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The components of energy expenditure are illustrated in figure 1. Metabolic rate is affected by many parameters such as eating (caloric consumption as well as dietary com-position), activity (dependent on type, intensity, and duration of activity), lean body mass, age, sex, hor-mones, and drugs .Since all of the energy expended by the body is ultimately converted to heat (except when work is performed outside the body), metabolic rate can be determined by the amount of heat energy liberated by the body (Guyton, 1976). A calorimeter can be used to directly measure the heat given off by the body. However, since greater than 95% of the energy lib-erated by the body is derived from the reaction of foods with oxygen, the metabolic rate can also be calculated from the rate of oxygen consumption (Guyton, 1976). In many studies metabolic rate, or energy expenditure, is expressed in terms of oxygen consumption.Thermic Effect of Feeding Medium Chain TriglyceridesAfter consuming a meal the food is digested, released into the bloodstream, and transported to all the cells of the body. There, it reacts with oxygen to produce en-ergy. Some of the energy is captured in ATP, the energy source used directly by cellular machinery performing work.

Calories consumed in excess of energy require-ments will be stored as body weight. About 55% of the energy contained in food is liberated as heat during the process of ATP formation (Guyton, 1976). This release of heat energy from the oxidation of foods rep-resents an increase in metabolic rate and is accompanied by increased oxygen consumption .Feeding different dietary items while maintaining caloric intake affects oxygen consumption (Baba, Bracco, and Hashim, 1982). That different foods, normalized for energy content, increase the metabolic rate to different extents probably reflects the tendency of a particular food to be burned for energy versus being stored as body weight, as well as its extent of digestion and absorption. That protein increases the metabolic rate more than carbohydrate and conventional fat sug-gests that certain amino acids may directly stimulate thermogenesis (Guyton, 1976). The increase in energy expenditure caused by feeding is known as diet-induced thermogenesis or the thermic effect of feeding (Van Zant, 1992). MCTs cause profound postprandial thermogen-esis because they are very caloric dense and are absorbed and metabolized very rapidly.

The rapid oxidation of MCFAs in the liver causes an increase in postprandial oxygen consumption, i.e. metabolic rate. The increase in metabolic rate resulting from MCT ingestion has been measured in humans as well as in rats, using LCTs as con-trols (Seaton et al, 1986; Hill et al, 1989; Baba, Bracco, and Hashim, 1982). The data seem straight forward, well controlled, and statistically significant. Baba, Bracco, and Hashim (1982) observed that rats overfed MCT gained significantly less fat than rats fed an isocaloric diet containing LCT as the fat source. This was attributed to higher resting oxygen consumption (metabolic rate) in the MCT group. The authors ex-plained this by pointing out that while conventional fats are transported as chylomicrons and are largely stored as body fat, MCTs are transported directly to the liver where they are oxidized extensively to produce energy. The rapid oxidation of MCTs results in increased oxygen consumption, increased heat generation, and increased metabolic rate. In 1986 Seaton and colleagues demonstrated in humans that a meal containing MCTs increased oxygen consump-tion 12% above basal levels for 6 hours following the meal, while the LCT-containing meal increased oxygen consumption by only 4%. This indicates that MCTs are burned faster than conventional fats and increase the metabolic rate more. The increase in energy expenditure accounted for 13% of the energy contained in the MCT meal and 4% of the energy contained in the LCT meal. Hill and coworkers (1989) also compared the thermo-genic effect of medium chain triglycerides with that of long chain triglycerides.

Ten male volunteers were hospitalized and fed diets containing 30% of calories from either MCT or LCT. Metabolic rate was measured before, during, and after the experiment. Each subject was studied for one week on each diet in a double-blind crossover design. The thermic effect of food (TEF) is defined as the difference between metabolic rate during a six hour period after eating and the resting metabolic rate. That is, it is a measure of the increase in metabolic rate caused by eating the test meal. On day one of the experiment, the TEF of the meal containing MCT ac-counted for 8% of the ingested energy, while the TEF of the LCT meal accounted for 5.5% of the ingested energy. On day six of the experiment, the TEF of the MCT meal had increased to 12% of ingested energy, and the TEF of the LCT meal was 6.6% of ingested energy (figure 2). This means that the MCT-enhancement of the metabolic rate increased during the course of the experiment as the subjects became acclimated to the MCTs. On the last day of the trial the subjects were fed a liquid diet by continuous tube feeding.

During this experiment it was found that the TEF of the MCT meal increased to 15.7% of ingested energy, and the TEF of the LCT meal was 7.3% of ingested energy. So the increase in metabolic rate was even greater when MCT was administered continually .Mechanisms of ThermogenesisThe chemical mechanism underlying this thermogenic effect is unknown at present, but several suggestions have been advanced. Hill and coworkers (1989 and 1990) demon-strated that MCT overfeeding results in in-creased hepatic de novo fatty acid synthesis in man. This process is energetically costly and could account for the lesser efficiency of storage of MCT-derived energy. The observed increase in thermogenesis agrees well with the energy cost associated with de novo lipogenesis (Hill et al, 1990). This observation was corroborated by Crozier (1988) working with isolated rat hepatocytes.Alternatively, if electron transport is uncoupled from oxidative phosphorylation the energy spent to es-tablish an electrochemical potential gradient across the mitochondrial membrane is dissipated as heat instead of being conserved as ATP (Baba, Bracco, and Hashim, 1987).

For example, in brown adipose tissue a pathway exists allowing proton leakage across the mitochondrial membrane (Nicholls, 1979).Another means of dissipating energy as heat, believed to occur in liver mitochondria, is redox cycling involv-ing the glycerophosphate and malate shuttles (Berry et al, 1985; Crozier et al, 1987). In the glycerophosphate shuttle, energy is spent to pump reducing equivalents outside the mitochondria to drive the reduction of di-hydroxyacetone phosphate to glycerol-3-phosphate in the cytoplasm. The glycerol-3-phosphate then diffuses into the mitochondria and is oxidized to reform dihy-droxyacetone phosphate, which then diffuses out of the mitochondria to complete the cycle . The net result is the shuttle of glycerol-3-phosphate and dihydroxyacetone phosphate across the mitochondrial membrane (Berry et al, 1985; Crozier et al, 1987; Zubay, 1983, p. 401). Free energy is consumed to drive the cycle, but since no net work is performed the energy ultimately appears as heat (Berry et al, 1985).

