lyle mcdonald - the ultimate diet 2.0

The Ultim e Die t 2.0 at

by Lyle McDonald

Page 1 http://www.bodyrecomposition.com

This book is not intende d for the treatmen t or preventio n medica l treatment , nor as an alternativ e to medica l advice . presente d for informatio n purpose s only. Recommendation adopte d withou t a full revie w of the scientifi c reference s physician . Use of the guideline s herei n is at the sole choice and

of disease , nor as a substitut e for It is a revie w of scientifi c evidence s outline d herei n shoul d not be provide d and consultatio n wit h a ris k of the reader.

Copyright : 2003 by Lyle McDonald . All right s reserved.

This book or any par t thereof , may not be reproduce d or recorde d in any form withou t permission in writin g from the publisher , excep t for brief quotation s embodie d in critica l article s or reviews. For informatio n contact: Lyle McDonald 7584 Chevy Chas e Dr. #210 Austin, Tx 78752 email : [email protected] ISBN: 0-9671456-2-7 FIRS T EDITION FIRS T PRINTING


AcknowledgementsAs always , withou t Dan Duchaine , neithe r thi s book nor any of my other s would have happened . I owe him a debt I can neve r repay. Anothe r acknowledgemen t to Shell y Hominu k for giving me permissio n to use the Ultimat e Diet titl e for thi s book, on top of everythin g else she' s done for me. Thanks , of course , to my tester s who gave invaluabl e feedbac k on the diet. And, once more , thank s to everyon e who continue s to buy and rea d my stuff , it keep s my ban k very happy.


ForewordAfter my las t littl e dru g book on Bromocriptine , I wante d to get back to my mai n are a of interes t and rea l are a of expertise : integrate d method s of trainin g and nutrition . I will be mentionin g some drug s tha t migh t be usefu l along the way, but that' s not the mai n focus of this book. Actually , the best way for me to introduc e thi s book is wit h a story/histor y lesson. The stor y of thi s book begin s jus t over twent y year s ago in 1982. Tha t year , Dan Duchain e and Michae l Zumpan o introduce d the Ultimate Diet to the world of bodybuilding . In a nutshell , the Ultimat e Diet was a 10 day cyclical diet and trainin g plan , incorporatin g three differen t trainin g and eatin g approache s in a coordinate d fashion . Dru g option s were suggested since the laws were less stringen t then . It was radica l and revolutionar y for its time combining cuttin g edge scienc e wit h good old intuitio n (and mayb e a littl e lucky guesswork ) to creat e a complet e plan for generatin g extraordinar y result s in ordinar y people . It achieve d somethin g few plan s could claim : fat loss wit h muscl e gain or at the very leas t fat loss wit h no muscl e loss. With sligh t adjustment s in calori e intak e it could be use d for muscl e gain wit h minima l fat gain. Fiftee n year s later , the sam e Dan Duchain e release d an "updated " versio n of tha t diet in his semina l book Underground Bodyopus: Militant Body Recomposition . Now a 7 day plan, withou t nearl y the complexit y as the origina l Ultimat e Diet, Bodyopu s kicke d off an entirel y new interes t in the bodybuildin g subcultur e regardin g cyclical diet s and cyclical ketogeni c diet s in particular . This is wher e I ente r the story. In 1997, I was terribl y bored wit h my life, lookin g for somethin g to do. I latche d onto the Bodyopu s diet like a drownin g ma n grabbin g a life preserve r and neve r looked back. In one sense, it mirrore d Duchaine' s origina l interactio n wit h Zumpan o and the Ultimat e diet back in the 80's. At tha t time , Zumpan o was the gur u and Duchain e was the bored detai l man lookin g for somethin g new to do wit h his life. In 1997, Dan was the gur u and I was the bored detai l man. That' s how I like to thin k of it anyhow ; I don' t know if Dan saw it like tha t or not. In any event , wha t starte d as a whim , writin g a weekl y diar y of my experience s on the diet turne d into somethin g far more. A couple of year s later , I wrot e the be-all , end-al l book on ketogeni c dieting . Eve n Dan admitte d I kne w more abou t "his" diet tha n he did which was as grea t an hono r as I could receive . I becam e the keto-gu y (a nicknam e I still can' t shak e no matte r how har d I try) even thoug h I neve r reall y advocate d the m in the sens e tha t you'd think. Agains t all odds, considerin g how badl y it was writte n and how borin g it was to read , the keto book actuall y sold decently . If nothin g else, it establishe d me as a "name " in the industry . A detailobsesse d geek, min d you, but a "name " nonetheless. In the 6 year s since tha t book, researc h into huma n physiology , nutrition , biochemistry, etc. has advance d at an amazin g and exponentia l pace. Scienc e is finall y gettin g to the mechanisti c reason s tha t thing s happe n in the body. Knowin g how thing s happe n in the body allow s for a certai n measur e of control . This book represent s an integrate d approac h to all of it. Page 4 http://www.bodyrecomposition.com

A not e on the titl e of thi s book In case you didnt look at the cover, the titl e of thi s book is The Ultimate Diet 2.0. Before I go any further , I wan t to explai n the reasonin g behin d the name . The firs t reason , min d you, is that I suck at coming up with creative names (the titles of my last two books prove that). At leas t I'm honest . Bu t eve n if I wer e creative , I stil l woul d hav e chose n to call it The Ultimate Diet 2.0, so that' s actuall y not the mai n reaso n thi s time. If there' s a primar y reaso n I chose the titl e I did, it's out of tribute . As above, thi s book is basicall y an updat e and revisio n to the dietar y approac h tha t helpe d me gain whateve r amount of respec t and importanc e I hold in the bodybuildin g or sport s nutritio n world. Fro m the Ultimate Diet came Bodyopus . From Bodyopus came my first book. From my first book came my career. Now, since I got involve d wit h this whole mess at the Bodyopu s stag e of things , you may be wonderin g why I didn' t call this Bodyopu s 2.0 instead . Ther e are a few reasons . First , it just seeme d a bit inappropriate . Bodyopu s was Dan' s brainchil d and the nam e held a very specific meanin g to him. The Ultimate Diet 2.0 is a littl e more generi c of a titl e and jus t seem s a littl e less pretentiou s in tha t respect . Or not. Also, Dan passe d awa y thre e year s ago (2000), and it jus t seeme d disrespectfu l to confuse people wit h two books calle d Bodyopus . Eve n thoug h it's a few year s out of dat e and had a minor numbe r of technica l mistakes , I still thin k everyon e shoul d own a copy of Bodyopus . Havin g two books w h tha t titl e would hav e confuse d the averag e person . Finally , I didn' t know who legally it owned the right s to the Bodyopu s name and didn' t wan t to get my ass sued. Perhap s more importantly , thi s book doesn' t reall y revis e the seve n day Bodyopu s plan, wit h its two type s of weigh t trainin g (tensio n and depletion ) and two distinc t dietar y period s (lowand high-carb) . My firs t book was closer to that , more of a detail/technica l manua l for keto/cyclica l keto diets . If anything , tha t firs t book shoul d hav e been calle d The Bodyopus Companio n or somethin g equall y silly. Rather , wha t I'm going to describ e her e comes directl y out of the origina l Ultimat e Diet pla n from 1982, which had thre e type s of weigh t training , thre e type s of eating , and a lot more complexit y (and potentia l source s of confusion) . On variou s levels , includin g the most fundamenta l ones, the origina l Ultimat e Diet was the impetu s for thi s book; as a tribute/revision to tha t diet, I thin k the name s shoul d be the same. The titl e of thi s book, The Ultimate Diet 2.0, has severa l meanings . The firs t is simpl y one of tribut e to Duchain e and Zumpano' s origina l Ultimat e Diet, release d all the way back in 1982. It' s fascinatin g readin g now and the y were ahea d of thei r time by man y years . This book is also an updat e to tha t sam e diet integratin g finding s abou t metabolism , fat loss and muscl e gain to optimiz e it. Anyone involve d wit h computer s know s that new version s of stuff get a new number. Henc e 2.0. Finall y (hopefully) , it will be the las t diet you need . Henc e the word "ultimate." Page 5 http://www.bodyrecomposition.com

IntroductionFace it, you'r e normal . Well, more norma l tha n you like. Eve n thoug h you've traine d like an animal , take n all the supplement s and done everythin g you'r e suppose d to, you'r e still closer to norma l tha n not. Sure , you carr y more muscl e tha n the averag e perso n on the stree t (whic h isn't sayin g much ) and you'r e leane r too (whic h is sayin g even less). You're as health y as it gets (physicall y anyhow ) and your doctor is thrilled. But we both know tha t there' s tha t naggin g voice tha t isn' t satisfied : norma l isn' t the same as content . Eithe r you don' t hav e as muc h muscl e as you'd like or you can' t get rid of the last littl e bit of fat. How do I know this ? Am I psychic ? Hav e I been watchin g you throug h your window ? No. I know thi s becaus e folks who hav e optimize d metabolism s and good genetic s don't buy books like thes e in the firs t place . We alway s notic e them in the gym, the folks who seem to brea k all the rule s of trainin g and diet and still look bette r tha n we can hope to. They do nothing but benc h and curls , eat a jun k food diet and jus t get big, symmetrica l and ripped . We can, and should , hat e them . No, it's the folks who are lookin g for salvatio n who keep me in business. In buyin g thi s book, you'r e continuin g a long-hel d traditio n of graspin g at anythin g that migh t offer a solution . If at all possible , it shoul d be simpl e and unobtrusive . Mayb e a pill. Well, I hat e to burs t your bubbl e but thi s is the truth : if it were simpl e and easy to become supranormal, everyon e would do it and you'd see a lot more example s walkin g around. Wha t I'm going to describ e in thi s book isn' t easy and it isn' t simple . It's also not magic . I hav e some physiologica l trick s tha t may look like magic , but they'r e not. Since my biggest bodypar t is my brain , I've use d it to (re)develo p an integrate d syste m of trainin g and nutrition (and some supplement s and drugs ) tha t let you sideste p some of the problem s inheren t in achievin g a supranorma l body. In redevelopin g the origina l Ultimat e Diet, I've applie d the most cuttin g edge research available , discusse d variou s element s of the diet wit h man y othe r smar t folks, and done cycle afte r cycle testin g the diet both in myself and in my multipl e guine a pigs. After man y year s of testing , desig n and redesign , I give you the Ultimat e Diet 2.0 (UD2 from her e on out).


