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Bulletin #20 – The Ultimate Formula For Losing Body Fat, Part 2

The pre-eminent consideration in de-termining body weight is energy balance,defined as energy consumption minusenergy expenditure. Conventional ap-proaches to obesity management fail be-cause they do not consider that the body’senergy expenditure changes in responseto caloric intake as well as macronutrientcomposition of the diet. If energy intakeis reduced, energy expenditure is reducedto compensate. This serves to enhancesurvival during famine by slowing thedepletion of stored energy. Since weightreduction strategies based on caloric re-striction are observed to fail, perhaps bet-ter success could be achieved in manipu-lating the expenditure side of the energyequation.Metabolic rate is the body’s rate ofenergy expenditure commonly expressedin calories per hour. It consists of severalcomponents: basal metabolic rate (BMR),the thermic effect of feeding (TEF), thethermic effect of activity (TEA) and adap-tive thermogenesis (1). The basal meta-bolic rate is the body’s rate of energy ex-penditure while at rest during the post-absorptive phase (several hours after eat-ing when all the food hasbeen digested and ab-sorbed). This representsthe energy requirements ofmaintaining life, consistingmostly of maintenance ofbody temperature, heartrate, breathing, nervetransmission, electro-chemical gradients acrossmembrane cells, and theenergy cost of proteinturnover required to main-tain cells.

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The basal meta-bolic rate accounts for 65-75% of daily energy re-quirements (1). Metabolicrate is affected by manyparameters including en-ergy intake, dietary com-position (the percent of calories from pro-tein, carbohydrate and fat), activity (de-pendent on type, intensity, and durationof activity), lean body mass, age, sex,hormones and drugs. Since greater than95% of the energy expended by the bodyis derived from the oxidation of foods,metabolic rate is proportional to oxygenconsumption (2).Perhaps one of the most significantdiscoveries in nutrition is that feeding dif-ferent dietary items while maintaining ca-loric intake affects oxygen consumption(3,4). That different foods, normalized forenergy content, increase the metabolic rateto different extents probably reflects ten-dency of a particular food to be burnedfor energy versus being stored as bodyweight, as well as its extent of digestionand absorption.

That protein increases themetabolic rate more than carbohydrateand fat suggests that certain amino acidsmay directly stimulate thermogenesis(3,2). The increase in energy expenditurecaused by feeding is known as diet-in-duced thermogenesis or the thermic ef-fect of feeding, TEF (1). Since differentfoods increase the metabolic rate to dif-ferent extents, this means that differentfoods, normalized for energy content,have characteristic tendencies to be storedas body weight versus being burned asenergy. This concept is known as “foodefficiency.” Food efficiency is defined asthe calories consumed of a particular fooddivided by the resulting weight gain (3,5,6)and is thus a measure of how efficiently aparticular food is converted to bodyweight. Ingested foods can experiencethree general fates: 1) they can be oxi-dized to release energy, 2) they can beretained as body weight (muscle, fat orglycogen), or 3) they can be excreted. Therelative balance between these possibili-ties determine a food’s efficiency. Foodswith a high food efficiency are readilystored as body weight while foods with alow food efficiency are more prone to beutilized as energy.This concept is the basis for use ofCapTri® for weight reduction. CapTri® isa highly fractionated medium chain trig-lyceride formulated especially for body-builders and other athletes. CapTri® is pro-foundly thermogenic (4,5,7,8,9) and hasa very low food efficiency. This meansthat it is preferentially burned for energyand has very little tendency to be storedas body weight. Calorie for calorie,CapTri® contributes less to body weightgain (fat gain) than carbohydrates or con-ventional dietary fat.