The malate/aspartate shuttle is analogous .  Finally, increased activity of Na-K ATPase has also been suggested as a thermogenic mechanism for wasting en-ergy as heat (Levin and Sullivan, 1985). It is estimated that 10-40% of the total energy expended by the cell is used to maintain the concentration gradient of sodium and potassium ions across the cell membrane (Vander, Sherman, and Luciano, 1980). Since these ions also can cross the membrane by passive diffusion, an increase in the activity of the enzyme could be a mechanism for spending ATP.In all of the models - de novo fatty acid synthesis, proton leakage, redox cycling (or other futile cycles), and Na-K ATPase - the MCFAs are rapidly oxidized (explaining increased oxygen consumption), energy is consumed (explaining the low efficiency of storage of MCT-derived energy) and heat is produced as a by-prod-uct (explaining the thermogenic effect). Considerable evidence exists to support the involvement of de novo fatty acid synthesis as a mechanism for MCT-induced thermogenesis (Hill et al, 1989; Hill et al, 1990; Crozier, 1988) but other mechanisms may be involved as well. The reader is referred to Levin and Sullivan (1985) and Van Zant (1992) for reviews on thermogenesis and en-ergy balance.

References

1. Baba, Bracco, and Hashim, Enhanced thermogen-esis and diminished deposition of fat in response to over-feeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35: 678-682 (1982).

2. Baba, Bracco, and Hashim, Role of brown adipose tissue in thermogenesis induced by overfeeding a diet containing medium chain triglyceride . Lipids 22: 442-444 (1987).

3. Berry, Clark, Grivell, and Wallace, The contribu-tion of hepatic metabolism to diet-induced thermogenesis . Metab. 34: 141-147 (1985).

4. Crozier, Medium chain triglyceride feeding over the long term: the metabolic fate of C-14 octanoate and C-14 oleate in isolated rat hepatocytes. J. Nutr. 118: 297-304 (1988).

5. Crozier, Bois-Joyeux, Chanez, Girard, and Peret, Metabolic effects induced by long-term feeding of medium chain triglycerides in the rat. Metabolism 36: 807-814 (1987).

6. Guyton, Textbook of Medical Physiology. Pub-lished by W.B. Saunders, chapter 71 (1976).

7. Hill, Peters, Yang, Sharp, Kaler, Abumrad, and Greene, Thermogenesis in humans during overfeeding with medium chain triglycerides. Metabolism 38: 641-648 (1989).

8. Hill, Peters, Swift, Yang, Sharp, Abumrad, and Greene, Changes in blood lipids during six days of over- feeding with medium or long chain tri-glycerides. J. Lipid Res. 31: 407-416 (1990).

9. Levin and Sullivan, Regulation of thermogenesis in obesity. In: Novel Approaches and Drugs for Obesity, eds. Sullivan and Garattini, John Libbey and Co. Ltd. (1985).

10. Nicholls, Brown adipose tissue mitochondria. Bio-chim. Biophys. Acta 549: 1-29 (1979).

11. Seaton, Welle, Warenko, and Campbell, Thermic effect of medium chain and long chain triglycerides in man. Am. J. Clin. Nutr. 44: 630-634 (1986).

12. Vander, Sherman, and Luciano, Human Physiology - The Mechanisms of Body Function, p. 236. Published by McGraw-Hill Book Company, 1980 .

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The reaction between hydrogen and oxygen to make water is extremely exergonic (this is the reaction that turned the Hindenburg into a fireball). This reaction releases energy because hydrogen and oxygen are more stable (i.e., have less energy) when they are joined together as water than when they exist separately. Most of the energy derived from the aero-bic metabolism of foods is from this reaction. Fats provide twice the caloric density of carbohydrates - 9 calories per gram for fat as compared to 4 calories per gram for carbohydrate. The reason fat contains more energy than carbohydrate is that in fat the carbon is in a more reduced form (Zubay, 1983, p. 482) - more hydrogen is packed in per carbon atom. In aerobic metabolism the carbon and hydrogen in foods react with oxygen to produce CO2 and H2O. This reaction releases energy because carbon diox-ide and water molecules contain less energy than the original food molecules and oxygen.

The same reac-tion occurs when a piece of food burns in the camp fire. In that situation the energy released by the reac-tion is simply liberated as heat to the surroundings. In the body the reaction is broken down into many small steps and the energy which is released is captured in a molecule called adenosine triphosphate, or ATP. About 67% of the energy obtained in glucose (the body’s chief fuel molecule) is captured by ATP and the rest is liberated as heat (Zubay, 1983, p. 395). This is a very impressive efficiency level compared to other machines. ATP is the immediate source of energy used to fuel nearly all cellular processes, including muscular contraction. The role of ATP is not to store energy (that is the role of body fat and glycogen) but rather to transfer energy from a food molecule to some other cellular molecule which is going to perform work (Vander, Sherman, Luciano, 1980, p. 80). Ener-gy is the ability to do work. Potential energy is energy which is stored and has the potential to perform work if it is released. The energy contained in a chemi-cal bond is a form of potential energy. The potential energy contained in the chemical bonds of food mol-ecules is released during oxidation, and this energy is transferred via ATP to other molecules which perform cellular work - everything from muscular contraction to protein synthesis .

Conceptually, it is convenient to break up this process into four stages, although in fact these stages are inti-mately linked in the cell. The first stage of carbohy-drate metabolism is glycolysis and the first stage of fat metabolism is beta-oxidation. The following stages of energy production are common to both fats and carbo-hydrates, and are the Krebs cycle, electron transport, and oxidative phosphorylation. The Krebs CycleThe central energy producing pathway in the body is the Krebs cycle (figure 1), named for the German chemist Hans Krebs. Krebs originally postulated this process, also known as the TCA cycle, in 1937 and was later awarded the Nobel Prize in 1953 for this work. Energy substrates derived from carbohydrates or fatty acids enter the Krebs cycle as the intermedi-ate acetyl-CoA. The ultimate end of the process is to convert the chemical energy contained in foods into ATP.

Adenosine triphosphate is an unstable molecule containing a high energy phosphate bond. When ATP is split, the energy contained in this phosphate bond is released and is available to perform work inside the cell. ATP is the immediate source of energy for nearly all cellular processes, and thus has earned its reputa-tion as “the energy currency of the cell.”Carbohydrates are initially metabolized via an anaerobic process known as glycolysis. Glu-cose enters the glycolytic pathway and is con-verted into two molecules of pyruvate, generat-ing a net yield of two ATP molecules. Under anaerobic conditions, as may be temporarily experienced in muscular tissue during weight training, pyruvate is reduced to lactate, or lactic acid, which causes a burning sensation in the muscle. Glycolysis is a relatively inefficient process, yielding only two ATPs per glucose molecule. The two lactate molecules account for roughly 93% of the energy present in the original glucose molecule, so only about 7% of the energy embodied in glucose is made avail-able for use. Of this, about 50% is captured in ATP (Zubay, 1983, p. 305).

