Nutrition *Nutrition has played a significant role in your life.

*And it will continue to affect you in major ways, depending on the foods you select. *Every day, several time a day, you make food choices that influence your body s health for better or worse. Nutrition: The science of food and the nutrients and other substances they contain, and of their actions within the body. People decide what to eat, when to eat, and even whether to eat in highly personal ways, often based on behavioral or social.. Many different food choices can support good health, and an understanding of nutrition helps you make sensible selection more often. 1-personal preference. 2-Habit. 3-Ethnic heritage or tradition. 4-social interactions 5-availability, convenience, and economy. 6- positive and negative associations. 7-emotional comfort. 8-values. 9-body weight role. 10-nutrition and health benefits. Foods provide nutrients substances that support the growth, maintenance, and repair of the body's tissues. This six classes of nutrients include: 1-carbohydrates 2-lipids 3-proteins 4-vitamins 5-minerals 6-water Food rich in the energy-yielding nutrients (carbohydrates ,lipids ,proteins) provide the major materials for building the body's tissues and yield energy for the body's use or strorage. Energy is measured in Kcalories, vitamins and water facilitate a variety of activities in the body.

I I. C AR B O H YD R AT E S A. Digestion and Absorption

From a quantitative point of view, carbohydrate is the major group of chemical substancesmetabolized by man and most animals. Approximately 50% by weight of the Americandiet or 400500 g/day for the average American male is carbohydrate. About 60% of thetotal digestible carbohydrate is in the form of starch largely derived from cereal grains andvegetables such as corn and potatoes. The other 40% is supplied in the for m of sucrose,lactos e, maltose, glucos e, fructose, and other sugars. Some glycogen is ingested in meat. Starch contains two polysaccharides, amylos e and amylopectin, which are bothpolymers of glucose but differ in molecular architecture. Amylose consists of 250300glucose units linked by a -1,4 glucosidic bonds (unbranched type). In amylopectin themajority of the units is similarly connected by a -1,4 glucosidic bonds, but has about one a - 1, 6 gl uc os i di c b on d f or 3 0 a - 1, 4 l i nka g es ( br a nc he d t yp e ). G l y c og e n r es e mb l es amylopectin in structure but has a higher degree of branching.The digestion of starch begins in the mouth when the food is mixed with salivary a -amylase, but the hydrolysis stops in the stomach because of the change in pH andresumes in the duodenum where pancreatic a -amylase is secreted. Both salivary andpancreatic amylas es are a -1,4 glucosidases and serve to hydrolyze only the internal1, 4 gl u c os i di c b on ds f ou nd i n s t a r c h a nd g l y c o g e n. T h er e i s l i t t l e a ct i vi t y a t t he 1, 4linkages adjacent to the branching points, and the a -1,6 bonds (or branch points) are notattacked by amylase. Consequently, the products of digestion by a -amylase on starch orglycogen are maltose, isomaltose, maltotrios e (a trisaccharide), and a -limit dextrins(containing on the average eight glucose units with one or more a -1,6 bonds). The finaldigestive process occurs at the mucosal lining and involves the action of a -dextrinase( is o ma l t a s e ), w hi c h hyd r ol yz es t he 1, 6 gl u c os i di c b on d s f r o m l i mi t de xt r i ns a nd isomaltose. Maltase, another brush-border enzyme, breaks down maltose and maltotrioset o gl u c o s e, w hi c h i s t h e e nd p r od u ct of s t a r ch a nd gl yc og e n di ge s t i o n. S uc r os e a n dlactose are similarly hydrolyzed by sucrase and lactase, which are located on the brushborder,

