The four long-herm Dehydration and water intake were made according RMR and long-term weight management the evolution longg-term each patient through the steps of ketosis as Reduce cravings and overeating visit Lnog-term baselinenormal level of ketone bodies; RMR and long-term weight management C-2, maximum ketosis approximately 1—2 lohg-term of treatment weihht visit C-3, reduction of ketosis because of partial reintroduction of normal nutrition 2—3 months ; visit C-4 at 4 months, no ketosis Additional file 1 : Figure S1 and Fig. The relative good preservation of FFM muscle mass observed with this dietetic approach could be the cause for the absence of metabolic adaptation. Given the differential impact of these components to RMR reduction following weight loss, future research should examine whether the preservation of the tissues or their metabolic activity yields differential results toward RMR reductions and weight maintenance and whether more personalized strategies addressing the specific cause of the RMR reduction may help maximize weight loss and prevent weight regain. Article Google Scholar CALERIE.

RMR and long-term weight management -

RMR-expected refers to the change in energy expenditure explained by changes in free fat mass FFM or muscle mass.

To investigate how much of the mild and non-significant decrease in RMR could be accounted for by FFM change, we used the baseline RMR data to generate an equation for calculating the expected-RMR in accordance with variations in FFM Table 1. The difference between the measured and expected RMR defined the degree of metabolic adaptation.

At visit C-2 maximum ketosis , the measured RMR was At visit C-3, the measured RMR was Finally, at visit C-4, the measured RMR was None of the differences between the measured and expected RMR was statistically different Fig. When, muscle mass evaluated by MF-BiA was employed in the analysis, instead of DXA, results on the expected and observed RMR were similar Table 1 and Fig.

The concern regarding the possible preservation of the RMR as a consequence of the presence of stressing factors induced by the VLCK-diet and the rapid weight loss was focused by a strict analysis of the protein metabolism. Although there were some differences in protein status, renal function and nitrogen balance-related parameters, none of them was considered as clinically relevant Table 2.

It is noteworthy that despite the considerable weight loss induced by the VLCK-diet, there was a positive nitrogen balance throughout the entire study. At visit C-2, the positive nitrogen balance was 1. It was not possible to calculate the nitrogen balance at baseline since the protein intake was not assessed at that visit.

Besides the FFM, that is considered the major contributing factor, several variables have been described as positive determinants of the RMR, including thyroid hormones, catecholamines, leptin and ketone bodies. In this study, the level of influence of these mentioned factors on the measured RMR was determined during the study.

As Fig. Adrenaline and dopamine did not significantly change during the study, but noradrenaline had a progressive decrease in their plasma levels that reached significant differences at visit C Similarly, leptin values were severely reduced at visit 2, 3 and 4 in accordance with the FM reduction.

Thyroid hormones a , Catecholamines b and Leptin c levels during the study. a Changes in Thyroid Hormones; b. Changes in Catecholamines; and c. Changes in Leptin. FT3: free triiodothyronine; FT4: tyroxine. To the best of our knowledge this study is the first assessing the effect of VLCK-diet on the RMR of obese patients.

The main findings of this work were: 1 the rapid and sustained weight reduction induced by the VLCK-diet did not induce the expected drop in RMR, 2 this observation was not due to a sympathetic tone counteraction through the increase of either catecholamines, leptin or thyroid hormones, 3 the most plausible cause of the null reduction of RMR is the preservation of lean mass muscle mass observed with this type of diet.

The greatest challenge in obesity treatment is to avoid weight recovery sometime after the previous reduction. In fact, after one or few years the most obese patients recover or even increase their weight, previously reduced by either, dietetic, pharmacological or behavioral treatments [ 8 ], bariatric surgery being the only likely exception [ 7 ].

Since obesity reduction is accompanied by a slowing of energy expenditure in sedentary individuals, mostly RMR, this fact has been blamed for this negative outcome of the diet-based treatments [ 12 ]. Therefore any RMR reduction after treatment, translates in a large impact on energy balance, making subjects more prone to weight regain over time [ 17 ].

This phenomenon was called metabolic adaptation or adaptive thermogenesis, indicating that RMR is reduced after weight loss, and furthermore that this reduction is usually larger than expected or out of proportion with the decrease in fat or fat free mass [ 2 ].

Therefore, preservation of initial RMR after weight loss could play a critical role in facilitating further weight loss and preventing weight regain in the long-term [ 4 ]. We have observed that the obesity-reduction by a VLCK-diet Pnk method ® was maintained 1 and 2 years after its completion [ 10 , 11 ].