In the presence of oxygen a different metabolic fate is available to pyruvate. Instead of being converted into lactate, pyruvate is decarboxylated to generate acetyl-CoA. Acetyl-CoA is also produced by beta-oxidation of fatty acids, as discussed Tech-nical Report #2.The basic point of the Krebs cycle is to provide the chemical means of completely oxidizing the carbon of glucose or fatty acids to CO2 and the hydrogen to H2O. This allows much more of the energy contained in the food molecule to be extracted and used by the cell, as compared to anaerobic metabolism. In each turn of the Krebs cycle two carbons enter as acetate and two carbons exit as CO2. The cycle involves eight intermediates, each of which is converted into the next by an enzyme specific for that step (figure 1). These reactions are localized in the mitochondria, the site of aerobic energy production within the cell. The first stage of carbohydrate metabolism, glycolysis, occurs in the cytoplasm and does not require oxygen.

The end-product of glycolysis, pyruvate, enters the mitochondria to be further metabolized. In the mi-tochondria pyruvate is converted into acetyl-CoA by pyruvate dehydrogenase. Fats are oxidized to produce acetyl-CoA within the mitochondria. Long chain fatty acids must be ferried across the mitochondrial mem-brane by the carnitine shuttle, while medium chain fatty acids can transverse the membrane by passive diffusion.Acetyl-CoA donates the two-carbon compound acetate to a four-carbon acceptor oxaloacetate thereby gener-ating citrate, a six-carbon compound. During one turn of the cycle two molecules of carbon dioxide are liber-ated, ultimately regenerating oxaloacetate. The Krebs cycle intermediates are not consumed in the cycle and there is no net loss of carbon in the process, ignoring any side reactions which may occur. The cycle can thus be viewed as catalytic, since a relatively small amount of oxaloacetate can be used to metabolize an arbitrary amount of acetyl-CoA.

The activity of this pathway is controlled by the levels of its substrates and products, so that its level of energy production matches the energy needs of the cell. As the concentration of substrates increases, or the concentration of end products decreases, the activ-ity of the cycle increases. The most sensitive factors which directly regulate the cycle’s activity are the NAD/NADH ratio and the ATP/ADP ratio. The activ-ity of the first step in the pathway is also sensitive to the concentration of oxaloacetate.Under normal conditions the concentration of interme-diates such as oxaloacetate is not limiting. Medium chain triglycerides enter mitochondria independent of the carnitine shuttle, and thus bypass an important regulatory step in fatty acid oxidation (refer to Techni-cal Report #2). Medium chain triglycerides are oxi-dized so rapidly that the acetyl-CoA which is produced can overwhelm the amount of oxaloacetate available to accept it (Bach and Babayan, 1982). Some portion of the acetyl-CoA is then diverted to another metabolic fate - ketogenesis. In ketogenesis two molecules of acetyl-CoA combine to form ketone bodies, primar-ily acetoacetic acid and beta-hydroxybutarate (refer to Technical Report #2). This process is diminished if oxaloacetate precursors, such as aspartate and pyru-vate, are co-administered with the MCTs (Bach and Babayan, 1982; Crozier, 1988).

This suggests that the ketogenic properties of MCTs are due, in fact, to their ability to overwhelm the capacity of the Krebs cycle at the level of oxaloacetate.Only one ATP molecule is produced directly by each turn of the Krebs cycle. This is referred to as “sub-strate level phosphorylation” since the generation of ATP is directly coupled to a specific chemical reaction. In other words, ADP participates as a substrate in the reaction. Most of the energy derived from aerobic metabolism comes from subsequent oxidation of the NADH and FADH2 produced by the cycle. This is referred to as “oxidative phosphorylation” since here ATP synthesis is coupled to the oxidation of NADH and FADH2. Aerobic metabolism can the be thought of as having two phases: the oxidative phase in which electrons (in the form of hydrogen atoms) are removed from organic substrates and transferred to coenzyme carriers (FAD and NAD), followed by the reoxidation of the reduced coenzymes (FADH and NADH2) by the transfer of electrons (again in the form of hydrogen) to oxygen, generating H2O (Zubay, 1983, p. 325).

The reduction of oxygen to water to extremely exergonic and most of the ATP is generated during this process. The oxidation of acetyl-CoA involves removal of electrons (as hydrogen) from the Krebs cycle inter-mediates and transfer of hydrogen to the coenzymes FAD and NAD. In the process, these coenzymes are reduced to FADH and NADH2. (In chemistry, “oxi-dation” is the removal of electrons and “reduction” is the addition of electrons.) Subsequently, the reduced coenzymes are reoxidized by transfer of the hydrogens to oxygen in the “electron transport chain.” Ultimate-ly, ATP is synthesized by oxidative phosphorylation of ADP, which is driven by a proton gradient generated in the process of electron transport (Zubay, 1983, p. 325).The reactions of the Krebs cycle can be summarized by the following equation (Zubay, 1983, p. 335):acetyl-CoA + 2 H2O + 3 NAD+ + FAD + ADP + Pi 2 CO2 + 3 NADH + 3 H+ + FADH2 + CoA + ATP Two carbons enter as acetate and exit as CO2, pro-ducing ATP, NADH, and FADH2 as byproducts. The FADH and NADH2 in turn enter the electron transport chain to be further metabolized.Electron Transport and Oxidative PhosphorylationAlthough some ATP is directly generated by the Krebs cycle, more significant products of the cycle are the reduced coenzymes NADH and FADH2. Most of the energy contained in the starting material is still pres-ent in these coenzymes. The primarily energy yield of aerobic metabolism occurs when NADH and FADH2 are re-oxidized to NAD and FAD.

This process is known as electron transport because electrons from NADH and FADH2 are transported via a chain of electron carriers and are ultimately transferred to mo-lecular oxygen.  Oxygen is a very electronegative element, meaning that it has a strong affinity for electrons. In essence, oxygen and hydrogen combine to form water because oxygen has a high affinity for electrons, and hydrogen represents an easy source. Hydrogen does not have a strong affinity for electrons and basically gets trapped into sharing its electrons with oxygen. The overall reactions can be summarized as (Zubay, 1983, p. 364): NADH + H+ + 1/2O2 NAD+ + H20 G = -52.6 kcal/mol FADH2 + 1/2O2 FAD + H20 G = -43.4 kcal/molThe reduced coenzymes NADH and FADH2 serve as donors of electrons (as hydrogen) which combine with oxygen to form water. The delta-G expression indicates that the reaction will proceed spontaneously with the release of energy. Enough energy is released to drive the synthesis of several ATPs. Therefore, rather than wasting energy, the above reaction is di-vided up into several small steps.

The energy release is thus parcelled out in small packets to allow ATP to be generated more efficiently (Zubay, 1983, p. 365).  To achieve this, electrons are transported from the reduced coenzymes to oxygen via a series of carri-ers, arranged in the order of increasing electron affin-ity (figure 2). These electron carriers are molecules (some of them proteins) capable of undergoing revers-ible oxidation-reduction reactions.These electron transporters are embedded within the mitochondrial inner membrane (mitochondria are double-membraned structures). The energy which is released as electrons are transported down the chain to acceptors of ever increasing electron affinity is not directly used to synthesize ATP. Instead, the energy is used to generate a proton gradient across the inner mitochondrial membrane. This results in an electric field across the membrane (about 0.14 V) as well as a pH gradient (about 1.4 units). Protons are actively pumped across the inner mitochondrial membrane us-ing the energy derived from electron transport. In or-der to establish a proton concentration gradient across the membrane, the membrane must be impermeable to passive diffusion of protons.

