In the previous bulletins, we have discussedhow to effectively lose body fat and whytraditional approaches to weight loss aredoomed to failure. To illustrate that thesetheoretical concepts are correct and reallywork in humans, I have selected one of thearticles in the reference list for detailed re-view. This will give you some idea of howthese experiments are performed. We do thesame sort of thing at Parrillo Performanceexcept out subjects are competitive body-builders and fitness athletes and out endpoints of measurement are lean body mass,body fat percentage and competitive wins.The study by Golay (1) was se-lected for review because it examines energymetabolism in the obese state, after weightloss by hypocaloric diet, and after relapse ofobesity following weight loss.
Thus, manyof the concepts previously discussed areempirically tested. The study was well con-trolled. measuring energy metabolism in thesame individuals before and afterhypocaloric diet (internal control) as well ascompared to lean controls (external controls).In addition, insulin resistance, which is as-sociated with obesity and impaired glucose-induced thermogenesis (GIT) was also ex-amined. The goal of the investigation was toexamine the impact of weight reduction byhypocaloric diet on glucose-induced ther-mogenesis and its relation to relapse of obe-sity.Methods: Energy expenditure wasmeasured by indirect calorimetry for threehours following administration of a 100g glu-cose load. The glucose-induced thermogen-esis was expressed as the percent of energycontained in the glucose dose. Obese sub-jects were divided into three groups accord-ing to their degree of glucose tolerance: nor-mal glucose tolerance, impaired glucose tol-erance, and diabetic (NIDDM). Thirty-twoobese individuals were studied before andafter body weight loss ranging from 9.6 to33.5 kg achieved by hypocaloric diet for fourto six months.
Eight obese non-diabetic pa-tients were examined six years later after re-lapse of obesity had occurred.Results and Discussions:Although energy expenditure wasincreased in all groups followingadministration of the glucose load,GIT was lower in obese patientsthan in nonobese controls. Further-more, diabetic obese patients hadsignificantly lower GIT than non-diabetic obese patients. Afterweight loss by hypocaloric diet,GIT was dramatically reduced innon-diabetic obese patients.Weight loss induced non diminu-tion of GIT in the diabetic group.After relapse of body weight gain,GIT returned to its original valuebefore weight loss. However, basalenergy expenditure failed to return to thesame level as before weight loss.These results confirm other reportsthat postprandial thermogenesis followingglucose ingestion is lower in obese than inlean subjects. Regression analysis showedthat the main factor in explaining the decreasein GIT observed in obesity is an increase inplasma insulin levels. This suggests that in-sulin resistance may play a role in suppress-ing GIT. This obviously could play a role inthe development of obesity since if less en-ergy is wasted as heat more is available forstorage. Reduction of body weight by ca-loric restriction is associated not only with adecrease in BMR but also with a bluntedthermic response to feeding (1,2,3). The fur-ther reduction in GIT in obese followingweight loss may thus be involved in relapseof obesity. Notably, while GIT returned to itspre-diet level following obesity relapse, BMRdid not.
This is likely to be due to loss oflean body mass (skeletal muscle) during ca-loric restriction, which was not replaced dur-ing obesity relapse, although this possibil-ity was not investigated.This experiment demonstratesmany of the principles discussed in the in-troduction. Caloric restriction reduces thebody’s rate of energy expenditure, so thatwhen normal caloric consumption is re-sumed, body weight (fat) is recovered. Thissort of compensation is exactly what onewould expect of a homeostatic mechanism.This report confirms that a hypocaloric dietfails to achieve body weight control and infact activates an “anti-starvation” responsewhich works by decreasing energy expendi-ture. That BMR was not recovered after obe-sity relapse suggests that repeated cyclesof hypocaloric dieting just make it evenharder to lose weight. This undesirable ef-fect can be overcome with exercise.An Integrated Approach To BodyWeight ControlThroughout this report it has been empha-sized that obesity is not a problem of excesscaloric consumption because, in fact, obesepeople do not, on average, consume morecalories than non-obese people (2,3). There-fore treatment of obesity by caloric restric-tion does not make sense on at least grounds:1) It is unrelated to the cause of obesity; 2)
The body has compensatory mechanisms toadapt to the low caloric diet and to recoverfat stores when caloric consumption is re-sumed; and most importantly, 3) It is empiri-cally observed to fail 90-95% of the time (2,3).Five great discoveries in nutritionnow make it possible to devise a successfulapproach to body weight control. These are:1) The body has a weight regulation mecha-nism located in the hypothalamus; 2) Differ-ent foods are converted to ATP with differ ent efficiencies; 3) The insulin:glucagon ra-tio is determined by diet composition(CHO:PRO) and can exert powerful influenceon body weight; 4) the sympathetic nervoussystem is activated by carbohydrate feed-ing and can direct partitioning of ingestedenergy; and 5) While carbohydrate and pro-tein stores are tightly regulated, the size ofadipose depots correlates most strongly withfat content of the diet.From these considerations a simpleprescription for long-term body weight con-trol follows:1) Caloric intake should not be dras-tically reduced below maintenance require-ments.