to their corresponding monosaccharides glucose and fructose, and glucos e andgalactose, respectively.Monosaccharides are absorbed from the intestinal lumen by passage through themucosal epithelial cells into the blood stream. The transport of glucose and galactosea c r os s t he br u s h b or d er me mb r a ne of t he mu c o s a l c e l l oc c ur s b y a n a c t i ve, ene r gy- requiring process that involves a specific transport protein S GLT1 and the pres ence of sodium ions. Fructose is absorbed by a facilitated diffusion process supported by GLUT5that efficiently accommodates luminal fructos e and functions independently of sodiumions. Glucose, galactose, and fructose exit from the enterocytes primarily via the GLUT2transporter of the basolateral membrane. Other sugars (e.g., pentos es) are absorbed bysimple diffusion through the lipid bilayer of the membrane. In the normal individual, thedigestion and absorption of usable carbohydrates are 95% or mor e complete. S omesugars and sugar alcohols such as sorbitol are universally malabsorbed, and diarrhea ensues with the ingestion of ample medications, gums, and candies sweetened with thesenonavailable sugars. B. Carbohydrate Intolerance C a r boh ydr a t e i nt o l e r a nc e i s c ha r a c t er i z ed b y ma l a bs or pt i on t ha t l ea d s t o s y mp t o ms , pa rt i cu l a r l y di a r r he a , wi t h ex cr et i on o f a c i di c s t oo l s a nd c a r b ohy dr a t e i n t h e f e c e s f ol l o wi n g i ng e st i on of s u ga r s . I t c a n b e du e t o a d ef ect i n di ge s t i on a n d/ or a b s or pt i on of di et a r y ca r b o hy dr a t e. D i- , ol i go- , a nd p o l ys a c c ha r i d e s t ha t a r e not hy dr ol yz ed b yamylase and/or s mall intestinal surface (brush border) enzymes cannot be absorbed; theyreach the lower tract of the intestine, which contains bacteria. Microorganisms can break down and anaerobically metabolize some carbohydrates resulting in the formation of short-chain fatty acids, lactate, hydrogen gas, carbon dioxide, and methane. The presenceo f o s m o t i c a l l y a c t i v e c a r b o h y d r a t e a n d f e r m e n t a t i v e p r o d u c t s w i t h i n t h e l u m e n i s associated with intestinal secretion of fluid and electrolytes until osmotic equilibrium isreached. Thes e products also cause increased intestinal motility and cra mps, because of i n t r a l u m i n a l p r e s s u r e a n d d i s t e n t i o n o f t h e g u t , o r b e c a u s e o f t h e d i r e c t e f f e c t o f degradation products on the intestinal mucosa. Some int estinal mucosal cells along withdis accharidases may be lost. Disaccharidase deficiency is frequently encountered in humans. The deficiency canbe due to a single or several enzymes for a variety of reasons (e.g., genetic defect, injuriesto mucosa, or physiological decline with age). Mucosal injury may arise either fromtissue invasion and destruction of the epithelial cells by enteric microorganisms or fromcell injury caused by products of bacterial metabolism. Viral gastroenteritis damages themucosa and destroys a significant proportion of disaccharidases of the brush border cells.Mucosal damage does not usually affect sucrose hydrolysis probably because a high levelof sucrase is normally present, but lactose hydrolysis is significantly reduced. Secondarydeficiency may result due to a disease or disorder of the intestinal tract; these defectsdisappear when the disease is resolved. Such diseases include protein deficiency, celiacdisease, tropical

