Dieettaaminen asiat, joilla EI ole merkityst

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

Usein sanotaan, ett sy ruokia, jotka sisltvt pienen glykeemisen indeksin/kuorman, koska ne lihottavat vhemmn mm. pienemmn insuliinierityksen takia. Katsotaanpa asiaa hieman tarkemmin. Vaikka matalan GI:n ja GK:n ruoat sisltvt yleens enemmn suojaravinteita, asia ei aina ole nin. Pelkll fruktoosilla on matala GI, mutta siin ei ole mitn ravinteita. Ja esim. jteln ja Coca-Colan GI on matalampi kuin porkkanalla ja perunalla. Selkesti GI ei kerro kaikkea. Ja esim. proteiini laskee GI:t, mutta nostaa insuliinia. Ja vaikka perunalla on erittin korkea GI, sen SI eli kyllisyysindeksi on mys erittin korkea. Ja maidolla on erittin matala GI, mutta erittin suuri II, insuliini indeksi. Vaikka GI usein korreloikin melko hyvin II:n kanssa, niin matala GI aiheuttaa pidemmn insuliinivasteen tosin matalamman. Korkea GI korkeamman, mutta lyhyemmn. Lopputulos on siis melko sama. Ja esim. erss tutkimuksessa GI ei tuonut eroja insuliinin olivat ateriat suuria tai pieni (1). Useat (uudet, vanhemmista lpikatsaus myhemmin) pitkaikaset tutkimukset eivt ole huomanneet mitn apua matalasta GI tai GK:sta (2-10). Ja osa hiilareista omaa matalan 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 Royal Veterinary and Agricultural University, Frederiksberg, Denmark. ar@kvl.dk 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 a low GI is recommended. The same is now often the case in lipid research. Recently, a new debate has arisen around whether a low-GI diet should also be advocated for appetite- and long-term body weight control. A systematic review was performed of published human intervention 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-GI foods reduced ad libitum food intake in seven studies, but not in eight other

Tss lpikatsaus GI:hin jokusen vuoden takaa. 31 tutkimusta tehtiin kyllisyyden suhteen, vain puolessa huomattiin, ett matalasta GI:st oli apua. Ja niss tutkitaan yleens vaikutusta tyhjn vatsaan aamulla, ilman muita makroravinteita. Ero olisi viel pienempi, jos nautittaisiin muita makroja ja eik tyhjn vatsaan. Samin vain puolessa tutkimuksissa GI:n huomattiin auttavan ad libutum-saantiin eli vapaaehtoiseen 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 on verrattu 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 tulevat olemaan viel pienempi - siis kehonrakentajille. Ja varsinkin kun proteiinin mr nostetaan 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 ja annettu kaikki ruoat ja heit on pyydetty olemaan symtt mitn muuta. Ainakaan oletettavasti, he ovat tehneet nin ja todennkisesti erot tasoittuisivat ryhmien vlill, vaikka jotkut olisivatkin ehk syneet. Joka tapauksessa kontrolloidumpia tutkimuksia 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 Food Technology (INTA), University of Chile, Ave. El Libano 5524, Macul, Santiago, Chile. ediaz@inta.cl The purpose of this review was to examine the role of glycaemic index in fuel partitioning and body composition with emphasis on fat oxidation/storage in humans. This relationship is based on the hypothesis postulating that a higher serum glucose and insulin response induced by high-glycaemic carbohydrates promotes lower fat oxidation and higher fat storage in comparison with low-glycaemic carbohydrates. Thus, high-glycaemic index meals could contribute to the maintenance of excess weight in obese individuals and/or predispose obesityprone subjects to weight gain. Several studies comparing the effects of meals with contrasting glycaemic carbohydrates for hours, days or weeks have failed to demonstrate any differential effect on fuel partitioning when either substrate oxidation or body composition measurements were performed. Apparently, the glycaemic index-induced serum insulin differences are not sufficient in magnitude and/or duration to modify fuel oxidation.

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

Tm on erittin merkittv paperi. Glykeemisen indeksin aiheuttamat erot insuliiniarvoissa eivt ole tarpeeksi suuria, ett niill olisi merkityst. Tss ers lpikatsaus 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

Lisksi on vahvaa dataa sen puolesta, ett verensokeri/glykeeminen vaste ei mrit nlntunnetta vaan aterian insulineeminen vaste (15,16) Kytnnss - Ei ole mitn merkityst kehonkoostumuksen kannalta syk nopeita vai hitaita hiilareita. Usein hitaissa hiilareissa on paremmat ravintoarvot. Mutta nm ruoat valitaankin juuri hyvien ravintoarvojen takia, ei matalan GI:n tai GK:n. Paras tapa on syd sit, mill kalorit pysyy parhaiten hallussa, kuitenkin panostaen posin ravinnerikkaisiin ruokiin.

The prevalence of obesity has increased over the last decades. Associated to this, there has been observed a chance in the dietetic pattern of the population in general, related to the increase in carbohydrate consumption. According to some authors, the glycemic index (GI) of food may affect body composition and body weight. The purpose of this review was to evaluate the effects of GI on appetite, satiety, and body composition. Based on the scientific evidences reviewed, it was possible to verify that the majority of the studies that observed a positive effect 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 has little application in clinical practice, as a useful tool to control satiety, reduce appetite, and consequently, to reduce the prevalence of obesity.

2. Aerobinen vs. HIIT ja aerobinen aamulla

Viime aikoina HIIT on kasvattanut suosiotaan runsaasti. Aerobinen on usein haukuttu lyttyyn. HIIT:in on vitetty olevan kytnnss katsoen joka tavalla parempi. Liikunnan tarkoitus on kuluttaa kaloreita. Ja kalorien kulutus on usein helpompi pit suurempana aerobisella kuin HIIT:ll. HIIT:iss on suurempi jlkikulutus, mutta sen vaikutus on melko pieni, vain reilut 6-15% kokonaiskulutuksesta, HIIT:in ollessa ylpss ja aerobisen alapss nist luvuista (17). Molemmissa on hyv puolensa ja huonot puolensa. HIIT:in hyvt puolet ovat lyhyt kesto, tehokkaampi proteiinisynteesille, eik ole niin tyls. Huonoja puolia on sitten mm. se ett dieetill kun palautumiskyvyt eivt muutenkaan ole ideaaleja - mites siihen jopa 3-5 kovia 2030 minuuttia kestvi juoksuvetotreenej jo ehkp 2-3 kovan jalkapunttitreeniin plle? Aerobisen hyvi puolia on suuri energiankulutus ja se ett toimivat tavallaan palauttavina. Huonoja puolia ovat kesto ja liiallisesti kytettyn mahdollinen ''katabolia''. Aerobinenhan aiheuttaa suuremman kortisolivasteen, mutta vain kroonisesti koholla olevista kortisolitasoista on haittaa - kortisoli on hy olla korkealla esim. aamulla ja treenin aikana. Kortisoli on hyv asia, mutta kuten kaikessa, hyv asiaa voi olla liikaa. Kytnnss kannattaa ottaa se, josta pit enemmn/sopii paremmin ja jos tekee paljon, niin kannattaa kytt molempia ja ottaa molempien hyvt puolet. Sitten aamuaerobinen. Aamuaerobinen tyhjll vatsalla *voi* tehostaa rasvaoksidaatiota. Mutta akuutit muutokset rasvaoksidaatiossa ovat melko merkityksettmi kun mietitn kokonaiskuvaa. Aerobisen (tai HIIT:in) tarkoitus on list kalorinkulutusta - silloin ei ole merkityst tekeek aerobista aamulla vai illalla tai milloin vaan. Aamulla mys proteiinisynteesi on alhainen ja maksan glykogeenitasot vhn matalalla, joten lihasten menettminen on hieman todennkisemp aamulla tehtess, jos ei sy mitn. Varsinkin kovaa sessiota tehdess jaksaa paremmin jos haukkaa jotain purtavaa. Kytnnss ei ole siis vlil milloin aerobisen tekee - kaloritase mritt laihdutko vai 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 aerobisessa rasva toimii muutenkin pasiallisena energialhteen.

