laihduttaminen asiat joilla ei ole merkitysta

8/3/2019 Laihduttaminen Asiat Joilla Ei Ole Merkitysta

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Dieettaaminen

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asiat, joilla EI ole merkityst

1. Glykeeminen indeksi/kuorma, nopeat hiilarit vs. hitaat

Usein sanotaan, ett sy ruokia, jotka sisltvt pienen glykeemisenindeksin/kuorman, koska ne lihottavat vhemmn mm. pienemmn insuliinierityksentakia. Katsotaanpa asiaa hieman tarkemmin.

Vaikka matalan GI:n ja GK:n ruoat sisltvt yleens enemmn suojaravinteita, asiaei aina ole nin. Pelkll fruktoosilla on matala GI, mutta siin ei ole mitnravinteita. Ja esim. jteln ja Coca-Colan GI on matalampi kuin porkkanalla japerunalla. Selkesti GI ei kerro kaikkea.

Ja esim. proteiini laskee GI:t, mutta nostaa insuliinia. Ja vaikka perunalla on erittinkorkea GI, sen SI eli kyllisyysindeksi on mys erittin korkea. Ja maidolla on erittinmatala GI, mutta erittin suuri II, insuliini indeksi. Vaikka GI usein korreloikin melko

hyvin II:n kanssa, niin matala GI aiheuttaa pidemmn insuliinivasteen tosinmatalamman. Korkea GI korkeamman, mutta lyhyemmn. Lopputulos on siis melkosama. Ja esim. erss tutkimuksessa GI ei tuonut eroja insuliinin olivat ateriatsuuria tai pieni (1).

Useat (uudet, vanhemmista lpikatsaus myhemmin) pitkaikaset tutkimukset eivtole huomanneet mitn apua matalasta GI tai GK:sta (2-10). Ja osa hiilareista omaamatalan GI:n koska ne aiheuttavat nopeasti erittin suuren insuliinivasteen (11).

Obes Rev. 2002 Nov;3(4):245-56.Should obese patients be counselled to follow a low-glycaemic index diet? No.

Raben A.

Research Department of Human Nutrition, Centre for Advanced Food Studies, The RoyalVeterinary and Agricultural University, Frederiksberg, [email protected]

Comment in:

* Obes Rev. 2002 Nov;3(4):233.* Obes Rev. 2003 Feb;4(1):73-4.

In diabetes research the glycaemic index (GI) of carbohydrates has long been recognized and alow GI is recommended. The same is now often the case in lipid research. Recently, a newdebate has arisen around whether a low-GI diet should also be advocated for appetite- andlong-term body weight control. A systematic review was performed of published humanintervention studies comparing the effects of high- and low-GI foods or diets on appetite, food

intake, energy expenditure and body weight. In a total of 31 short-term studies (< 1 d),low-GI foods were associated with greater satiety or reduced hunger in 15 studies,whereas reduced satiety or no differences were seen in 16 other studies. Low-GIfoods reduced ad libitum food intake in seven studies, but not in eight other
mailto:[email protected]:[email protected]:[email protected]


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studies. In 20 longer-term studies (< 6 months), a weight loss on a low-GI diet wasseen in four and on a high-GI diet in two, with no difference recorded in 14. Theaverage weight loss was 1.5 kg on a low-GI diet and 1.6 kg on a high-GI diet. Toconclude, there is no evidence at present that low-GI foods are superior to high-GIfoods in regard to long-term body weight control. However, the ideal long-term studywhere ad libitum intake and fluctuations in body weight are permitted, and the diets are similarin all aspects except GI, has not yet been performed.

Tss lpikatsaus GI:hin jokusen vuoden takaa. 31 tutkimusta tehtiin kyllisyyden

suhteen, vain puolessa huomattiin, ett matalasta GI:st oli apua. Ja niss tutkitaanyleens vaikutusta tyhjn vatsaan aamulla, ilman muita makroravinteita. Ero olisiviel pienempi, jos nautittaisiin muita makroja ja eik tyhjn vatsaan.

Samin vain puolessa tutkimuksissa GI:n huomattiin auttavan ad libutum-saantiin elivapaaehtoiseen mttkisaan. Samat pointit kuin edelliseen.

Ja 20 pitkaikaisessa tutkimuksessa vain neljss matalasta GI:st oli apua,kahdessa haittaa ja 14:ssa ei huomattu mitn merkittv eroa.

Useat nist tutkimuksista eivt ole olleet edes kalorikontrolloituja. Ja niss onverrattu pelkstn korkeaa ja pelkstn matalaa GI:t ja GK:ta. Todellisuudessa

kukaan ei sy niin. Erot tulevat olemaan viel pienempi kun nautitaan sek matalaa,ett korkeaa ja sydn runsaasti kuituja. Tietenkin liikkuvalle kansalle, erot tulevatolemaan viel pienempi - siis kehonrakentajille. Ja varsinkin kun proteiinin mrnostetaan ja hiilihydraattien mr ehk lasketaan. Eroja tulee siis viel vhemmn -eroja joita ei edes alunperin ollutkaan.

Ja kalorikontrolloituja tutkimuksia on mys tehty - eli koehenkilille on tehty jaannettu kaikki ruoat ja heit on pyydetty olemaan symtt mitn muuta. Ainakaanoletettavasti, he ovat tehneet nin ja todennkisesti erot tasoittuisivat ryhmienvlill, vaikka jotkut olisivatkin ehk syneet. Joka tapauksessa kontrolloidumpiatutkimuksia ei ole tehty. Niss ei ole huomattu mitn merkittv eroa (12-14).

Obes Rev. 2006 May;7(2):219-26.Glycaemic index effects on fuel partitioning in humans.

Daz EO, Galgani JE, Aguirre CA.

Laboratory of Energy Metabolism and Stable Isotopes, Institute of Nutrition and FoodTechnology (INTA), University of Chile, Ave. El Libano 5524, Macul, Santiago,[email protected]

The purpose of this review was to examine the role of glycaemic index in fuel partitioning andbody composition with emphasis on fat oxidation/storage in humans. This relationship is basedon the hypothesis postulating that a higher serum glucose and insulin response induced byhigh-glycaemic carbohydrates promotes lower fat oxidation and higher fat storage incomparison with low-glycaemic carbohydrates. Thus, high-glycaemic index meals couldcontribute to the maintenance of excess weight in obese individuals and/or predispose obesity-prone subjects to weight gain. Several studies comparing the effects of meals with

contrasting glycaemic carbohydrates for hours, days or weeks have failed todemonstrate any differential effect on fuel partitioning when either substrateoxidation or body composition measurements were performed. Apparently, theglycaemic index-induced serum insulin differences are not sufficient in magnitudeand/or duration to modify fuel oxidation.

Tm on erittin merkittv paperi. Glykeemisen indeksin aiheuttamat erotinsuliiniarvoissa eivt ole tarpeeksi suuria, ett niill olisi merkityst. Tss erslpikatsaus parin vuoden takaa.

Arq Bras Endocrinol Metabol. 2007 Apr;51(3):382-8.[Effects of glycemic index on energy balance]

[Article in Portuguese]

Guttierres AP, Alfenas Rde C.