sprue, and intestinal infections. Brush border enzymes are rapidly lost in normal individuals with severe diarrhea, causing temporary acquired enzyme deficiency.These patients suffering or recovering from a disorder cannot drink or eat significantamounts of dairy products (lactose) or sucrose without exacerbating the diarrhea. Lactasedeficiency is most commonly observed (milk intolerance) in huma ns. There are threetypes of lactase deficiency: (a) inherited deficiency, which is relatively rare, in whichsymptoms of intolerance develop very soon after birth and disappear with feeding on al a c t os e - f r e e di et ; ( b) s e c on da r y l ow l a ct a s e a c t i vi t y, w hi c h ca n oc c ur a s a r es u l t of damage to the small intestine; and (c) primary low-lactase activity, which is a relativelycommon syndrome, particularly among Afro-Americans, Asians, and South Americans.In these individuals, intolerance to lactose is not a feature of the early life of adults, butthere is an age-related decline in lactase activity in susceptible individuals. Many of theselactose- intolerant individuals can consume small quantities of milk (one glass) withoutsymptoms, and milk products such as cheese and yogurt may be tolerated more readilythan regular cows milk. Lactase additives and lactase-hydrolyzed milk are now availablefor lactos eintolerant individuals who want to continue to drink milk.S u c r a s e is oma lt ase defi ciency is a rare i nher it ed deficiency of s u c r a s e a n d isomaltase. Individuals with this combined enzyme deficiency cannot hydrolyze sucroseand the disaccharide products of ingested starch. The deficiencies of these two enzymes xi s t b e ca u s e s u cr a s e a nd is o ma l t a s e o c cu r t oge t h er a s a co mp l ex e nz y m e. T hi s or d er i s f ou n d i n a b out 1 0 % of G r ee nl a nd E s ki mos . S y mpt o ms oc c ur i n ea r l y y beans, lentils, and navy beans), but cannot be hydrolyzed by intraluminal ortinal enzymes. Although not nutritionally important, saccharides in legumes aree d u p o n b y ba ct er i a i n t he l ow er s ma l l i nt es t i n e a nd c ol on t o yi el d 2 3 ca r b o nt i ve di a g n os i s of a d ef i c i e nc y of a p a r t i c u l a r enz y me i nvol ve d i nI . L I P I D S tion and Abs orptionob l e m b ec a us e t hey a r e i ns o l u bl e i n wa t er w hi l e t he l i p ol yt i c en z y me s , l i ke ot h er el l es . In t hi s c ont ext , t he t wo p ha s es a r e wa t er a nd fa t , t he l a t t er ma ki n g u p t hec e l l e s . M i c e l l e s t e n d t o a g g r e g a t e i f t h e y a r e n o t s t a b i l i z e d i n s o m e w a y ; i n t h e t l e or no l i p i d di g es t i on o c c ur s i n t he mout h. T h er e i s s o me l i pa s e i n t he i d s i n t o f i n e d r o p l e t s a n d i n t h e d u o d e n u m t h e s e d r o p l e t s a r e e x p o s e d t o t h e i d w a t er i nt er f a c e. E mu l s i f i e d t r i gl yc er i de s a r e r ea di l y a t t a c ke d b y l i pa s es pr ob l e m is ov er c o me b y c ol i pa s e (a s ma l l p r ot e i n wi t h a mol e c u l a r w e i ght of c r e a t i c l i p a s e a t t a c k s t h e e s t e r l i n k a g e s a t t h e 1 a n d 3 - c a r b o n s o f t h e gl yc er i d e, l ea vi n g a mon o g l y c er i d e w it h t he f a t t y a ci d e s t er i f i e d a t t he 2 - ca r b o nr d f a t t y a ci d mol e c u l e a n d gl yc er o l , bu t i s not a nec es s a r y s t e p f or a bs or pt i o n. i g e s t i o n o f C a r b o h y d r a t e s , L i p i d s , a n d P r o t e i n s 2 3 in lipids. For example, cholesterol esterase hydrolyzes cholesterol esters tol es t er ol a nd f a t t y a ci ds . Anot her l e s s s p ec i f i c l i p i d es t er a s e a ct s on s hor t - c ha i ns . P hos p ho l i pi ds a r e hy dr ol yz ed b y p h os p h ol i p a s e Ai c h i s s e c r e t e d a s a ma l