Think of CapTri® asan immediate energy source that will getburned before the body has time to storeit. If eating regular food is like throwing alog on the fire, eating CapTri® is like pour-ing gasoline on the fire.How does this work? Medium chaintriglycerides enter the mitochondria bypassive diffusion independent of the car-nitine shuttle and thus are immediatelyoxidized as fuel, bypassing regulation(4,5,7,8,9). Mitochondria are the little fur-naces inside cells where foods are burnedto produce energy. Normal fats cannot getinside mitochondria by themselves, but have to be carried inside by a transportsystem called the carnitine shuttle. Thisresults in regular fats being burned rela-tively slowly, giving them more time tobe stored as body fat. Also, this serves asa way of regulating fat metabolism. Regu-lar fats are not used as fuel to a signifi-cant extent as long as carbohydrates areavailable, since the carnitine shuttle is in-hibited by malonyl-CoA, a byproduct ofcarbohydrate metabolism. CapTri®, on theother hand, is used as fuel even in thepresence of available  carbohydrates, andspares carbohydrate for glycogen storage.This means more carbohydrates are avail-able for strength and more endurance. TheTEF and low food efficiency of CapTri®is due to its rapid oxidation (burning). Asfats are converted to energy, the initialbreakdown product is acetyl-CoA, whichthen feeds into the pathways of the Krebscycle, electron transport and oxidativephosphorylation. (The biochemistry of allthis is explained in much greater detail inour technical series.) As CapTri® is beingburned, acetyl-CoA is produced so fastthat as to overwhelm the capacity of theKrebs Cycle in the liver. This excessacetyl-CoA is converted to ketone bodies(6,10,11). Ketone bodies produced in theliver are then used as fuel by skeletalmuscle. The strategy is to replace con-ventional dietary fat with CapTri®, therebyreducing food efficiency of the diet.

Wehave used this technique at Parrillo Per-formance to convert amateur bodybuild-ers into professionals (12). Our secret isCapTri® — the most powerful MCT onthe market. By replacing regular dietaryfat with CapTri®, you can achieve lowerbody fat levels. Before contests, bodybuild-ers also substitute CapTri® for starchy car-bohydrates. This increases the glucagonto insulin ratio generated by the diet aswell as further reducing food efficiency.This all works together to shift your meta-bolic pathways into a fat-burning mode.Ask for our technical series on CapTri®or consult our Nutrition Program orCapTri® Manual if you want the scientificdetails on how it works and how to useit.The thermic effect of food (TEF) isdefined as the postprandial (after eating)increment in energy expenditure above theresting rate and is expressed as a fractionof the energy content of the food con-sumed (3). A substantial part of the TEF(50-75%) is simply the energy used todigest, transport and store food (3). Thisis termed the obligatory component ofTEF. Carbohydrate feeding is known tostimulate the sympathetic nervous systemand the ensuing catecholamine-mediatedincrease in metabolic rate is known as thefacultative component of TEF (3). Thiseffect can be blocked by propanolol (abeta-adrenergic antagonist).Mechanisms which may be involvedin facultative thermogenesis include stimu-lation of sympathetic activity, increasedsubstrate cycling of three-carbon com-pounds such as lactate (from anaerobicmetabolism) and alanine (from branchedchain amino acid metabolism), increasedredox cycling and stimulation of proteinand fat synthesis (3). The relative contri-bution of each of these probably variesaccording to the fuel substrate being oxi-dized. The most important player in glu-cose-induced thermogenesis (GIT) isprobably activation of the sympatheticnervous system, since this effect can beblocked by propanolol (3).

The majorcontributor to  MCT-induced thermogen-esis appears to be increased de novo fattyacid synthesis. Hill and co-workers(10,11) demonstrated that MCT overfeed-ing results in increased hepatic de novofatty acid synthesis is man. This processis energetically costly and could accountfor the lesser efficiency of storage ofMCT-derived energy. The observed in-crease in thermogenesis agrees well withthe energy cost associated with de novolipogenesis (10,11). This observation wascorroborated by Crozier (13) workingwith isolated rat hepatocytes (liver cells).This means that some of the excessacetyl-CoA produced during the rapidoxidation of MCTs is used to build newfat molecules. What is the net result ofstarting with a fat molecule (MCT), tak-ing it apart and using the parts to buildnew fat molecules? Think of taking ahouse apart brick by brick, moving it ahundred yards, then putting it all back to-gether just as it was before. The househasn’t changed but a tremendous amountof energy was expended in the process.This is the biochemical basis for part ofthe thermogenic effect of MCTs. Doesthis mean that MCTs will make me fat?NO! REMEMBER, LESS BODY FAT ISMADE FROM EATING MCTs THANFROM EATING AN EQUAL NUMBEROF CARBOHYDRATES. Rather than con-tributing to fat stores, this effect reducesfat storage because a higher percentageof dietary energy is converted to heat.Alternatively, if electron transport isuncoupled from oxidative phosphoryla-tion, the energy spent to establish an elec-trochemical potential gradient across themitochondrial membrane is dissipated asheat instead of being conserved as ATP(14). For example, in brown adipose tis-sue, a pathway exists allowing protonleakage across the mitochondrial mem-brane (15).Another method of dissipating energyas heat, believed to occur in liver mito-chondria, is redox cycling involving theglycerophosphate and malate shuttles(6,13,16).