Chapte r 1: Wha t thi s boo k is an d wh o it's for

So her e we are again , anothe r book, anothe r chapte r on definin g the problems . If you read my las t book, you alread y probabl y hav e some idea wha t I'm going to say. In short , dietin g to low bodyfa t levels sucks . Actually , dietin g suck s acros s the boar d but the rea l problem s star t when you star t to get far below normal . So what' s normal? In moder n times , an averag e mal e may be carryin g 18-25% bodyfat , an averag e female 21-28%. Many, many (too many) people are much fatter than that. Health y bodyfa t levels are considere d to be 11-18% for men and 18-25% for women . To the body-obsessed , excep t mayb e at the lower levels , that' s still fat. Male bodybuilder s (and other athletes ) thin k in term s of sub-10 % bodyfa t levels , female s typicall y in the low to mid teens. Researcher s would probabl y debat e the validit y of such belief s but who cares ; if you believ e it, it's tru e to you. Perhap s more importan t is tha t it is your goal. Most diet s or diet books are aime d at the folks who are tryin g to get somewher e in the real m of average . Ther e are tons to choose from out there . Any discover y or piece of research tha t migh t affect thes e folks can be turne d into a quick fix diet book. One of thes e days , I'm going to writ e my own, mak e a zillion dollar s and retire. For obese folks jus t tryin g to lose weight , prett y muc h any non-retarde d diet will work. The mai n issue s to deal wit h ther e hav e more to do wit h anxiet y and the issue s involve d in changing long-ter m eatin g and activit y patterns . And even thoug h some reader s migh t disagree , gettin g a mal e to 12-15% bodyfa t or a femal e into the 18-22% rang e usuall y isn' t tha t difficult . Basic food control , adequat e protei n and exercis e will usuall y get it done withou t too muc h trouble . This book isn' t aime d at eithe r group. By the time folks get to the 12-15% (18-22% for women ) range , anxiety , food contro l and changin g habit s usuall y aren' t the problem . For bodybuilder s and athlete s meticulou s food contro l and trainin g is par t of the lifestyle . It's whe n folks star t tryin g to achiev e the lower extremes of bodyfat percentage that other problems start to occur. Ravenous hunger, severe muscl e loss, metaboli c slowdow n and screwe d up hormone s are a few of the usua l problems. Wome n and some men hav e an additiona l proble m mobilizin g and gettin g rid of stubbor n fat (hip/thig h are a for women , ab/low-bac k fat for men). In presentin g the UD2, I'm going to assum e tha t you alread y hav e the disciplin e and anxiet y issue s well unde r control . While the y are less of a proble m on thi s diet tha n on many others , it's the real physiologica l problem s I'm settin g out to addres s and fix.


Who am I? I imagin e most reader s know me as the autho r of The Ketogenic Diet, which is more or less considere d to be the be-all , end-al l book on low-carbohydrat e dieting . Fewe r reader s seem to be awar e of my secon d book, which deal t wit h the dru g Bromocriptine . If you've rea d eithe r book, you'll hav e a bette r backgroun d to understan d the informatio n in thi s book. If not, don' t worry , I'll try to give you enoug h backgroun d to understan d the UD2. To be honest , to give the rational e for everythin g in detai l would tak e more page s tha n I wan t to take . I'm going to cover the basics and you'll jus t hav e to tak e my word for the rest.

Who are you? So who are you, the idea l UD2 candidate ? Actually , let me backpeda l a bit and tal k about who thi s diet isn' t for. It's not for ran k beginners . The trainin g and dietar y recommendations simpl y aren' t appropriat e for someon e jus t startin g out. Get 3-6 month s of basic trainin g under your belt and get your basic diet deal t wit h firs t before even considerin g the syste m describe d in thi s book. As above, it's not for the genera l fat folks out there . In general , unti l male s hit 12-15% bodyfa t and female s 20-22% bodyfat , a more standar d approac h is probabl y fine (and desirable). I recommen d folks use the simples t approache s the y can unti l thos e approache s stop working. Firs t and foremost , if you'r e a male , you shoul d hav e no more tha n 15% bodyfat , femal e no more tha n 22% bodyfat . Most likely you wan t to get leane r while maintainin g or even increasing muscl e mass . This could be for a bodybuildin g contest , for some specia l event , or simpl y because you wan t to see wher e the body has veins . Alternately , you may wan t to gain muscl e withou t the accompanyin g fat gain (or even sligh t fat loss). Perhap s you'r e a performanc e athlet e like a powerlifte r or an enduranc e athlet e who need s to lea n out while maintainin g performance . The UD2 can be use d for all thos e goals. It shoul d go withou t sayin g tha t you hav e to be exercisin g for the diet to work. By exercise, tha t mean s weigh t trainin g (I'll tal k abou t enduranc e athlete s separately) . Again , if you'r e new to weigh t training , the UD2 isn' t appropriate ; get 3-6 month s of trainin g unde r your belt first . If you'r e not plannin g on exercising , this diet will not do you any good. In fact, it'll probabl y just make you fatter. You'll need a reasonabl e (but not insane ) amoun t of diet disciplin e and you shoul d hav e a basic understandin g of nutritio n and diet setup . If you don' t know wha t a protei n or carbohydrate is, or how to set up a diet, you'r e going to be totall y lost readin g this . I've trie d my best to provide all the informatio n you need but I'm going to mak e some assumption s abou t basic knowledge . If you mee t thi s rathe r narro w set of criteria , rea d on. Page 8 http://www.bodyrecomposition.com

Why no t jus t us e standar d dietin g approaches? You may be wonderin g why you shouldn' t jus t use one of the myria d standar d dieting program s out there . I mean , pick up any bodybuildin g magazine , and ther e are tons of plan s that claim to let you achiev e everythin g the UD2 does withou t all of the hassle . Why is the UD2 superior? The mai n proble m I hav e wit h the standar d advic e is tha t it's jus t so standard . High protein , low to moderat e fat, low to moderat e carbohydrates , weigh t trainin g and aerobic s is the standar d prescriptio n for gettin g rippe d up. If all of the magazine s are writin g it, it m t work, us right ? Well, yes, up to a point. Frankly , I hav e no proble m wit h the standar d advic e as long as it's producin g results . As I said above, I actuall y prefe r simple r approache s as long as the y work. In man y people , who frequentl y hav e geneti c advantage s tha t the y migh t not even be awar e of, the y work jus t fine. Bu t base d on observation s at the gym and the feedbac k I get, not everybod y is so lucky (I'll talk abou t some of the reason s the geneticall y lucky are lucky nex t chapter) . The realit y is, only a smal l portio n of the people who try actuall y achiev e thei r goals usin g the standar d advice . That tell s me that , standar d or not, it's not effective. And don' t get me starte d on the advic e given by pro bodybuilders . It shouldn' t even be take n into consideratio n unles s you've got the arra y of steroids , thyroi d medications, thermogenic s and appetit e suppressant s tha t the y use to get read y for a contest . A curren t pro is reporte d to hav e said the followin g abou t contes t dietin g "Ther e is no magic diet, buy as many drug s as you can afford and starv e yoursel f for as long as you can stan d it." For the majority , the geneticall y averag e (or disadvantaged) , any numbe r of problem s can stop the diet in its tracks . A metabolicall y averag e diete r may lose 1 lb of muscl e for every 3 lbs of fat lost tryin g to get to singl e digit bodyfa t levels . Wome n have even more problem s with muscl e loss, not to mentio n issue s wit h lower bodyfa t mobilization . For some, metabolic adaptatio n cause s fat loss to slow or stop completel y long before goals are reached . Ther e are all kind s of reason s thes e problem s occur, most of which can be trace d to the body's man y annoying ways of adaptin g to a diet. Those same individual s hav e an equall y har d time addin g muscle withou t gainin g too muc h bodyfa t at the sam e time . Fundamentally , thi s is an issu e of partitioning , wher e the calorie s are going (or coming from) whe n you eat (or diet). W t you shoul d expec t durin g the diet ha I'll say up fron t tha t the UD2 is not an easy diet. You'll hav e to count/decreas e calories and carbohydrate s 3-5 days out of every 7. While you don' t get to eat everythin g in sigh t on the othe r days , it'll sur e seem like it. On some days you can even eat some jun k food. If you use the fat loss variant , you shoul d be losing a poun d or more of fat per week, while Page 9 http://www.bodyrecomposition.com

gainin g some muscle . At the very leas t you'll maintai n muscl e withou t loss which can be an improvemen t for most people . Performanc e athlete s can lea n out while maintainin g or even increasin g performanc e as well. For the muscl e gain variant , it's a littl e harde r to predict. Women , of course , will hav e slightl y smalle r change s overal l for wha t shoul d be obvious reasons. Despit e wha t you may be use d to, you'll only be liftin g 4 days per week. Eac h workout shoul d tak e abou t an hou r or so, wit h one runnin g mayb e an hou r and a half. If you can' t find 4 hour s per week to trai n consistently , thi s diet won't do you muc h good. Cardi o is optiona l for men, but generall y necessar y for wome n to lose thei r lower bodyfa t at any decen t rate . Still , you shouldn' t need a ton of cardi o wit h thi s diet, not nearl y as muc h as you thin k anyhow. Ther e are only one or two require d supplements , althoug h ther e are some tha t can be genuinel y helpful . Beyon d that , the diet revolve s aroun d basic foods tha t you can get at any supermarke t (I assum e tha t bodybuilder s and athlete s hav e no proble m wit h protei n powder). While I'll mentio n dru g option s to furthe r optimiz e the diet, the y are by no mean s required.