3. Variaatiot rasvan ja hiilihydraattien mrss

Usein kuulee vitteit kuten: 'l sy hiilareita, koska ne lihottavat', 'varo piikkaamasta insuliinia, koska se lihottaa'. No kyll ja ei. Kun sydn vhemmn kuin kulutetaan, keho on vhemmn aikaa varastoivassa tilassa - pienemmn kalorimrn takia. Keho varastoi aterian jlkeen AINA rasvaa. Insuliinin erittyminen hiilihydraattien jlkeen on juuri tm vaikutusmekanismi. Mutta mys proteiinin syminen aiheuttaa tarpeeksi suuren insuliinipiikin lopettamaan rasvanpoltto. Niin, mutta eiks glugakoni tasapainota tt insuliinipiikki? Tavallaan kyll, tavallaan ei koska glugakoni ei polta rasvaa. Mutta mites sitten rasvaisen aterian jlkeen? Silloin ei erity paljoa insuliinia. Ei, mutta ASP: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 triacylglycerol clearance. As discussed previously, important differences in the metabolism of chylomicrons and VLDL have become apparent. The ASP pathway has also been recognized and appears to play a critical role in chylomicron metabolism. The ASP pathway is activated in order to trap the fatty acids released from chylomicrons by the action of LPL and there is now unequivocal in vivo evidence in human subjects that ASP is generated by adipocytes in the postprandial period. These findings match the in vitro data showing that chylomicrons, but not the other plasma lipoproteins or fatty acids, activate the generation of ASP by cultured human adipocytes. An inverse relationship appears to exist between the proportion of fatty acids taken up by adipocytes and that released into the general circulation. Too great a release into the general circulation because of diminished trapping of fatty acids released from chylomicrons appears to be critical in the pathogenesis of the dyslipoproteinaemias associated with hyperapo B or FCHL and omental obesity. Evidence has been presented that dysfunction of the ASP pathway may be one of the causes of this disorder. Put differently, the ASP pathway is essential for the normal clearance and disposition of dietary fatty acids. Binding of chylomicrons to capillary endothelium followed by lipolysis by LPL results in the sudden liberation of fatty acids, and in the marked generation of ASP by adipocytes. The ASP 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 rather than exit into the general circulation. The transport vehicle, the chylomicron, therefore stimulates the formation of the peptide, ASP, which is responsible for its successful metabolism. Thus, the ASP pathway provides the metabolic coordination between the chylomicron and the adipocyte, which we describe as microenvironmental metabolic regulation and which we believe is essential for the normal 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 is considered to be the most potent stimulant of triglyceride synthesis. In this paper, we report on the effect of a small (14000 Da), basic (pI 9.0) protein isolated from human serum. This protein has been called acylation stimulating protein (ASP). It is a potent stimulant of

triglyceride synthesis in adipocytes from both normal weight and morbidly obese subjects. Its stimulatory effect on adipocytes is both rapid, occurring between 15-30 min after the start of incubation, and prolonged, lasting for up to 3 hr. Compared to insulin, it is sixfold more potent in its effect on triglyceride synthesis. As well as acting on isolated cells, ASP also has a fourfold stimulatory effect on triglyceride synthesis in human adipose microsomes at a concentration of 25 micrograms/ml. This study indicates that ASP is a potent stimulant of triglyceride synthesis and therefore may play a role in the pathogenesis of morbid 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 OX3 9DU, UK. We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001). There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids. There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty 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. allan.sniderman@muhc.mcgill.ca The storage and release of energy by adipocytes is of fundamental biologic importance. Not surprisingly, therefore, the rate at which these processes occur can be modulated by a variety of physiologic molecules. A newly recognized participant is produced by adipocytes themselves: acylation-stimulating protein (ASP). This article focuses on the most recent in-vivo evidence regarding how the ASP pathway may influence energy storage and release. In brief, the rate at which triglycerides are cleared from plasma (i.e. the rate at which they are hydrolysed) is determined by lipoprotein lipase and insulin, which is the principal hormone that regulates lipoprotein lipase. By contrast, the ASP pathway modulates the rate at which fatty acids are taken 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 the process. 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 on energy storage and release by adipocytes, the effects of both insulin and ASP must be 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, and there are now considerable in vitro data indicating that the ASP pathway is a major determinant of de novo triglyceride synthesis in human and murine adipocytes. Also, ASP is a major determinant of the rate at which fatty acids are released from adipocytes. It does so, principally, by increasing re-esterification, but also by reducing hormonesensitive 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.

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) is generated 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 an anterior abdominal wall vein that drains adipose tissue. Veno-arterial (V-A) gradients across the subcutaneous adipose tissue bed were calculated. The data demonstrate that ASP is produced in vivo (positive V-A gradient) With maximal production at 3-5 h postprandially. The plasma triacylglycerol (TAG) clearance was evidenced by a negative V-A gradient. 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 TAG clearance. 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 VA glycerol and non-esterified fatty acid (NEFA) differences postprandially. FIAT was negative during 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 TAG clearance. 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 by human adipocytes and that this process is accentuated postprandially, supporting the concept that ASP plays an important role in clearance of TAG from plasma and fatty 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 C3 production 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 triacylglycerol storage. In vivo studies have shown that ASP production by adipocytes increases locally after a fat meal. Initial in vitro studies demonstrated increased production of ASP 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) were capable of stimulating C3 (the precursor protein) or ASP production. Rather, the active component is a nonlipid, loosely associated, trypsin-sensitive molecule. High pressure liquid chromatography fractionation of the CHYLO infranate proteins identified the critical protein as transthyretin (TTR), which binds retinol-binding protein and complexes thyroxine and retinol. Addition of TTR alone, with lipid emulsion, or with respun CHYLO to human differentiated adipocytes had little effect on C3 and ASP production. By contrast, when transthyretin was added to CHYLO, C3 and ASP production were substantially enhanced up to 75- and 7. 5-fold respectively, compared with the effect of native CHYLO alone. Finally, a polyclonal antibody against 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 hypothesize that TTR mediates the transfer of the active components from CHYLO to adipocytes, which then stimulates increased C3 and ASP production. Thus the CHYLO provides the physiologic trigger of the ASP pathway.

Yksinkertaistettuna - ASP on merkittv tekij rasvan varastoimisessa. Ja rasvan syminen aiheuttaa ASP:n erityst. Vitteet siis, ett pelkstn insuliinia hillitsemll saa metabolisen edun tai laihtuu, eivt yksinkertaisesti ole totta, koska insuliini ei ole ainoa tekij, joka hillitsee lipolyysi ja edist triglyseridisynteesi (rasvan varastoitumista). Keho varastoi rasvaa, vaikka insuliinia ei pikkaisi ollenkaan (insuliiniahan erittyy, vaikka ei sisi mitn), ASP:n kautta. Ja sama jos ei sy ollenkaan rasvaa - insuliinin kautta. Esim. insuliinin erityst laskevassa lkkeest ei ole mitn apua, kun kalorien mr on sama (18). Ja joissain tutkimuksissa insuliiniarvot laskevat huonommin tai jopa nousevat hiilihydraattipitoisella dieetill, kun ne laskevat vhhiilihdyraattisella, mutta silti ei tule eroja painonpudotuksen suhteen (mm. 19-23). Ja esimerkiksi insuliiniresistenssist 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.