This simply reduces BMR, TEF andincreases lipoprotein lipase. One cannotmake the body healthier by depriving it offood. It is infinitely preferable to achievenegative energy balance by increasing en-ergy expenditure through exercise. This doesnot activate the starvation response, and infact increases BMR as well as increasing en-ergy expenditure in activity. For the averageobese person consuming the typical Ameri-can diet (40% fat, no caloric restriction isneeded. The simplest way to determine totaldaily energy expenditure is to weigh yourfood and calculate how many calories youare consuming per day during a time whenyou weight is not changing. This representsthe energy intake required to maintain yourpresent body weight. In general, this is pro-portional to lean body mass and activitylevel. Try to lose fat at the rate of one poundper week. Since one pound of body fat equals3500 calories, this represents a daily energydeficit of 500 calories. It is best to achievethis deficit by performing 500 calories worthof aerobic exercise per day (which is aboutone hour of moderately intense activity). If areduction in energy intake is needed, limit itto 10% of the of the maintenance require-ment. It is best to lose weight slowly, sincethis seems to achieve more permanent re-sults (2,3) and minimizes loss of lean bodymass and consequent reduction of BMR.Monitor body composition (percent bodyfat) during weight loss to ensure muscle isnot being lost.2) Increase the CHO:FAT ratio inthe diet.
This increases thermogenesis andFQ. (A diet with a low fat content has a highFQ.) Remember that fat deposition is relatedto fat consumption.3) Perform regular low to moderateintensity aerobic exercise. This decreasesRQ. When RQ is less than FQ this meansthat the body is burning more fat than it isconsuming. This fat comes from adiposestores. Low to moderate intensity aerobicexercise is fueled primarily by fat, and if littlefat is provided by the diet, stores will be re-duced.4) Consume a CHO:PRO ratio whichwill result in an insulin:glucagon ratio com-patible with fat loss. Remember that insulinpromotes fat storage while glucagon in-creases use of fat for energy. Empirically, adiet consisting of 30% protein, 65% carbo-hydrate and 5% fat (as energy) has provenvery successful for many people (4). TheParrillo Performance Nutrition Manual hasall the details of how to fine tune the diet tofit your particular needs.5) Choose complex carbohydratesand limit refined carbohydrates, especiallysimple sugars. Selection carbohydrates witha low glycemic index will reduce insulin lev-els and decrease fat storage. Limit fructoseconsumption, which is profoundly lipogeniceven though it has a low glycemic index (5).Fructose enters the glycolytic pathway be-yond the phosphofructokinase step and thusits metabolism is largely unregulated.
It israpidly metabolized to acetyl-CoA whichserves as a substrate for de novo fatty acidsynthesis. While excess calories from car-bohydrates are readily stored as glycogen,excess calories from fructose are convertedto fat.In summary, obesity is not a prob-lem of excess energy consumption, but ratheris a direct consequence of the Americanlifestyle. This is supported by the observa-tion of increased incidence of obesity inAmerican immigrants from Asia and Japan.A person may consume an appropriate num-ber of calories, but if he is sedentary andderives 40% of his calories from fat, his RQwill be greater than his FQ and he will neces-sarily accumulate excess body fat. Caloricrestriction in such an individual would serveno useful purpose. What is called for is adiet low in fat and high in complex carbohy-drates combined with regular exercise. Thesuccessful dieter will realize that permanentweight loss requires a lifelong commitmentto healthy diet and exercise habits. The strat-egy presented here will work for anyone try-ing to get in better shape, from the man onthe street to the Olympia competitor. Youwant results? Get with the program.
1. Golay A. Blunted glucose-induced ther-mogenesis: a factor contributing to relapseof obesity. Intl. J. Obesity 17 (Suppl 1) s23s27, 1993
4. Bjorntorp P, and Brodoff BN. Obesity. J.B.Lippincott Co., Philadelphia, 1992.
5. Remington DW, Fisher AG, and ParentAG. How to lower your Fat Thermostat. Vi-tality House International, Provo, 1983.
22. Parrillo Performance, Cincinnati, Ohio,original research results by John Parrillo andArthur Roberson, PhD.
24. Shafrir E. Fructose/sucrose metabolism,its physiological and pathological implica-tions. Sugars and Sweeteners , KretchmerN, and Hollenbeck CB, Eds. p. 63-98. CRCPress, 1991.