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Bulletin #19 – The Ultimate Formula For Losing Body Fat

Everyone is concerned about theirbody fat level. Whether you’re a competi-tive bodybuilder trying to get down to 4%body fat or just someone trying to get inbetter shape, everybody wants to knowthe best way to lose fat and keep it off.It’s no exaggeration to say that we atParrillo Performance are world class ex-perts at getting in shape. Here in Cincin-nati we work with competitive bodybuild-ers pushing the human body to itslimit. Our greatest satisfaction isseeing our athletes improve andwin contests. We convert begin-ners into winners, amateurs intoprofessionals and professionalsinto champions.Many people have had aweight problem all their lives andhave tried all the diets without suc-cess. For every competitive body-builder, there are probably a thou-sand other people who have beencutting calories in a desperate at-tempt to get rid of a few (or a lot)excess pounds. This approach isdoomed to fail.In this series of articles aboutenergy metabolism and thermo-genesis, we explore in great detail the bio-chemistry and physiology of weight loss,and explain how to do it correctly.

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Wecan teach you how to lose fat and keep itoff for the rest of your life. The strategy of how to lose fat whilemaintaining lean body mass is the sameregardless of whether you’re obese or al-ready in great shape. There are a few ex-tra tricks you can use to get into com-petitive shape, but the foundation of theprogram is the same.As you read, keep in mind that thisarticle is written for anyone wanting tolose fat and get lean. The same conceptsapply to everyone. We will discuss theprocess of fat loss and how to controlbody composition by diet and exercise.We will discuss the effects of low caloriediets and explain why they fail in 95% ofthe cases. We will explain the proper wayto structure your diet to fuel your me-tabolism, so you can increase metabolicrate while dieting instead of decreasing it.As a natural result of this program, yourbody will be leaner and have more energythan ever before.This series of articles represents thescientific basis for the diet described inthe Parrillo Performance Nutrition Manual.The manual contains the nuts and boltsof how to build your diet, describing ex-actly which foods to eat, how much toeat and how to structure your meals. Italso comes with a food scale, which youwill need to weight your food. The Nutri-tion Manual is really the only piece ofequipment you will need. Supplements youmay find helpful include CapTri, Hi-Pro-tein Powder, Pro-Carb Formula, and Ad-vanced Lipotropic Formula. The place tostart, however, is with the proper diet.Without that as the foundation, you willnever achieve your goal.Results. That’s what we’re about.Everybody has a dream. We can help youmake it come true. We’ll start with a dis-cussion of obesity and low calorie diet-ing, since this is a major medical problemin the U.S.ObesityCurrent estimates indicate that 35million people in the United States areobese, defined as 20% above idealbody weight (1). Obesity is a riskfactor for diabetes, hypertension,coronary artery disease and sometypes of cancer, as well as being anindependent risk factor for prema-ture mortality (3,4).

Furthermore,weight loss reduces the risk forthese same diseases (4). These ob-servations suggest that obesity mayplay a causal role in some cases ofthese diseases or that obesity sharesa common cause with these dis-eases. Among the obese, hyperten-sion is three times more commonand hypertriglyceridemia and diabe-tes are two times more commonthan in the nonobese (1). In addi-tion, obesity is often associated withlow HDL cholesterol levels (1). While re-markable progress has been made in re-cent decades in many arenas of medicine,the successful treatment of obesity re-mains an enigma. Given the widespreadprevalence of obesity and its associationwith serious disease states, a re-evalua-tion of current approaches to obesity man-agement seems warranted.It is generally assumed that obesity isthe result of excess caloric consumption.However, most obese people do not haveincreased caloric intakes over those ofnonobese people (3,4). In fact, long-termstudies of deliberate over-feeding and un-der-feeding in humans and rats demon-strate that body weight is regulated to return to some “programmed” value follow-ing periods of altered food intake (4).Furthermore, the observed increase ordecrease in body weight following over-feeding or under-feeding is smaller thanpredicted by simple considerations of en-ergy balance (5). These observations sug-gest that the body has some way of regu-lating its weight in the face of altered en-ergy intake. Many theories and experi-ments have been devised to elucidate this“weight regulation mechanism.” The mostimportant of these will be discussed be-low. A synthesis of the available literaturesuggests that perhaps a successful ap-proach to long-term weight control is nowwithin reach.Low-Calorie DietsThe conventional treatment for obe-sity consists of a hypocaloric (low-calo-rie) diet (3,4). This approach derives fromthe assumptions that obesity is caused byhypocaloric (high calorie) consumption,and that weight reduction can be achievedby reducing calories. The empirical real-ity is that 90-95% of people who loseweight by restricting calories experiencerelapse of obesity within five years (2,3).This is not necessarily a consequence ofhyperphagia (overeating following caloricrestriction, but occurs even when reason-able form of caloric intake is resumedfollowing weight loss. This is explainedintuitively by saying that the body inter-prets periods of caloric deprivation as star-vation (i.e., adequate food is not available),so that when eucaloric consumption re-sumes, the body repletes its fat stores asa defense mechanism to withstand thenext bout of famine.This makes perfect sense from anevolutionary point of view. Individualswho have adapted to the stress of famineby maintaining fat stores in times of plentyhave been selected through evolution.Fortunately, the biochemical mechanismsby which this occurs are now understood.Chronic caloric restriction causeschanges in the body’s pattern of energymetabolism and substrate utilization whichfavors weight gain (especially fat gain)when normal caloric consumption is re-sumed (3,4,5).