Chapte r 2: You r bod y hate s you

As I'm fond of saying , your body hate s you. Actually , that' s backwards , your body loves you. It loves you so muc h tha t it will do everythin g in its power to keep you alive even if that mean s keepin g you small(er ) and fat(ter) . Becaus e to your body, tha t gives you a bette r chance of survival . Tha t you wan t to do somethin g differen t doesn' t matte r as far as your body is concerned. I wan t you to put thi s book down and go look in the mirro r for a second . Don't get so caught up in throwin g most muscula r poses tha t you forge t to come back. Wha t you jus t saw is perhap s the most complicate d machin e in existence . Over million s of year s (or 7 days , depending on your persona l cosmology), it has develope d ways of adaptin g to jus t abou t anythin g tha t you can thro w at it. This most complicate d machine , your body, the one tha t hate s you (but reall y loves you) still think s tha t you'r e living the rathe r plebeia n existenc e of our ancestors . Our moder n lifestyle has only been aroun d for the las t couple of thousan d year s or so, far too shor t a time for our bodie s to adapt . As far as your body is concerned , you migh t as well be a paleolithi c ma n named Og (no jokes abou t the menta l capacitie s of athletes , please ) living on the plains. Let' s look at the implication s of thi s by tryin g to see thing s from your body's perspective. For the most part , your body has one overwhelmin g goal which is to keep you alive long enoug h to hav e childre n and ensur e the surviva l of your genes . Everythin g else is prett y secondar y to that goal. So wha t does tha t mean ? Again , a few things. Firs t it mean s tha t your body need s a nice space-efficien t way to stor e scad s of energy. That' s to get you throug h the time s whe n ther e isn' t food availabl e (as it frequentl y wasn' t prior to the adven t of 7-11). Tha t energ y stor e exists , it's calle d bodyfat , and your body think s it's great . Fa t is spac e efficient , easy to store , doesn' t tak e muc h energ y to sustain , and can hold an unlimite d numbe r of calories . If your fat cells get full, your body can even mak e new ones to store more incomin g calories . The new fat cells are a lot harde r to get rid of the n the y were to gain , by the way, which is a very good reaso n not to get too fat in the firs t place . Bodyfa t is trul y an ideal way to stor e energy. Fro m your body's perspectiv e it looks like this : If food become s unavailable , the more fat you have , the more likely you are to surviv e long enoug h unti l food become s availabl e again . In societie s wit h seasona l food availability , being able to stor e a lot of fat whe n food was plentiful was the only way to get throug h the time s whe n it wasn't . The extr a fat also helpe d keep folks war m durin g the winter . No centra l hea t or Gorte x parka s back then. In man y societie s people would fatte n up in the summe r so tha t the y could survive throug h the winte r and repea t for as long as the y lived. Now, we jus t sta y in one long fattening cycle (if you'r e a powerlifter , you can call thi s a bulkin g cycle and not feel guilty ) withou t a break. Page 11 http://www.bodyrecomposition.com

That' s at the root of the moder n proble m of obesity : constan t availabilit y of high calorie , highsugar , high-fa t foods. Decrease s in daily activit y is the othe r big part . Thoug h our genetic s are the sam e as the y were 10,000 + year s ago, our environmen t has change d drastically. Lea n individual s would hav e been at a big disadvantag e hundred s of thousand s of years ago whe n gettin g your nex t mea l wasn' t as simpl e as drivin g down to the local fast-food restaurant . Folk s who didn' t fatte n up wouldn' t hav e survive d the food shortages , for the most part , so thei r genetic s usuall y got weede d out of the pool. This probabl y isn' t true for ethnic group s tha t lived in area s of the world wher e food was availabl e yea r round : thos e are the ethnic group s tha t ten d to sta y lea n prett y naturally. The people who could stor e fat the best , who were most likely to surviv e the famines , were the ones who survive d and passe d on thei r geneti c code down the line to us. In our curren t society, bodyfa t is jus t a health-risk , not a necessar y elemen t to keep us alive for the most part . This fact is clearl y show n in the surviva l time s of lea n versu s obese folks durin g tota l starvation . A lean individua l may die afte r 60 days of tota l starvatio n while an obese individua l may mak e it for six month s or longer . Extrem e leannes s is generall y incompatibl e wit h surviva l if food becomes unavailable . I'll come back to thi s in a bit. But wha t abou t muscle , that' s usefu l right ? You've got to be able to kill stuff to survive and tha t mean s muscle . Yes and no. Althoug h it's wonderfu l to imagin e Paleolithi c ma n taking down wild animal s wit h his bar e hand s like in all the "Tarzan " movies , it's more likely tha t man use d his bigge r brai n to outfox animal s whe n it came to hunting . Our brain s are staggeringly larg e (relativ e to our bodyweight ) than thos e of othe r animals ; most likely we use d our brain s to compensate for relatively less muscle mass. So while a modicu m of muscl e was necessar y for survival , and our ancestor s are thought to hav e had more muscl e tha n the averag e America n couch potat o (whic h isn' t reall y saying much) , excessiv e muscl e mas s was probabl y a liability . Sure , you need enoug h to get aroun d and get food but anythin g more tha n tha t is basicall y dea d weight . In the wild, wit h the possible exceptio n of impressin g a potentia l mate , an 18 inch arm wouldn' t hav e been muc h of a benefit. If anything , it migh t hav e slowed down your spear-throwin g a bit. In contras t to fat, muscl e require s a lot of energ y to build , require s a lot of energ y to sustain , and doesn' t provid e muc h energ y whe n it is broke n down. Eve n then , your body will happil y brea k it down whe n you diet. My poin t is tha t you run into an equall y difficul t set of adaptation s occurrin g whe n you try to pus h your muscl e mas s beyon d a certai n point. The end resul t of all of thi s is that , to your body, which think s its still on the plain s eking out an existence , being fat and smal l are beneficial , becaus e they mean t greate r survivability. Our physiolog y reflect s this which make s thing s reall y suck for folks who wan t to be bigge r and leaner . In short , we're fightin g agains t million s of year s of evolutio n and adaptatio n to reac h our goals of bigge r and leaner . Usually , the body wins. Now, you may be thinkin g tha t I'm full of it already , becaus e you can look at any magazine Page 12 http://www.bodyrecomposition.com

and find man y sterlin g example s of individual s who are both hug e and lean . They are calle d pro bodybuilders . Ther e are a few reason s why the image s in the majorit y of the magazine s aren't very relevan t to the res t of us. Firs t and foremost , pro bodybuilder s (or athlete s in general ) have bette r genetic s tha n the res t of us. They are the geneti c elite . This isn' t some type of personal grous e or whine , simpl y a statemen t of fact and reality . If you had thei r genetics , you wouldn' t be readin g thi s book. If you look at pro bodybuilder s in thei r earl y stages , the y are still typicall y leane r and bigge r tha n the norma l individual . Fro m a physiologica l standpoint , they probabl y hav e higher tha n averag e testosteron e levels and don' t overproduc e cortisol . Thyroi d levels are probably optima l or close to it, helpin g to naturall y optimiz e metaboli c rate , fat burnin g and protein synthesis. They hav e good skeleta l muscl e insuli n sensitivit y and ten d to put calorie s into muscle more effectivel y (i.e. the y partitio n calorie s toward s muscl e instea d of fat). They probabl y have fewer fat cells tha n most people and tha t fat is evenl y distribute d (althoug h even femal e pros hav e problem s wit h lower bodyfat) . Whe n they diet, the y don' t hav e as man y problem s with metaboli c slowdown . Thei r evenl y distribute d fat comes off easil y and , since the y can use fatty acids easil y for fuel, the y don' t lose as muc h muscl e whe n they diet. All of thes e factors contribute to their success. We can contras t tha t to the averag e individua l who could hav e any numbe r of potential metaboli c defect s tha t prevent s the m from reachin g thei r desire d goals. Testosteron e migh t be on the low side of normal , cortiso l productio n is elevated , thyroi d or nervou s syste m outpu t may be low (meanin g a lower tha n optima l metaboli c rate) . Skeleta l muscl e insuli n sensitivit y is low which mean s tha t excess calorie s get pushe d toward s fat cells more effectively . Whe n thes e folks diet, the brai n tend s to overreact , lowerin g metaboli c rat e (whic h probabl y wasn' t optima l to begin with) . Fa t loss slows to a crawl . Difficultie s mobilizin g bodyfat , along wit h problem s with testosteron e and cortisol , lead to increase d muscl e loss. I could keep going but you get the idea. I'm not jus t tellin g you thi s to depres s you; conside r it more of a realit y check to mak e you awar e of wha t is and isn' t possible . My poin t is tha t pro bodybuilder s (hell, pro athlete s of any sort) are the geneti c elite . You are not like the m and the y hav e advantage s naturall y tha t you don't . Most importantly , tryin g to mimic wha t the y do, or expectin g thei r results , can only lead you down an endles s pat h of frustration.

And the n ther e ar e drugs All professiona l bodybuilder s (and most athletes ) use drugs . Anyone who says differently is lying or tryin g to sell you something . Again , thi s isn' t a grous e or whine , but rathe r a statement of fact. Whe n you introduc e the myria d anaboli c drug s into the equation , it become s possibl e to Page 13 http://www.bodyrecomposition.com

not only side-ste p but almos t ignor e "normal " huma n physiology . Coupl e bette r than average genetic s wit h enoug h drug s and you get professiona l bodybuilders . You are not one of them , you will not be one of them . No amoun t of wishfu l thinkin g can chang e that . Eve n if you had access to all of thei r drugs , there' s no guarante e you'd get as big; it's likely tha t one of the genetic advantage s that professiona l bodybuilder s hav e is a high sensitivit y to the drug s tha t the y do take. Anyone who tell s you tha t the variou s bodybuildin g drug s (anaboli c steroids , insulin, clenbuterol , etc.) don' t work, or aren' t necessar y to reac h a monstrou s level of development , is bullshittin g you. Usuall y the y hav e an all-natura l supplemen t or steroi d replacemen t to sell you in the firs t place (I jus t hav e a book). I'd be lying if I told you tha t anythin g you'll rea d in thi s book could tak e you to the developmen t level of even the wors t pro. It can't . Withou t both their genetic s and thei r drugs , it simpl y can' t be done. At best proper/meticulous/craft y nutritio n and trainin g will let your maximiz e your own potentia l and move beyon d ordinary . To go above your geneti c potentia l require s drugs . The soone r you come to term s wit h this , the bette r off you'll be. The fact is tha t drugs , even the relativel y simpl e testosterone , can tak e you to a level of developmen t otherwis e unachievabl e by any natura l training , diet and supplemen t methods . At even moderat e doses, testosteron e allow s you to sideste p your norma l physiolog y and reac h a highe r level. It raise s the "setpoint " of how muc h muscl e you can carry ; it reduce s your fat mass at the sam e time . Once you introduc e all the othe r drug s endemi c to pro-bodybuilding , you get a physiolog y that is unattainabl e in non-dru g usin g individuals. Still not convinced ? A singl e exampl e shoul d help to mak e my point . In natura l (read : non dru g using ) individual s who hav e diete d down to extremel y low bodyfa t levels , say 5%, you see a commo n hormona l pattern . Testosteron e levels are typicall y bottome d out (some studie s even find castrat e levels , which is why a lot of natura l contes t bodybuilder s can' t get thei r dick hard, not tha t the y hav e a sex driv e in the firs t place), thyroi d levels are bottome d out, IGF-1 levels are bottome d out, sympatheti c nervou s syste m outpu t is way down meanin g decrease d caloric and fat burning , appetit e is throug h the roof, cortiso l is throug h the roof, on and on it goes. This make s good evolutionar y sense : at 5% bodyfat , you are starvin g to death . Your body is turning off every syste m (metabolic , reproductive , immune , etc.) tha t it can to keep you alive unti l you get some food. Contras t tha t to a dietin g professiona l bodybuilder . With the choice of the righ t drugs , he can eliminat e prett y muc h all of the above problems . Anaboli c steroid s replac e natural testosterone , syntheti c thyroi d replace s wha t the body is no longe r making , injectabl e insulin, GH, and IGF-1 fix the insulin , GH and IGF-1 problem , clenbutero l replace s sympatheti c nervous syste m output , appetit e suppressant s can deal wit h appetit e and anti-cortiso l drug s deal with the cortiso l problem . That' s only a partia l dru g list, by the way.