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 insulin resistance in populations with a high prevalence of a "thrifty genotype." An alternative hypothesis is that obesity-induced hyperinsulinemia is an adaptation which, by increasing central 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 risk of weight gain, we examined whether any of three different measures of the level of insulin secretion (the area under the plasma insulin curve during both a meal tolerance test and an oral glucose tolerance test, and the acute insulin secretory response to iv glucose) was predictive 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%/yr in males and 3.5 +/- 3.6%/yr in females, reflecting a mean annual increase in body fat content of 6.9%/yr in both sexes. Insulin secretion was negatively associated with the rate of weight gain, whether assessed by the insulin response during the meal tolerance test (r = -0.35; P < 0.001), the oral glucose tolerance test (r = -0.30; P = 0.004), or the acute insulin secretory response to iv glucose (r = -0.28; P = 0.002). Moreover, the significance of the relationship between each measure of insulin secretion and weight gain persisted after controlling for differences in age, sex, initial body weight, and insulin sensitivity. Relatively reduced insulin secretion, therefore, is a significant and independent predictor of the tendency to gain weight and adiposity in Pima Indians. The presence of relative insulin resistance also conferred an independent reduction in the risk of weight gain in some regression analyses. We conclude that insulin resistance and hyperinsulinemia are unlikely to play a causal role in the development of obesity, and that relatively reduced insulin secretion is a marker of an increased risk of weight gain in this population. These conclusions support the hypothesis that the level of insulin secretion plays an important role in long term body weight regulation. Baillieres Clin Endocrinol Metab. 1994 Jul;8(3):527-48. Energy and macronutrient metabolism. Swinburn BA, Ravussin E. Department of Community Health, University of Auckland, New Zealand. In general, obesity is a state of high energy stores, high energy intake, and high energy expenditure. The high energy expenditure is largely due to the increased fat-free mass. The failure to find a positive relationship between reported energy intake and body size reflects a greater under-reporting of calorie intake among obese individuals. Obesity, therefore, develops as a consequence of a chronic imbalance between intake and expenditure, although the cause of this is not apparent from the energy balance equation. However, this equation can be dissected into its component nutrient balance equations because net de novo lipogenesis is negligible in free-living humans. Fat calories are handled very differently from non-fat calories. Non-fat nutrient oxidation rates rise and fall to match the fluctuations in non-fat intake so that non-fat calorie balance is actively maintained. In contrast, changes in fat intake do not acutely affect fat oxidation but are matched by changes in storage. Therefore, within the fat balance equation there is ample scope for a chronic imbalance between fat intake and oxidation. Also, there is some evidence that carbohydrate balance may be an important signal for hunger and satiety. These concepts imply that, under free-living, ad libitum eating conditions, changes in nutrient intake composition (e.g. an increased proportion of fat in the diet) or changes in nutrient oxidation composition (e.g. a decrease in the proportion of fat oxidized) will lead to body weight change (in these cases, to weight gain). Considering obesity as a consequence of normal physiology (with its normal variation between individuals) in a 'pathological' environment (high fat diet, low exercise) offers an important perspective for explaining the interpopulation and interindividual differences in obesity and for formulating treatment and prevention options. Low energy expenditure (relative to body size), high respiratory quotient and insulin sensitivity have been shown to be predictors of weight gain, although upon gaining weight these metabolic factors tend to 'normalize'. Metabolic responses to underfeeding or overfeeding are largely predictable from the changes in calorie intake and changes in body composition, but some adaptive changes may occur.

Koko kehon insuliiniresistenssi (maksa, rasva, lihakset) saa dieettaamisen aikana kehon vapauttamaan valtavan mrn rasvahappoja. Koska rasva on insuliiniresistentti ei ravinteet imeydy sinne helposti. Ja koska lihaksetkin ovat, kyttvt ne valtavia mri nit rasvahappoja energiaksi, etenkin dieetill ja viel

salitreenin ja muun liikunnan ohella. Mutta samalla kun paino laskee, paranee insuliiniherkkyys ja laihtuminen hidastuu, lihominen on helpompaa ja tulee vaikeammaksi pit lihasta. Esim. insuliiniherkkyys on parempi jos rasvaprosentti on 5 kuin 35. Ja tietenkin edellisess on paljon vaikeampaa laihduttaa ja pit yll lihasta kyseisen prosessin aikana.
Effect of diet composition on metabolic adaptations to hypocaloric nutrition: comparison of high carbohydrate and high fat isocaloric diets SB Lewis, JD Wallin, JP Kane and JE Gerich The metabolic consequences of two hypocaloric diets were assessed in 10 obese men. The study, performed on a metabolic ward, compared the response of these men to two cholesterol-free liquid formula diets of differing composition [B](10 kcal/kg per day, 70% carbohydrate, 20% protein, 10% fat versus 70% fat, 20% protein, 10% carbohydrate) but identical in calories. These were administered for 14 days in a random order and each diet was preceded by a 7-day control weight maintenance diet (30 kcal/kg per day, 40% carbohydrate, 20% protein, 40% fat). The low calorie diets were well tolerated by the men and effected similar losses of nonaqueous body weight. Fasting glucose and insulin decreased significantly in these men after they ingested either weight loss diet for 14 days, but the change in each parameter was greater for high fat as compared to high carbohydrate (15% versus 7% and 67% versus 35%, respectively, P less than 0.01). In contrast, fasting glucagon concentration decreased in these subjects to a greater extent in respo nse to the high carbohydrate diet (35% versus 16%, P less than 0.01). This adaptive response thus resulted in a 50% fall in insulin:glucagon molar ratio for high fat and no change for high carbohydrate weight loss. Despite these hormonal alterations no change in glucose tolerance was observed. Fasting serum triglyceride and cholesterol levels declined in these subjects to a greater extent following the high fat compared to the high carbohydrate regimen (45% versus 28%, P less than 0.01 and 8% versus 3%, not significant, respectively). These changes reflected decrements in very low density lipoproteins alone. Despite similar increments in free fatty acid levels, (350% versus 270%, not significant) serum ketone body (betahydroxybutyrate and acetoacetate) concentrations increased 7-fold on the high fat diet compared to the high carbohydrate diet, P less than 0.001. The hyperketonemia of these men in response to the high fat, low calorie diet suggested the occurrence of a shift in hepatic free fatty acid metabolism toward ketogenesis rather than triglyceride synthesis. The associated decrease in the insulin: glucagon molar ratio raised the question of a possible role for these hormones in the adaptation.

Ja kun kaloreita ja proteiinin mr kontrolloidaan tarkasti - joko antamalla koehenkilille kaikki ateriat tai jopa tarkkailemalla viikkojen ajan heidn aktiivisuustasojaan ja energian kulutusta ja saantia (ns. metabolic ward- tutkimukset) rasvan mr vhenee kytnnss katsoen yht tehokkaasti, koostui ruokavalio sitten hiilihydraateista tai rasvasta, olivat variaatiot niden makrojen vlill suuria tai pieni. Eli kytnnss koehenkilit on valvottu viikkojen ajan ja kaikki kalorit mit he ovat saaneet on laskettu tarkasti ja jopa aktiivisuutta on kontrolloitu, ett se ei tosii eroja - mik on mahdollista jos koehenkilille vain valmistetaan ja annetaan ruoat, mutta muuten elvt normaalia elm. Joka tapauksessa kummallakaan tavalla, laihtuminen ei ole merkittvsti tehokkaampaa, sis sitten hiilihydraatteja tai rasvapainoitteista ruokavaliota. Kun kalorien ja proteiinin mr on sama, ei ole mitn vli syk rasvaa tai hiilihydraatteja, laihtuminen on kuitenkin yht tehokasta (mm. 26-33). Mikn tutkimus ei ole ikin huomannut metabolista etua rasvapainoitteisella ruokavaliolla taikka tehokkaampaa laihtumista kalorikontrolloiduissa tiloissa, proteiinin mrn ollessa sama. Toistan. Ikin. Ja koska nit tutkimuksia on tehty niin monta ja nykyn tutkimusmetodit ovat niin kehittyneit, ei rasvapainoitteinen ruokavalio laihduta tehokkaammin (paitsi ern tutkimuksen mukaan tm voisi olla mahdollista imettvill ideill). Sama ptee tokii hiilihydraattipainoitteiseen ruokavalioon, vaikka hiilihydraattien terminen vaikutus on hieman suurempi kuin rasvan, ero ei ole kuitenkaan kovinkaan merkittv. Tosin sydess yli kulutuksen, rasva lihottaa enemmn tai vhintn yht paljon kuin hiilihydraatit (34-36). Monet ihmiset, urheilijat ja kehonrakentajat ovat laihtuneet hiilihydraattipainoitteisella ruokavaliolla ja rasvapainoitteisella ruokavaliolla. Miksi sitten useat laihtuvat niin tehokkaasti vhhiilihydraattisella ruokavaliolla?