In the glycerophosphate shuttle,energy is spent to pump reducing equiva-lents outside the mitochondria to drive thereduction of dihydroxyacetone phosphateto glycerol-3-phosphate in the cytoplasm.The glycerol-3-phosphate then diffuses into the mitochondria and is oxidized toreform dihydroxyacetone phosphate,which then diffuses out of the mitochon-dria to complete the cycle. The net resultis the shuttle of glycerol-3-phosphate anddihydroxyacetone phosphate across themitochondrial membrane. Free energy isconsumed to drive the cycle, but sinceno net work is performed, the energy ul-timately appears as heat (16). The malate/aspartate shuttle works in the same man-ner.Finally, increased activity of        NA-K ATPase has also been suggested as athermogenic mechanism for wasting en-ergy as heat (17). It is estimated that 10-40% of the total energy expended by thecell is used to maintain the concentrationof gradient of sodium and potassium ionsacross the cell membrane (18). Sincethese ions also can cross the membraneby passive diffusion, an increase in theactivity of the enzyme could be a mecha-nism for spending ATP (5,7,18).Notably, BMR is increased followingexcess feeding of a mixed diet, but not ifonly excess

[conventional] fat is con-sumed (3). Since different fuel substratesfollow different metabolic pathways, it isperhaps not surprising that carbohydrate,fat and protein are converted to usable en-ergy (ATP) with differing efficiencies.Energy from carbohydrate is convertedto ATP with an overall yield of 75% effi-ciency, energy from dietary fat is con-verted to ATP at 90% efficiency and en-ergy from protein is converted to ATP at45% efficiency (detailed calculations canbe found in reference 3, chapter 8). It isevident from these considerations that theenergy expenditure required to replace 1mol of ATP will vary depending on thesubstrate mix being oxidized (3). Thisexplains, in part, the increase in BMR ob-served when subjects are changed froma mixed diet to a high carbohydrate diet(3).

We see the same thing at Parrillo Per-formance in our bodybuilders. When weswitch them to a high protein, high car-bohydrate, low fat diet, the rapidly losebody fat and gain muscle. We know thatenergy expenditure has increased becausethey are eating more calories than everand still losing fat. Of course, we trainthem harder than they’ve ever trained be-fore too.Thus, we see that maintenance of con-stant body weight requires not only thatlong term energy balance be maintained,but also that the average composition ofthe fuel mix oxidized be equivalent to thenutrient distribution in the diet (3). In otherwords, the energy intake required to main-tain body weight varies according to di-etary composition, since different fuels areconverted to ATP with different efficien-cies. The respiratory quotient (RQ) de-scribes the substrate mix being oxidizedby the body, while the food quotient (FQ)describes the ratio of CO2 produced toO2 consumed during oxidation of a rep-resentative sample of the diet (3). If en-ergy intake equals energy expenditure,constant body weight will be maintainedonly if RQ equals FQ. If RQ is less thanFQ, weight will be lost even in energybalance because the fuel mix being oxi-dized is inefficiently converted to ATP.Thus, more dietary energy will be lost asheat and less will be available as ATP tomaintain body weight. By reducing foodefficiency and while maintaining energybalance, one can bring about weight losswithout activating the body’s homeostaticmechanisms to maintain constant bodyweight. This concept is at the heart ofsuccessful weight reduction, but it’s notthe whole story.In intuitive terms, if RQ is less thanFQ this means that more fat is beingburned by the body than is being suppliedby the diet.