Gettin g to the point The dru g usin g bodybuilde r has completel y shut the door in the face of his normal physiolog y while the natura l bodybuilde r is basicall y fucke d (physiologicall y speaking) . Again , my poin t in explainin g thi s isn' t so muc h to give you a metaphorica l kick in the nut s before we get started ; it's to explai n the basic realitie s of the situation . One of the wors t thing s tha t a natural athlet e or bodybuilde r can hope to do is to emulat e the pros in term s of thei r results , trainin g or diet. Pro athlete s and bodybuilder s hav e at leas t two majo r advantage s tha t you don' t have: geneti c and drugs . Hopin g tha t you can achiev e wha t the y achiev e or, even worse , tryin g to use thei r approac h to do it, is destine d for failure. But all is not lost. One of the goals of the UD2 is to mimic , to as grea t a degre e as possible, some of the processe s tha t occur normall y in the geneti c elite . We may not be able to do it 100%, but we can get in the ballpar k and thi s will improv e results . By usin g specific nutritiona l and trainin g practices , the occasiona l supraphysiologica l level of supplement s and even the occasiona l drug , we can duplicat e some of what' s going on.


Chapte r 3: Why is it so har d (Par t 1)After las t chapter , you'r e thinkin g one of two things . Eithe r you can' t wai t to get into the nut s and bolts of thi s diet, or you'r e still not convinced . I mean , you can open any of the muscle magazine s (or shoul d we call them supplemen t catalogs? ) and see any numbe r of diet plans, trainin g programs , or nutritiona l supplement s all of which promis e everythin g I told you thi s diet could accomplish . So how come I'm righ t and they'r e wrong? As I said in chapte r 1, the bigges t proble m wit h the standar d advic e is simpl y tha t it is generall y so standard . Most bodybuildin g writers , nutritionist s and guru s are more concerned wit h maintainin g the statu s quo, mayb e refinin g it a bit, tha n going out on a limb and suggesting somethin g new and radical . So let's look at the statu s quo and see why it won't ultimatel y let you achiev e your goal (again , if it did, you wouldn' t hav e gotte n or even neede d thi s book). The standar d prescriptio n to do wha t I've describe d (more muscle , less bodyfat ) is usually a fairl y standar d moderat e to high carb, moderat e to high protein , and low to moderat e fat diet (dependin g on the persona l philosoph y of the magazin e and the write r in question) . High fiber, clea n carbs , lots of qualit y protein , fats seem to be the most variabl e althoug h everyon e is finally gettin g onto the health y fat bandwago n like the y shoul d hav e done year s ago. Coupl e that with weigh t trainin g and cardi o and magic will happen , right ? Well, sort of. Most people remembe r thos e wonderfu l beginne r days , whe n muscl e gain and fat loss come withou t too muc h effort. It's true , beginner s can pull off wha t seem s like a magica l body compositio n transformatio n withou t muc h difficulty . Folk s coming back from a layoff or injury, wher e they typicall y gain fat and lose muscle , can do thi s too. Muscl e memor y allow s the muscle to be regaine d while the fat is coming back off. As people become more advanced , gainin g more muscle , or reachin g lower bodyfa t levels , this tric k become s more and more difficul t unti l the poin t tha t it is more or less impossible . You usuall y end up eithe r havin g to focus purel y on muscl e gain (acceptin g that some fat will come wit h it) or fat loss (acceptin g that you'll lose some muscle) . Bulkin g and cuttin g phases , basically. I say more or less impossibl e becaus e ther e are a lot of inefficien t ways of accomplishin g it usuall y involvin g month s and month s of teeny-tin y caloric deficits(lik e 200 calories/da y under maintenance ) couple d wit h intensiv e trainin g to achiev e fairl y smal l changes . Personally , I don't hav e tha t kin d of patience . I've alway s wante d a faste r solutio n even if it was more complicated. Eve n withou t tryin g to gain muscl e while you'r e losing fat, simpl y losing fat withou t losing muscl e is problematic . This is especiall y true once you try to pus h the boundarie s of normalcy (again , abou t 12-15% bodyfa t in men and 20-22% bodyfa t in women) . Gettin g to thos e levels withou t muscl e loss isn' t too muc h of a proble m but gettin g leane r tend s to caus e muscl e loss at faste r and faste r rates . The usua l advic e is to up protei n (whic h only work s up to a point ) or lose fat so abysmall y slowly (0.5 pound s per week) tha t you go nut s dietin g for month s on end. Gainin g muscl e withou t puttin g on too muc h fat is another , somewha t differen t problem, Page 16 http://www.bodyrecomposition.com

althoug h the same advic e is usuall y given. Mayb e wit h less cardio , or slightl y differen t training, but the sam e nonetheless . Once again , pas t the beginne r stage , lifter s find tha t puttin g on muscle at any sort of appreciabl e rat e (withou t drug s anyhow ) usuall y mean s gainin g some bodyfa t as well. The ones who don' t wan t to gain any fat are the ones who will tell you tha t 3-5 lbs of muscle/yea r is the most you can gain pas t the beginne r stage. The n there' s the folks who wan t to lea n out significantl y while gainin g muscl e (or strength) at the sam e time . As I said above, thi s is prett y easy in beginners , folks who are very fat, or thos e coming back from a layoff. For everybod y else, it's more difficult , approachin g impossible. For shor t periods , the UD2 will let you do it.

Definin g th e proble m again If you go aroun d into any commercia l gym, you typicall y see folks in a lot of different conditions . Ther e are typicall y some big but fat guys, some smal l but lea n guys, some smal l and fat guys, and a few big and lea n guys. But , unles s you belong to a gym wit h a larg e bodybuilder contingent , the las t grou p ten d to be few and far between . The questio n is why? Why is it so difficul t to get both big and lea n at the sam e time ? It's almos t as if the body can do one or the othe r well, but not both , which reall y isn' t far from the truth . Relate d to that, why is it so difficul t to lose fat and gain muscl e at the sam e time ? Or to gain muscl e without gainin g fat at the sam e time ? Hell, even losing fat withou t losing muscl e is difficul t enough . To answe r the questio n of why thing s are so difficult , let's star t simpl e and move toward s more comple x explanations , since tha t will lead us to an understandin g of how to solve the problem. The simples t answe r I could give, I've alread y discusse d in the las t chapte r and in my last book: evolution . To restat e it all quickl y and simply , 10 million + year s of evolutio n have left us wit h geneti c propensitie s and physiologie s tha t wan t us to sta y smallis h and fat, becaus e that mean s bette r survival . On top of that , once you'r e pas t puberty , your body is far more concerned wit h homeostasi s (remainin g the same ) tha n wit h anythin g else. To one degre e or another , it tend s to defen d your bodyweigh t and bodyfa t percentag e at a certai n level (whic h appear s to be programme d in the brain) . You can chang e tha t set poin t to some degre e wit h trainin g and diet, but your body alway s strive s to maintai n the statu s quo more tha n anythin g else. But both of thos e are reall y jus t statement s of the amazingl y obvious , withou t really tellin g us much . So let's move a level deepe r and star t to get into the physiolog y of why accomplishin g our goals is so difficult . Tha t will lead us toward s the solution.


Doin g two thing s at once One fundamenta l proble m is tha t our bodies aren' t typicall y good at doing two thing s at once, especiall y whe n thos e thing s are at odds wit h one another , or hav e differen t fundamental requirements. For example , stud y afte r stud y has show n that combinin g heav y strengt h trainin g with heav y enduranc e trainin g compromise s the overal l results . Why? Strengt h trainin g send s the muscl e an adaptiv e signa l to become bigge r and stronge r and more efficien t at usin g glucos e for fuel; enduranc e trainin g sen d a signa l to become more energ y efficien t (whic h typicall y means smalle r becaus e smalle r muscl e fiber s can get energ y more readily ) and use more fat for fuel. End resul t is tha t the body can' t do both optimall y and you get less tha n stella r result s whe n you try to do both. How does thi s appl y to losing fat and gainin g muscle ? In short , the y hav e differen t (and , in fact, mutuall y exclusive ) requirements . Tha t is, gainin g muscl e and losing fat requir e different scenario s in term s of nutrition , hormones , etc. In fact, the specific requirement s for gaining muscl e are also the reaso n tha t you ten d to gain fat at the same time . Similarly , the requirement s for fat loss are par t of the reaso n (along wit h your body's adaptations ) tha t you will lose muscl e at the sam e time . I'll discus s thi s in detai l nex t chapter. Synthesizin g new tissu e (whethe r muscl e or fat) require s energ y and tha t energ y can' t just magicall y appear . Synthesizin g new muscl e tissu e is especiall y costly, at leas t whe n compared to synthesizin g new fat. While it's wonderfull y idyllic to thin k tha t the calorie s for muscl e growth will magicall y be generate d from burnin g fat, it rarel y happen s tha t way, at leas t not without powerfu l repartitionin g drug s like clenbuterol . Which make s a rathe r nice segu e into the next chapter.