Departamento de Nutrio e Sade, Universidade Federal de Viosa, MG.paulagutti@@yahoo.com.br


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The prevalence of obesity has increased over the last decades. Associated to this, there hasbeen observed a chance in the dietetic pattern of the population in general, related to theincrease in carbohydrate consumption. According to some authors, the glycemic index (GI) offood may affect body composition and body weight. The purpose of this review was to evaluatethe effects of GI on appetite, satiety, and body composition. Based on the scientific evidencesreviewed, it was possible to verify that the majority of the studies that observed a positiveeffect of GI in that matter have a lot of methodological limitations. Well-designed studies have

not observed any benefit of GI on these parameters. Therefore, it is concluded that GI haslittle application in clinical practice, as a useful tool to control satiety, reduceappetite, and consequently, to reduce the prevalence of obesity.

Lisksi on vahvaa dataa sen puolesta, ett verensokeri/glykeeminen vaste ei mritnlntunnetta vaan aterian insulineeminen vaste (15,16)

Kytnnss - Ei ole mitn merkityst kehonkoostumuksen kannalta syk nopeitavai hitaita hiilareita. Usein hitaissa hiilareissa on paremmat ravintoarvot. Mutta nmruoat valitaankin juuri hyvien ravintoarvojen takia, ei matalan GI:n tai GK:n. Parastapa on syd sit, mill kalorit pysyy parhaiten hallussa, kuitenkin panostaenposin ravinnerikkaisiin ruokiin.

2. Aerobinen vs. HIIT ja aerobinen aamullaViime aikoina HIIT on kasvattanut suosiotaan runsaasti. Aerobinen on usein haukuttulyttyyn. HIIT:in on vitetty olevan kytnnss katsoen joka tavalla parempi.

Liikunnan tarkoitus on kuluttaa kaloreita. Ja kalorien kulutus on usein helpompi pitsuurempana aerobisella kuin HIIT:ll. HIIT:iss on suurempi jlkikulutus, mutta senvaikutus on melko pieni, vain reilut 6-15% kokonaiskulutuksesta, HIIT:in ollessaylpss ja aerobisen alapss nist luvuista (17). Molemmissa on hyv puolensaja huonot puolensa. HIIT:in hyvt puolet ovat lyhyt kesto, tehokkaampiproteiinisynteesille, eik ole niin tyls. Huonoja puolia on sitten mm. se ett dieetill

kun palautumiskyvyt eivt muutenkaan ole ideaaleja - mites siihen jopa 3-5 kovia 20-30 minuuttia kestvi juoksuvetotreenej jo ehkp 2-3 kovan jalkapunttitreeniinplle?

Aerobisen hyvi puolia on suuri energiankulutus ja se ett toimivat tavallaanpalauttavina. Huonoja puolia ovat kesto ja liiallisesti kytettyn mahdollinen''katabolia''. Aerobinenhan aiheuttaa suuremman kortisolivasteen, mutta vainkroonisesti koholla olevista kortisolitasoista on haittaa - kortisoli on hy olla korkeallaesim. aamulla ja treenin aikana. Kortisoli on hyv asia, mutta kuten kaikessa, hyvasiaa voi olla liikaa.

Kytnnss kannattaa ottaa se, josta pit enemmn/sopii paremmin ja jos tekeepaljon, niin kannattaa kytt molempia ja ottaa molempien hyvt puolet.

Sitten aamuaerobinen. Aamuaerobinen tyhjll vatsalla *voi* tehostaarasvaoksidaatiota. Mutta akuutit muutokset rasvaoksidaatiossa ovat melkomerkityksettmi kun mietitn kokonaiskuvaa. Aerobisen (tai HIIT:in) tarkoitus onlist kalorinkulutusta - silloin ei ole merkityst tekeek aerobista aamulla vai illallatai milloin vaan. Aamulla mys proteiinisynteesi on alhainen ja maksanglykogeenitasot vhn matalalla, joten lihasten menettminen on hiemantodennkisemp aamulla tehtess, jos ei sy mitn. Varsinkin kovaa sessiotatehdess jaksaa paremmin jos haukkaa jotain purtavaa.

Kytnnss ei ole siis vlil milloin aerobisen tekee - kaloritase mritt laihdutkovai et. Monet tuntevat olonsa koko pivn virkeksi tehdessn aamulla aerobisen -

silloin sen tekeminen on ihan perusteltua. Kannattaa kuitenkin syd jotain -HIIT:iss ei kuitebnkaan kytet rasvaa akuutisti niin paljoa energiaksi ja aerobisessarasva toimii muutenkin pasiallisena energialhteen.


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3. Variaatiot rasvan ja hiilihydraattienmrss

Usein kuulee vitteit kuten: 'l sy hiilareita, koska ne lihottavat', 'varopiikkaamasta insuliinia, koska se lihottaa'. No kyll ja ei.

Kun sydn vhemmn kuin kulutetaan, keho on vhemmn aikaa varastoivassatilassa - pienemmn kalorimrn takia. Keho varastoi aterian jlkeen AINA rasvaa.Insuliinin erittyminen hiilihydraattien jlkeen on juuri tm vaikutusmekanismi. Muttamys proteiinin syminen aiheuttaa tarpeeksi suuren insuliinipiikin lopettamaanrasvanpoltto. Niin, mutta eiks glugakoni tasapainota tt insuliinipiikki? Tavallaankyll, tavallaan ei koska glugakoni ei polta rasvaa.

Mutta mites sitten rasvaisen aterian jlkeen? Silloin ei erity paljoa insuliinia. Ei, muttaASP:t erittyy.

Acylation stimulating protein. Tm vuonna 1989 lydetty hormoni on merkittvin

rasvaa varastoiva hormoni.Proc Nutr Soc. 1997 Jul;56(2):703-12.The acylation-stimulating protein pathway and regulation of postprandial metabolism.

Sniderman AD, Cianflone K, Summers L, Fielding B, Frayn K.

McGill Unit for the Prevention of Cardiovascular Disease, Royal Victoria Hospital, Montreal,Quebec, Canada.

Much has recently been learned about the processes involved in postprandial triacylglycerolclearance. As discussed previously, important differences in the metabolism of chylomicronsand VLDL have become apparent. The ASP pathway has also been recognized and appears toplay a critical role in chylomicron metabolism. The ASP pathway is activated in order to trap thefatty acids released from chylomicrons by the action of LPL and there is now unequivocal invivo evidence in human subjects that ASP is generated by adipocytes in thepostprandial period. These findings match the in vitro data showing that chylomicrons, butnot the other plasma lipoproteins or fatty acids, activate the generation of ASP by culturedhuman adipocytes. An inverse relationship appears to exist between the proportion of fattyacids taken up by adipocytes and that released into the general circulation. Too great a releaseinto the general circulation because of diminished trapping of fatty acids released fromchylomicrons appears to be critical in the pathogenesis of the dyslipoproteinaemias associatedwith hyperapo B or FCHL and omental obesity. Evidence has been presented that dysfunctionof the ASP pathway may be one of the causes of this disorder. Put differently, the ASPpathway is essential for the normal clearance and disposition of dietary fattyacids. Binding of chylomicrons to capillary endothelium followed by lipolysis by LPL results inthe sudden liberation of fatty acids, and in the marked generation of ASP by adipocytes. TheASP that is generated is essential if LPL is to continue to form fatty acids at a normal rate. It is

essential also if the fatty acids which are formed are to enter the adipocyte ratherthan exit into the general circulation. The transport vehicle, the chylomicron,therefore stimulates the formation of the peptide, ASP, which is responsible for itssuccessful metabolism. Thus, the ASP pathway provides the metabolic coordinationbetween the chylomicron and the adipocyte, which we describe asmicroenvironmental metabolic regulation and which we believe is essential for thenormal clearance of dietary triacylglycerol from plasma.J Surg Res. 1989 May;46(5):470-3.The effect of ASP on the adipocyte of the morbidly obese.