This fat is coming from adi-pose stores. Thus, one can draw uponstored fat for energy even when energyconsumption equals energy intake. Forexample, consider someone who main-tains absolutely constant body weight andwhose energy intake exactly equals en-ergy output. Let’s say this person is eat-ing 3,000 calories per day, provided as40% fat, 40% carbohydrate and 20% pro-tein. Now imagine this person continuesto consume 3,000 calories per day anddoes not modify his activity level, butchanges his diet to 10% fat, 70% carbo-hydrate and 20% protein. This person willlose weight because energy from carbo-hydrate is converted to ATP with less ef-ficiency than energy from fat is convertedto ATP. More of his dietary energy will belost as heat and less will be available forATP production. Not only will he loseweight while maintaining energy balance,but this weight will come from fat storessince his activity level dictates a certainRQ (within the constraints of substrateavailability). Aerobic activity is preferen-tially fueled by fat (a low RQ) while highintensity anaerobic activity (weight lifting)is fueled primarily by carbohydrate (a highRQ). Increasing lean body mass will alsohelp you burn more fat, since skeletalmuscle is the main site of fat oxidation.So while weight lifting is largely fueledby carbohydrates, the increase in leanbody mass will increase BMR and resultin greater fat metabolism.It is known from nitrogen balancestudies that the adult body maintains anearly constant protein content (as longas the diet provides sufficient protein) re-gardless of the proportions of fat and car-bohydrate in the diet (4). It is also knownthat the body’s glycogen reserve is on thesame order as on the daily turnover ofcarbohydrate (200-400 g) (4). Given theimportance of maintaining blood glucose,proper control of the carbohydrateeconomy is of critical importance (4).

Theglucostatic theory of food intake regula-tion describes the priority given to main-tenance of carbohydrate balance. Theadjustment of carbohydrate oxidation tocarbohydrate intake is carefully regulatedto result in stable glycogen reserves un-der widely varying dietary intakes (4). RQincreases following feeding, demonstrat-ing an increase in the proportion of car-bohydrate being oxidized in the fuel mix.The change in RQ following feeding isdetermined by the test meal’s carbohy-drate and protein content, but not its fatcontent (4). Thus, while protein and car-bohydrate feeding promotes carbohydrateoxidation, fat feeding does not promotefat oxidation (4). On days when carbo-hydrate excess carbohydrate is con-sumed, carbohydrate oxidation is in-creased to limit excess glycogen deposition, but if excess fat is consumed it issimply stored in adipose depots (4).

Thus,while protein and carbohydrate stores areclosely regulated, fat stores are generallynot regulated, and increase in response toover-consumption of fat. (If fat storeswere regulated we wouldn’t have obesepeople.)Of course, excess calories from pro-tein or carbohydrate can also be convertedto fat, but this is quantitatively  insignifi-cant for most people consuming an Ameri-can diet (4). Thirty percent of excess car-bohydrate calories are wasted as heat, andsince glycogen stores are generally farfrom full (especially in exercising individu-als), an excess carbohydrate load of 500g. can be accommodated without an in-crease in body fat. Notably, not all carbsare created equal. Complex carbohydrateswhich are broken down slowly are moreeffectively stored as glycogen than aresimple sugars, which are released into thebloodstream faster than they can be con-verted to glycogen. This means some ofthe simple sugars will be converted intofat and will “spill over” into body fatstores. Also, fructose is famous for itstendency to be converted to fat, and that’swhy we limit fruit and juice on our diet— more on that in a future article.In effect, oxidation is determined bythe difference between energy expendi-ture and energy consumed in the form ofcarbohydrate and protein (4). Since theaverage RQ is influenced by the degreeof repletion of glycogen stores and by thefat mass, weight  maintenance occurs onlywhen a particular body composition hasbeen reached (4).