Chapter 4: Why is it so hard (Part 2) Partitioning

At a very fundamenta l level, the proble m natura l bodybuilder s and athlete s hav e is one of partitioning . At its simplest , partitionin g refer s to wher e the calorie s go (into muscl e or fat cells) whe n you eat more of the m or come from (from muscl e or fat cells) whe n you eat less of them. In an idea l universe , every calori e you ate would go to muscl e tissue , wit h none going into fat cells; you'd gain 100% muscl e and no fat. In tha t sam e idea l universe , every calori e used durin g dietin g would come from fat stores ; you'd lose 100% fat and no muscle . Unfortunately , we don' t live in an idea l universe. As I mentione d earl y in thi s book, some haples s individual s will lose as muc h as one pound of muscl e for every 2-3 pound s of fat tha t the y lose whe n the y diet. Typically , thos e same individual s will put on abou t the sam e amoun t of fat and muscl e whe n they gain weight . Thu s is the balanc e of the univers e maintained . More geneticall y advantage d individual s ten d to put mor e calorie s into muscl e (meanin g less into fat) whe n the y overea t and pull more calorie s out of fat cells (and less out of muscle ) whe n they diet. They sta y naturall y lea n and hav e few problems dieting . Once again , you aren' t one of them , or you wouldn' t be readin g thi s book. Whe n talkin g abou t calori e partitioning , researcher s refe r to somethin g calle d the P-ratio. Essentially , P-rati o represent s the amoun t of protei n tha t is eithe r gaine d (or lost) durin g over (or under ) feeding . So a low P-rati o whe n dietin g would mea n you use d very littl e protei n and a lot of fat. A high P-rati o would m n tha t you use d a lot of protei n and very littl e fat. It looks like, for ea the most part , P-rati o is more or less the sam e for a given individual : the y will gain abou t same amoun t of muscl e whe n they overfee d as the y lose whe n the y diet. P-rati o can vary between individuals , of course , but for any given person , it appear s to be relativel y constant. So wha t control s P-ratio ? As depressin g as thi s is, the majorit y of of the P-rati o is out of our control ; it's mostl y genetic . We can contro l mayb e 15-20% of it wit h how we eat or train. Supraphysiologica l amount s of certai n compound s (supplements ) and , of course , drugs , can also affect the P-ratio . Exercis e is perhap s the most significan t weapo n we hav e in battlin g wit h our body and affectin g P-ratio. So wha t are the mai n determinant s of calori e partitioning ? Hormone s are crucially important . High testosteron e levels ten d to hav e positiv e partitionin g effects (more muscle , less fat) while chronicall y high levels of cortiso l hav e the opposit e effect (less muscle , more fat). Thyroi d and nervou s syste m activit y affect not only metaboli c rat e but also fat burning . Thyroid also affect s protei n synthesis . Optima l levels of thes e hormone s not only mea n bette r fat loss (and less muscl e loss) whe n you diet but bette r muscula r gain s (and less fat gain) whe n you gain weight . Unfortunately , levels of thes e hormone s are basicall y "set" by our genetics ; the only way to chang e the m significantl y is wit h supplement s or drugs . Beyon d that , there' s not a whole lot Page 19 http://www.bodyrecomposition.com

we can do to contro l them. Anothe r facto r controllin g P-rati o is insuli n sensitivit y which refer s to how well or how poorly a given tissu e respond s to the hormon e insulin . High insuli n sensitivit y mean s tha t a smal l amoun t of insuli n will generat e a larg e response ; insuli n resistanc e indicate s tha t it takes more insuli n to caus e the sam e effects to occur. Now, insuli n is a storag e hormone , affectin g nutrien t storag e in tissue s such as liver, muscl e and fat cells. In tha t sam e idea l world, we'd hav e high insuli n sensitivit y in skeletal muscl e (as thi s would ten d to driv e more calorie s into muscle ) and poor insuli n sensitivit y in fat cells (makin g it harde r to stor e calorie s there) . This is especiall y true whe n you'r e tryin g to gain muscle. Whe n you diet, it's actuall y bette r to be insuli n resistan t (note tha t two of the most effectiv e diet drugs , GH and clenbuterol/ephedrin e caus e insuli n resistance) . By limitin g the muscle' s use of glucos e for fuel, insuli n resistanc e not only spare s glucos e for use by the brain, but also increase s the muscle s use of fatt y acids for fuel. In additio n to hormona l advantages , it's likely tha t the geneti c elite hav e high skeletal muscl e insuli n sensitivity . They stor e tremendou s amount s of calorie s in thei r muscles , which leave s less to go to fat cells. Thei r bodies also don' t hav e to releas e as muc h insuli n in respons e to food intake. In contrast , individual s wit h poor skeleta l muscl e insuli n sensitivit y tend to overproduce insulin , don' t stor e calorie s in muscl e well (thi s is par t of why the y hav e troubl e gettin g a pump: poor glycogen storag e in muscl e cells) and ten d to spill calorie s over to fat cells more effectively. So wha t control s insuli n sensitivity ? As always , ther e are a host of factors . One is simply genetic , folks can vary 10 fold in thei r sensitivit y to insuli n even if everythin g abou t the m is the same . Anothe r is diet. Diet s high in carbohydrate s (especiall y highl y refine d carbohydrates), saturate d fats and low in fiber ten d to impai r insuli n sensitivity . Diet s wit h lowered carbohydrate s (or less refine d sources) , healthie r fats (fish oils and monounsaturate d fats like olive oil) and highe r fiber intake s ten d to improv e insuli n sensitivity. Anothe r majo r facto r is activit y which influence s insuli n sensitivit y in a numbe r of ways. The firs t is tha t muscula r contractio n itself improve s insuli n sensitivity , facilitatin g glucose uptak e into the cell. Glycoge n depletio n (remembe r this, it's important ) improve s insulin sensitivit y as well. So wha t else control s the P-ratio ? As it turn s out, the primar y predicto r of P-rati o during over- and underfeedin g is bodyfa t percentage . The more bodyfa t you carry , the more fat you tend to lose whe n you diet (meanin g less muscle ) and the leane r you are , the less fat you ten d to lose (meanin g more muscle) . The sam e goes in reverse : naturall y lea n (but no t folks who hav e dieted down) individual s ten d to gain more muscl e and less fat whe n they overfee d and fatte r individuals ten d to gain more fat and less muscl e whe n they overfeed. The questio n is why, why does bodyfa t percentag e hav e such a profoun d impac t on PPage 20 http://www.bodyrecomposition.com

ratio ? Ther e are a few easy answers . One is tha t bodyfa t and insuli n sensitivit y ten d to correlate : the fatte r you get, the more insuli n resistan t you ten d to get and the leane r you are the more insuli n sensitiv e you ten d to be. A secon d is that , the fatte r you are , the more fatt y acids you hav e availabl e for fuel. In general , whe n fatt y acids are availabl e in larg e amounts , the y get used . This spare s both glucose and protein . By extension , the leane r you get, the more problem s you ten d to have ; as it gets harde r to mobiliz e fatt y acids , the body has less to use. Since ther e is less glucos e available (becaus e you'r e dieting ) thi s increase s the relianc e on amin o acids (protein ) for fuel. The original Ultimat e Diet advocate d mediu m chai n triglyceride s (a specia l type of fatt y acid tha t is used mor e easil y for fuel tha n standar d fats) and thi s can be a good strateg y unde r certain circumstances . I'll mentio n some othe r option s late r on in the book. But that' s not all. It turn s out tha t bodyfa t percentag e is controllin g metabolis m to a muc h greate r degre e tha n jus t by providin g fatt y acids . Researc h over the pas t 10 year s or so has identifie d fat cells as an endocrin e tissu e in thei r own right , secretin g numerou s hormone s and protein s tha t hav e majo r effects on othe r tissues . Perhap s the most important , and certainl y the one most talke d abou t is leptin , but that' s far from the only one. Tumo r necrosi s factor-alpha, the variou s interleukins , adiponecti n and othe r compound s release d from fat cells are sending signal s to othe r tissue s in the body which affect metabolism. Withou t gettin g into all of the nitpick y detail s (man y of which haven' t been worke d out yet), I jus t wan t to tal k a littl e abou t lepti n (if you rea d my las t book, thi s will all be familiar ground).

Leptin , the shor t course Lepti n is a protei n release d primaril y from fat cells althoug h othe r tissue s such as muscle also contribut e slightly . Lepti n levels primaril y correlat e wit h bodyfa t percentage , the more fat you hav e the more lepti n you ten d to hav e (note: differen t depot s of fat, viscera l versus subcutaneous , show differen t relationship s wit h leptin) . At any given bodyfa t percentage , women typicall y produc e 2-3 time s as muc h lepti n as men. In additio n to being relate d to the amoun t of bodyfa t you have , lepti n levels are also related to how muc h you'r e eating . For example , in respons e to dieting , lepti n levels may drop by 50% withi n a week (or less) althoug h you obviousl y haven' t lost 50% of your bodyfat . After tha t initial rapi d drop, ther e is a slowe r decreas e in lepti n relate d to the loss of bodyfa t tha t is occurring . In respons e to overfeeding , lepti n tend s to reboun d equall y quickl y (muc h faste r than you'r e gaining bodyfat) . In contras t to wha t you migh t think , it looks like lepti n productio n by fat cells is mainly determine d by glucos e availabilit y (you'd thin k it was fat intake) . So wheneve r you star t pulling glucos e out of the fat cell (dieting) , lepti n levels go down; whe n you driv e glucos e into fat cells, it Page 21 http://www.bodyrecomposition.com

goes up. Basically , lepti n represent s two differen t variables : how muc h bodyfa t you'r e carryin g and how muc h you'r e eating . Tha t is, it acts as a signa l to the res t of your body abou t your energy stores . I'll come back to thi s in a second. Like most hormone s in the body, lepti n has effects on most tissue s in the body. Leptin receptor s hav e been found all over the place , in the liver, skeleta l muscle , in immun e cells; you nam e a site in the body and ther e are probabl y lepti n receptor s there . Ther e are also leptin receptor s in the brai n but I'll come back to tha t below. For now, let's look at a few of the effects tha t lepti n has on othe r tissue s in the body. In the liver, lepti n tend s to reduc e insuli n secretio n from the beta-cells . In skeleta l muscle, lepti n promote s fat burnin g and tend s to spar e glucos e (and therefor e amin o acid use). In fat cells , lepti n may promot e fat oxidatio n as well as makin g the fat cell somewha t insuli n resistant. Lepti n also affect s immun e cell function , decreasin g lepti n impair s the body's abilit y to moun t an immun e response . Now you know at leas t par t of the reaso n you ten d to get sick more whe n you diet. On and on it goes. An entir e book could and shoul d be writte n abou t leptin.