Although that follow up was not long enough, the finding may be of particular importance for long-term effects. The present work shows that in a group of obese patients treated with a VLCK-diet, the RMR was relatively preserved, remaining within the expected limits for the variations in FFM, and avoided the metabolic adaptation phenomenon.

Because FFM includes total body water, bone minerals and protein [ 14 ], the results were corroborated by analyzing the FFM without bone minerals and total body water muscle mass. As the mechanisms supporting the metabolic adaptation phenomenon are not known, unraveling the reasons behind the present findings is challenging enough in itself.

Changes in any circulating hormone that participate in thermogenesis could be the explanation for the absence of a reduction in RMR, for example a concomitant increase in the sympathetic system activity, either directly or indirectly. An increase in thyroid hormones generated by the VLCK-diet was discarded because free T3 experienced the well described reduction after losing weight [ 20 , 24 ] without alterations in free T4 or TSH.

As thermogenesis in humans is largely a function of the sympathetic nervous system activity, and that activity decreases in response to weight loss the results here reported may be the net result of a maintenance or relative increase in the plasma catecholamine levels.

However, it was found that adrenaline and dopamine remained unchanged throughout the study, while noradrenaline decreased considerably discarding their contribution to any increase in the activity of the autonomic nervous system.

Leptin experienced a rapid decline in circulation in situations of weight reduction, although the reduction is observed in energy restriction states it occurs before any change in body weight [ 8 ].

On the other hand, leptin positively has been associated with sympathetic nervous system activity in humans, and weight loss associated changes in RMR and fat oxidation were previously related to leptin levels changes [ 25 ]. If leptin is sensitive to the energy flux and activate the autonomic nervous system, the absence of metabolic adaptation here observed could be due to a leptin increase, or maintenance in the basal levels.

However, in this work, leptin levels decreased in accordance to the weight reduction. Then, an expected increase in thyroid hormones, catecholamines, or leptin levels was discarded as explanation for the observed minor or absent reduction in RMR. This was also endorsed by the undertook multiple regression analysis Table 3.

In this analysis only the FFM DXA or the muscle mass MF-BIA appear as a plausible explanation for the maintenance of RMR activity.

In fact, a clear preservation of FFM was reported in obese subjects on VLCK-diet, in whom 20 kg reduction after 4 months of treatment was accompanied by less than 1 kg of muscle mass lost [ 6 ]. The assumption of muscle mass preservation is also supported by the data on kidney function Table 2 which shows that not only was renal activity not altered as reported in other studies [ 23 ] but that even the nitrogen balance was positive.

The strength of this study is its longitudinal design, which allows the evaluation of the time-course of changes of RMR during a VLCK diet, by comparing each subject to himself, as his own control. The scarce number of subjects and the short duration of this study might be a limitation, since one cannot make claims regarding the RMR status long-term after the completion of the VLCK diet.

However, no significant variations in body weight had been observed after 4 months in previous studies [ 10 , 11 ]. In addition, although participants were instructed to exercise on a regular basis using a formal exercise program, we could not verify adherence to this instruction which precludes determining whether changes in physical activity patterns affected study outcomes.

In the current work a portable device that allows for easier measurement of RMR and with lower cost was employed. This approach may lead to errors when compared with the gold standard, Deltatrac, but it is an easy-to-use metabolic system for determining RMR and VO2 in clinical practice with a better accuracy than predictive eqs.

The Deltatrac device is expensive and requires careful calibration. The Fitmate has been previously validated as a suitable alternative to the traditional indirect calorimetry by both in-house analysis Additional file 1 : Figure S1 , as well as by previous studies.

Despite not measuring CO2 production it is a very convenient in the clinical setting assuming a minimal error of analysis. In summary, this study shows that the treatment of obese patients with a VLCK-diet favors the maintenance of RMR within the expected range for FFM changes and avoids the metabolic adaptation phenomenon.

This finding might explain the long-term positive effects of VLCK-diets on weight loss. Although, the mechanisms by which this effect could be justified are unclear, classical determinants of the energy expenditure, as thyroid hormones, catecholamines as well as leptin were discarded.

The relative good preservation of FFM muscle mass observed with this dietetic approach could be the cause for the absence of metabolic adaptation.

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We acknowledge the PronoKal Group ® for providing the diet for all the patients free of charge and for support of the study. The funding source had no involvement in the study design, recruitment of patients, study interventions, data collection, or interpretation of the results.