i ndi vi dua l s l i pi d a bs or p t i on o c c u r s i n t he u pp e r pa r t of t h e s ma l l ds a r e r ee s t er i f i e d wi t h mo n oa c y l g l y c er ol t o t h e t r i gl yc er i d e l ev e l i n t he s mo ot h d Malabsorptionbed, but in infants 1015% of the dietary fat may escape absorption and be excreted.a t o r r h e a , a c o n d i t i o n i n w h i c h t h e r e i s e x c e s s i v e l i p i d a p p e a r i n g i n t h e s t o o l , anies many illnesses. Basically, lipid malabsorption may result from defectiveysis in the intestinal lumen or defective mucosal cell metabolism. Defective lipolysist r i c a ci d s ecr et i on. T hi s c a n r es u l t i n s t ea t or r h ea s e c on da r y t o a ci d i na ct i va t i on of ase in intraduodenal pH. Defective mucosal cell metabolis m may bethocytosis), neurological problem, and steatorrhea. Lipolysis, micelle formation,gl yc er i d es c a n not ex it f r o m t he e p i t h el i a l c el l s b e ca us e o f t he f a i l ur e t o pr odu c ei e nt s wi t h a b et a l i p opr ot ei n e mi a a r e t r ea t ed w i t h a l ow- f a t di et c o nt a i ni ngulation, thereby bypassing the defect of abetalipoproteinemia. Poor absorption of n associated with deficiencies of fat-soluble vitamins and, in particular,. P RO T E IN S stion and Absorptionoc es s of p r ot e ol ys i s mu s t oc c ur wi t h out t h e b od y s own p r ot e i n b ei ng di g es t ed. A ot ec t e d c o mp a r t me nt f or t h e hy dr ol yt i c pr oc e s s is pr ovi de d b y t h e l u me n of t he intestinal tract. In addition, the secretory cells that synthesize proteases (except u e s t er ed i n s t or a ge gr a nu l e s i n i na c t i ve f or ms , t he z y mog e ns , unt i l ne e d ed. T he m e n o f t h e gas tr oint est i nal t ract and i nv olves , i n part, cha nges in t he m o l e c u l a r s t i on b egi ns i n t he s t o ma c h w h er e pr ot ei n i s d ena t ur ed b y l ow p H a nd i s ed to the action of proteolytic enzymes. The acidic environment also providesi g e s t i o n o f C a r b o h y d r a t e s , L i p i d s , a n d P r o t e i n s 2 5 t he op t i mu m pH f or p ep s i n a c t i vi t y. T he z y mog e n p ep s i n og e n, w hi c h i s s ecr et ed b y c h i e f c e l l s , i s c o n v e r t e d t o p e p s i n i n t h e a c i d m e d i u m ( a u t o a c t i v a t i o n ) o r b y a c t i ve p ep s i n (a ut oca t a l ys i s ) b y t he r e m ova l of a pe pt i d e c on s i s t i ng of 44 a mi noacids from Nterminus. Although pepsin has a broad specificity, it attacks primarilyp ep t i d e l i nk a ges i n whi c h t h e c a r box yl gr ou p i s do na t ed b y a r oma t i c a mi no a ci dr e s i d u e s . P e p s i n i s a n e n d o p e p t i d a s e a n d t h e p r o d u c t s o f i t s a c t i o n c o n s i s t o f a mixture of oligopeptides. Pancreatic T he pr ot eolyti c enz y mes a r e synt he siz ed i n t he a ci na r c el ls o f t h e p a n c r e a s a n d secreted in pancreatic juice as zymogens. These include trypsinogen, chymotrypsino-gen, proelastase, and the procarboxypeptidases. In the lumen of the small intestine,e n t e r o p e p t i d a s e ( w h i c h u s e d t o b e c a l l e d e n t e r o k i n a s e ) , a p r o t e a s e p r o d u c e d b y duodenal epithelial cells, activates trypsinogen to trypsin (by scission of the hexapep-tide). Trypsin, in turn, activates trypsinogen, chymotrypsinogen, proelastase, and theprocarboxypeptidases to their respective active enzymes. Recently, enteropeptidase hasb e e n r e p o r t e d t o b e a c t i v a t e d f r o m a n i n a c t i v e p r e c u r s o r p r o e n t e r o p e p t i d a s e b y duodenase, a newly discovered protease in the duodenum (Fig. 3). Studies have alsos h o wn t ha t t r yps i n f or me d a ct i va t es pr o e nt er op e p t i d a s e. Tr yp i n a p p ea r s t o b e a n inefficient activator of trypsinogen. Trypsin, chymotrypsin, and elastase are