Walsh MJ, Sniderman AD, Cianflone K, Vu H, Rodriguez MA, Forse RA.

Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.

The control of triglyceride synthesis within the adipocyte is not fully understood. Insulin isconsidered to be the most potent stimulant of triglyceride synthesis. In this paper, we report onthe effect of a small (14000 Da), basic (pI 9.0) protein isolated from human serum. Thisprotein has been called acylation stimulating protein (ASP). It is a potent stimulant of


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triglyceride synthesis in adipocytes from both normal weight and morbidly obese subjects. Itsstimulatory effect on adipocytes is both rapid, occurring between 15-30 min afterthe start of incubation, and prolonged, lasting for up to 3 hr. Compared to insulin, itis sixfold more potent in its effect on triglyceride synthesis. As well as acting onisolated cells, ASP also has a fourfold stimulatory effect on triglyceride synthesis in humanadipose microsomes at a concentration of 25 micrograms/ml. This study indicates that ASP is apotent stimulant of triglyceride synthesis and therefore may play a role in the pathogenesis ofmorbid obesity.

Am J Physiol. 1999 Feb;276(2 Pt 1):E241-8.Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism.

Evans K, Clark ML, Frayn KN.

Nuffield Department of Clinical Biochemistry, John Radcliffe Hospital, Headington, Oxford OX39DU, UK.

We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuringarteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Sixsubjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as anintravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) wassuppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulatorof HSL activity, showed little change after either oral or intravenous fat load,suggesting that suppression of HSL action occurred independently of insulin. Therate of action of LPL (measured as triacylglycerol extraction) increased with both oral andintravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001). There wasincreased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown bylack of reesterification of fatty acids. There was no release into the circulation of LPL-derivedfatty acids from skeletal muscle. These results suggest that insulin is not essential forHSL suppression or increased triacylglycerol clearance but is important inreesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affectingfatty acid partitioning between adipose tissue and the circulation, postprandial nonesterifiedfatty acid concentrations, and hepatic very low density lipoprotein secretion.Of mice and men (and women) and the acylation-stimulating protein pathway.

Sniderman AD, Maslowska M, Cianflone K.

Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Centre,Royal Victoria Hospital, Montreal, Quebec, Canada. [email protected] storage and release of energy by adipocytes is of fundamental biologic importance. Notsurprisingly, therefore, the rate at which these processes occur can be modulated by a varietyof physiologic molecules. A newly recognized participant is produced by adipocytes themselves:acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidenceregarding how the ASP pathway may influence energy storage and release. In brief, the rate atwhich triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) isdetermined by lipoprotein lipase and insulin, which is the principal hormone that regulateslipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids aretaken up and converted to triglycerides by adipocytes. Under certain circumstances, however,reduction of activity of the ASP pathway may negatively impact on the first step of theprocess.ASP also influences the rate at which fatty acids are released by adipocytes,and it is clear that insulin and ASP interact in a variety of ways that involve energy

storage and release. Accordingly, to understand the impact of any intervention onenergy storage and release by adipocytes, the effects of both insulin and ASP mustbe taken into account.

Acylation stimulating protein (ASP) results from the interaction of three proteins: factor B,adipsin, and the third component of complet C3. All three are secreted by adipocytes, andthere are now considerable in vitro data indicating that the ASP pathway is a majordeterminant of de novo triglyceride synthesis in human and murine adipocytes.Also, ASP is amajor determinant of the rate at which fatty acids are released from adipocytes. Itdoes so, principally, by increasing re-esterification, but also by reducing hormone-sensitive lipase activity.J Lipid Res. 1998 Apr;39(4):884-91.Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by

human adipose tissue in vivo in the postprandial period.

Saleh J, Summers LK, Cianflone K, Fielding BA, Sniderman AD, Frayn KN.
mailto:[email protected]:[email protected]


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McGill Unit for the Prevention of Cardiovascular Diseases, Royal Victoria Hospital, Montreal,Quebec, Canada.

The objective of this study was to determine whether Acylation Stimulating Protein (ASP) isgenerated in vivo by human adipose tissue during the postprandial period.After a fat meal,samples from 12 subjects were obtained (up to 6 h) from an arterialized hand vein and ananterior abdominal wall vein that drains adipose tissue. Veno-arterial (V-A) gradients across thesubcutaneous adipose tissue bed were calculated. The data demonstrate that ASP is

produced in vivo (positive V-A gradient) With maximal production at 3-5 hpostprandially. The plasma triacylglycerol (TAG) clearance was evidenced by a negative V-Agradient. It increased substantially after 3 h and remained prominent until the final time point.There was, therefore, a close temporal coordination between ASP generation and TAGclearance. In contrast, plasma insulin and non-esterified fatty acid (NEFA) had an early (1-2 h)postprandial change. Fatty acid incorporation into adipose tissue (FIAT) was calculated from V-A glycerol and non-esterified fatty acid (NEFA) differences postprandially. FIAT was negativeduring the first hour, implying net fat mobilization. FIAT then became increasingly positive,implying net fat deposition, and overall followed the same time course as ASP and TAGclearance. There was a direct positive correlation between total ASP production and total FIAT(r = 0.566, P < 0.05). These data demonstrate that ASP is generated in vivo byhuman adipocytes and that this process is accentuated postprandially, supportingthe concept that ASP plays an important role in clearance of TAG from plasma andfatty acid storage in adipose tissue.J Biol Chem. 1998 Aug 14;273(33):20903-9.Chylomicron-specific enhancement of acylation stimulating protein and precursor protein C3production in differentiated human adipocytes.

Scantlebury T, Maslowska M, Cianflone K.

Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Center,McGill University, Montreal, Quebec H3A 1A1, Canada.

Acylation stimulating protein (ASP) is a potent stimulator of adipocyte triacylglycerolstorage. In vivo studies have shown that ASP production by adipocytes increaseslocally after a fat meal. Initial in vitro studies demonstrated increased production ofASP in the presence of chylomicrons (CHYLO). The present aim was to define the CHYLO

component responsible. None of the apoproteins tested (AI, AII, AIV, CI, CII, CIII, and E) werecapable of stimulating C3 (the precursor protein) or ASP production. Rather, the activecomponent is a nonlipid, loosely associated, trypsin-sensitive molecule. High pressure liquidchromatography fractionation of the CHYLO infranate proteins identified the critical protein astransthyretin (TTR), which binds retinol-binding protein and complexes thyroxine and retinol.Addition of TTR alone, with lipid emulsion, or with respun CHYLO to human differentiatedadipocytes had little effect on C3 and ASP production. By contrast, when transthyretin wasadded to CHYLO, C3 and ASP production were substantially enhanced up to 75- and 7. 5-foldrespectively, compared with the effect of native CHYLO alone. Finally, a polyclonal antibodyagainst TTR could inhibit stimulation of C3 and ASP production by CHYLO (by 98 and 100%,respectively) and by CHYLO infranate proteins (by 99 and 94%, respectively). We hypothesizethat TTR mediates the transfer of the active components from CHYLO to adipocytes, whichthen stimulates increased C3 and ASP production. Thus the CHYLO provides thephysiologic trigger of the ASP pathway.