1. He syvt vhemmn kaloreita. He jttvt hiilihydraatit pois eli eliminoivat (ainakin lhes) kokonaan yhden makroravinteen. Kaloriovaje on helpompi saavuttaa. 2. He lisvt aktiivisuutta eli kuluttavat enemmn. Monien olo paranee selkesti kun hiilihydraatit jtetn pois ja insuliinitasot eivt heittele. Tmn takia voi hyvinkin tulla huomaamataa listty aktiivisuutta, vaikkapa hytyliikunnan muodossa. Nill henkilill insuliiniherkkyys on huonontunut. Yleens insuliiniresistenteille henkilille sopii paremmin rasvapainoitteinen ruokavalio ja sama pinvastoin. Ja *voi ehk* olla mahdollista, ett nille henkilille tulisi mys metabolinen etu, heille sopivia diettej noudatettaessa - insuherkille hiilariptioista, resist. rasvapitoista. Lisdataa tst aiheesta vaaditaan ennen kuin voidaan olla varmoja. 3. He syvt enemmn proteiinia. Proteiinilla on pieni termogeeninen etu muihin makroihin nhden ja muiden etujen lisksi, tm hieman auttaa laihduttamaan tehokkaammin, hieman suuremman kokonaiskulutuksen takia. 4. Nestetasapaino huijaa. Insuliini, hiilihydraatit ja suola saavat kehon sitomaan vett. VHH:lla nit tulee usein vhemmn, joten nestett poistuu aluksi tehokkaammin, joskus jopa erittin rajusti.
Efficacy and safety of low-carbohydrate diets: a systematic review. Bravata DM, Sanders L, Huang J, Krumholz HM, Olkin I, Gardner CD, Bravata DM. Center for Primary Care and Outcomes Research, Stanford University School of Medicine, Stanford, Calif 94305-6019, USA. bravata@healthpolicy.stanford.edu Comment in: * JAMA. 2003 Apr 9;289(14):1853-5. * JAMA. 2003 Apr 9;289(14):1767-8, 1773. * ACP J Club. 2003 Nov-Dec;139(3):70. CONTEXT: Low-carbohydrate diets have been popularized without detailed evidence of their efficacy or safety. The literature has no clear consensus as to what amount of carbohydrates per day constitutes a low-carbohydrate diet. OBJECTIVE: To evaluate changes in weight, serum lipids, fasting serum glucose, and fasting serum insulin levels, and blood pressure among adults using low-carbohydrate diets in the outpatient setting. DATA SOURCES: We performed MEDLINE and bibliographic searches for English-language studies published between January 1, 1966, and February 15, 2003, with key words such as low carbohydrate, ketogenic, and diet. STUDY SELECTION: We included articles describing adult, outpatient recipients of lowcarbohydrate diets of 4 days or more in duration and 500 kcal/d or more, and which reported both carbohydrate content and total calories consumed. Literature searches identified 2609 potentially relevant articles of low-carbohydrate diets. We included 107 articles describing 94 dietary interventions reporting data for 3268 participants; 663 participants received diets of 60 g/d or less of carbohydrates--of whom only 71 received 20 g/d or less of carbohydrates. Study variables (eg, number of participants, design of dietary evaluation), participant variables (eg, age, sex, baseline weight, fasting serum glucose level), diet variables (eg, carbohydrate content, caloric content, duration) were abstracted from each study. DATA EXTRACTION: Two authors independently reviewed articles meeting inclusion criteria and abstracted data onto pretested abstraction forms. DATA SYNTHESIS: The included studies were highly heterogeneous with respect to design, carbohydrate content (range, 0-901 g/d), total caloric content (range, 525-4629 kcal/d), diet duration (range, 4-365 days), and participant characteristics (eg, baseline weight range, 57-217 kg). No study evaluated diets of 60 g/d or less of carbohydrates in participants with a mean age older than 53.1 years. Only 5 studies (nonrandomized and no comparison groups) evaluated these diets for more than 90 days. Among obese patients, weight loss was associated with longer diet duration (P =.002), restriction of calorie intake (P =.03), but not with reduced carbohydrate content (P =.90). Lowcarbohydrate diets had no significant adverse effect on serum lipid, fasting serum glucose, and fasting serum insulin levels, or blood pressure. CONCLUSIONS: There is insufficient evidence to make recommendations for or against the use of low-carbohydrate diets, particularly among participants older than age 50 years, for use longer than 90 days, or for diets of 20 g/d or less of carbohydrates. Among the published studies, participant weight loss while using low-carbohydrate diets was principally associated with decreased caloric intake and increased diet duration but not with reduced carbohydrate conte Horm Metab Res. 2005 Dec;37(12):734-40. No difference in lipolysis or glucose transport of subcutaneous fat cells between moderate-fat and low-fat hypocaloric diets in obese women.

Lfgren P, Andersson I, Wahrenberg H, Hoffstedt J. Karolinska Institutet, Clinical Research Center and Department of Medicine, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Sweden. patrik.lofgren@ki.se The objective of the present study was to evaluate the effect of two different diets on lipolysis and lipogenesis in subcutaneous fat cells from obese women. In a ten-week nutritional intervention study, forty women were randomly assigned to a hypoenergetic-2,514 kJ (600 kcal/day) diet of either moderate-fat/moderate-carbohydrate or low-fat/highcarbohydrate content. Body weight was equally reduced by approximately 7.5 % in both diet groups (p = 0.58). A subcutaneous adipose tissue biopsy was obtained for subsequent measurement of triglyceride breakdown (lipolysis) using drugs active at different steps of the lipolytic signaling cascade, and lipid synthesis (glucose transport) before and after intervention. No difference was found between the two diet groups at the maximum rate of either lipolysis or adrenoceptor sensitivity (p-values: 0.14 - 0.97). Inhibition of lipolysis by insulin was also similar in both diet groups before and after intervention. Finally, insulin-stimulated glucose transport did not show any changes that could be attributed to the type of diet. In conclusion, our data suggest that macronutrient diet composition has no major influence on glucose transport or mobilization of triglycerides in human subcutaneous fat cells of obese women. Metabolism. 1983 Aug;32(8):757-68. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. To study the metabolic effects of ketosis without weight loss, nine lean men were fed a eucaloric balanced diet (EBD) for one week providing 35-50 kcal/kg/d, 1.75 g of protein per kilogram per day and the remaining kilocalories as two-thirds carbohydrate (CHO) and one-third fat. This was followed by four weeks of a eucaloric ketogenic diet (EKD)--isocaloric and isonitrogenous with the EBD but providing less than 20 g CHO daily. Both diets were appropriately supplemented with minerals and vitamins. Weight and whole-body potassium estimated by potassium-40 counting (40K) did not vary significantly during the five-week study. Nitrogen balance (N-Bal) was regained after one week of the EKD. The fasting blood glucose remained lower during the EKD than during the control diet (4.4 mmol/L at EBD, 4.1 mmol/L at EKD-4, P less than 0.01). The fasting whole-body glucose oxidation rate determined by a 13Cglucose primed constant infusion technique fell from 0.71 mg/kg/min during the control diet to 0.50 mg/kg/min (P less than 0.01) during the fourth week of the EKD. The mean serum cholesterol level rose (from 159 to 208 mg/dL) during the EKD, while triglycerides fell from 107 to 79 mg/dL. No disturbance of hepatic or renal function was noted at EKD-4. These findings indicate that the ketotic state induced by the EKD was well tolerated in lean subjects; nitrogen balance was regained after brief adaptation, serum lipids were not pathologically elevated, and blood glucose oxidation at rest was measurably reduced while the subjects remained euglycemic.

Termodynamiikan lait ptevt kaikkiin, niit ei voi kiert. Kalorit sisn - kalorit ulos = diettaamisen lopputulos. Tmn takia samanpainoiset henkilt laihtuvat suurinpiirtein saman verran samalla kalorivajeella (data laitettu jo aiemmin) ja kun energian saantia ja kulutusta kontrolloidaan tarkasti pystytn kaloritaseesta laskemaan/arvioimaan kuinka paljon kehonkoostumus muuttuu (37-40). On naurettavaa vitt, ett kalorit eivt merkitsisi, kun sill on nin vankkumaton perusta, sek labrassa, ett tutkimuksissa, ett kytnnss. Sitten kytntn - paras dieetti on se, jota pystyt noudattamaan ja tuo parhaat tulokset. Rasva ei voi aivan nolliin vet, ainakaan pitkksi aikaa. Hiilihydraatit taas voi, tai ainakin erittin lhelle. Mrittele kalorvaje, sy paljon proteiinia ja muut makrot eivt tuo merkittv eroa.

4. Makrojen erottelu
Makrojen erottelussa jtetn yleens yhdelt tai useammalta aterialta pivss jokin makroravinne pois. Teoria tmn takana on se, ett kun sy rasvaa, on hyv minimoida insuliinipiikki, ett rasva ei menisi suoraan rasvakudokseen. No rasva

varastoituu ASP:n ansiosta ilman insuliiniakin, ett tll ei ole merkityst. Ja hiilihydraatit ja proteiinit insuliinin ansiosta, vaikka rasvaa ei sisikn. Keho varastoi aterian jlkeen rasvaa, si mit si. Eli teoria on olemattomalla pohjalla, mutta ent kytnt?
Int J Obes Relat Metab Disord. 2000 Apr;24(4):492-6. Similar weight loss with low-energy food combining or balanced diets.