Protons re-enter the mitochondrial matrix (driven by the concentration gra-dient) through a protein structure embedded within the membrane known as F0. F0 is physically attached to another protein structure known as F1-ATPase, which directly synthesizes ATP from ADP and phosphate. The precise mechanism by which energy is transferred from F0 to F1 and subsequently used to drive ATP synthesis is still under investigation, but may involve protein conformational changes or channeling of pro-tons through the enzyme active site (Zubay, 1983, p. 393). In summary, ATP is a molecule used to transfer energy from fuel substrates to cellular machinery performing work. The specific way in which this is accomplished is simple in principle but complicated in its actual ex-ecution. In principle, energy is derived from foods by their reaction with oxygen, just as when food is burned in a fire. Instead of being released as heat to the sur-roundings, some of the energy is captured as ATP. To achieve this efficiently, the process is broken down into several small steps. The first stage is to convert food molecules into a two-carbon compound, acetyl-CoA. For carbohydrates this is achieved by glycolysis followed by decarboxylation of pyruvate; fatty acids are converted to acetyl-CoA by beta-oxidation.

The acetyl-CoA, whether derived from carbohydrate or fat, is next metabolized in the Krebs cycle. One ATP molecule is generated per acetyl-CoA directly in the Krebs cycle, by “substrate level phosphorylation.” The carbon entering the Krebs cycle is released as CO2. Hydrogen present in the original food is now in the form of the reduced coenzymes NADH or FADH2. Most of the energy from aerobic metabolism is de-rived from oxidation of these reduced coenzymes in the electron transport chain . The summary reactions of the electron transport chain suggest that the hydro-gen from NADH and FADH2 combine with oxygen to form water, a well known exergonic reaction. How-ever, this does not happen directly. Instead, the energy released as electrons are transported down the chain (to electron acceptors of increasing electron affinity) is used to generate a proton gradient across the mito-chondrial membrane. The movement of protons back inside the membrane through the F0-F1 complex pro-vides the driving force for ATP synthesis by F1. This is referred to as “oxidative phosphorylation” because the phosphorylation of ADP to form ATP is coupled to the oxidative events occurring in the electron transport chain .

Energy Production and the AthleteAthletes experience increased energy need as com-pared to sedentary people . Bicycle racers and other endurance athletes can require as much as 10,000 calories per day to support their activity level. Body-builders commonly consume in excess of 8,000 calories daily to fuel their training and support gains in body weight. The body draws on three different types of food as energy substrates: fats, carbohydrates, and protein. Of these, carbohydrate is the most preferred. Carbohydrates are easily digested and rapidly enter the bloodstream as glucose. Glucose is immediately used as fuel by the cell. A byproduct of glucose metabo-lism is malonyl-CoA, which inhibits carnitine acyl-transferase I. Since long chain fatty acids require the carnitine shuttle in order to be transported inside the mitochondria, they are not used as fuel to a significant extent until the carbohydrates are depleted. Similarly, amino acids can be also oxidized to produce energy but are not used as fuel to a significant extent until carbohydrate is depleted. Of course, one of the primary goals of bodybuilders is to increase muscle mass.

Therefore amino acids are more valuable to use as protein rather than as fuel. Conventional fats are not a good energy source for bodybuilders either since they cannot be metabolized anaerobically and are not burned rapidly enough to meet the energy demands of high intensity exercise such as weight lifting (Coleman, 1991). Medium chain triglycerides are absorbed and metabolized much more rapidly than conventional fats and are immediately available for energy (Bach and Babayan, 1982). MCTs are an excellent quick energy source, harnessing the caloric density of fat but being metabo-lized as rapidly as glucose (Bach and Babayan, 1982).  Furthermore, MCTs and the ketone bodies they pro-duce decrease glucose uptake and utilization (Lavau and Hashim, 1978) and this seems to result in a glu-cose-sparing effect (Cotter et al, 1987). MCTs also have a protein-sparing effect and may reduce skeletal muscle protein catabolism, leaving amino acids avail-able for use as protein instead of being oxidized as fuel (Babayan, 1987; Haymond, Nissen, and Miles, 1983). Medium chain triglycerides are an excellent energy source for anyone experiencing increased en-ergy needs (Bach and Babayan, 1982) and are ideally suited to the special needs of athletes.

References

1. Babayan. Medium chain triglycerides and structured lipids. Lipids 22: 417-420 (1987).

2. Bach and Babayan. Medium chain triglycer-ides: an update. Am. J. Clin. Nutr. 36:950-962 (1982).

3. Coleman. Carbohydrates: the master fuel. In: Sports Nutrition for the 90s, eds.Berning and Steen. Aspen Publishers, 1991.

4. Cotter, Taylor, Johnson, and Rowe, A meta-bolic comparison of pure long chain triglyceride lipid emulsion (LCT) and various medium chain tri-glyceride (MCT)-LCT combination emulsions in dogs Am. J. Clin. Nutr. 45: 927-939 (1987).

5. Crozier. Medium chain triglyceride feeding over the long term: the metabolic fate of C-14 octano-ate and C-14 oleate in isolated rat hepato-cytes. J. Nutr. 118: 297-304 (1988).

6. Guyton. Textbook of Medical Physiology. Published by W.B. Saunders, 1976.

7. Haymond, Nissen, and Miles, Effects of ketone bodies on leucine and alanine metabolism in normal man. In: Amino Acids - Metabolism and Medical Applications, Eds. Blackburn, Grant, and Young. Published by John Wright PSG Inc., pages 89-95 (1983).

8. Lavau and Hashim, Effect of medium chain triglyc-eride on lipogenesis and body fat in the rat. J. Nutr. 108: 613-620 (1978).

9. Vander, Sherman, and Luciano. Human Physiology - The Mechanisms of Body Function. Published by McGraw-Hill Book Company, 1980.

10. Zubay. Biochemistry. Addison-Wesley Publishing Company, 1983 .

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First, the fatty acid is converted to its active form, acyl-CoA. The long chain acyl-CoA is then transesterified to L-carnitine by carnitine acyltransferase I (CAT I), generating acylcarnitine. A protein carrier embed-ded within the mito-chondrial membrane acts as a shuttle to transport the LCFA-carnitine complexes into the inner mito-chondrial space . Once there, carnitine acyl-transferase II (CAT II) releases the fatty acid in its activated form, acyl-CoA (figure 1).The enzymes respon-sible for oxidation of fatty acids are located inside the mitochon-dria. Therefore, if fatty acids are not permitted to enter the mitochondria they cannot be burned for energy. Entry into the mitochon-dria is regulated by the activity of the carnitine shuttle. This transport system is not very active if carbohy-drates are available because carbohydrate metabolism generates malonyl-CoA, which inhibits CAT I. In addition, glucagon (the hormonal antagonist of insu-lin) is involved in stimulating mobilization of body fat stores and use of fat for energy. Following carbo-hydrate ingestion insulin is released and glucagon is suppressed, so very little body fat is used for energy.