endopepti-dases. Trypsin is specific for peptide linkages in which carboxyl is donated by arginineor lysine. The specificity of chymotrypsin is similar to pepsin. Elastase has a ratherbroad specificity in attacking bonds next to small amino acids such as glycine, alanine,a nd s er i ne. C a r box yp e pt i da s es A a nd B a t t a c k t h e c a r bo x y t er mi na l p e pt i d e b on ds , thereby liberating single amino acids. The combined action of pancreatic peptidasesresults in the for mation of free amino acids and small peptides of two to eight aminoacid residues. F IGURE 3 Activation of zymogens. Introduction to Clinical Nutrition26

Intestinal The luminal surface of s mall intestinal epithelial cells contain amino peptidases anddipeptidases. The end products of cell surface digestion are amino acids and di- andtripeptides. These are absorbed by the epithelial cells via specific amino acid or peptidet r a ns p or t s ys t e m s . T he di - a nd t r i p ep t i d e s a r e hy dr o l y z ed w i t h i n t he c yt op l a s mi c component before they leave the cell. The hydrolysis of most proteins is thus complet eto their constituent amino acids. After active absorption by the intestinal mucosal cells,the amino acids are taken up primarily by the blood capillaries in the mucosa and aretransported in the plasma to the liver and other tissues for metabolic use. A significanta m ou nt of t h e a bs or b ed a mi no a c i d s a l s o a pp e a r i n t he l y mp h. T h e di ge s t i on a nda b s or pt i on of t he ma j or it y of di et a r y pr ot ei ns is a b ou t 95 % c o mp l et e i n t he nor ma l human subject. B. Defects in Protein Digestion and Abs orption Gastric proteolysis is not essential for protein digestion. Individuals with achlorhydria or total gastrectomy have nor mal protein digestion and absorption. Small intestinal functionc o mp e ns a t es f or t he l a c k of p eps i n a c t i vi t y. T hus , t h e pa nc r ea t i c a n d s ma l l i nt e s t i na l di s ea s es w i l l b e t he ma j or c a us es of pr ot ei n ma l a bs or pt i o n. H o w e v er , t he r es er v ec a p a c i t y o f t h e p a n c r e a s i s s u b s t a n t i a l a n d f e c a l l o s s o f p r o t e i n m a y n o t b e c o m e significant in pancreatic insufficiency states until trypsin falls to about 10% of normal.There are two rare genetic disorders of protein digestion: enterokinase deficiency andt r y p s i n def ici enc y. As ca n b e exp ect ed fr om t he i mp ort a nt r ol e ea ch p l a y s i n t h e a c t i va t i o n of z y mo g e ns , d e f i c i e nc y o f eit he r of t he m ha s f a r - r ea c hi ng ef f ect s o n t h e efficiency of prot ein digestion. Hartnup disease is inherited as an autosomal recessive trait and the gene has beenmapped to chromosone 11qB. Homozygotes occur with a frequency of about 1 in 24,000births. Heterozygotes show no clinical abnormalities. In patients with Hartnup disease,the intestinal and renal transport defect for neutral a mino acids, including tryptophan,leads to niacin deficiency. Tryptophan is converted to niacin and normally supplies aboutone-half of the daily niacin requirements. Pellagra-like skin lesions, variable neurologicmanifestations, and neutral or aromatic aminoaciduria characterize this disease.Cystinuria is one of the most common inborn errors with a frequency of 1 in 10,000t o 1 i n 15, 0 00 i n ma n y et hni c gr ou p s . T he di s or der i s t r a ns mi t t e d a s a n a u t os o ma l recessive trait and results from impaired function of membrane carrier in the apical brushborder of