Yksinkertaistettuna - ASP on merkittv tekij rasvan varastoimisessa. Ja rasvansyminen aiheuttaa ASP:n erityst. Vitteet siis, ett pelkstn insuliinia hillitsemllsaa metabolisen edun tai laihtuu, eivt yksinkertaisesti ole totta, koska insuliini ei oleainoa tekij, joka hillitsee lipolyysi ja edist triglyseridisynteesi (rasvanvarastoitumista). Keho varastoi rasvaa, vaikka insuliinia ei pikkaisi ollenkaan(insuliiniahan erittyy, vaikka ei sisi mitn), ASP:n kautta. Ja sama jos ei syollenkaan rasvaa - insuliinin kautta.

Esim. insuliinin erityst laskevassa lkkeest ei ole mitn apua, kun kalorien mron sama (18). Ja joissain tutkimuksissa insuliiniarvot laskevat huonommin tai jopanousevat hiilihydraattipitoisella dieetill, kun ne laskevat vhhiilihdyraattisella, muttasilti ei tule eroja painonpudotuksen suhteen (mm. 19-23). Ja esimerkiksiinsuliiniresistenssist on jopa apua laihduttamiseen (24, 25) Kyll, luit aivan oikein.

J Clin Endocrinol Metab. 1995 May;80(5):1571-6.Reduced insulin secretion: an independent predictor of body weight gain.


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Schwartz MW, Boyko EJ, Kahn SE, Ravussin E, Bogardus C.

Department of Medicine, University of Washington, Seattle 98108, USA.

A causal role in the pathogenesis of obesity has been proposed for hyperinsulinemia and insulinresistance in populations with a high prevalence of a "thrifty genotype." An alternativehypothesis is that obesity-induced hyperinsulinemia is an adaptation which, by increasingcentral nervous system insulin signaling (which suppresses food intake), confers resistance to

weight gain. To characterize the relationship between the level of insulin secretion and the riskof weight gain, we examined whether any of three different measures of the level of insulinsecretion (the area under the plasma insulin curve during both a meal tolerance test and anoral glucose tolerance test, and the acute insulin secretory response to iv glucose) waspredictive of weight gain in a prospective study of 97 Pima Indians (64 males and 33 females)with normal glucose tolerance. During a mean (+/- SD) follow-up period of more than 3 yr(males, 3.58 +/- 1.46 yr; females, 3.02 +/- 1.73 yr), average weight increased 2.1 +/- 3.0%/yrin males and 3.5 +/- 3.6%/yr in females, reflecting a mean annual increase in body fat contentof 6.9%/yr in both sexes. Insulin secretion was negatively associated with the rate of weightgain, whether assessed by the insulin response during the meal tolerance test (r = -0.35; P 0.05; lipolysis: 25% W(max)102 +/- 19 vs. 55 +/- 14 nmol x 100 g(-1) x min(-1), P = 0.06; 55% W(max) 86 +/- 11 vs. 50

+/- 20 nmol x 100 g(-1) x min(-1), P > 0.05; 85% W(max) 88 +/- 31 vs. -9 +/- 25 nmol x 100g(-1) x min(-1), P < 0.05). In conclusion, blood flow and lipolysis are generally higher in SCATadjacent to contracting than adjacent to resting muscle irrespective of exercise intensity. Thusspecific exercises can induce "spot lipolysis" in adipose tissue.

Jep, paikallista rasvanpolttoa tapahtuu. Mutta kuinka paljon?Assuming a molecular weight of 860 g/mol for TG, this corresponds to an extra breakdown of0.62.1 mg of TG in 30 min/100 g of adipose tissue adjacent to contracting muscles

Eli rasvaa kytettiin suoraan rasvavarastoista energiaksi 30 minuutin treenin aikanaperti 0.6-2.1 milligrammaa 100 grammaa rasvaa kohden. Jos tekisi jopa kymmenentuollaista sessiota viikossa, puolen vuoden ajan tulisi tst perti 156-546milligrammaa/100 grammaa rasvaa. Eli lhes puoli grammaa rasvaa kymmennellpuolen tunnin treenill puolen vuoden ajan. Tuossa samassa ajassa, samalla treenillkuluisi kaloreita n. (olettaen, ett tuo sessio kuluttaisi 250 kaloria, mit ei ole kovin

vaikeaa saavuttaa) 65000. Kilossa rasvaa on n. 7000 kaloria eli hieman yli 9 kiloarasvaa olisi mahdollista polttaatuon liikunnan kalorinkulutuksen ansiosta. Hieman enemmn kuin puoli grammaa.


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Kalorit kunnon/roskaruoastaKalori on kalori. Aivan sama mist kalorit tulevat. Tietenkin on aina parempi sydruokaa, joissa olisi suojaravinteita. Esim. kaliumin krooninen puute laskeelepoaineenvaihduntaa. Mutta olettaen, ett mistn mikroravinteesta ei tule puutetta(mihin tietenkin jokaisen ruokavalion pitisi thdt), ei ole merkityst,

mist kalorit tulevat. Pieni/kohtuullinen mr voi tulla mist vaan ilman, ett sillolisi suurta merkityst. Useissa tutkimuksissa isokalorisessa tilassa suurestasokerinmrstkn ei ole ollut haittaa (47,48).

Sitten erittin merkittv paperi.Ann Nutr Metab. 2007;51(2):163-71. Epub 2007 May 29.Hormonal responses to a fast-food meal compared with nutritionally comparable meals ofdifferent composition.

Bray GA, Most M, Rood J, Redmann S, Smith SR.

Pennington Biomedical Research Center, Baton Rouge, LA, USA. [email protected]

BACKGROUND: Fast food is consumed in large quantities each day. Whether there are

differences in the acute metabolic response to these meals as compared to 'healthy' meals withsimilar composition is unknown. DESIGN: Three-way crossover. METHODS: Six overweight menwere given a standard breakfast at 8:00 a.m. on each of 3 occasions, followed by 1 of 3lunches at noon. The 3 lunches included: (1) a fast-food meal consisting of a burger,French fries and root beer sweetened with high fructose corn syrup; (2) an organicbeef meal prepared with organic foods and a root beer containing sucrose, and (3)a turkey meal consisting of a turkey sandwich and granola made with organic foodsand an organic orange juice. Glucose, insulin, free fatty acids, ghrelin, leptin, triglycerides,LDL-cholesterol and HDL-cholesterol were measured at 30-min intervals over 6 h. Salivarycortisol was measured after lunch. RESULTS: Total fat, protein and energy content weresimilar in the 3 meals, but the fatty acid content differed. The fast-food meal had moremyristic (C14:0), palmitic (C16:0), stearic (C18:0) and trans fatty acids (C18:1) than the other2 meals. The pattern of nutrient and hormonal response was similar for a given

subject to each of the 3 meals. The only statistically significant acute difference observedwas a decrease in the AUC of LDL cholesterol after the organic beef meal relative to that forthe other two meals. Other metabolic responses were not different. CONCLUSION: LDL-cholesterol decreased more with the organic beef meal which had lesser amounts of saturatedand trans fatty acids than in the fast-food beef meal.

Hormonaaliset vasteet 'roskaruoan' ja 'kunnon ruoan' vlill eivt ole merkittvi.Toisessa 'kunnon ateriassa' LDL-kolesterolin piikki oli pienempi. Mitn muita eroja eiollut. Ateriat olivat kalori - ja makroarvoiltaan melko samanlaiset. Kalorit sisn -kalorit ulos.

Kytntn - valtaosa kaloreista olisi hyv tulla ravinnerikkaista lhteist. Pelkkmultivitamiini ei riit. Imeytyminen ei ole niin tehokasta ja ne voivat jopa listmirkoravinteiden eptasapainoa. Esim. lytyy paljon jotain ravinnetta, jota saa

huonosta ruokavaliosta paljon ja vhn, jota saa sitten vhn taiei ollenkaan. Ja vihanneksia ei voi rutistaa pilleri muotoon.