Lepti n and the brain Now, I wan t you to thin k back to the firs t couple of chapter s of thi s book, wher e I talked abou t the evolutionar y reason s it's so har d to get extremel y lean . To your body, becomin g too lea n is a very rea l threa t to your survival . Fro m a physiologica l standpoint , tha t mean s that your body need s a way to "know" how muc h energ y you hav e stored. As you may hav e guessed , or know n from my las t book, lepti n is one of the primar y signals (along wit h man y other s includin g ghrelin , insulin , peptid e YY and othe r as of yet undiscovered compounds ) that signal s the brai n abou t how muc h energ y you hav e store d and how muc h you're eating. All of thes e hormone s sen d an integrate d signa l to a par t of the brai n calle d the hypothalamu s tha t "tell" it what' s going on elsewher e in your body. Change s in levels of these hormone s cause s othe r change s in variou s neurochemical s such as neuropeptide- Y (NPY), corticotrophi n releasin g hormon e (CRH), pro-opiomelanocorti n (POMC) and severa l other s to occur. Thes e neurochemical s regulat e metaboli c rate , hunge r and appetite , hormone s and a host of other processes. So whe n you restric t calories , causin g change s in all of the hormone s and neurochemicals mentione d above, and a numbe r of physiologica l processe s change , mostl y for the worse . Levels of thyroi d stimulatin g hormone , leutinizin g hormon e and follicle stimulatin g hormon e (TSH, LH and FSH respectively ) go down. This result s in lowere d levels of thyroi d and testosterone . Levels of growt h hormon e releasin g hormon e (GHRH ) go down meanin g GH outpu t can be impaired. Page 22 http://www.bodyrecomposition.com

Sympatheti c nervou s syste m activit y goes down which , along wit h the drop in thyroid , has a huge impac t on metaboli c rate . Cortiso l levels go up as does hunge r and appetite . You get the idea. Wha t you end up seein g is an all purpose s system s cras h whe n you try to take bodyfa t to low levels . I shoul d note tha t thes e processe s are occurrin g to one degre e or anothe r durin g all diets, the y simpl y become more pronounce d at the extrem e low levels of bodyfat. Ideally , the opposit e effects shoul d occur whe n you rais e calories . However , for reason s I detaile d in my las t book, the syste m is asymmetrical : fallin g lepti n (and change s in all of the other hormones ) has a muc h large r impac t on the body's metabolis m tha n raisin g lepti n does (unless you'r e raisin g it back to normal) . So the body end s up fightin g weigh t loss to a far greate r degree tha n weigh t gain . Generall y speaking , people find tha t it a lot easie r to get fat tha n to get lean. Of course , ther e are exceptions , folks who seem to resis t obesit y (or weigh t gain altogether). Researc h will probabl y find tha t the y are extremel y sensitiv e to the effects of lepti n (and other hormones) , so whe n calorie s go up, the y simpl y bur n off the excess calorie s withou t gettin g fat. Most of us aren' t tha t lucky. Rather , like insuli n sensitivit y discusse d above, researchers will probabl y find tha t lepti n sensitivit y is a hug e facto r influencin g how change s in caloric intake affect metabolism . Someon e wit h good lepti n sensitivit y will ten d to sta y naturall y lea n and have an easy time dieting ; folks wit h worse lepti n sensitivit y (lepti n resistance ) won't. You migh t be thinkin g tha t the quick and dirt y solutio n would be lepti n injections . As I pointe d out in my las t book, injectabl e lepti n is a pipe-drea m at thi s point , an effectiv e dose costin g nearl y $1000/da y (not to mentio n requirin g twice daily injections) . Usin g bromocriptin e or othe r dopamin e agonist s seem to fix at leas t par t of the proble m by sendin g a false signa l to the brai n by makin g it thin k lepti n levels are normal. Recen t studie s tha t hav e given injectabl e lepti n to dieter s show tha t the fall in lepti n is one of the primar y signal s in initiatin g the adaptatio n to dieting . However , unlik e in rats , injecting lepti n into human s doesn' t fix all of the problems. This is because , in humans , ther e is more of an integrate d respons e to both over and underfeeding . To understan d thi s better , I wan t to tak e a snapsho t of wha t happen s whe n you eithe r reduc e or increas e calories.

Dieting So you decide to diet, reducin g carbs , calorie s or both . Vary rapidly , blood glucos e and insuli n levels are going to be reduced . This is good as it release s the "block" on fat mobilization. Additionally , catecholamin e releas e typicall y goes up (at leas t initially) , furthe r increasin g fat mobilizatio n from fat cells. This cause s blood fatt y acid levels to increase . This is also good, as it tend s to promot e fat burnin g in tissue s such as liver and muscle . This effect is facilitate d if you deplet e liver and muscl e glycogen , as glycogen depletio n tend s to increas e the use of fatt y acids Page 23 http://www.bodyrecomposition.com

for fuel. The increas e in blood fatt y acid levels also has the short-ter m effect of causin g insulin resistance . As I mentioned , thi s is a good thin g on a diet since it spare s glucos e and help s promote fat oxidation . So far, so good, right? Unfortunately , along wit h thes e good effects , a lot of bad thing s star t to happen . I already describe d man y of the centra l adaptation s above: change s in leptin , ghrelin , Peptid e YY (and certainl y othe r hormones ) "tell" your brai n tha t you'r e not eatin g enough . This cause s change s in the variou s neurochemical s stimulatin g a numbe r of negativ e adaptations . I wan t to note that the respons e is not immediate , ther e is a lag time betwee n the change s in all of thes e hormones and the body's response . But that' s not all. Ther e are also man y othe r adaptation s which occur whe n you diet, so let's look at some of those . Firs t and foremost , the drop in lepti n directl y affect s liver, skeleta l muscl e and fat cell metabolism , mostl y for the worse. While the drop in insuli n mentione d above cause s bette r fat mobilization , it cause s other problems . One is tha t testosteron e will bind to sex-hormon e bindin g globuli n (SHBG) better, lowerin g free testosteron e levels (thi s is in additio n to the drop in tota l testosterone) . As well, insuli n is anti-cataboli c to muscle , inhibitin g muscl e breakdown . The increas e in cortiso l that occurs wit h dietin g enhance s protei n breakdow n as well as stimulatin g the conversio n of protein to glucos e in the liver. Additionally , a fall in energ y stat e of the muscl e impair s protei n synthesis (althoug h it increase s fatt y acid oxidation) . The mechanis m behin d thi s is more detai l tha n I wan t to get into here . But the combine d effect of thes e processe s is tha t protei n synthesi s is decrease d and breakdow n is accelerated ; thi s cause s muscl e loss. On top of that , high blood fatt y acid levels ten d to impai r the uptak e of T4 (inactive thyroid ) into the liver. Ther e are also change s in liver metabolis m tha t impai r the conversio n of T4 to T3 (activ e thyroid) . Both of thes e processe s caus e decrease d blood levels of T3. Ther e is some evidenc e tha t high blood fatt y acid levels cause s tissue s to become resistan t to thyroid hormon e itself (thi s is par t of why jus t takin g extr a thyroi d on a diet doesn' t fix all of the problems) . After the initia l increase , ther e is also a drop in nervou s syste m outpu t (tha t can occur in as littl e as 3-4 days afte r you star t a diet). Along wit h the drop in thyroid , insuli n and leptin , thi s explain s a majorit y of the metaboli c slowdow n that occurs . The chang e in liver metabolis m (and the reductio n in insulin ) also impair s the productio n of IGF-1 from GH. All of thes e adaptation s serv e two mai n purposes . The firs t is to slow the rat e of fat loss, as thi s will ensur e your surviva l as long as possible . Relate d to that , the body tend s to shu t down caloricall y costly activities . This include s protei n synthesis , reproductio n and immun e function; there' s littl e poin t keepin g any of thes e functionin g whe n you'r e starvin g to death . The drop in leptin , and the change s in hormone s tha t occur are a hug e par t of why men ten d to lose thei r sex driv e (and ability ) and wome n lose thei r perio d whe n the y get lean/die t hard. The secon d is to prim e your body to put fat back on at an accelerate d rat e whe n calories become availabl e again . Decrease d metaboli c rat e and fat burning , along wit h improve d caloric Page 24 http://www.bodyrecomposition.com

storag e all conspir e to put the fat back on whe n you star t eatin g again . As I mentione d earlier, thi s make s perfec t evolutionar y sense , even if it present s a hug e pai n in the ass to us. I haven' t even mentione d the hunge r and appetit e issu e which is a topic worth y of an entir e book. The combinatio n signa l sen t by leptin , ghrelin , insulin , glucose , and a host of other hormone s (cholecystokinin , glucagon-lik e peptid e 1 and 2, bombesi n and man y man y others ) are all involve d in both hunge r and appetite . The change s tha t occur wit h dietin g ten d to mak e both shoot throug h the roof: you ten d to get and sta y hungry , thinkin g abou t food nearl y constantly. Bodybuilder s and athlete s may hav e unbelievabl e food contro l but it still suck s being hungry constantl y whe n you try to diet. Ok, enoug h abou t dieting , wha t abou t overfeeding?