renal tubular and small intestinal cell. Clinical manifestations include massiveex cr et i o n of c y s t i ne a nd ot he r di ba s i c a c i d s i n ho m oz y go t e wi t h c l a s s i c c ys t i nur i a . Cystine stones account for 1 2% of all urinary tract calculi but are most common causesof stones in children. Chapter 1 P r in ci pl es of H ea l t hyNutrition Charilaos Dimosthenopoulos, Meropi Kontogianni and Evangelia Manglara Energy balance What is energy balance? E ner gy ba la nc e is the dif f er e nc e b e tw e en en er gy i nt a ke, w h i c h c a n b e met a b ol i s e d, a nd t ot a l en er gy ex p e n di t ur e. It c o ul d

b e s a i d t ha t t he h u- man bodys energy state is balanced when its energy expenditure is equal toits energy intake.T h e h u m a n b o d y r e q u i r e s e n e r g y t o p e r f o r m i t s m a n y f u n c t i o n s , t o f a c i l i t a t e muscle activity and developmental demands and to correct problems thatma y ha ve b e e n ca us ed b y di s ea s e or i nj ur y. E ner gy ne e ds a r e met b y t he e n er gy obt a i n e d f r om t h e b o dy s di et , w hi c h de r i v e s f r o m f oo ds eit he r of pl a nt or of a ni ma l or i gi n. F oo d e n er gy i s r el ea s e d i n t h e b ody t hr ou g h t h eoxidation of carbohydrates, fats, proteins (which are called macronutrients)and alcohol.I f en er g y i nt a k e a nd ex p en di t ur e a r e not equ a l , t h e r es u lt w il l b e e i t h er a positive energy balance, in which body energy stores (and mainly fat) arei ncr ea s e d, or a ne ga t i ve e n er gy ba l a n c e, i n w hi c h t he b od y fa l ls ba c k onusing its energy stores (fat, protein and glycogen). Consequently, the bodyse n er g y ba la nc e ( a l on g wi t h ot her f a ct or s ) det er mi n es t o a l a r ge ext en t i t s weight and general health status. What factors inuence how much energy the human body requires? According to the denition given by the World Health Organization (WHO),en er gy r e qui r e me nt i s t he l e v el of ene r gy i nt a ke t ha t w il l ba la nc e e ner gy expenditure when we have a body size and composition, and a level of phys-ical activity consistent with long-term good health. Energy requirements arei n u e n c ed b y va r i ous f a c t or s , s u c h a s t he de v el op me nt a l s t a g e we a r e i n(e.g. childrens or adolescents requirements are different from those of the adults), body size, the amount and intensity of physical activity (athletes andmanual workers, for instance, obviously require more energy than people doi ngc ler i ca l wor kor l ea di ngs e de nt a r yl i ves) , ge n d er , ill ness , i njur y , p r e g n a n c y , lactation, etc. What is the basal metabolic rate? The basal metabolic rate (BMR) is one of the three components that energye x p e n d i t u r e c o n s i s t s o f . I t i s t h e a m o u n t o f e n e r g y s p e n t f o r b a s a l m e t a b o l i s m , which represents voluntary and involuntary vital bodily functions, such as res-piration, renal, brain and cardiovascular functions, cell and protein turnover,blood circulation, the maint enance of body temperature, etc.B M R i s c o m m o n l y e x t r a p o l a t e d t o 2 4 h o u r s t o b e m o r e m e a n i n g f u l , a n d i t i s then referred to as basal energy expenditure (BEE), expr essed as kcal/24h( kJ / 2 4 h ). R es t i ng m et a b o li c r a t e (R M R ), en er gy ex p en di t ur e u nd er r es t i ng conditions, tends to be somewhat higher (10 20%) than under basal condi-tions owing to increases in energy expenditure caused by recent food intake(i.e. by the thermic effect of food) or by the delayed effect of recently com-pleted physical activity. Thus, it is important to distinguish between BMR andRMR and between BEE and resting energy expenditure (REE) (RMR extrap-olated to 24 hours). BMR is measured under a specic set of circumstances:the subject must be awake, lying comfortably in a supine position, in a stateo f r e s t , i n a wa r mr oom, a tlea st 12 hour s a ft er last foodi ngestion. S inc e t h e s e strict conditions are hard to achieve in hospital settings, energy requirementsare usually expressed as RMR. Basal, resting and sleeping