After carbohydrate reserves have been diminished, the body releases glucagon as a signal to begin burning fat. These are the reasons why fat stores are drawn upon for energy only after glycogen has been depleted.The inhibition of CAT I by malonyl-CoA represents a regulatory mechanism to prevent the wasteful use of energy substrates. Generally speaking, the body uses carbohydrate fuels first and stores fat as an energy reserve. Fat contains twice the energy density of car-bohydrate (9 calories per gram versus 4 calories per gram) and does not require water for storage, as does carbohydrate. Fat is thus a more efficient molecule for energy storage. Ani-mals are able to store only a small amount of energy as carbohydrate (in the form of liver and muscle glycogen) but can store a virtually unlimited amount of energy as fat.In contrast to long chain fats, MCFAs (includes MCTs) are immediately available for energy. Me-dium chain fatty acids are retained by the liver, where they are rapidly and extensively oxidized (Bach and Babayan, 1982). Medium chain fatty acids can en-ter the mitochondria by passive diffusion and do not require the carnitine transport system (Record et al, 1986; Bach and Babayan, 1982).

MCFAs thus can be used for energy even in the presence of carbohydrates, and in fact have a carbohydrate-sparing effect (Lavau and Hashim, 1978; Cotter et al, 1987). Once inside the mitochondria all fatty acids are burned in a process tion. During beta-oxidation, blocks of two carbon atoms are removed from the activated fatty acid (acyl-CoA) to form acetyl-CoA (figure 2). The intermediate acetyl-CoA can then undergo several metabolic fates: i) it can enter the Krebs cycle to generate ATP; ii) it can be used to generate ketone bodies; iii) it can be used as a substrate for fatty acid synthesis or elonga-tion; or iv) it can be consumed in an energy trans-forming process known as reversed electron transfer (Bach and Babayan, 1982; Berry et al, 1985; Crozier et al, 1987).The vast majority of MCFAs (includes MCTs) are re-tained in the liver where they undergo beta-oxidation, producing acetyl-CoA. To enter the Krebs cycle (the body’s central energy producing pathway) the acetyl-CoA combines with oxaloacetate, producing citrate. Me-dium chain fatty acids are oxidized in the liver so rapidly that the supply of oxaloacetate becomes limiting.

As a result, the capacity of the Krebs cycle is overwhelmed and a large proportion of the acetyl-CoA is directed to-ward the synthesis of ketone bodies (Bach and Babayan, 1982). This process is known as “ketogenesis” (figure 3). Ketone bodies are released from the liver into the blood and are subsequebtly taken up by muscles and used as fuel. LCT ingestion also causes an increase in blood levels of ketone bodies during fasting, but only MCT will still produce ketone bodies if carbohydrates are con-currently ingested (Sucher, 1986). Once inside muscle cells, ketone bodies are converted back to acetyl-CoA, which then enters the Krebs cycle to produce ATP. The conversion of MCFAs to ketone bodies occurs even in the presence of carbohydrates. This additional source of energy decreases glucose uptake and utilization (Lavau and Hashim, 1978) and thus may extend endurance by sparing glycogen (Cotter et al, 1987).

References

Bach and Babayan, Medium chain triglycerides: an update. Am. J. Clin. Nutr. 36:950-962 (1982).

Berry, Clark, Grivell, and Wallace, The contribution of hepatic metabolism to diet-induced thermogenesis. Metab. 34: 141-147 (1985).

Cotter, Taylor, Johnson, and Rowe, A metabolic com-parison of pure long chain triglyceride lipid emulsion (LCT) and various medium chain triglyceride (MCT)

LCT combination emulsions in dogs. Am. J. Clin. Nutr. 45: 927-939 (1987).

Crozier, Bois-Joyeux, Chanez, Girard, and Peret, Metabolic effects induced by long-term feeding of medium chain triglycerides in the rat. Metabolism 36: 807-814 (1987).

Lavau and Hashim, Effect of medium chain triglycer-ide on lipogenesis and body fat in the rat. J. Nutr. 108: 613-620 (1978).

Record, Kolpek, and Rapp, Long chain versus medium chain length triglycerides - a review of metabolism and clinical use. Nutr. Clin. Prac. 1:129-135 (1986).

Sucher, Medium chain triglycerides: a review of their enteral use in clinical nutrition. Nutr. Clin. Prac. 44: 146-150 (1986).

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Medium chain triglycerides (MCTs) are comprised of medium chain fatty acids (MCFAs), which are 6-12 carbons in length. Although the carboxylic acid part of fatty acids is soluble in water, the hydrocarbon chain is not. Thus, LCFAs are not water soluble. Since the hydrocarbon chains of MCFAs are shorter, MCFAs are more water soluble than LCFAs. Likewise, MCTs are also relatively soluble in water, due to ionization of the carboxylic acid groups and the small size of the hydrocarbon chains . Their small molecular size and greater water solu-bility cause MCTs to undergo a differ-ent metabolic path than that experienced by LCTs (Bach and Babayan, 1982).

Occurrence and Purification of MCTsMedium chain triglycerides occur naturally in small quantities in a variety of foods, and are present naturally in the blood of the human fetus and in human milk (Bach and Babayan, 1982; Souci, Fachmann, Kraut, 1989/90). In cow’s milk, C6-C14 fatty acids together account for 20% of the total fatty acid composition (Christensen et al, 1989). Commercially, medium chain fatty acids are prepared by the hydrolysis of coconut oil (an abundant source) and are fractionated by steam distillation. The MCFAs so obtained consist of predominantly C8:0, with lesser amounts of C10:0, and minute amounts of C6:0 and C12:0. The fractionated MCFAs are re-esterified with glycerol to generate MCTs (Bach and Babayan, 1982). MCT oil softens or splits certain plastics such as polyethylene and polystyrene, but not polypropylene. It is recommended that MCT oil be stored in metal, glass, or ceramic containers (Sucher, 1986). MCT oil has a caloric density of 8.3 calories per gram; one tablespoon equals 14 grams and contains 115 calories. MCTs are not drugs and have no pharmacological effects (Bach and Babayan, 1982). Historical Uses of MCTsSince their introduc-tion in 1950 for the treatment of fat malab-sorption problems, me-dium chain triglycer-ides have enjoyed wide application in enteral and parenteral nutri-tion regimens (Bach and Babayan, 1982).