Golay A, Allaz AF, Ybarra J, Bianchi P, Saraiva S, Mensi N, Gomis R, de Tonnac N. Division of Therapeutic Patient Education for Chronic Diseases, University Hospital Geneva, Switzerland. Alain.Golay@hcuge.ch OBJECTIVE: The goal of this study was to evaluate the effect of two diets ('food combining' or dissociated vs balanced) on body weight and metabolic parameters during a 6-week period in an in-hospital setting. SUBJECTS AND DESIGN: 54 obese patients were randomly assigned to receive diets containing 4.5 MJ/day (1100 kcal/day) composed of either 25% protein, 47% carbohydrates and 25% lipids (dissociated diet) or 25% protein, 42% carbohydrates and 31% lipids (balanced diet). Consequently, the two diets were equally low in energy and substrate content (protein, fat and carbohydrate) but widely differed in substrate distribution throughout the day. RESULTS: There was no significant difference in the amount of weight loss in response to dissociated (6.2 +/- 0.6 kg) or balanced (7.5 +/- 0.4 kg) diets. Furthermore, significant decreases in total body fat and waist-to-hip circumference ratio were seen in both groups, and the magnitude of the changes did not vary as a function of the diet composition. Fasting plasma glucose, insulin, total cholesterol and triacylglycerol concentrations decreased significantly and similarly in patients receiving both diets. Both systolic and diastolic blood pressure values decreased significantly in patients eating balanced diets. The results of this study show that both diets achieved similar weight loss. Total fat weight loss was higher in balanced diets, although differences did not reach statistical significance. Total lean body mass was identically spared in both groups. CONCLUSION: In summary at identical energy intake and similar substrate composition, the dissociated (or 'food combining') diet did not bring any additional loss in weight and body fat.

Eli minknlaista apua ei ole makrojen erottelulla kalorimrn ollessa identtinen. Miksi sitten monet ovat laihtuneet tll metodilla? Koska kaloreita tulee tietenkin syty selkesti vhemmn kun yksi makroravinne jtetn kokonaan pois. Kytntn - makrojen erottelu ei ole milln tavalla vlttmtnt, mutta jos se auttaa pitmn kalorit hallussa, on sen kytt perusteltua.

5. Iltasyminen

Iltasymist, varsinkin hiilihydraattien, on jo pitkn pidetty lihottavana tekijn. Tosin tysin ilman perusteita. Iltasyminen ei lihota sen enemp kuin syminen minn muuna aikana. Monet vittvt, ett hiilihydraatit illalla lihottavat, koska ne estvt yllisen kasvuhormonipiikin erityksen. Mutta unohtava, mainita sen ett kasvuhormonin suhteen tulee jlkipiikki (41). Sitten on vitteit, ett koska illalla tulee liikuttua vhemmn, nin silloin ei kannata syd niin paljoa. Mutta jos kalorien mr on sama syk aamu - tai iltapainoitteisesti, on iltapainoitteisella ruokavaliolla oltu kalorivajeessa aamulla ja iltasyminen pelkstn tasapainottaa tt vajetta verrattuna aamulla symiseen. Lopputulos on sama, rasvaa kertn ja poltetaan enemmn vain eri aikaan. Ja kun suuri osa ihmisist istuu pulpetiin tai tietokoneen takana pitkin piv, niin eip usein aamulla/pivll sen enemp tule liikuttua. Jos taas tulee aikaisemmin pivll liikuttua enemmn, niin kalorien ajoittaminen niihin hetkiin *voi* tuoda apua kehonkoostumuksen suhteen. Mutta silloinkaan vaikutus ei tule iltasymisen huonoudesta vaan siit, ett sydn paljon kuin treenit eivt ole lhell. Eli samat tilanne ptisi toisinpin. Ja useimmat viel treenaavat illalla, joten senkin takia on hyv syd illalla, ett maksimoitaisiin palautuminen.

On mys tutkittu, ett tuoko identtisell kalorimrll, ilta - tai aamupainoitteinen syminen apua diettaamisen suhteen (42, 43). Toisessa ei huomattu mitn eroja. Toisessa aamupainoitteisella laihduttiin hieman enemmn, mutta ei merkittvsti. Mutta aamupainoitteisella mys lihasta lhti merkittvsti enemmn, tuoden iltapainoitteiselle symisen jopa edun. Miksi sitten monet laihtuvat usein helposti jttessn iltapalan pois/vhemmlle? No kalorimr laskee. Sama vanha virsi. Kytntn - mikli runsas iltasyminen sopii pivn kaloritavoitteeseen ja on viel, vaikka treenattukkin illalla, voi illalla syd vallan mainiosti runsaastikin. Kalorit sisn - kalorit ulos. Henkilkohtaiset mieltymykset ovat trkein seikka.

6. Paikallinen rasvanpoltto
Ensimmiseksi - paikallinen rasvanpoltto ei ole myytti, vaan se on hyvinkin mahdollista toteuttaa. Toiseksi, sen vaikutus on kuitenkin niin pieni, ett sill ei ole mitn merkityst. Spot reductionia on huomattu tapahtuvan pariinkin otteeseen ja termogeeniset voiteet *voivat* auttaa minimaalisen merkityksettmn spot reductionin saavuttamisessa (44-46) Tss yksi paperi.
Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E394-9. Epub 2006 Sep 19. Are blood flow and lipolysis in subcutaneous adipose tissue influenced by contractions in adjacent muscles in humans? Stallknecht B, Dela F, Helge JW. Department of Medical Physiology, The Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark. B.Stallknecht@mfi.ku.dk Aerobic exercise increases whole body adipose tissue lipolysis, but is lipolysis higher in subcutaneous adipose tissue (SCAT) adjacent to contracting muscles than in SCAT adjacent to resting muscles? Ten healthy, overnight-fasted males performed one-legged knee extension exercise at 25% of maximal workload (W(max)) for 30 min followed by exercise at 55% W(max) for 120 min with the other leg and finally exercised at 85% W(max) for 30 min with the first leg. Subjects rested for 30 min between exercise periods. Femoral SCAT blood flow was estimated from washout of (133)Xe, and lipolysis was calculated from femoral SCAT interstitial and arterial glycerol concentrations and blood flow. In general, blood flow and lipolysis were higher in femoral SCAT adjacent to contracting than adjacent to resting muscle (time 15-30 min; blood flow: 25% W(max) 6.6 +/- 1.0 vs. 3.9 +/- 0.8 ml x 100 g(-1) x min(1), P < 0.05; 55% W(max) 7.3 +/- 0.6 vs. 5.0 +/- 0.6 ml x 100 g(-1) x min(-1), P < 0.05; 85% W(max) 6.6 +/- 1.3 vs. 5.9 +/- 0.7 ml x 100 g(-1) x min(-1), 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 100 g(-1) x min(-1), P < 0.05). In conclusion, blood flow and lipolysis are generally higher in SCAT adjacent to contracting than adjacent to resting muscle irrespective of exercise intensity. Thus specific exercises can induce "spot lipolysis" in adipose tissue. Assuming a molecular weight of 860 g/mol for TG, this corresponds to an extra breakdown of 0.62.1 mg of TG in 30 min/100 g of adipose tissue adjacent to contracting muscles

Jep, paikallista rasvanpolttoa tapahtuu. Mutta kuinka paljon?

Eli rasvaa kytettiin suoraan rasvavarastoista energiaksi 30 minuutin treenin aikana perti 0.6-2.1 milligrammaa 100 grammaa rasvaa kohden. Jos tekisi jopa kymmenen tuollaista sessiota viikossa, puolen vuoden ajan tulisi tst perti 156-546 milligrammaa/100 grammaa rasvaa. Eli lhes puoli grammaa rasvaa kymmennell puolen tunnin treenill puolen vuoden ajan. Tuossa samassa ajassa, samalla treenill kuluisi 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 kiloa rasvaa olisi mahdollista polttaa tuon liikunnan kalorinkulutuksen ansiosta. Hieman enemmn kuin puoli grammaa.