Overfeeding To a grea t degree , most of the adaptation s tha t occur wit h dietin g revers e whe n you overeat . Actually , tha t depend s a lot on the situation . As I mentione d above, the body as a whole tend s to defen d agains t underfeedin g bette r tha n it does agains t overfeedin g which is why it's generall y easie r to gain weigh t tha n to lose it. Studie s wher e lepti n has been increase d above norma l (i.e. to try and caus e weigh t loss in overweigh t individuals ) hav e generall y born e thi s out: excep t at massiv e doses, raisin g lepti n above norma l does very little. Ther e are a couple of theorie s as to why thi s migh t be the case. One theor y is tha t normal lepti n levels sen d essentiall y a 100% signal , tha t is the y tell the body tha t all system s are normal . It shoul d seem clea r tha t raisin g lepti n above 100% isn' t going to do much . Another possibilit y is relate d to somethin g I allude d to above: lepti n sensitivit y and resistance . It's though t tha t people hav e varyin g degree s of lepti n resistanc e which means , in essence , tha t they don' t respon d as well to lepti n as the y should . On top of this , whe n lepti n levels go up, it appears to stimulat e resistanc e to itself . Tha t is, whe n lepti n gets and stay s high , it cause s you to become resistan t to its effects. Both explanation s for the failur e of high lepti n levels to defen d agains t weigh t gain make good evolutionar y sense . Your body doesn' t wan t to be lea n but it doesn' t reall y min d gettin g fat. This is because , durin g our evolution , being fat was neve r a risk , while being lea n was. If anything , gettin g fat was a benefi t which is why our bodies ten d to be so good at it. It's only in moder n time s whe n people can get and , more importantly , sta y fat for extende d periods , that being fat is a problem . Ten thousan d year s from now, perhap s we will evolve defense s against being fat. Anyhow , if calorie s are availabl e all the time , it would mak e littl e sens e for you to get full and/o r star t burnin g the m off. This is wha t would happe n if you were extremel y sensitiv e to lepti n (and does happe n in a smal l percentag e of individuals) . So high levels of lepti n induce Page 25 http://www.bodyrecomposition.com

resistanc e to itself , keepin g you hungr y and eatin g while the food is available . Lepti n can induce resistanc e to itself in only a few days of overeating. But we're not reall y talkin g abou t raisin g lepti n above norma l here , we're talkin g about reversin g or preventin g the drop tha t occurs wit h dieting . In tha t situation , man y of the above adaptation s to dietin g will revers e to one degre e or another . Wha t degre e will depen d on how lean you are , how long you diet, and how long you overeat. So now you increas e your calorie s and carbs . Let' s look at some of wha t happen s when you do so. Firs t ther e are all of the centra l adaptation s tha t occurre d durin g dieting , tha t will revers e to some degre e while overfeeding . Lepti n will go up (notin g agai n tha t it goes up more quickl y than bodyfa t comes on) along wit h insuli n and peptid e YY, ghreli n goes down. This signals the hypothalamu s tha t you'r e eatin g agai n signalin g tha t the body can revers e the adaptations tha t had occurre d in the firs t place. In addition , the increas e in insuli n will revers e the bindin g of testosteron e to SHBG; cortisol also goes down. With increase d carbohydrates , you increas e both liver and muscl e glycogen. Whil e thi s decrease s fat oxidatio n in the muscle , you get improve d protei n synthesi s (the increase in insuli n and testosteron e and the drop in cortiso l hav e an additiona l effect). Of course , wit h increasin g insulin , ther e is a decreas e in blood fatt y acid concentrations which improve s insuli n sensitivity . Skeleta l muscl e insuli n sensitivit y is enhance d even more by exercise. The decreas e in blood fatt y acids , along wit h change s in liver metabolis m will improv e both the uptak e and conversio n of T4 to T3; along wit h improvement s in nervou s syste m output , this will help to increas e metabolism . You get the idea: wit h overfeeding , the body reverse s the basic adaptation s tha t occurre d to dietin g in the firs t place.

Summin g up for now Lookin g at the char t on the nex t page, you may star t to appreciat e the problem s involved, especiall y for the geneticall y normal . Underfeedin g is necessar y for fat loss but will alway s have a negativ e impac t on muscl e mass . Dietin g also induce s a numbe r of adaptation s tha t ten d to preven t furthe r fat loss. Overfeedin g is necessar y to gain muscl e but will alway s hav e a negative impact on fat mass. However, it can reverse many of the adaptations that occur with dieting.


Calories Protein Carbs/fa t (energy) Insulin Tota l testosterone Fre e testosterone GH IGF-1 Thyroid Catecholamines Cortisol Leptin Ghrelin Cellula r energ y state Protein synthesis Bodyfat levels Muscl e mass Net effect

Overfeeding Up Up Up Up Up or no change Up Up Up Up Down Down Up Down Up Up Up Up Body is systemically anabolic

Underfeeding Down No chang e or Up Down Down Down Down Up Down Down Up Up Down Up Down Down Down Down Body is systemically catabolic

A fina l not e on leptin Hopefull y the above section s hav e mad e you realiz e tha t ther e is far more to the adaptation s to eithe r dietin g or overfeedin g tha n just leptin . Rather , ther e is an integrated respons e involvin g leptin , insulin , ghrelin , fatt y acids , liver, fat cell and skeleta l muscle adaptations , and probabl y factor s tha t haven' t been discovere d yet. This probabl y explain s why injectin g lepti n into dietin g human s reverse s only some but not all of the adaptation s to dieting. For example , jus t injectin g lepti n would be expecte d to fix a defect in TSH (and thyroid output ) and it does do this . But injectabl e lepti n won't fix the problem s wit h conversio n that occur at the liver. Similarly , while injectin g lepti n would normaliz e LH and FSH output , it won't correc t the proble m wit h increase d bindin g of testosteron e to SHBG cause d by lowere d insulin. Hopefull y you get the picture . Now we know the problem . What' s the solution?

Cyclica l dieting Wha t I've basicall y done over the previou s page s is mak e a long-winde d argumen t for cyclical dieting , tha t is period s wher e you alternat e a low-calori e intak e wit h a high-calori e intake. More specificall y I'm describin g a diet wher e you alternat e betwee n period s of low calories/carbs Page 27 http://www.bodyrecomposition.com

wit h period s of high calories/carb s to alternat e betwee n period s of anabolis m (tissu e building ) and catabolis m (tissu e breakdown) . Of course , thi s is nothin g new. Ther e hav e been numerou s othe r scheme s over the year s tha t alternate d period s of low and high calories . DiPasquale' s Anaboli c Diet, Rob Faigan' s NH E and man y other s hav e come and gone over the years. Severa l year s ago, whe n I firs t starte d makin g some of the connection s betwee n lepti n and everythin g else, thi s reall y pointe d out the need to do periodi c refeed s (or chea t days or whatever you wan t to call them ) on a diet. I thin k it explain s par t of why people got bette r result s wit h the Bodyopu s diet: it wasn' t the ketogeni c phas e so muc h as the two day carb-loa d which refilled muscl e glycogen , mayb e instille d an anaboli c response , and helpe d to revers e some of the adaptation s inheren t to dieting. Since the Bodyopu s days , a numbe r of approache s hav e come and gone. In general , short refeeds , lastin g from 5 to 24 hour s done anywher e from once per week to every othe r day (dependin g on such variable s as bodyfa t percentag e and how har d you'r e dieting ) while dieting hav e been used . I've trie d the m all wit h varyin g degree s of success. One of the factor s I've been considerin g latel y has to do wit h the duratio n of the overfeeding period . While it's tru e tha t 5 (or 12 or 24) hour s of concentrate d overfeedin g will rais e leptin , the more importan t questio n is whethe r that' s sufficien t to "tell" the brai n tha t you'r e fed. While data (especiall y in humans ) is nonexistent , my hunc h is tha t it is not. My basic reasonin g is this : there' s a lag time of severa l days betwee n the drop in lepti n and the drop in metaboli c rat e (nervou s syste m output ) for example ; I'd be surprise d if a mer e 12 or 24 hour s was sufficien t to revers e this . Rather , I'd expec t it to tak e a simila r amoun t of time for the reversa l to occur. The more extende d logic of my reasonin g is beyon d wha t I wan t to put in thi s book, emai l me if you mus t know. Now, thi s isn' t to say that shor t carb-loads/refeed s aren' t of benefit . They refill glycogen, tur n off catabolis m briefl y and mayb e induc e an anaboli c respons e to boot. They also let you eat some of the crap you'r e reall y cravin g which help s psychologically . But I doub t the y are sufficien t to affect metabolis m very much . Instead , a longe r refee d is most likely necessary . The drawback , of course , is tha t longe r refeed s hav e a tendenc y to put too muc h bodyfa t back on whic h goes agains t the entir e goal of dieting. Perhap s the bigges t proble m wit h man y cyclical dietin g approache s is tha t the y don't coordinat e trainin g wit h the diet. Bodyopu s was an exceptio n but , for variou s reasons , I thin k the workou t pla n was screwy . If anything , it was backwards , puttin g tensio n workout s on lowcalorie/low-car b days (wher e you aren' t very anabolic ) and glycogen depletio n workout s before you are eatin g a lot. This seeme d wron g to me year s ago and more wron g to me now tha t I've delve d into it in more detail . This will mak e more sens e as you rea d the nex t chapters. Ultimately , all of thi s introductor y stuff , bring s us to the final question : how do we optimize the entir e syste m to maximiz e fat loss and eithe r muscl e maintenanc e or muscl e gain (or, if Page 28 http://www.bodyrecomposition.com

you'r e a performanc e athlete , how do we generat e fat loss while maintainin g performance) ? To understan d that , I need to get into a few more detail s regardin g muscl e gain and fat loss, which will help you to understan d the overal l system.


Chapter 5: Fat basicsAsk most people how to lose fat and you'll usuall y get a prett y generi c answer : eat less and exercise . I've mad e comment s along thos e line s myself . Fundamentally , there' s not muc h wrong wit h tha t particula r soun d bite, at leas t withi n a certai n rang e of bodyfa t percentages . Basically, if you creat e a defici t betwee n the energ y your body need s and wha t it has availabl e and at least some fat will be mobilize d to be use d for energy . How muc h is use d and wher e it comes from depend s on more tha n jus t simpl y reducin g calories . That' s the partitionin g issu e I talke d about last chapter. Wha t we're reall y intereste d in, more so tha n jus t calori e balance , is fat balance . Losin g fat require s a negativ e fat balance . A negativ e fat balanc e simpl y mean s tha t you mus t be burning more fat tha n you'r e eatin g (or producing) ; we wan t to try and optimiz e thi s proces s to maximize the rat e of fat loss. It is possible , unde r the righ t condition s for shor t period s of time , to be losing fat while eatin g above maintenanc e calories , as long as you maintai n a negativ e fat balance. Now, as I've mentione d in previou s chapters , geneti c superior s seem to be able to mobilize and utiliz e fatt y acids more effectivel y than the res t of us. This has a protei n sparin g effect because , the more you can force your body to rely on fatt y acids for fuel, the less it need s to use glucos e or amin o acids . So is ther e any way we can mimic thi s in the non-geneticall y elite ? To answe r thi s question , we need to look at some of the detail s of fat, both dietar y and bodyfat.