Fat emulsions can be used to provide up to 60% of nonprotein calories. Before the availability of lipid emulsions suitable for intravenous use, glucose was used as the only nonprotein source of calories (Mascioli et al, 1987). Not only did this result in essential fatty acid deficiencies, but it was also undesirable because it increased hepatic lipogenesis and respiratory work. Although inclusion of LCTs in intravenous feedings represented an improvement, problems remained with slow clearance of LCTs from the bloodstream and inter-ference with the RES component of the immune system. When medium chain triglycerides or structured lipids (triglycerides containing both MCFAs and LCFAs) are added to the regimen, calories are provided in a more readily oxidizable form (Schmidl, Massaro, and Labuza; 1988), and less interference with the RES is observed (Mascioli et al, 1987). In one case, MCT was fed as the exclusive source of fat (along with a small amount of LCT to provide essential fatty acids) to a patient with chyluria (a fat malabsorption disease) for over 15 years without producing side effects (Geliebter et al, 1983).

Sports NutritionAlthough MCTs have been used in hospital environments for years, their use by healthy individuals is relatively new. Recently, athletes have begun to use MCTs to II. MetabolismDigestion and Absorption of FatsSince LCTs are not very soluble in water, the body has to go through an elaborate digestive process in order to absorb these nutrients. Bile salts are secreted by the gall bladder to help dissolve the LCTs. Upon ingestion, LCTs interact with bile in the duodenum (upper small intes-tine) and are incorporated into mixed micelles (Record et al, 1986). Enzymes called lipases (pancreatic lipase and phospholipase A2) remove the fatty acid molecule from the glycerol backbone. The mixed micelles are passively absorbed into the intestinal mucosa where the free fatty acids are re-esterified with glycerol. The in-testinal mucosa synthesizes a lipoprotein carrier called a chylomicron to transport the reformed triglyceride. Chy-lomicrons are secreted into the lymph and are released into the venous circulation via the thoracic duct. In the bloodstream, lipoprotein lipase again breaks down the triglycerides into two free fatty acids and a monoglyc-eride.

The monoglycerides go to the liver to be further degraded, while many of the circulating free fatty acids are taken up and stored by adipocytes (fat cells). When carbohydrates are consumed insulin is released, and in-sulin stimulates adipocytes to re-esterify the fatty acids into triglycerides and store them as body fat. In general, body fat stores are not mobilized and used for energy to any significant extent in the presence of insulin.In contrast, since MCFAs are more water soluble they are more easily absorbed and do not require this complicated digestive process. MCTs can be absorbed intact and do not require the action of pancreatic lipase or incorpo-ration into chylomicrons. Instead, a lipase within the intestinal cell degrades the MCT into free MCFAs and glycerol. The MCFAs are bound to albumin, released into the bloodstream, and transported directly to the liver by the portal vein. The vast majority of MCFAs are retained by the liver where they are rapidly and extensively oxidized. Whereas conventional fats are largely deposited in fat cells, MCTs are transported directly to the liver and used for energy. Very little of the MCFAs ever escape the liver to reach the general circulation (Bach and Babayan, 1982). Only 1-2% of MCTs are incorporated into depot fat (Geliebter et al, 1983; Baba, Bracco, and Hashim, 1982). Medium chain triglycerides are digested and absorbed much faster than conventional fats (in fact, as rapidly as glucose) and are immediately available for energy.

References

Baba, Bracco, and Hashim, Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglyceride. Am. J. Clin. Nutr. 35: 678-682 (1982).

Bach and Babayan, Medium chain triglycerides: an up-date. Am. J. Clin. Nutr. 36:950-962 (1982).Christensen, Hagve, Gronn, and Christophersen, Beta-oxidation of medium chain (C8-C14) fatty acids studied in isolated liver cells.

Biochem. et Biophys. Acta 1004: 187-195 (1989).Geliebter, Torbay, Bracco, Hashim, and Van Itallie, Overfeeding with medium chain triglyceride diet results in diminished deposition of fat. Am. J. Clin. Nutr. 37: 1-4 (1983).

Mascioli, Bistrian, Babayan, and Blackburn, Medium chain triglycerides and structured lipids as unique non-glucose energy sources in hyperalimentation . Lipids 22: 421-423 (1987).

Record, Kolpek, and Rapp, Long chain versus medium chain length triglycerides - a review of metabolism and clinical use. Nutr. Clin. Prac. 1:129-135 (1986).

Schmidl, Massaro, and Labuza, Parenteral and enteral food systems. Food Tech. 77-87 (July, 1988).Souci, Fachmann, and Kraut, Food Composi-tion and Nutrition Tables 1989/90. Published by Wissenschaftliche Verlagsgesellschaft (1989).

Sucher, Medium chain triglycerides: a review of their enteral use in clinical nutrition. Nutr. Clin. Prac. 44: 146-150 (1986).Zubay, Biochemistry, chapter 13: “Metabolism of Fatty Acids and Triacylglycerols,” by Denis E. Vance. Published by Addison-Wesley Publishing Company

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Here’s the latest, greatest news on MCTs: A 2008 study published in Journal of the American College of Nutrition found that substituting mod-erate amounts of MCT oil for other fats in a weight-loss program resulted in fat loss, including around the waist, with no adverse impact on cardiovas-cular risk factors.In the 16-week study, 31 overweight patients consumed either olive oil or MCT oil in muffins. All of the subjects participated in dietitian-led weekly group weight-loss counseling sessions that stressed following a prudent diet, and encouraged healthy eating pat-terns. The oils accounted for roughly 12 percent of participants’ calorie prescription.

At 16 weeks, the MCT group had lost significantly more weight: an average of 7 pounds, or 3.8 percent of their baseline body weight, compared with 1.7 percent in the olive oil group. That’s 200% better than the control group for all you math whiz-zes. That’s over twice the weight loss of the control group. The MCT group also had a 1.5 percent decrease in total fat mass as measured by CT scan, including a reduction in intra-abdominal fat. (1) Unlike conven-tional oils, MCT oil gets burned im-mediately by the liver before it even has a chance to get stored as body fat, and many researchers feel that it has a place in weight management. Of course, I agree!CapTri® is a unique high thermo-genic ultra pure MCT available exclusively from Parrillo Perfor-mance. CapTri® comes unflavored for cooking or making salad dress-ings, etc. or butter flavored for driz-zling over vegetables, fish, popcorn and more. CapTri® contains around 115 calories per tablespoon. I have very specific recommendations for how to use CapTri® in a weight-loss program, and it is Parrillo Perfor-mance’s own version of the low-carb diet (but without the side effects of typical low-carb diets).