Mutta pieni osa, vaikka 10-15% voi tulla mist vaan, ett sill olisi ratkaisevaamerkityst.

SstliekkiJep. Kyseess on myytti, ainakin normaalioloissa. Diettaaminen aiheuttaaaineenvaihdunnan hidastumista. Koska kevyempi keho kuluttaa vhemmn energiaa.

Entisill lihavilla on joskus havaittu olevan n. 3-5% pienempi lepoaineenvaihduntakuin samankokoisilla henkilill, jotka eivt ole olleet lihavia (49). Mutta sitten taas

toisaalta, tt ei todellakaan oel huomattu aina eli painonpudottaneila janormaalipainoisilla ei ole ollut mitn eroa tai mitn merkittv eroalepoaineenvaihdunnassa - melko vahvaa dataa sstliekki vastaan (50-58).
mailto:[email protected]:[email protected]


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Tosin on paljon dataa, ett sstliekki voi tapahtua, mutta sen vaikutus ei oletodellakaan niin suuri kuin yleisesti luullaan ja se vain ehk hidastaa laihduttamista,ei ikin pysyt sit ja 'keho ei polta rasvaa, koska se on sstliekill'. Tm on uhka,jos nnnytt itsen puolisen vuotta parilla sadalla kalorilla. Sit kovin moni tllfoorumilla tuskin tekee. Suurin sstliekki on tainnut olla juuri henkilill, joitannnytettiin puolisen vuotta. Heidn rasvaprosenttinsa laski johonkin viidenpaikkeille tai alle ja aineenvaihdunta hidastui joku 30-40%. Melko merkittv

hidastuminen, mutta ei silti stoppaa laihduttamista. Termodynamiikan lait ptevtsstliekisskin. Varmaan kuuluisin sstliekki tutkimus on Ancel Keysin tekemtutkimus joskus 1940-luvulla. Aineenvaihdunta hidastui merkittvsti, mutta vainpuolet tst tuli sstliekin kautta - toinen puoli hidastumisesta johtuiyksinkertaisesti siit, ett kevyempi keho kuluttaa vhemmn energiaa.

Sstliekki, eli ylimrist aineenvaihdunnan hidastumista, mit kevyempi kehotuo tullessaan, on havaittu useasti, mutta vaikutus ei ole mitenkn suuri, kutenuseasti jo mainittu. Erss tutkimuksessa kulutuksen laskun havaittiin olevan 6% ylimit sen olisi pitnyt olla tai lepoaineenvaihduntahidastui noin 100 kalorin verran 10% painonpudotukseen tai lasku on muuten vainniin pieni, ett sill ei ole merkityst (59-68).

Ja on mys dataa sen puolesta, ett sstliekki ei tapahtuisi ollenkaan (69-73).Sstliekki nimittin nyttisi tapahtuvan (merkittviss mrin) vain silloin kuntodella nnnytettn ihmist kuoliaaksi tai ollaan vuosia kalorivajeessa (74).

Am J Clin Nutr. 1985 Apr;41(4):753-9.Energy expenditure before and during energy restriction in obese patients.

Ravussin E, Burnand B, Schutz Y, Jquier E.

Twenty-four hour energy expenditure (24 EE), resting metabolic rate (RMR), spontaneousphysical activity and body composition were determined in 7 obese patients (5 females, 2males, 174 +/- 9% IBW, 38 +/- 2% fat mass) on 2 different occasions: before weightreduction, and after 10 to 16 weeks on a hypocaloric diet as outpatients, the recommendedenergy intake varying from 3500 to 4700 kJ/day depending on the subject. Mean body weight

loss was 12.6 +/- 1.9 kg, ie 13% of initial body weight, 72% being fat. Twenty-four hourenergy expenditure (24 EE) was measured in a respiration chamber with all the subjectsreceiving 10418 kJ/d before weight reduction and an average of 3360 +/- 205 kJ/d while onthe diet. When expressed in absolute values, both 24 EE and RMR decreased during thehypocaloric diet from 9819 +/- 442 to 8229 +/- 444 and from 7262 +/- 583 to 6591 +/- 547kJ/d respectively. On the basis of fat-free-mass (FFM), 24 EE decreased from 168 +/- 6 to 148+/- 5 kJ/kg FFM/d whereas RMR was unchanged (approximately 120 kJ/kgFFM/d).Approximately one half of the 24 EE reduction (1590 kJ/d) was accountedfor by a decrease in RMR, the latter being mainly accounted for by a reduction inFFM. Most of the remaining decline in 24 EE can be explained by a decreasedthermic effect of food, and by the reduced cost of physical activity mainly due to alower body weight. Therefore, there seems little reason to evoke additionalmechanisms to explain the decline in energy expenditure during dieting.Int J Obes. 1989;13 Suppl 2:189-92.

Maintenance of weight loss with recovery of resting metabolic rate following 8 weeks of verylow calorie dieting.

Rattan S, Coxon A, Kreitzman S, Lemons A.

Howard Foundation Research, Cambridge, UK.

The challenge to maintain lost weight is particularly relevant for advocates of VLCD, since theseinduce a high rate of weight loss. It has been argued that excessive lean body mass is lost withvery restricted energy intake regimens which compromises metabolic rate and sabotagesweight maintenance. Thirty-nine subjects who had lost an average of 12.3 +/- 2 kg during an8-week VLCD trial were transferred immediately to a 1500 kcal per day maintenance formulawhich included solid foods. RMR was determined at four intervals: (1) before dieting; (2) after2 weeks of VLCD; (3) end of 8 weeks dieting; (4) end of 8 weeks maintenance period. It wasobserved that the metabolic rate dropped to 86 per cent of original by the end of the 8 weeksof VLCD. Metabolic rate recovered to 93 per cent of prediet values by the end of 8 weeks ofweight maintenance on 1500 kcal/day. Following an average 2 kg weight regain within the firstweek of maintenance, there was no further weight regain.VLCD did not produce losses of


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RMR beyond that expected from the loss of weight. No difficulty was observed inmaintaining weight for 8 weeks on 1500 kcal/day.Am J Clin Nutr. 2000 Nov;72(5):1088-94.Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? Anexamination of the set-point theory.

Weinsier RL, Nagy TR, Hunter GR, Darnell BE, Hensrud DD, Weiss HL.

Departments of Nutrition Sciences and Human Studies, the General Clinical Research Center,University of Alabama at Birmingham, and the Mayo Clinic, Rochester, MN,[email protected]

Comment in:

* Am J Clin Nutr. 2001 Mar;73(3):655-8.