Kalorit kunnon/roskaruoasta
Kalori on kalori. Aivan sama mist kalorit tulevat. Tietenkin on aina parempi syd ruokaa, joissa olisi suojaravinteita. Esim. kaliumin krooninen puute laskee lepoaineenvaihduntaa. 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 sill olisi suurta merkityst. Useissa tutkimuksissa isokalorisessa tilassa suuresta sokerinmrstkn 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 of different composition. Bray GA, Most M, Rood J, Redmann S, Smith SR. Pennington Biomedical Research Center, Baton Rouge, LA, USA. brayga@pbrc.edu 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 with similar composition is unknown. DESIGN: Three-way crossover. METHODS: Six overweight men were given a standard breakfast at 8:00 a.m. on each of 3 occasions, followed by 1 of 3 lunches 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 organic beef 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 foods and 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. Salivary cortisol was measured after lunch. RESULTS: Total fat, protein and energy content were similar in the 3 meals, but the fatty acid content differed. The fast-food meal had more myristic (C14:0), palmitic (C16:0), stearic (C18:0) and trans fatty acids (C18:1) than the other 2 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 observed was a decrease in the AUC of LDL cholesterol after the organic beef meal relative to that for the other two meals. Other metabolic responses were not different. CONCLUSION: LDLcholesterol decreased more with the organic beef meal which had lesser amounts of saturated and 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 ei ollut. Ateriat olivat kalori - ja makroarvoiltaan melko samanlaiset. Kalorit sisn kalorit ulos. Kytntn - valtaosa kaloreista olisi hyv tulla ravinnerikkaista lhteist. Pelkk multivitamiini ei riit. Imeytyminen ei ole niin tehokasta ja ne voivat jopa list mirkoravinteiden eptasapainoa. Esim. lytyy paljon jotain ravinnetta, jota saa huonosta ruokavaliosta paljon ja vhn, jota saa sitten vhn tai ei ollenkaan. Ja vihanneksia ei voi rutistaa pilleri muotoon. Mutta pieni osa, vaikka 10-15% voi tulla mist vaan, ett sill olisi ratkaisevaa merkityst.

Sstliekki
Jep. Kyseess on myytti, ainakin normaalioloissa. Diettaaminen aiheuttaa aineenvaihdunnan hidastumista. Koska kevyempi keho kuluttaa vhemmn energiaa. Entisill lihavilla on joskus havaittu olevan n. 3-5% pienempi lepoaineenvaihdunta kuin samankokoisilla henkilill, jotka eivt ole olleet lihavia (49). Mutta sitten taas toisaalta, tt ei todellakaan oel huomattu aina eli painonpudottaneila ja normaalipainoisilla ei ole ollut mitn eroa tai mitn merkittv eroa lepoaineenvaihdunnassa - melko vahvaa dataa sstliekki vastaan (50-58).

Tosin on paljon dataa, ett sstliekki voi tapahtua, mutta sen vaikutus ei ole todellakaan 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 tll foorumilla tuskin tekee. Suurin sstliekki on tainnut olla juuri henkilill, joita nnnytettiin puolisen vuotta. Heidn rasvaprosenttinsa laski johonkin viiden paikkeille tai alle ja aineenvaihdunta hidastui joku 30-40%. Melko merkittv hidastuminen, mutta ei silti stoppaa laihduttamista. Termodynamiikan lait ptevt sstliekisskin. Varmaan kuuluisin sstliekki tutkimus on Ancel Keysin tekem tutkimus joskus 1940-luvulla. Aineenvaihdunta hidastui merkittvsti, mutta vain puolet tst tuli sstliekin kautta - toinen puoli hidastumisesta johtui yksinkertaisesti siit, ett kevyempi keho kuluttaa vhemmn energiaa. Sstliekki, eli ylimrist aineenvaihdunnan hidastumista, mit kevyempi keho tuo tullessaan, on havaittu useasti, mutta vaikutus ei ole mitenkn suuri, kuten useasti jo mainittu. Erss tutkimuksessa kulutuksen laskun havaittiin olevan 6% yli mit sen olisi pitnyt olla tai lepoaineenvaihdunta hidastui noin 100 kalorin verran 10% painonpudotukseen tai lasku on muuten vain niin 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 kun todella 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), spontaneous physical activity and body composition were determined in 7 obese patients (5 females, 2 males, 174 +/- 9% IBW, 38 +/- 2% fat mass) on 2 different occasions: before weight reduction, and after 10 to 16 weeks on a hypocaloric diet as outpatients, the recommended energy 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 hour energy expenditure (24 EE) was measured in a respiration chamber with all the subjects receiving 10418 kJ/d before weight reduction and an average of 3360 +/- 205 kJ/d while on the diet. When expressed in absolute values, both 24 EE and RMR decreased during the hypocaloric diet from 9819 +/- 442 to 8229 +/- 444 and from 7262 +/- 583 to 6591 +/- 547 kJ/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/kg FFM/d). Approximately one half of the 24 EE reduction (1590 kJ/d) was accounted for by a decrease in RMR, the latter being mainly accounted for by a reduction in FFM. Most of the remaining decline in 24 EE can be explained by a decreased thermic effect of food, and by the reduced cost of physical activity mainly due to a lower body weight. Therefore, there seems little reason to evoke additional mechanisms 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 very low 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 these induce a high rate of weight loss. It has been argued that excessive lean body mass is lost with very restricted energy intake regimens which compromises metabolic rate and sabotages weight maintenance. Thirty-nine subjects who had lost an average of 12.3 +/- 2 kg during an 8-week VLCD trial were transferred immediately to a 1500 kcal per day maintenance formula which included solid foods. RMR was determined at four intervals: (1) before dieting; (2) after 2 weeks of VLCD; (3) end of 8 weeks dieting; (4) end of 8 weeks maintenance period. It was observed that the metabolic rate dropped to 86 per cent of original by the end of the 8 weeks of VLCD. Metabolic rate recovered to 93 per cent of prediet values by the end of 8 weeks of weight maintenance on 1500 kcal/day. Following an average 2 kg weight regain within the first week of maintenance, there was no further weight regain. VLCD did not produce losses of

RMR beyond that expected from the loss of weight. No difficulty was observed in maintaining 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? An examination 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, USA. weinsier@shrp.uab.edu Comment in: * Am J Clin Nutr. 2001 Mar;73(3):655-8. BACKGROUND: Obese persons generally regain lost weight, suggesting that adaptive metabolic changes favor return to a preset weight. OBJECTIVE: Our objective was to determine whether adaptive changes in resting metabolic rate (RMR) and thyroid hormones occur in weightreduced persons, predisposing them to long-term weight gain. DESIGN: Twenty-four overweight, postmenopausal women were studied at a clinical research center in four 10-d study phases: the overweight state (phase 1, energy balance; phase 2, 3350 kJ/d) and after reduction to a normal-weight state (phase 3, 3350 kJ/d; phase 4, energy balance). Weightreduced women were matched with 24 never-overweight control subjects. After each study phase, assessments included RMR (by indirect calorimetry), body composition (by hydrostatic weighing), serum triiodothyronine (T(3)), and reverse T(3) (rT(3)). Body weight was measured 4 y later, without intervention. RESULTS: Body composition-adjusted RMR and T(3):rT(3) fell during acute (phase 2) and chronic (phase 3) energy restriction (P: < 0.01), but returned to baseline in the normal-weight, energy-balanced state (phase 4; mean weight loss: 12.9 +/- 2.0 kg). RMR among weight-reduced women (4771 +/- 414 kJ/d) was not significantly different from that in control subjects (4955 +/- 414 kJ/d; P: = 0.14), and lower RMR did not predict greater 4-y weight regain (r = 0.27, NS). CONCLUSIONS: Energy restriction produces a transient hypothyroid-hypometabolic state that normalizes on return to energy-balanced conditions. Failure to establish energy balance after weight loss gives the misleading impression that weight-reduced persons are energy conservative and predisposed to weight regain. Our findings do not provide evidence in support of adaptive metabolic changes as an explanation for the tendency of weight-reduced persons to regain weight.

Vhkaloriset ja erittin vhkaloriset dieetit hidastuttavat aineenvaihduntaa enemmn kuin pienemmll vajeella tehtvt dieetit, mutta se johtuu yksinkertaisesti siit, ett ne aiheuttavat suuremman pudotuksen painossa (75). Pitkaikaisia vhkalorisia dieettej ei voi oikein suositella kehonrakennukseen tai voimailuun panostavalle henkillle, mutta viikon tai muutaman seteisse eivt aiheuta lihaskatoa tai sstliekki oikein suoritettuna. On mys dataa sen puolesta, ett aineenvaihdunnan hidastuminen korreloi leptiinin laskun 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 mr vhenee, leptiini laskee. Kun ruoan mr vhenee leptiini laskee. Ja kun leptiini laskee tulee juuri edell mainittu ongelma - aineenvaihdunta hidastuu ja nlntunne kasvaa, tehden diettaamisen vaikeammaksi ja vaikeammaksi. Leptiini kontrolloi mys CCK:ta, kolekystokiniinia, joka on yksi merkittv kyllisyyshormoni. Leptiinin on mys huomattu aktivoivan AMPK:ta, joka on yksi toinen trke tekij dietatessa, hoitaen lukuisia tehtvi. Leptiinill nyttisi olevan mys vaikutus ghreliinin, joka on yksi trkeimmist tekijist nlnhallinnassa, ollen merkittv nlkhormoni. Leptiinitasot olisi trke pit normaaleina, ei liian suurina eik liian pienin. Heti dieetin alussa leptiini alkaa laskemaan. Silloin sill ei ole viel suurta merkityst, mutat pidemmn plle on. Leptiini on nimittin trkempi hormoneja, pitkaikaisen nlnhallinnan suhteen. Leptiini ei vaihtele niin kovinkaan merkittvsti aterioiden vlill. Paitsi hiilihydraatteihin.