The calo-ries from CapTri® provide the en-ergy you need to keep training hard, while you’re trying to lose body fat. Also, by substituting CapTri® for an equivalent number of calories from carbohydrates you avoid the slow-down in metabolic rate which inevi-tably results from calorie-restricted diets.My approach to low-carb dieting al-lows you to utilize the power of the low carb diet without resorting to using regular fat as a food source. Instead of regular fat, you use high thermogenic CapTri®, which be-haves more like a carbohydrate in the body, except that it doesn’t in-crease insulin levels. This means you can use CapTri® in place of carbs to decrease insulin levels and shift your metabolism into a fat-burning mode. This is very similar to the strategy of low-carbdiets except without relying on conventional fat as an energy source.To use CapTri® for fat loss, con-tinue to keep your protein intake high at about one to 1.5 grams per pound of body weight per day, then reduce carbohydrate intake and provide an equivalent number of calories from CapTri®.

For ex-ample, if you normally consume 300 grams of carbs per day (1200 calories worth), reduce that to 150 grams per day and add 5 table-spoons of CapTri® per day (pro-viding 570 calories). By reducing carbs and always combining your starches with protein, vegetables, and CapTri® at each meal, you will dramatically reduce insulin levels and maximize fat loss. One more point: Unlike conventional fats, CapTri® also works well dur-ing weight gain because it doesn’t contribute to fat stores (2, 3).Of course, CapTri® isn’t just for weight loss; it’s also for building and maintaining lean mass, since it has a positive effect on your me-tabolism. CapTri® is very thermo-genic and dramatically increases the rate of oxygen consumption after a meal. It’s no accident that we’ve incorporated CapTri® at the core of our supplement program. The reason? As you know, CapTri® is a very con-centrated source of calories – calories that can be used for energy and to support weight gain. The increase in oxygen consumption that occurs after you eat CapTri® means that it is be-ing burned very fast (4, 5).

Remember, foods are burned by reacting with the oxygen we breathe, so the reason oxy-gen consumption increases after you eat is to supply enough oxygen to burn the food to produce energy. Some of the energy from CapTri® is converted into body heat in a process known as thermogenesis (4, 5).This is the single most important rea-son why excess calories from CapTri® have less of a tendency to make you fat than excess calories from other foods. CapTri® is burned so fast that excess calories from it are turned into body heat instead of being converted into fat. This is why I’ve called CapTri® the best supplement ever developed for active people – it’s an excellent way tosupply extra calories but has very little tendency to make you fat. CapTri® is available exclusively from Parrillo Performance. You can use CapTri®: 1. To maintain energy levels while diet-ing. 2. To add clean calories for gain-ing muscle. 3. To replace regular fat with healthier CapTri®.

References

1. St. Onge, M.P. et al. 2008. Mediumchain triglyceride oil consumption as part of a weight loss diet does not lead to an adverse metabolic profile when compared to olive oil. Journal of the American College of Nutrition 27(5):547-552.2. Baba, N., Bracco, E.F., and Hashim, S.A. 198

2. Enhanced thermogenesis and diminished deposition of fat in response to overfeeding with diet containing medium chain triglycer-ide. American Journal of ClinicalNutrition 35: 678-682.

3. Bach, A.C. and Babayan, V.K. 1982. Medium chain triglycerides: an update. American Journal of Clinical Nutrition 36: 950-962.

4. Hill, J.O., et al. 1989. Thermogen-esis in humans during overfeeding with medium chain triglycerides. Metabolism 38: 641-648.5. Seaton, T.B., et al. 1986. Welle, Warenko and Campbell, Thermic effect of medium chain and long chain triglycerides in man. Ameri-can Journal of Clinical Nutrition 44: 630-634.

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Over the past several years, many popu-lar diets have suggested that increasing or decreasing a single nutrient in your diet can dramatically affect your weight loss. Some diets have focused on carbo-hydrates, others on protein, still others on fat. Unfortunately though, highlight-ing one nutrient to the exclusion of oth-ers misses the boat. Weight loss through nutrition depends upon on a carefully designed balance of all of these nutri-ents and on the specific types of food in which those nutrients are found – which is exactly how the Parrillo Nutrition Program is put together. Why is this true? Both factors positively influence the action of your hormones – chemical messengers that regulate a world of functions in your body.

They also influence your metabolism, your body’s food-to-fuel processes. Thus, the interplay of food balance and food choices can greatly accentuate your ability to burn fat. It is this approach to weight loss that has the backing of med-ical science. A simplified explanation of these issues is provided below.The Role of Food Balance and Food Choice in Fat-BurningIf you desire to burn fat – and who doesn’t – then you require a carefully designed balance of certain types of protein, carbohydrates, and fat in your diet – with enough calories to keep your metabolism running in high gear. Remember on the Parrillo Nutrition Program, we do not advocate cutting calories. Doing so only slows down your metabolism. But back to nutrient balance, let’s start with protein.Protein As A Fat-BurnerWhen provided in your diet at higher levels, protein can clearly be nick-named a “fat burner” – for two impor-tant reasons. First, your body requires ample pro-tein to develop and maintain muscle.

If you don’t get enough protein, your body can start breaking down muscle tissue for the provision of energy. Con-sequently, you’ll lose metabolically active muscle, and this will sabotage your fat-loss efforts. Second, protein boosts your metabo-lism, and it does this by stepping up the action of your thyroid gland. (One of the main duties of the thyroid is to regulate metabolism.) This benefit of a higher-protein diet was observed in a study of dieters conducted by the University of Illinois at Urbana-Champaign, released in 2001. In this study, 24 mid-life women went on a liberal 1,700 calorie-a-day diet for 10 weeks. Half followed a diet based on the USDA Food Guide Pyramid – 55 percent carbohydrates, 15 percent pro-tein, and 30 percent fat. The other half followed a high-protein diet of 40 percent carbohydrates, 30 percent  protein, and 30 percent fat.Both groups lost the same amount of weight – 16 pounds, but the compo-sition of that weight differed greatly. The high-protein group shed 12.3 pounds of pure pudge and only 1.7 pounds of lean muscle, while the Food Pyramid dieters lost 10.4 pounds of fat and 3 pounds of mus-cle.

Translation: High protein means better, more fat loss. With a higher-protein diet, you don’t have to sacri-fice muscle. Also important in this study: The researchers detected an increase in the thyroid function of the high-protein dieters, and this was the concrete evidence for protein’s metabolism-boosting effect. Do you realize the significance in all of this? With more protein in your diet, in the right balance, you can almost double your weight-loss and fat-burning efforts!Carbohydrate Differentiation: Carbohydrates also play a role in fat-burning, as long as you choose the right types of carbohydrates. This is where food choice becomes all-important to your weight-loss success.For a very long time, carbohydrates have been classified as either simple or complex. Simple sugars are found in candies, syrups, many fruits and fruit juices, and processed foods, and complex carbohydrates are found in whole grains, beans, and vegetables. This classification is based on the molecular structure of the carbo-hydrate, with simple carbohydrates constructed of either single or dou-ble molecules of sugar, and complex carbohydrates made of multiple numbers of sugar molecules. Simple sugars send your blood sugar soaring, and this sets off a hormonal reaction that can lead to weight gain.

