources (vegetables, legumes, etc.). However, before and immediately after resistance exercise take a sugar-free low-carb protein drink to boost muscle protein anabolism.
    • Useful supplements: multivitamin-mineral complex and pure creatine powder or low-carb creatine formula.
    • Possibly useful supplements: HMB (3 grams/day) and CLA (3.4-6 grams/day).
    • Drink a lot of water and other calorie-free fluids.

Protein Update: Harvard Nutritionists Endorse High-Protein Diets

Recently, Drs. Thomas Halton and Frank Hu at the prestigious Harvard School of Public Health published an excellent review of high-protein diets and weight loss in the well-respected Journal of the American College of Nutrition. The take-home messages were the following:

1. There is convincing evidence that proteins exert an increased thermogenic effect (production of heat) and that high-protein diets increase satiety compared to lower-protein diets. High-protein diets can also facilitate weight loss/fat loss.

2. Exchange of protein for carbs has been shown to improve blood lipids and higher-protein diets have been associated with lower blood pressure and reduced risk of coronary heart disease.

3. There is little if any evidence that high-protein intake has adverse effects.

Similarly, the recent paper by Dr. Klaas Westerterp at Maastricht University in the Netherlands published in Nutrition and Metabolism ( concluded, “Protein plays a key role in bodyweight regulation through satiety related to diet-induced thermogenesis.”

Richard Fleming: The Ultimate Fake, in My Opinion

So, how the heck is it possible that some health care professionals and even scientists still claim high-protein diets do not facilitate fat loss and may have significant health risks? Hmm… I believe the main reason is the pseudo-scientific propaganda distributed by the animal rights activists. For example, Richard Fleming at the Fleming Heart and Health Institute has published two high-protein/low-carbohydrate diet studies (that I believe are fake) in lesser-known journals.

The “study” by Fleming published in Preventive Cardiology was supposedly designed to investigate the effects of several diets on weight loss, serum lipids and other cardiovascular disease risk factors. According to Fleming, 100 men and women followed one of four dietary programs for one year. However, there’s every reason to believe that this report was fabricated. For example:

1. Fleming is the sole member of “The Fleming Heart and Health Institute.”

2. Although this study supposedly followed 100 men and women, the report lists no co-authors, nurses, dietitians or technicians who may have assisted in the trial. Obviously, such a large clinical trial would require substantial manpower.

3. Conducting randomized intervention trials is extremely costly. Nevertheless, the paper does not list a single source of funding, even though funding acknowledgement is standard procedure in any respected, peer-reviewed scientific journal.

4. Fleming claims the participants “were randomly assigned to one of the four dietary regimens based upon dietary preferences.” However, if patients were assigned to diets based on their dietary preferences, they weren’t randomly assigned.

5. This is the only published paper to have ever reported greater weight loss among high-carb dieters. Also, the high-carb dieters supposedly recorded marked triglyceride (harmful blood lipid) reductions and the low-carb dieters supposedly experienced an initial modest decrease, which then reversed itself and ended up slightly higher than baseline levels by the end of this “study.” Oddly, all other studies published in the leading medical journals have reported that low-carb diets produce either similar or greater reductions in blood triglycerides than calorie-restricted high-carb diets.

6. Richard Fleming is an active member of the Physician Council for Responsible Medicine (PCRM), a group of radical vegetarian zealots with a long history of distorting scientific facts in order to advance their nonsensical agenda. And PCRM has long-standing ties with People for the Ethical Treatment of Animals (PETA), an extreme animal rights organization that has funneled over $850,000 to its pseudo-medical front group. According to the PCRM website, “A sincere thank-you to the countless physicians and others who have lent their time and expertise in 2003, including… Richard Fleming.”

7. Richard Fleming wrote to the New York medical examiner’s office requesting a copy of Robert Atkins’ death report. And after receiving the report, he passed a copy along to his friends at the PCRM. The PCRM in turn contacted The Wall Street Journal.

Questions or comments on this article? Post them in the Avant Labs Forums for live feedback from Anssi H. Manninen, as well as the Mind and Muscle staff and fellow readers!


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2. Manninen AH. High-protein weight loss diets and purported adverse effects: where is the evidence? Sports Nutr Rev J, 2004;1:45-51. Free full-text article available

3. Frayn KN. Metabolic Regulation: A Human Perspective. Oxford, UK: Blackwell Science, 2003.

4. Ganong WF. Review of Medical Physiology. New York: Lange Medical Books/McGraw-Hill, 2001.

5. Young CM, Scanlan SS Im HS et al. Effect on body composition and other parameters in obese young men of carbohydrate level of reduction diet. Am J Clin Nutr, 1971;24:290-296.

6. Volek JS. Sharman MJ, Love DM et al. Body composition and hormonal responses to a carbohydrate-restricted diet. Metabolism, 2002; 51:864-870.

7. Nair KS Welle SL, Halliday D, Cambell RG. Effect of b-hydroxybutyrate on whole-body leucine kinetics and fractional mixed skeletal muscle protein synthesis in humans. J Clin Invest, 1988;82:198-205.

8. Mathieson RA, Walberg JL, Gwazdauskas FC et al. The effect of varying carbohydrate content of a very-low-calorie diet on resting metabolic rate and thyroid hormones. Metabolism, 1986;35:394-398.

9. Meckling KA, Gauthier M, Grubb R, Sanford J. Effects of a hypocaloric, low-carbohydrate diet on weight loss, blood lipids, blood pressure, glucose tolerance, and body composition in free-living overweight women. Can J Physiol Pharmacol, 80:1095-1105, 2002

10. Turpin A, Talbott SM, Feliciano J, Bucci LR. Systematic and critical evaluation of benefits and possible risks of nutritional ergogenic aids. In: Wolinsky I, Driskell JA, eds. Nutritional Ergogenic Aids. Boca Raton, FL: CRC Press, pp. 469-504.

11. Halton TL, Hu FB. The effects of high-protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr, 23:373-385, 2004.

*** This article originally appeared in Muscular Development magazine, January 2005

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