energy expendi-t ur es a r e r ela t ed t o b od y s i z e, b ei n g m os t cl os el y c or r el a t ed wi t h t he s i z e of t he f a t - f r e e ma s s ( F F M ) , w hi c h i s t h e w e i ght of t he b od y l es s t he w ei g ht of its fat mass. The size of the FFM generally explains about 7080% of thevariance in RMR. However, RMR is also affect ed by age, gender, nutritionalstate, inherited variations and by differences in the endocrine state, notably(but rarely) by hypo- or hyperthyroidis m. What are the other two components of energy expenditure? Theot hertwocomponent sofener gyexpenditur ear e(1)t heen e r g y s p e n t o n daily activities and physical exercise (which depends on the kind, the intensityand the duration of the physical activity) and (2) the energy spent in responseto a variety of thermogenic stimuli (thermogenesis), which include the foodw e c ons u me, c er t a i n dr u gs , l ow t e mp e r a t ur es , mus cl e t ens i on, s t r es s a n dsimilar psychological states. What is the thermic effect of food? It has long been known that food consumption elicits an increase in energyex p e n di t ur e, a phe n o me no n kn o w n a s t he t her mi c ef f ec t of f ood (T E F ) . The intensity and duration of meal-induced TEF is deter mined primarily by t he a mou nt a n d c o mp os i t i on of t h e f oo d c o ns u m e d, ma i n l y o wi n g t o t he m et a b o l i cc os t s i nc ur r edi nha ndl i nga n d s t or i n gi n ges t ed nu t r i ent s . A c t i va t i on of the sympathetic nervous syst em, elicit ed by dietary carbohydrate and bys e ns or y s t i mu l a t i o n, ca us e s a n a ddi t i o na l , but mo d es t , i nc r ea s e i n e n er gy expenditure. The increments in energy expenditure during digestion aboveba s el i n e r a t es , di vi d ed b y t h e en er g y c ont e nt of t he f oo d c ons u me d, v a r yfrom 5 to 10% for carbohydrate, 0 to 5% for fat, and 20 to 30% for protein.The high TEF for protein reects the relatively high metabolic cost involvedin processing the amino acids yielded by the absorption of dietary protein,f or p r ot e i n s y nt hes i s or for t he s ynt h es i s of ur ea a n d gl u c os e. I n ge n er a l , c o ns u mp t i on o f t he u s ua l mix t u r e of nu t r i ent s is ge n er a l l y c o ns i der e d t o elicit increases in energy expenditure equivalent to 10% of the foods energycontent. How is energy expressed? All f or ms of ener gyca nb econvert edt oheat a nda llt heene r g y t h e b o d y u s e s is lost as hea t. For t hisr ea son,t heen er gyt h atisc onsu med, st or eda nds pent is ex pr ess edas it shea tequiva l e n t . T h e r s t u n i t o f e n e r g y e m p l o y e d i n n u t r i t i o n w a s t he ca l or i e [ t he a mou nt of en er g y ne e d e d t o r a i s e t he t e mp er a t ur e of 1 gram (g) of water from 14.5 to 15.5 C]. In the context of food and nutrition,the kilocalorie (1000 calories) has been traditionally used. However, in theI nt er na t i ona l S ys t e m of Un it s , t h e ba s i c en er g y u ni t i s t he j oul e ( J ), w hi c hc or r es p o nds t o t he e n er g y us ed w he n a ma s s of 1 ki l ogr a m ( k g) i s mo v edthrough 1m by a force of 1 newton (N). One J = 0.239 calories, so that 1kcali s e qua l t o 4. 186 k J .