Here is a closer look at exactly what happens: After you eat carbohydrate foods, your body breaks them down into glucose. Simple sugars are dis-mantled more quickly than others, and this causes a huge spike in your blood glucose. Complex carbohydrates take longer to break down, and conse-quently, blood glucose stays relatively even during the digestion process. When glucose shoots upward in re-sponse to simple sugars, so does the hormone insulin. The problem with an overload of insulin in your system is that it activates fat cell enzymes. These enzymes move fat from the bloodstream into fat cells for storage and trigger your body to create more fat cells. Simple sugars thus create conditions in your body that are con-ducive to gaining fat.What all of this tells us is very simple: Simple sugars promote fat storage; complex carbs like those recommend-ed on the Parrillo Nutrition Program do not. Choosing complex carbo-hydrates makes it possible to lose weight more easily. If you base your carbohydrate selections on this nutri-tional element, you will lose weight more quickly. The Parrillo Nutrition Program is based on the selection of complex carbohydrates.

These include certain whole grain cereals, brown rice, beans, legumes, potatoes, yams, and vegetables.The Fat Factor: For decades, we were taught that in order to lose weight, we had to slash the amount of dietary fat in our diets. Since the 1980s, Americans did reduce their fat consumption, but at the same time, they got fatter. More than 60 percent of our population is now considered overweight or obese.  Cutting the fat from our diets was clearly not the “magic answer” to weight loss.Scientists studying this alarming trend probed the reasons. What could explain this confusing phe-nomenon? After much research, they discovered that people had been replacing the fat in their diets with too many simple sugars. This was the impetus – the main common de-nominator – behind the expanding waistlines of the American public, along with the fact that Americans are becoming increasingly inactive.

So from a nutritional standpoint, simple sugars are among the prime culprits in weight gain, and dietary fat shoulders far less of the blame.   Taking all of this important infor-mation into account, the Parrillo Nutrition Program supplies roughly 10-20% percent of your daily calo-ries from fat, with special emphasis on the essential fatty acids we rec-ommend you have each day. A Final Point: The foods allowed on the Parrillo Nutrition Program provide what has been scientifically proven to be an effective combina-tion of specific types of protein, carbohydrate, and fat. This combi-nation of easily available and deli-cious foods, in the right proportions, stimulates increased body fat me-tabolism, while supplying nutrients required to support your health. The food you will eat will be more sat-isfying and nutritionally rewarding, plus will provide the metabolic and hormonal catalyst you need to shed surplus fat.

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This is followed by two or three days of carbing up to provide an anabolic growth spurt. Another program is more moderate, suggesting a diet of 30 percent protein, 40 percent carbs, and 30 percent fat, with-out cycling. There is a lot of science and theory behind these diets, although the high-fat recommendation is quite contro-versial. Without getting too bogged down in the biochemical details, the fundamental idea behind these approaches is to reduce carbohydrate intake in order to reduce insulin levels. Insulin is a potent inhibitor of lipolysis, or fat breakdown. By reducing insulin levels, you can take the brakes off fat metabolism and encourage the use of stored body fat for energy. In my work with bodybuilders, I have found that reducing carbs does indeed help to promote fat loss, especially in people who have a hard time getting lean. I don’t have a problem with carb reduction – as long as it’s done right (I’ll get to that in a moment). But what I have a problem with is that with high fat diets, the dietary fat is VERY prone to be stored as body fat.

Sev-eral studies have demonstrated that body fat percentage is more highly determined by dietary fat intake than by calorie intake (1,2,3,4,6,8,9,10). Not only does dietary fat contribute more to fat stores than protein or carbohydrate (1-13), but dietary fat (es-pecially long chain saturated fat) increases your cholesterol level and your risk for heart disease . Back to carbs for a moment: A prob-lem with the very low carb approach is that energy levels fall dramatically. Anaerobic exercise, such as weight lifting, is fueled almost exclusively by carbs. Fat cannot be used as an anaerobic energy source; it can only be oxidized aerobically. Therefore, strength and energy levels fall dramatically without carbs. This results in more muscle catabolism (breakdown and loss), as the muscles turn to branched chain amino acids as fuel. In addition, low carbohydrate diets have been found to reduce thyroid hormone level, which is one of the chief controllers of metabolic rate.If you’re familiar with my work at all, you know that I advocate, in general, a diet high in protein, high in complex carbo-hydrates, and very low in fat. I agree that hard-training athletes need more protein than sedentary people, at least one gram to 1.5 grams or more per pound of body weight per day.

This is a good general guideline, especially during weight gain. As you decrease calories to lose fat, it helps to increase this amount to as much as 1 .5 to 2 grams or more per pound of bodyweight per day. The higher dietary protein intake helps prevent catabolism of muscle protein during energy-restricted diets . Next, you should allot 5 to 10 percent of your daily calories to come from fat. The remainder of your calories come from complex carbohydrates, which I divide into starches (potatoes, rice, beans, and so forth) and fibrous carbs (vegetables and salad greens). By combining protein and fibrous vegetables with your starch at each meal you can greatly slow the rate of release of glucose into the bloodstream. This in turn decreases insulin levels, taking the brakes off fat metabolism. You will find that by proper food combining you can stimulate a powerful fat burning effect without elimi-nating too many carbs from your diet. But because carbohydrate reduction is such a powerful tool for fat loss, I’ve devel-oped an approach to low-carb dieting that allows you to utilize the power of the low carb diet without resorting to using regular fat as a food source. Instead of regular fat, you use CapTri®, a specially engineered fat with a unique molecular structure which causes it to follow a different metabolic route than regular fats (14,15). It behaves more like a carbohydrate in the body, ex-cept that it doesn’t increase insulin levels.

This means you can use CapTri® in place of carbs to decrease insulin levels and shift your metabolism into a fat-burning mode. This is very similar to the strategy of the high fat diets except without relying on conventional fat as an energy source. In short, CapTri® lets you reap the benefits of the high fat approach without the problems that go along with conventional dietary fat. To use CapTri® for fat loss, continue to keep your protein intake high at about 1.5 to 2 grams or more per pound of body weight per day, then reduce starchy carbo-hydrate intake and provide an equivalent number of calories from CapTri® while making sure you still eat plenty of fibrous carbs.For example, if you normally con-sume 300 grams of carbs per day (1200 calories worth), reduce that to 150 grams per day and add 5 tablespoons of CapTri® per day (providing 570 calories). By re-ducing carbs and always combining your starches with protein, vegetables, and Cap-Tri® at each meal, you will dramatically reduce insulin levels and maximize fat loss. One more point: Unlike conventional fats, CapTri® also works well during weight gain because it doesn’t contribute to fat stores (14,15).