BACKGROUND: Obese persons generally regain lost weight, suggesting that adaptive metabolicchanges favor return to a preset weight. OBJECTIVE: Our objective was to determine whetheradaptive changes in resting metabolic rate (RMR) and thyroid hormones occur in weight-reduced persons, predisposing them to long-term weight gain. DESIGN: Twenty-fouroverweight, postmenopausal women were studied at a clinical research center in four 10-dstudy phases: the overweight state (phase 1, energy balance; phase 2, 3350 kJ/d) and afterreduction to a normal-weight state (phase 3, 3350 kJ/d; phase 4, energy balance). Weight-reduced women were matched with 24 never-overweight control subjects. After each studyphase, assessments included RMR (by indirect calorimetry), body composition (by hydrostaticweighing), serum triiodothyronine (T(3)), and reverse T(3) (rT(3)). Body weight was measured4 y later, without intervention. RESULTS: Body composition-adjusted RMR and T(3):rT(3) fellduring acute (phase 2) and chronic (phase 3) energy restriction (P: < 0.01), but returned tobaseline in the normal-weight, energy-balanced state (phase 4; mean weight loss: 12.9 +/- 2.0kg). RMR among weight-reduced women (4771 +/- 414 kJ/d) was not significantly differentfrom that in control subjects (4955 +/- 414 kJ/d; P: = 0.14), and lower RMR did not predictgreater 4-y weight regain (r = 0.27, NS). CONCLUSIONS: Energy restriction produces atransient hypothyroid-hypometabolic state that normalizes on return to energy-balancedconditions. Failure to establish energy balance after weight loss gives the misleadingimpression that weight-reduced persons are energy conservative and predisposed to weight

regain. Our findings do not provide evidence in support of adaptive metabolicchanges as an explanation for the tendency of weight-reduced persons to regainweight.

Vhkaloriset ja erittin vhkaloriset dieetit hidastuttavat aineenvaihduntaaenemmn kuin pienemmll vajeella tehtvt dieetit, mutta se johtuu yksinkertaisestisiit, ett ne aiheuttavat suuremman pudotuksen painossa (75). Pitkaikaisiavhkalorisia dieettej ei voi oikein suositella kehonrakennukseen tai voimailuunpanostavalle henkillle, mutta viikon tai muutaman seteisse eivt aiheuta lihaskatoatai sstliekki oikein suoritettuna.

On mys dataa sen puolesta, ett aineenvaihdunnan hidastuminen korreloi leptiininlaskun kanssa (76,77). Leptiini on yksi trkeimmist hormoneissa dietatessa, tai

pikemminkin trkein. Se toimii viestinviejn. Leptiini lhett aivoille signaaleja,kertoen kuinka paljon sin syt ja kuinka paljon rasvaa sinulla on. Kun rasvan mrvhenee, leptiini laskee. Kun ruoan mr vhenee leptiini laskee. Ja kun leptiinilaskee tulee juuri edell mainittu ongelma - aineenvaihdunta hidastuu ja nlntunnekasvaa, tehden diettaamisen vaikeammaksi ja vaikeammaksi. Leptiini kontrolloi mysCCK:ta, kolekystokiniinia, joka onyksi merkittv kyllisyyshormoni. Leptiinin on mys huomattu aktivoivan AMPK:ta,joka on yksi toinen trke tekij dietatessa, hoitaen lukuisia tehtvi. Leptiinillnyttisi olevan mys vaikutus ghreliinin, joka on yksi trkeimmist tekijistnlnhallinnassa, ollen merkittv nlkhormoni.

Leptiinitasot olisi trke pit normaaleina, ei liian suurina eik liian pienin. Hetidieetin alussa leptiini alkaa laskemaan. Silloin sill ei ole viel suurta merkityst,mutat pidemmn plle on. Leptiini on nimittin trkempi hormoneja, pitkaikaisennlnhallinnan suhteen. Leptiini ei vaihtele niin kovinkaanmerkittvsti aterioiden vlill. Paitsi hiilihydraatteihin.


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Ylisymiset tai tankkaukset tai mttpivt ovat siis hydyllisi leptiinin nostamisenkautta. Estvt nin aineenvaihduntaa hidastumasta ja auttavat pidempiaikaisessanlnhallinnassa ja tekee vlill pkopallekkin hyv.

Tankkauksissa on hyv panostaa juuri runsaaseen hiilihydraattien saantiin, koska nenostavat lyhyell vlill leptiini parhaiten. Dietatessa taas sitten ei ole niin suurta

merkityst mitk makrot valitsee, ainakaan leptiinin kannalta. Fruktoosin ja sokerin(josta puolet fruktoosia) runsasta saantia kannattaa kuitenkin vltt, koska fruktoosiei nosta leptiini.

Leptiini tietenkin laskee sitten taas melko nopeasti. Varsinkin jos tankkaus on vainmuutaman aterian tai yhden pivn. Jos kunnolla haluaa nostaa leptiini, olisiparempi pit parin pivn tankkausjakso tai jopa viikon, jolloin mentisiin maltillisillaplussilla. Tst olisi apua paitsi leptiinin kautta, mys pkopalleja auttaisi lihasmassan sstmisesskin paremmin. Paasto tai kalorivaje ja senjlkeinen tankkaus ovat osoittautuneet erittin tehokkaiksi metodeiksi diettaamisen,lihasmassan sstmiseen dieetill tai jopa kasvattamiseen. Nit metodeja ovat mm.CKD ja IF.

Tankkausten lisksi mys runsaasta proteiinin saannista on havaittu olevan apuasstliekki vastaan (78-80) sek liikunnasta/punttitreenist (81). Molemmat asiatpitisi olla dieetill mukana oikeastaan aina.

Miksi sitten monet kuvittelevat sstliekin olevan olemassa?

1. Tekosyy.2. Nestetasapaino huijaa. Painohan voi vhkalorisella dieetill, vaikka nousta samallakun rasvan mr laskee.3. Ei lasketa kaloreita/arvioida aktiivisuustasoja oikein.

Kytntn - sstliekist ei tarvitse murehtia, ellei ole nnnyttmss itsen

kuoliaaksi, viet vuosia kalorivajeessa tai ole erittin pitkn aikaa erittinvhkalorisella dieetill ja liikkuu jrkyttvi mri tn aikana. Ja sstliekinvaikutus korostuu sitten hieman enemmn, kun lhestytn jotain vitosenrasvaprosentteja. Normaalin dieettajan ei tst kuitenkaan tarvitse murehtia,varsinkaan jos tulee liikuttua ja treenattua, syty runsaasti proteiinia ja vedettytankkauksia.

AteriatiheysUsein symisen on usein vitetty kiihdyttvn aineenvaihduntaa ja pitvn kehon poiskatabolisesta tilasta. Eli ideaalia olisi tmn ksityksen mukaan syd vhintn 6-7kertaa pivss 2-3 tunnin vlein.

Usein symisen ei ole kuitenkaan havaittu kiihdyttvn aineenvaihduntaa lukuisissatutkimuksissa (87-92). Sama todettiin erss viime vuonna tehdyss tarkassa,kontrolloidussa tutkimuksessa, jossa mitattiin mys kehonkoostumusta (93).

Itse asiassa usein syminen ei ole missn tutkimuksessa osoittautunut isokalorisessatilassa paremmaksi kuin harvoin syminen. Sama tietenkin pinvastoin. Vain yhdesstutkimuksessa on saatu erilaisia tuloksiaeri ateriatiheyksien vlill, mutta se johtuikin kyseisen tutkimuksen huonostasuunnittelusta, eik mistn yksityisest, maagisesta ateriavlist.

Br J Nutr. 1997 Apr;77 Suppl 1:S57-70. LinksMeal frequency and energy balance.

Bellisle F, McDevitt R, Prentice AM.INSERM U341, Hotel Dieu de Paris, France.Several epidemiological studies have observed an inverse relationship between people'shabitual frequency of eating and body weight, leading to the suggestion that a 'nibbling' meal


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pattern may help in the avoidance of obesity. A review of all pertinent studies shows that,although many fail to find any significant relationship, the relationship is consistently inverse inthose that do observe a relationship. However, this finding is highly vulnerable to the probableconfounding effects of post hoc changes in dietary patterns as a consequence of weight gainand to dietary under-reporting which undoubtedly invalidates some of the studies. We concludethat the epidemiological evidence is at best very weak, and almost certainly represents anartefact. A detailed review of the possible mechanistic explanations for a metabolic advantageof nibbling meal patterns failed to reveal significant benefits in respect of energy expenditure.