[“Normal caloric con-sumption” refers to the level of food in-take consumed by healthy, nonobesepeople, about 2,400 calories per day formen and about 1,500 for women (4).]Specifically, 25-50% of weight lost bycaloric restriction is muscle mass (3,4).This result is observed even when using“protein-sparing” low calorie diets. Leanbody mass (LBM) is the single most im-portant determinant of basal metabolic rate(BMR), and BMR is the largest compo-nent of energy expenditure (3,4,6,7).

Thus, when weight is lost by reducingcalories, the body’s energy requirementis also reduced, so that a normal diet thenresults in positive energy balance andweight gain occurs (3).Unfortunately, the weight gainwhich ensues following a hypocaloricregimen is not solely a replacement ofmuscle mass, but in fact is biasedtoward the fat compartment (4). Fatstores are preferentially repleted toprepare the body for the next famine.The net result is to return to the originalbody weight before dieting (or slightlyabove), albeit at a higher body fatpercentage (4). This weight cyclingphenomenon is commonly referred to as“yo-yo dieting.”How is weight gain following caloricdeprivation biased toward the fat compart-ment? Hypocaloric consumption increasesthe activity of lipoprotein lipase (LPL), thekey enzyme regulating fat storage(3,4,8,9,10). When body weight returnsto its pre-dieting level (i.e., when fat storesare repleted), LPL activity also returns toits normal level (5). This is one enzymaticmechanism underlying relapse of obesity,and presumably represents an evolution-ary strategy to survive bouts of famine.In addition, caloric restriction de-creases the thermic effect of food (TEF),the amount of food energy wasted as heat(3,4,11). During over-feeding, a signifi-cant proportion of the excess calories isliberated as body heat. This effect is largelymediated by stimulation of the sympatheticnervous system by carbohydrate inges-tion (3). During under-feeding, TEF isreduced and the efficiency of conversionof food energy to body weight (food effi-ciency) is increased. This also contrib-utes to obesity relapse following low calo-rie diets. Finally, hypocaloric diets alsodecrease the level of thyroid hormones(specifically T3) and this further decreasesbasal metabolic rate (3,12).In summary, hypocaloric diets areempirically observed to fail in the treat-ment of obesity in 90-95% of cases (3,4)and would be expected to do so on theo-retical grounds. Historically, obesity hasbeen attributed to consumption of calo-ries in excess of needs, but in fact obesepeople do not consume more calories thannonobese people nor do they have reducedenergy requirements (3,4). This simplis-tic thermodynamic approach fails to takeinto account that the human body is not abomb calorimeter but is rather aHomeostatically regulated machine whichstrives to maintain the steady state. If ca-loric intake is reduced, changes in hor-mones, enzymes, nervous system activ-ity, and body composition occur so as tocompensate and try to recover the origi-nal steady state. A more fruitful approachmight be to consider that body weight andbody composition are homeostatically regulated just like every other parameterof body function. The successful ap-proach to obesity management involveschanging the steady state which the bodystrives to maintain, rather than reducingenergy intake and setting into play thebody’s compensatory mechanisms, whichcannot be overcome.In the next bulletin, we continue ourseries on fat loss with a look at how en-ergy metabolism affects your ability to getlean and musclular.

References

1. Kaplan NM. The deadly quartet:upper body obesity, glucose intolerance,hypertriglcyeridemia, and hypertension.Arch. Intern. Med. 149: 1514-1520, 1989.

2. U.S. Preventive Services TaskForce. Guide to Clinical Preventive Ser-vices, Fisher M. (Ed.), chapters 1, 2, 3,16 and 18. Williams and Wilkins, Balti-more, 1989.

3. Bjorntorp P, and Brodoff BN. Obe-sity. J.B. Lippincott Co., Philadelphia,1992.Energy Metabolism and Thermogenesis: The Ultimate Formula For Losing Body Fat

4. Remington DW, Fisher AG, andParent AG. How to lower your Fat Ther-mostat. Vitality House International,Provo, 1983.

5. Nelson KM, Weinsier RL, JamesLD, Darnell B, Hunter G, and Long CL.Effect of weight reduction on energy ex-penditure, substrate utilization, and ther-mic effect of food in moderately obesewomen. Am. J. Clin. Nutr. 55: 924-933,1992.

6. 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.

7. Van Zant RS. Influence of diet andexercise on energy expenditure —  a re-view. Int. J. Sports Nutr. 2: 1-19, 1992.

8. Cryer A. Tissue lipoprotein lipaseactivity and its action in lipoprotein me-tabolism. Int. J. Biochem. 13: 525-541,1981.

9. Eckel RH. Lipoprotein lipase: amultifunctional enzyme relevant to com-mon metabolic diseases. New Engl. J.Med. 320: 1060-1067, 1990.

10. Kern et al. the effects of weightloss on the activity and expression of adi-pose tissue lipoprotein lipase in very obesehumans. New Engl. J. Med. 322: 1053,1990.

11. Golay A. Blunted glucose-inducedthermogenesis: a factor contributing torelapse of obesity. Intl. J. Obesity 17(Suppl 1) s23 s27, 1993

12. Tyzbir RS, Kunin AS, SimsNM, et al. Influence of diet compositionon serum triiodothyronine (T3) concen-tration, hepatic mitochondrial metabo-lism and shuttle system activity in rats.J. Nutr. 111: 252-289, 1981.

2018-03-13T11:10:38-04:00 May 13th, 2009|Technical Supplement Bulletins|

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