Dietar y fat Let' s star t wit h dietar y fat, the fat that' s found in your food. Dietar y fat is technicall y a triglyceride , which is a molecul e of glycerol (a sugar ) boun d to thre e fatt y acids . All fatt y acids are not the same , though . They can differ in lengt h from shor t to mediu m to long chain , depending on how man y carbon s are present . They also differ in the numbe r of doubl e bond s which are present . Saturate d fats (found mainl y in anima l foods) hav e no doubl e bonds , monounsaturated fats (olive oil) hav e a singl e doubl e bond, and polyunsaturate d fats (fish oils, flax oil) hav e multiple doubl e bonds . Chemica l difference s in fat can affect metabolis m and physiology. Unlik e protein s and carbohydrates , dietar y fats aren' t wate r soluble , the y hav e to be digeste d in the stomac h wit h the help of bile acids release d from the pancreas . After a good bit of processin g (the detail s of which are unimportan t here) , most dietar y fats are package d as chylomicron s which ente r the lymphati c system . In contrast , carbohydrate s and protei n go to the liver, via the porta l system , afte r digestio n and absorption. After abou t 3 hours , thes e chylomicron s will reac h the fat cells. There , the y are acted upon by an enzym e calle d lipoprotei n lipas e (LPL), which liberate s the fatt y acids from the Page 30 http://www.bodyrecomposition.com

chylomicron . Those fatt y acids can eithe r be store d in the fat cell or take n up into the bloodstrea m for use by othe r tissue s such as muscl e and liver. Whethe r the y are store d or release d depend s on the metaboli c stat e of the dieter . The mai n poin t is tha t dietar y fat isn't going to be readil y availabl e by tissue s such as muscl e and liver, even unde r the best of circumstances . At best it migh t become availabl e 3 hour s afte r ingestion. But remembe r from above, one of our goals is to mak e fatt y acids as readil y availabl e to the body as possible . Is ther e any way to increas e the rat e at which dietar y fat is available ? The answe r is yes, havin g to do wit h two weir d exception s to the above. The firs t exception , and probabl y the compoun d most reader s hav e at leas t hear d of, are mediu m chai n triglyceride s (MCTs). Unlik e longe r chai n fats , MCTs go the liver and are available for use far more rapidl y by othe r tissue . In addition , MCTs are preferentiall y use d to produce keton e bodies which can be use d instea d of glucose , amin o acids or fatt y acids by most tissue s of the body. In some studie s thi s has a protei n sparin g effect and thi s is especiall y true in the initial period s on a low-calori e low-carbohydrat e diet. A secon d potentia l exceptio n is the newly availabl e diacylglycero l (DAG) oil put out by a compan y calle d ENOVA (http://www.enova.com) . Unlik e triglycerides , DAG oil is mad e available to the body more rapidl y than long-chai n fats . Usin g eithe r MCT or DAG oil shoul d allow calories to be reduce d to lower tha n norma l levels withou t causin g as muc h muscl e loss.

So wha t abou t bod y fat? Whe n people tal k abou t body fat, wha t the y mea n are triglyceride s which are store d in your fat cells (ther e is also some store d in your muscles , calle d intramuscula r triglyceride , but it is a tiny amoun t compare d to what' s store d on your fat but t or stomach) . An averag e individual may hav e 30 billio n fat cells which are compose d of abou t 90% triglycerid e store d as one big droplet . The remainin g 10% is wate r and the enzymati c machiner y which control s cellular metabolism. Now, not all fat cells on your body are the same . Researcher s hav e identifie d at leas t 4 differen t "types" of bodyfat , althoug h we can actuall y mak e at leas t one furthe r distinction. Firs t is essentia l bodyfat , which exist s in smal l quantitie s (abou t 3% of the tota l in men, and 9-12% of the tota l in women ) in the brain , spina l cord, etc. You can' t lose it, and if you did you'd be dead . The amoun t of essentia l bodyfa t set s the ultimat e lower limi t for bodyfat percentage . So tha t shoul d be 3% for men and 9% for women . I shoul d note tha t you will occasionall y see claim s of bodyfa t percentage s less tha n 3% for men or less tha n 9% for women. It's not tha t the folks are lying, so muc h as the fact tha t the measuremen t method s being used aren' t as accurat e as the y need (or are claimed ) to be. We don' t need to worr y abou t essentia l fat in thi s book. Like I said , you can' t lose it and even if you could, you'd be dead. Page 31 http://www.bodyrecomposition.com

A secon d type of fat is brow n fat which is a specialize d type of fat tha t actuall y burn s up the othe r type s of fat, producin g hea t in the process . In contras t to whit e fat (all the other types) , which is primaril y triglycerid e wit h a littl e bit of othe r stuff , brow n fat is mad e up mainly of mitochondri a (the powerhous e of the cell), wit h very littl e triglyceride . The high mitochondrial conten t make s brow n fat idea l for burnin g fatt y acids for heat . The proble m is, while animals hav e a lot of brow n fat (the y need it to keep body temperatur e up agains t the cold and such), humans lose most of their brown fat once they move past the baby stage of life. We can pretty muc h ignor e it for the res t of thi s book. You shoul d also questio n any supplement s tha t claim to caus e fat loss via brow n fat activation ; it will probabl y work wonderfull y in your pet hamste r or mouse but that's about it. Next up is viscera l fat. This is a type of fat tha t surround s your interna l organs . In excess it gives you a pregnan t look becaus e it make s your gut stic k out. Viscera l fat has a numbe r of differen t characteristic s from subcutaneou s fat (whic h I'll discus s nex t chapter ) which has some consequence s for both healt h and dieting . Men ten d to hav e more viscera l fat tha n wome n as testosteron e and cortiso l tend s to promot e its growth . Wome n who use anaboli c steroids , or who hav e highe r tha n norma l testosteron e for whateve r reason , ten d to accumulat e viscera l fat as well. By the time men reac h the 12-15% bodyfa t range , it is unlikel y tha t the y will carr y much viscera l fat unles s the y hav e been usin g androgens. The type of fat most dieter s are concerne d wit h is subcutaneou s fat which is found under the skin . In men, subcutaneou s fat tend s to accumulat e aroun d the midsectio n and low-back ; in women , it tend s to be on the hips and thighs . This occurs unde r the influenc e of the hormones testosterone/cortiso l and estrogen/progesteron e in men and wome n respectively . This is why kids before pubert y hav e the sam e bodyfa t pattern s and kids afte r don't. In fact, whe n researcher s pum p sex-chang e patient s up wit h hormones , the y see a shif t in bodyfat : men tak e on femal e bodyfa t pattern s and vice versa . Wome n who don' t go on hormone replacemen t afte r menopaus e (meanin g the y produc e no estrogen ) tend to lose the fat in their hip s and thigh s and gain it in thei r stomac h area . As I've mentioned , some lucky individual s have more even fat distribution s and still look ok even whe n they'r e carryin g a lot of fat; the y are simpl y smoot h all over. If you'r e readin g thi s book, odds are you aren' t one of them. We (not the researchers ) can subdivid e subcutaneou s fat into two types : norma l and stubborn . Norma l fat is jus t norma l subcutaneou s fat tha t comes off withou t too muc h effort. A littl e calori e cutting , a littl e cardio , and it comes off withou t too muc h trouble . Stubbor n fat is the othe r kind , tha t stuff tha t goes on first , and comes off last , if it ever comes off at all. Stubbor n fat is generall y ab and low back fat for men and hip and thig h fat for women . Ther e are reason s that stubbor n fat is so stubbor n tha t you'll lear n abou t soon. Now tha t you know the basic s of both dietar y fat metabolis m and bodyfat , let's get into the detail s of how fat is burne d off and how we can optimiz e the process. Page 32 http://www.bodyrecomposition.com

Chapte r 6: Fa t cel l metabolism

The ultimat e goal of a diet is to lose bodyfa t of cours e so let's look at the processes controllin g that . Tha t mean s examinin g the step s involve d in mobilizin g fat from fat cells and burnin g the m off. First , let me elaborat e on wha t it mean s to lose or "burn " bodyfat . Wha t thi s mean s is tha t the fat store d in your fat cells is remove d from thos e cells and converte d to energ y elsewhere in the body. Most tissue s in the body (ther e are a few exception s such as the brain ) can use fatty acids for fuel, but the mai n ones we are intereste d in are skeleta l muscl e and the liver. I wan t to mentio n tha t even thoug h the brai n can' t use fatt y acids directly , it can use ketone s which are mad e from fatt y acid metabolis m in the liver. Let' s look at the mechanism s underlyin g the proces s of fat loss. Althoug h the proces s can be furthe r subdivided , we are only intereste d in thre e majo r step s of fatt y acid metabolism: mobilization , transport , and oxidatio n (burning).

Ste p 1: M obilization The firs t ste p in burnin g off bodyfa t is gettin g it out of your fat cells. You migh t even argue tha t thi s is the most importan t ste p since, if you can' t get it out of the fat cell, you can' t bur n it off. Recall from las t chapte r that bodyfa t is primaril y store d triglyceride , wit h a smal l amount of wate r and some enzymati c and cellula r machinery . Mobilizin g bodyfa t require s that we first brea k down the store d triglycerid e into thre e fatt y acids and a molecul e of glycerol . The rate limitin g step in thi s proces s is an enzym e calle d hormon e sensitiv e lipas e (HSL). So wha t regulate s HSL? Althoug h a numbe r of hormone s such as testosterone , cortisol, estrogen , and growt h hormon e hav e modulatin g effects on HSL activit y (mainl y increasin g or decreasin g tota l level s of HSL in the fat cell), the only hormone s tha t we need to be concerned wit h in term s of HSL activit y are insuli n and the catecholamines. The primar y inactivato r of HSL is the hormon e insuli n and it only take s very tiny amount s (dependin g on insuli n sensitivity ) to hav e an effect. Eve n fastin g insuli n levels are sufficien t to inactivat e HSL by nearl y 50%. Smal l increase s in insuli n (from eithe r protei n or carbohydrat e intake ) inactivat e HSL further . Additionally , the mer e presenc e of triglyceride s in the bloodstrea m (via infusio n or by jus t eatin g dietar y fat by itself ) also inhibit s HSL activit y so thi s isn' t as simpl e as jus t blamin g insulin . One way or another , any time you eat, HSL is going to be inactivated , eithe r by the increas e in insuli n from protei n or carb s or the presenc e of fat in the bloodstrea m from eatin g fat. Page 33 http://www.bodyrecomposition.com

The primar y hormone s which activat e HSL are the catecholamines : adrenalin e and noradrenaline . Adrenalin e is release d from the adrena l cortex , travelin g throug h the bloodstream to affect numerou s t

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