Although some short-term studies suggest that the thermic effect of feeding is higher when anisoenergetic test load is divided into multiple small meals, other studies refute this, and mostare neutral.More importantly, studies using whole-body calorimetry and doubly-labelled water to assess total 24 h energy expenditure find no difference betweennibbling and gorging. Finally, with the exception of a single study, there is noevidence that weight loss on hypoenergetic regimens is altered by meal frequency.We conclude that any effects of meal pattern on the regulation of body weight arelikely to be mediated through effects on the food intake side of the energy balanceequation.

Ja yhdesskn tutkimuksessa, jossa on mitattu energiankulutusta, ei ole huomattumitn merkityst usein vs. harvoin symisell.

Normaalin aterian imeytyminen on kesken viel 5 tuntia aterian jlkeen (94). Eli

normaalin aterian imeytymiseen menee yli viisi tuntia. Eli ei tarvitse pelt, ett alleviiden tunnin ateriavlit aiheuttaisivat kataboliaa. Pidemmt ateriavlit voivat listproteiinidegredaatiota, mutta proteiinisynteesi kiihtyytaas sitten kuin sydn. Mikli proteiinin saanti on runsasta, voi selvit hyvinkinparilla tai kolmella aterialla pivss ja saavuttaa hyvi tuloksia ja niin onkin tehty.Mutta varmaan sopivana ateriavlin voisi pit juuri tuota viitt tuntia. Pidemmtateriavlit eivt *ehk* ole en optimaalisia.

Itse asiassa liian usein symisest voi olla jopa haittaa lihastenkasvatukselle. Muttase on sitten aivan toinen aihe.

Yhteenveto

Mutta miten sitten syd?

Kaikista trkeint on miinuskalorit pitkll aikavlill. Vlill voi ja kannattaakin kydplussilla. Seuraavaksi tulee riittv proteiinin saanti. Joka voi vaihdella 2-4 g/kgvlill. Pahasti ylipainoiselle, vhn treenaavalle ja hitaasti diettaavalle 2 g/kg voi ollatarpeeksi. 3g/kg on enemmn optimaalinenhenkillle, joka treenaa 4-5 kertaa viikossa ja vhintn saman verran aerobistaplle ja jonka rasvaprosentti on alle 10. Tt suuremmat annokset eivttodennkisesti tuo enemp hytyj kuin haittoja, ainakaan natuille. Ellei sitten sypelkstn proteiinia, jolloin proteiinin mrn voi/kannattaa nostaa 4 g/kg.

Runsas proteiinin saanti on erittin trke dieetill. Paitsi ett se tuo suurtakyllisyytt, se voi tukea aineenvaihduntaa. Ja mikn makroravinne ei sstlihasproteiinia paremmin kuin proteiini. Proteiinilla on mys suurin termogeeninenvaikutus, joten sekin voi tuoda pieni apuja laihduttamisen tehokkuudensuhteen. Proteiinin tarvehan kasvaa dieetill. Massan kasvatukseen riittpienemmtkin mrt. Mutta sekin sitten aivan on toinen aihe.

Eli ensiksi aseta kalorivaje. Toiseksi aseta proteiinin mr (2-3 (4)g/kg). Sitten pidhuoli riittvst vlttmttmien rasvahappojen, rasvan (n. 1g/kg) ja vihannestensaannista. Sitten hiilihydraatteja aktiivisuuden mukaan. Tietenkin rasvan mr voiolla suurempikin, mutta pitkll vlill sen olisi hyv olla vhintn tuo 1g/kg.

Lhteet1 Acute effect of meal glycemic index and glycemic load on blood glucose and insulin


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responses in humans, Galgani et al. 20062 No effect of a diet with a reduced glycaemic index on satiety, energy intake andbody weight in overweight and obese women, Ston et al. 20083 Comparison of 4 diets of varying glycemic load on weight loss and cardiovascularrisk reduction in overweight and obese young adults: a randomized controlled trial.McMillan-Price et al. 20064 Differences in glycaemic status do not predict weight loss in response to hypocaloric

diets in obese patients, de Luis et al. 20065 Diets high and low in glycemic index versus high monounsaturated fat diets: effectson glucose and lipid metabolism in NIDDM, Luscombe et al. 19996 An 18-mo randomized trial of a low-glycemic-index diet and weight change inBrazilian women, Sichieri et al, 20077 Influence of glycemic index/load on glycemic response, appetite, and food intake inhealthy humans, Alfenas et al, 20058 The effect of dietary glycemic index on weight maintenance in overweight subjects:a pilot study, Philippou et al, 20099 The effect of high- and low-glycemic index energy restricted diets on plasma lipidand glucose profiles in type 2 diabetic subjects with varying glycemic control,Heilbronn et al, 200210 Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized

trial, Ebbeling et al. 200711 Different glycemic indexes of breakfast cereals are not due to glucose entry intoblood but to glucose removal by tissue, Schenk et al. 2003.12 Long-term effects of 2 energy-restricted diets differing in glycemic load on dietaryadherence, body composition, and metabolism in CALERIE: a 1-y randomizedcontrolled trial. Das et al. 200713 Reduced glycemic index and glycemic load diets do not increase the effects ofenergy restriction on weight loss and insulin sensitivity in obese men and women.Raatz et al. 200514 No difference in body weight decrease between a low-glycemic-index and a high-glycemic-index diet but reduced LDL cholesterol after 10-wk ad libitum intake of thelow-glycemic-index diet, Sloth et al. 2004

15 Effect of glycemic carbohydrates on short-term satiety and food intake, Andersonet al. 200316 Glycemic and insulinemic responses as determinants of appetite in humans, Flintet al. 200617 Effects of exercise intensity and duration on the excess post-exercise oxygenconsumption, LaForgia et al, 200618 No effect of inhibition of insulin secretion by diazoxide on weight loss inhyperinsulinaemic obese subjects during an 8-week weight-loss diet, Due et al, 200719 Comparison of the effects on insulin resistance and glucose tolerance of 6-mohigh-monounsaturated-fat, low-fat, and control diets, Due et al, 200820 Comparison of a Low-Fat Diet to a Low-Carbohydrate Diet on Weight Loss, BodyComposition, and Risk Factors for Diabetes and Cardiovascular Disease in Free-Living,Overweight Men and Women, Meckling et al, 2004

21 A Randomized Trial Comparing Low-Fat and Low-Carbohydrate Diets Matched forEnergy and Protein, Segal-Isaacson et al, 200422 Similar weight loss with low- or high-carbohydrate diets, Golay et al, 200623 Comparison of isocaloric very low carbohydrate/high saturated fat and highcarbohydrate/low saturated fat diets on body composition and cardiovascular risk,Noakes et al, 200624 Predictors of weight change in a bi-ethnic population. The San Antonio HeartStudy, Valdez et al, 199425 Insulin resistance associated with lower rates of weight gain in Pima Indians,Swimburn et al, 199126 Cognitive effects of ketogenic weight-reducing diets, Wing et al, 199527 Energy balance trials with a diet rich in fats in the human, Wolfram et al, 1985

28 Metabolic differences in response to a high-fat vs. a high-carbohydrate diet,Bandini et al, 199429 Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogeniclow-carbohydrate diets, Johnston et al, 2006