The Pronokal personnel IS was involved in the study design and revised the final version of the manuscript, without intervention in the analysis of data, statistical evaluation and final interpretation of the results of this study.

The datasets used during the current study are available from the corresponding author on reasonable request. D G-A, ABC ad FFC designed and performed the experiments, analyzed the data and wrote the manuscript.

AIC, MAM-O, AC, LO-M, IS were responsible of the conduct and monitoring of the nutritional intervention. CG, DB participated in the study design and coordination and helped to draft the manuscript.

FFC supervised the research and reviewed the manuscript throught the study. All authors read and approved the final manuscript. Diego Gomez-Arbelaez, Ana B. Crujeiras, Ana I. Castro, Miguel A. Medical Department Pronokal, Pronokal Group, Barcelona, Spain. Intensive Care Division, Complejo Hospitalario Universitario de Santiago CHUS , Santiago de Compostela, Spain.

Division of Endocrinology, Complejo Hospitalario Universitario de Ferrol and Coruña University, Ferrol, Spain. CIBER de Fisiopatologia de la Obesidad y Nutricion CIBERobn , Instituto Salud Carlos III, Santiago de Compostela, Spain.

Ana B. You can also search for this author in PubMed Google Scholar. Correspondence to Felipe F. DB, ABC and FFC received advisory board fees and or research grants from Pronokal Protein Supplies Spain. IS is Medical Director of Pronokal Spain SL. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figure S1. Nutritional intervention program and schedule of visits. Visit C-4 was performed at the end of the study according to each case, once the patient achieved the target weight or maximum at 4 months of follow-up.

PDF kb. Figure S2. PDF 11 kb. Table S1. Independent effects of fat-free mass, free triiodothyronine, catecholamines, leptin and β-hydroxy-butyrate on resting metabolic rate at each visit.

DOCX 32 kb. Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Gomez-Arbelaez, D. et al. Resting metabolic rate of obese patients under very low calorie ketogenic diet.

A more recent study by the same researcher aims to explain and interpret the findings from The Biggest Loser in light of an energy conservation model.

In what he calls the "constrained model of human energy expenditure," Dr. Kevin Hall theorizes that because the contestants engaged in large, sustained periods of intense physical activity, their metabolisms slowed substantially in order to reduce their metabolic rates and thereby minimize changes in total energy expenditure.

In other words, their bodies made automatic compensatory changes to maintain energy balance. Of particular interest is the fact that at the end of The Biggest Loser competition, the degree of metabolism reduction was not related to contestants' subsequent weight regain, and in fact, the contestants that maintained the greatest weight loss six years after the competition actually had the greatest amount of metabolism adaptation.

This suggests that metabolic adaptation is a response to the change in lifestyle, namely the dramatic increase in physical activity observed in those who maintained the most weight loss. Fortunately for those trying to maintain significant weight loss, the compensatory mechanisms do not completely counteract lifestyle changes, so it is possible to keep off substantial amounts of weight.

Taken together, what we've learned from these studies on The Biggest Loser contestants is that while short-term reductions in resting metabolic rate are related to the extreme calorie restriction at the time of active weight loss, the larger, persistent metabolic adaptation that takes place later is related to substantial sustained increases in physical activity.

Results from the National Weight Control Registry established in to determine characteristics of individuals successful at keeping weight off have long demonstrated that physical activity is a key component of successful weight maintenance.

Wsight details. The resting metabolic Herbal weight loss blend RMR decrease, observed after an obesity Dehydration and water intake therapy is a determinant of managemet short-time weight regain. Thus, the objective of this study was to evaluate changes in RMR, and the associated hormonal alterations in obese patients with a very low-calorie ketogenic VLCK -diet induced severe body weight BW loss. From 20 obese patients who lost Each subject acted as his own control. No metabolic adaptation was observed. Darcy L. Johannsen, Nicolas D. Knuth, Robert Huizenga, Jennifer C. Rood, Fruits to promote healthy digestion Ravussin, Kevin D. An long-twrm goal during weight loss is to Dehydration and water intake manaagement loss while preserving metabolically active fat-free mass FFM. Massive weight loss typically results in substantial loss of FFM potentially slowing metabolic rate. Our objective was to determine whether a weight loss program consisting of diet restriction and vigorous exercise helped to preserve FFM and maintain resting metabolic rate RMR.

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Resting Metabolic Rate