In other words, for agiven dietary intake with some average FQ,body composition will change until RQequals FQ. The steady state is achievedwhen energy intake equals energy expen-diture and when the substrate mix beingoxidized is the same as the fuel mix beingconsumed. Simply put, since protein andcarbohydrate stores are narrowly regu-lated, to lose fat one must consume lessfat than one burns. This is achieved byconsuming a low fat diet and by perform-ing aerobic exercise. Weight training helpsby increasing lean mass and therefore theBMR.These arguments show that a mealwith a high carbohydrate:fat ratio(CHO:FAT) is more thermogenic than ameal with a low ratio. While carbohydrateand protein balance are closely regulated,fat balance is related to the amount of fatin the diet (3). During over-feeding,weight gain is closely related to fat intake.The body’s inability to regulate fat storesexplains why the incidence of obesity risesas the fat content of the diet increases (3).

References

1. Van Zant RS. Influence of diet andexercise on energy expenditure —  a re-view. Int. J. Sports Nutr.

2: 1-19, 1992.2. Guyton AC. Textbook of MedicalPhysiology. W.B. Saunders 1991.

3. Bjorntorp P, and Brodoff BN. Obe-sity. J.B. Lippincott Co., Philadelphia,1992.

4. Baba N, Bracco EF, and HashimSA. Enhanced thermogenesis and dimin-ished depositions of fat in response tooverfeeding with diet containing mediumchain triglycerides. Am. J. Clin. Nutr. 35:678-682, 1982.

5. Bach AC and Babayan VK. Mediumchain triglycerides: and update. Am. J.Clin. Nutr. 36: 950-962, 1982.

6. Crozier G, Bois-Joyeux B, ChanezM, Girard J, and Peret J. Metabolic ef-fects of induced by long-term feeding ofmedium chain triglycerides in the rat.Metab. 36: 807-814, 1987.

7. Geliebter A, Torbay N, Bracco EF,Hashim SA, and Van Ittalic TB. Overfeed-ing with medium chain triglyceride dietresults in diminished deposition of fat.Am. J. Clin. Nutr. 37: 1-4, 1983.

8. Lavau MM, and Hashim SA. Effectof medium chain triglyceride on lipogen-esis and body fat in the rat. J. Nutr. 108:613-620, 1978.

9. Seaton EB, Welle SL, Warenko MK,and Campbell RG. Thermic effect of me-dium chain and long chain triglycerides inman. Am. J. Clin. Nutr. 44: 630-634,1986.

10. Hill JO, Peters JC, Swift LL, YangD, Sharp T, Abumrad N, and Greene HL.Changes in blood lipids during six days ofoverfeeding with medium or long chaintriglycerides. J. Lipid Res. 31: 407-416,1990.

11. Hill JO, Peters JC, Yang D, SharpT, Kaler M, Abumrad N, and Greene HL.Thermogenesis in humans during over-feeding with medium chain triglycerides.Metab. 38: 641-648, 1989.

12. Parrillo Performance, Cincinnati,Ohio, original research results by JohnParrillo and Arthur Roberson, PhD.

13. Crozier. Medium chain triglycer-ide feeding over the long term: the meta-bolic fate of the C-14 octanoate and C-14oleate in isolated rat hepatocytes. J. Nutr.118: 297-304, 1988.

14. Baba, Bracco and Hashim. Role ofbrown adipose tissue in thermogenesisinduced by overfeeding a diet containingmedium chain triglyceride. Lipids 22: 442-444, 1987.

15. Nicholls. Brown adipose tissuemitochondria. Biochem. Biophys. Acta549: 1-28, 1979.

16. Berry, Clark, Grivell, and Wallace.The contribution of hepatic metabolismto diet-induced thermogenesis. Metab. 34:141-147, 1985.

17. Levin BE, and Sullivan AC. Regu-lation of thermogenesis in obesity. Novelapproaches and Drugs for Obesity,Sullivan AC, and Garrantini S, Eds. pg.159-180. John Libbey and Co. Ltd., 1985.

18. Vander, Sherman, andLuciano. Human Physiology —The Mechanisms of BodyFunction, p. 236. Published byMcGraw-Hill Book Company,1980.

2018-03-13T11:10:38+00:00 May 14th, 2009|Technical Supplement Bulletins|

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