Ylisymiset tai tankkaukset tai mttpivt ovat siis hydyllisi leptiinin nostamisen kautta. Estvt nin aineenvaihduntaa hidastumasta ja auttavat pidempiaikaisessa nlnhallinnassa ja tekee vlill pkopallekkin hyv. Tankkauksissa on hyv panostaa juuri runsaaseen hiilihydraattien saantiin, koska ne nostavat 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 fruktoosi ei nosta leptiini. Leptiini tietenkin laskee sitten taas melko nopeasti. Varsinkin jos tankkaus on vain muutaman aterian tai yhden pivn. Jos kunnolla haluaa nostaa leptiini, olisi parempi pit parin pivn tankkausjakso tai jopa viikon, jolloin mentisiin maltillisilla plussilla. Tst olisi apua paitsi leptiinin kautta, mys pkopalle ja auttaisi lihasmassan sstmisesskin paremmin. Paasto tai kalorivaje ja sen jlkeinen 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 apua sstliekki vastaan (78-80) sek liikunnasta/punttitreenist (81). Molemmat asiat pitisi olla dieetill mukana oikeastaan aina. Miksi sitten monet kuvittelevat sstliekin olevan olemassa? 1. Tekosyy. 2. Nestetasapaino huijaa. Painohan voi vhkalorisella dieetill, vaikka nousta samalla kun 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 erittin vhkalorisella dieetill ja liikkuu jrkyttvi mri tn aikana. Ja sstliekin vaikutus korostuu sitten hieman enemmn, kun lhestytn jotain vitosen rasvaprosentteja. Normaalin dieettajan ei tst kuitenkaan tarvitse murehtia, varsinkaan jos tulee liikuttua ja treenattua, syty runsaasti proteiinia ja vedetty tankkauksia.

Ateriatiheys
Usein symisen on usein vitetty kiihdyttvn aineenvaihduntaa ja pitvn kehon pois katabolisesta tilasta. Eli ideaalia olisi tmn ksityksen mukaan syd vhintn 6-7 kertaa pivss 2-3 tunnin vlein. Usein symisen ei ole kuitenkaan havaittu kiihdyttvn aineenvaihduntaa lukuisissa tutkimuksissa (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 isokalorisessa tilassa paremmaksi kuin harvoin syminen. Sama tietenkin pinvastoin. Vain yhdess tutkimuksessa on saatu erilaisia tuloksia eri ateriatiheyksien vlill, mutta se johtuikin kyseisen tutkimuksen huonosta suunnittelusta, eik mistn yksityisest, maagisesta ateriavlist.
Br J Nutr. 1997 Apr;77 Suppl 1:S57-70. Links Meal 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's habitual frequency of eating and body weight, leading to the suggestion that a 'nibbling' meal

Ja yhdesskn tutkimuksessa, jossa on mitattu energiankulutusta, ei ole huomattu mitn 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 alle viiden tunnin ateriavlit aiheuttaisivat kataboliaa. Pidemmt ateriavlit voivat list proteiinidegredaatiota, mutta proteiinisynteesi kiihtyy taas sitten kuin sydn. Mikli proteiinin saanti on runsasta, voi selvit hyvinkin parilla tai kolmella aterialla pivss ja saavuttaa hyvi tuloksia ja niin onkin tehty. Mutta varmaan sopivana ateriavlin voisi pit juuri tuota viitt tuntia. Pidemmt ateriavlit eivt *ehk* ole en optimaalisia. Itse asiassa liian usein symisest voi olla jopa haittaa lihastenkasvatukselle. Mutta se on sitten aivan toinen aihe.

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 in those that do observe a relationship. However, this finding is highly vulnerable to the probable confounding effects of post hoc changes in dietary patterns as a consequence of weight gain and to dietary under-reporting which undoubtedly invalidates some of the studies. We conclude that the epidemiological evidence is at best very weak, and almost certainly represents an artefact. A detailed review of the possible mechanistic explanations for a metabolic advantage of 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 an isoenergetic test load is divided into multiple small meals, other studies refute this, and most are neutral.More importantly, studies using whole-body calorimetry and doublylabelled water to assess total 24 h energy expenditure find no difference between nibbling and gorging. Finally, with the exception of a single study, there is no evidence 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 are likely to be mediated through effects on the food intake side of the energy balance equation.

Yhteenveto
Mutta miten sitten syd? Kaikista trkeint on miinuskalorit pitkll aikavlill. Vlill voi ja kannattaakin kyd plussilla. Seuraavaksi tulee riittv proteiinin saanti. Joka voi vaihdella 2-4 g/kg vlill. Pahasti ylipainoiselle, vhn treenaavalle ja hitaasti diettaavalle 2 g/kg voi olla tarpeeksi. 3g/kg on enemmn optimaalinen henkillle, joka treenaa 4-5 kertaa viikossa ja vhintn saman verran aerobista plle ja jonka rasvaprosentti on alle 10. Tt suuremmat annokset eivt todennkisesti tuo enemp hytyj kuin haittoja, ainakaan natuille. Ellei sitten sy pelkstn proteiinia, jolloin proteiinin mrn voi/kannattaa nostaa 4 g/kg. Runsas proteiinin saanti on erittin trke dieetill. Paitsi ett se tuo suurta kyllisyytt, se voi tukea aineenvaihduntaa. Ja mikn makroravinne ei sst lihasproteiinia paremmin kuin proteiini. Proteiinilla on mys suurin termogeeninen vaikutus, joten sekin voi tuoda pieni apuja laihduttamisen tehokkuuden suhteen. Proteiinin tarvehan kasvaa dieetill. Massan kasvatukseen riitt pienemmtkin mrt. Mutta sekin sitten aivan on toinen aihe. Eli ensiksi aseta kalorivaje. Toiseksi aseta proteiinin mr (2-3 (4)g/kg). Sitten pid huoli riittvst vlttmttmien rasvahappojen, rasvan (n. 1g/kg) ja vihannesten saannista. Sitten hiilihydraatteja aktiivisuuden mukaan. Tietenkin rasvan mr voi olla suurempikin, mutta pitkll vlill sen olisi hyv olla vhintn tuo 1g/kg.

Lhteet 1 Acute effect of meal glycemic index and glycemic load on blood glucose and insulin

responses in humans, Galgani et al. 2006 2 No effect of a diet with a reduced glycaemic index on satiety, energy intake and body weight in overweight and obese women, Ston et al. 2008 3 Comparison of 4 diets of varying glycemic load on weight loss and cardiovascular risk reduction in overweight and obese young adults: a randomized controlled trial. McMillan-Price et al. 2006 4 Differences in glycaemic status do not predict weight loss in response to hypocaloric diets in obese patients, de Luis et al. 2006 5 Diets high and low in glycemic index versus high monounsaturated fat diets: effects on glucose and lipid metabolism in NIDDM, Luscombe et al. 1999 6 An 18-mo randomized trial of a low-glycemic-index diet and weight change in Brazilian women, Sichieri et al, 2007 7 Influence of glycemic index/load on glycemic response, appetite, and food intake in healthy humans, Alfenas et al, 2005 8 The effect of dietary glycemic index on weight maintenance in overweight subjects: a pilot study, Philippou et al, 2009 9 The effect of high- and low-glycemic index energy restricted diets on plasma lipid and glucose profiles in type 2 diabetic subjects with varying glycemic control, Heilbronn et al, 2002 10 Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized trial, Ebbeling et al. 2007 11 Different glycemic indexes of breakfast cereals are not due to glucose entry into blood but to glucose removal by tissue, Schenk et al. 2003. 12 Long-term effects of 2 energy-restricted diets differing in glycemic load on dietary adherence, body composition, and metabolism in CALERIE: a 1-y randomized controlled trial. Das et al. 2007 13 Reduced glycemic index and glycemic load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women. Raatz et al. 2005 14 No difference in body weight decrease between a low-glycemic-index and a highglycemic-index diet but reduced LDL cholesterol after 10-wk ad libitum intake of the low-glycemic-index diet, Sloth et al. 2004 15 Effect of glycemic carbohydrates on short-term satiety and food intake, Anderson et al. 2003 16 Glycemic and insulinemic responses as determinants of appetite in humans, Flint et al. 2006 17 Effects of exercise intensity and duration on the excess post-exercise oxygen consumption, LaForgia et al, 2006 18 No effect of inhibition of insulin secretion by diazoxide on weight loss in hyperinsulinaemic obese subjects during an 8-week weight-loss diet, Due et al, 2007 19 Comparison of the effects on insulin resistance and glucose tolerance of 6-mo high-monounsaturated-fat, low-fat, and control diets, Due et al, 2008 20 Comparison of a Low-Fat Diet to a Low-Carbohydrate Diet on Weight Loss, Body Composition, 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 for Energy and Protein, Segal-Isaacson et al, 2004 22 Similar weight loss with low- or high-carbohydrate diets, Golay et al, 2006 23 Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated fat diets on body composition and cardiovascular risk, Noakes et al, 2006 24 Predictors of weight change in a bi-ethnic population. The San Antonio Heart Study, Valdez et al, 1994 25 Insulin resistance associated with lower rates of weight gain in Pima Indians, Swimburn et al, 1991 26 Cognitive effects of ketogenic weight-reducing diets, Wing et al, 1995 27 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, 1994 29 Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets, Johnston et al, 2006