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30 Dietary carbohydrate-to-fat ratio: influence on whole-body nitrogen retention,substrate utilization, and hormone response in healthy male subjects, McCargar et al,198931 Composition of weight lost during short-term weight reduction. Metabolicresponses of obese subjects to starvation and low-calorie ketogenic and nonketogenicdiets, Yang et al, 197632 Energy intake required to maintain body weight is not affected by wide variation in

diet composition. Leibel et al, 199233 Low-Fat versus Low-Carbohydrate Weight Reduction Diets: Effects on Weight Loss,Insulin Resistance and Cardiovascular Risk A Randomised Control Trial, Bradley et at,200934 Fat and carbohydrate overfeeding in humans: different effects on energy storage,Horton et al, 199535 Spontaneous overfeeding with a 'cafeteria diet' in men: effects on 24-hour energyexpenditure and substrate oxidation, Larson et al, 199536 Ad libitum food intake on a "cafeteria diet" in Native American women: relationswith body composition and 24-h energy expenditure, Larson et al, 199537 Short-term, mixed-diet overfeeding in man: no evidence for "luxuskonsumption",Ravussin et al, 198538 Metabolic response to experimental overfeeding in lean and overweight healthy

volunteers, Diaz et al, 199239 Weight loss in 108 obese women on a diet supplying 800 kcal/d for 21 d, Websteret al, 198940 Body composition, nitrogen metabolism, and energy utilization with feeding ofmildly restricted (4.2 MJ/d) and severely restricted (2.1 MJ/d) isonitrogenous diets,Stanko et al, 199241 Pathophysiology of the Neuroregulation of Growth Hormone Secretion inExperimental Animals and the Huma, Giustina et al, 199842 Chronobiological aspects of weight loss in obesity: effects of different meal timingregimens, Sensi et al, 198943 Weight Loss is Greater with Consumption of Large Morning Meals and Fat-FreeMass Is Preserved with Large Evening Meals in Women on a Controlled Weight

Reduction Regimen, Keim et al, 199744 Topical fat reduction from the waist, Caruso et al, 200745 Glycyrrhetinic acid, the active principle of licorice, can reduce the thickness ofsubcutaneous thigh fat through topical application, Armanini et al, 200546 Subcutaneous fat alterations resulting from an upper-body resistance trainingprogram, Kostek et al, 200747 Effect of eucaloric high- and low-sucrose diets with identical macronutrient profileon insulin resistance and vascular risk: a randomized controlled trial, Black et al. 200648 Metabolic and behavioral effects of a high-sucrose diet during weight loss, Surwitet al, 199749 Meta-analysis of resting metabolic rate in formerly obese subjects, Astrup et al,199950 Energy expenditure and free-living physical activity in black and white women:

comparison before and after weight loss, Weinsier et al. 200051 Resting energy expenditure in reduced-obese subjects in the National WeightControl Registry, wyatt et al, 199952 No differences in rates of energy expenditure between post-obese women andtheir matched, lean controls, de Peuter et al, 199253 Total and resting energy expenditure in obese women reduced to ideal bodyweight, Amatruda et al, 199354 Low plasma leptin concentration and low rates of fat oxidation in weight-stablepost-obese subjects, Filozof et al 200055 Do adaptive changes in metabolic rate favor weight regain in weight-reducedindividuals? An examination of the set-point theory, Weinsier et al, 200056 Changes in resting energy expenditure after weight loss in obese African American

and white women, Foster et al, 199957 Energy metabolism in weight-stable postobese individuals, Larson et al, 199558 Why do obese patients not lose more weight when treated with low-calorie diets?A mechanistic perspective, Heymsfield, et al, 2007


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59 Effect of 6-month calorie restriction on biomarkers of longevity, metabolicadaptation, and oxidative stress in overweight individuals: a randomized controlledtrial, Heilbronn et al, 2006.60 Effect of Calorie Restriction on Resting Metabolic Rate and Spontaneous PhysicalActivity, Martin et al, 200761 Metabolic fuel utilisation in obese women before and after weight loss, Burstein etal, 1996

62 Energy expenditure and physical performance in overweight women: response totraining with and without caloric restriction, Keim et al, 199063 Changes in resting energy expenditure after weight loss in obese African Americanand white women, Foster et al, 199964 Dietary recommendations after weight loss: how to avoid relapse of obesity, Jameset al, 199765 Weight loss and change in resting metabolic rate, Heshka et al, 199066 Resting metabolic rates of obese women after rapid weight loss, Welle et al, 199467 Underfeeding and body weight regulation in normal-weight young men, Heyman etal, 199268 Energy expenditure, fat oxidation, and body weight regulation: a study ofmetabolic adaptation to long-term weight change, Weyer et al, 200069 Long-term changes in energy expenditure and body composition after massive

weight loss induced by gastric bypass surgery, Das et al, 200370 Factors determining energy expenditure during very-low-calorie diets, Van Gaalf,et al 199271 Metabolic and Behavioral Compensations in Response to Caloric Restriction:Implications for the Maintenance of Weight Loss, Redman et al, 200972 Diet, exercise, weight loss, and energy expenditure in moderately overweightwomen, Belko et al, 198773 Adaptation of energy metabolism of overweight women to alternating andcontinuous low energy intake, de Groot et al, 198974 Energy metabolism after 2 y of energy restriction: the biosphere 2 experiment,Weyer et al, 200075 Rapid weight loss and lean tissue: evidence for comparable body composition and

metabolic rate in differing rates of weight loss, Coxon et al, 198976 Changes in energy expenditure and substrate oxidation resulting from weight lossin obese men and women: is there an important contribution of leptin, Doucet et al,200077 Greater than predicted decrease in energy expenditure during exercise after bodyweight loss in obese men, Doucet et al, 200378 The effect of a high protein-low calorie diet on the energy expenditure of obeseadolescents, Stallings et al, 199279 The effect of protein intake on 24-h energy expenditure during energy restriction,Whitehead et al, 199680 Maintenance of resting energy expenditure after weight loss in premenopausalwomen: potential benefits of a high-protein, reduced-calorie diet, Pasiakos et al, 200881 Effects of resistance vs. aerobic training combined with an 800 calorie liquid diet

on lean body mass and resting metabolic rate, Byrner er al, 199982 Exercise-training enhances fat-free mass preservation during diet-induced weightloss : a meta-analytical finding, Ballor et al, 199483 Meta-analysis: effect of exercise, with or without dieting, on the body compositionof overweight subjects, Garrow et al, 199584 Resistance weight training during caloric restriction enhances lean body weightmaintenance, Ballor et al, 198885 Exercise with or without dietary restriction and obesity treatment, Saris et al, 199586 The role of diet and exercise for the maintenance of fat-free mass and restingmetabolic rate during weight loss, Stiegler et al, 200687 Influence of the feeding frequency on nutrient utilization in man: consequences forenergy metabolism, Westerterp et al, 1991

88 Frequency of feeding, weight reduction and energy metabolism, Westerterp et al,199389 Compared with nibbling, neither gorging nor a morning fast affect short-termenergy balance in obese patients in a chamber calorimeter, Taylor et al, 2001


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90 Effect of the pattern of food intake on human energy metabolism, Westerterp etal, 199391 Feeding frequency and energy balance in adult males, Dallosso et al, 198292 Effect of isoenergetic intake of three or nine meals on plasma lipoproteins andglucose metabolism, Arnold et al, 199393 Increased meal frequency does not promote greater weight loss in subjects whowere prescribed an 8-week equi-energetic energy-restricted diet, Cameron et al, 2009

94 Splanchnic and leg substrate exchange after ingestion of a natural mixed meal inhumans, Capaldo et al, 1999

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