30 Dietary carbohydrate-to-fat ratio: influence on whole-body nitrogen retention, substrate utilization, and hormone response in healthy male subjects, McCargar et al, 1989 31 Composition of weight lost during short-term weight reduction. Metabolic responses of obese subjects to starvation and low-calorie ketogenic and nonketogenic diets, Yang et al, 1976 32 Energy intake required to maintain body weight is not affected by wide variation in diet composition. Leibel et al, 1992 33 Low-Fat versus Low-Carbohydrate Weight Reduction Diets: Effects on Weight Loss, Insulin Resistance and Cardiovascular Risk A Randomised Control Trial, Bradley et at, 2009 34 Fat and carbohydrate overfeeding in humans: different effects on energy storage, Horton et al, 1995 35 Spontaneous overfeeding with a 'cafeteria diet' in men: effects on 24-hour energy expenditure and substrate oxidation, Larson et al, 1995 36 Ad libitum food intake on a "cafeteria diet" in Native American women: relations with body composition and 24-h energy expenditure, Larson et al, 1995 37 Short-term, mixed-diet overfeeding in man: no evidence for "luxuskonsumption", Ravussin et al, 1985 38 Metabolic response to experimental overfeeding in lean and overweight healthy volunteers, Diaz et al, 1992 39 Weight loss in 108 obese women on a diet supplying 800 kcal/d for 21 d, Webster et al, 1989 40 Body composition, nitrogen metabolism, and energy utilization with feeding of mildly restricted (4.2 MJ/d) and severely restricted (2.1 MJ/d) isonitrogenous diets, Stanko et al, 1992 41 Pathophysiology of the Neuroregulation of Growth Hormone Secretion in Experimental Animals and the Huma, Giustina et al, 1998 42 Chronobiological aspects of weight loss in obesity: effects of different meal timing regimens, Sensi et al, 1989 43 Weight Loss is Greater with Consumption of Large Morning Meals and Fat-Free Mass Is Preserved with Large Evening Meals in Women on a Controlled Weight Reduction Regimen, Keim et al, 1997 44 Topical fat reduction from the waist, Caruso et al, 2007 45 Glycyrrhetinic acid, the active principle of licorice, can reduce the thickness of subcutaneous thigh fat through topical application, Armanini et al, 2005 46 Subcutaneous fat alterations resulting from an upper-body resistance training program, Kostek et al, 2007 47 Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial, Black et al. 2006 48 Metabolic and behavioral effects of a high-sucrose diet during weight loss, Surwit et al, 1997 49 Meta-analysis of resting metabolic rate in formerly obese subjects, Astrup et al, 1999 50 Energy expenditure and free-living physical activity in black and white women: comparison before and after weight loss, Weinsier et al. 2000 51 Resting energy expenditure in reduced-obese subjects in the National Weight Control Registry, wyatt et al, 1999 52 No differences in rates of energy expenditure between post-obese women and their matched, lean controls, de Peuter et al, 1992 53 Total and resting energy expenditure in obese women reduced to ideal body weight, Amatruda et al, 1993 54 Low plasma leptin concentration and low rates of fat oxidation in weight-stable post-obese subjects, Filozof et al 2000 55 Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory, Weinsier et al, 2000 56 Changes in resting energy expenditure after weight loss in obese African American and white women, Foster et al, 1999 57 Energy metabolism in weight-stable postobese individuals, Larson et al, 1995 58 Why do obese patients not lose more weight when treated with low-calorie diets? A mechanistic perspective, Heymsfield, et al, 2007

59 Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial, Heilbronn et al, 2006. 60 Effect of Calorie Restriction on Resting Metabolic Rate and Spontaneous Physical Activity, Martin et al, 2007 61 Metabolic fuel utilisation in obese women before and after weight loss, Burstein et al, 1996 62 Energy expenditure and physical performance in overweight women: response to training with and without caloric restriction, Keim et al, 1990 63 Changes in resting energy expenditure after weight loss in obese African American and white women, Foster et al, 1999 64 Dietary recommendations after weight loss: how to avoid relapse of obesity, James et al, 1997 65 Weight loss and change in resting metabolic rate, Heshka et al, 1990 66 Resting metabolic rates of obese women after rapid weight loss, Welle et al, 1994 67 Underfeeding and body weight regulation in normal-weight young men, Heyman et al, 1992 68 Energy expenditure, fat oxidation, and body weight regulation: a study of metabolic adaptation to long-term weight change, Weyer et al, 2000 69 Long-term changes in energy expenditure and body composition after massive weight loss induced by gastric bypass surgery, Das et al, 2003 70 Factors determining energy expenditure during very-low-calorie diets, Van Gaalf, et al 1992 71 Metabolic and Behavioral Compensations in Response to Caloric Restriction: Implications for the Maintenance of Weight Loss, Redman et al, 2009 72 Diet, exercise, weight loss, and energy expenditure in moderately overweight women, Belko et al, 1987 73 Adaptation of energy metabolism of overweight women to alternating and continuous low energy intake, de Groot et al, 1989 74 Energy metabolism after 2 y of energy restriction: the biosphere 2 experiment, Weyer et al, 2000 75 Rapid weight loss and lean tissue: evidence for comparable body composition and metabolic rate in differing rates of weight loss, Coxon et al, 1989 76 Changes in energy expenditure and substrate oxidation resulting from weight loss in obese men and women: is there an important contribution of leptin, Doucet et al, 2000 77 Greater than predicted decrease in energy expenditure during exercise after body weight loss in obese men, Doucet et al, 2003 78 The effect of a high protein-low calorie diet on the energy expenditure of obese adolescents, Stallings et al, 1992 79 The effect of protein intake on 24-h energy expenditure during energy restriction, Whitehead et al, 1996 80 Maintenance of resting energy expenditure after weight loss in premenopausal women: potential benefits of a high-protein, reduced-calorie diet, Pasiakos et al, 2008 81 Effects of resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body mass and resting metabolic rate, Byrner er al, 1999 82 Exercise-training enhances fat-free mass preservation during diet-induced weight loss : a meta-analytical finding, Ballor et al, 1994 83 Meta-analysis: effect of exercise, with or without dieting, on the body composition of overweight subjects, Garrow et al, 1995 84 Resistance weight training during caloric restriction enhances lean body weight maintenance, Ballor et al, 1988 85 Exercise with or without dietary restriction and obesity treatment, Saris et al, 1995 86 The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss, Stiegler et al, 2006 87 Influence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism, Westerterp et al, 1991 88 Frequency of feeding, weight reduction and energy metabolism, Westerterp et al, 1993 89 Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter, Taylor et al, 2001

90 Effect of the pattern of food intake on human energy metabolism, Westerterp et al, 1993 91 Feeding frequency and energy balance in adult males, Dallosso et al, 1982 92 Effect of isoenergetic intake of three or nine meals on plasma lipoproteins and glucose metabolism, Arnold et al, 1993 93 Increased meal frequency does not promote greater weight loss in subjects who were 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 in humans, Capaldo et al, 1999