In my last research article review titled “Muscle strength gains during resistance exercise training are attenuated with soy compared with dairy or usual protein intake in older adults – part 1” (see here), no additional benefit for improvements in strength, body composition, physical function, or quality of life when additional protein from either dairy or soy versus usual protein intake were seen after 12 weeks of progressive resistance training exercise in healthy older adults.
The focus of this article – part 2 of this review – is to discuss the findings that suggest that increased soy protein intake attenuated improvements in muscular strength compared to dairy protein and usual protein. I want to explore some of the results of this study that are discordant with the conclusions reached by the authors. Their take-home message I believe is therefore misleading and misrepresents what the study actually showed.
The biggest problem with this is that the vast majority of media (print, TV, social media etc), websites, blogs and other avenues used to report on this study, haven’t taken the time to analyse or assess whether or not the conclusions reached are valid. In fact, when I Googled the net for websites, pages or blogs that wrote about, and reported the results of the study in question, I could not find ONE that had even questioned or scrutinised the conclusion against the actual results produced.
This highlights a bigger issue regarding the veracity of health, exercise, fitness and nutrition news that is reported and shared – following publication – in the blink of an eye. Whilst I do not want to explore this further today, it is certainly something that bothers me and something I would like to write about soon.
Let’s look at some of the issues with the conclusions reached by the authors of this paper.
Problem #1 – One of the main findings claimed to have been shown by this research was that:
Increased soy protein intake attenuated gains in muscle strength during resistance training in older adults compared with increased intake of dairy protein or usual protein intake” (pg. 27).
Now unless you read the whole study and scrutinised the results there would be no way of knowing if this conclusion is well-founded or not; so let’s have a look at the results table to see if this is a fair assessment of their data (click on table to expand).
Strength improvement results for each diet intervention
The first thing you’ll notice is that the only exercise that soy protein attenuated gains in muscle strength was leg press 8RM (RM; maximum weight lifted for eight repetitions); for all other exercises no differences were found for protein source and subsequent strength improvement. More specifically, there were no significant differences between the soy, diary and usual protein group for strength improvement in isometric knee extensor strength, handgrip strength, chest press, knee extension, lat pulldown and leg curl. Thus, strength training adaptation from resistance training in older adults for all exercises, bar one (leg press), was the same irrespective of the protein source provided. The significant difference found therefore for the sum total 8RM lifted for all 8RM exercises was most likely due to the difference in leg press 8RM. (Note: percentage improvement in lat pulldown 8RM was greater in usual protein vs dairy but with no difference vs soy; this doesn’t, however, detract from the core proposal above).
Leg Press for increasing lower body muscle strength
If that is the case, the question that needs to be asked is, why was this ignored and not explored in the discussion? There are certainly some intriguing possibilities regarding this result. Does soy protein, for example, possibly attenutate gains in lower body but not upper body strength? Is there any other explanation for the attenuated strength for Leg press and, if so, would that mean that there are essentially no differences between the source of the protein and the strength improvement? I’m not sure what mechanism of action you would propose to explain a differential for strength gain between lower and upper body when consuming soy versus dairy protein? The authors do hypothesise that the inhibition of strength gain due to soy protein could have been hormonally based by stating:
Instead, it is more likely that the attenuation of the strength increase in the HP-S group was due to some effect of the soy inhibiting the increase in strength. Soy foods not only contain soy protein, but also contain isoflavones, which exhibit estrogenic properties [Barnes 2012]. A recent study demonstrated that 14 days of soy protein supplementation in resistance trained young men during training reduced serum testosterone concentrations in the first 30 min post-exercise compared with whey protein or a carbohydrate control [Kraemer et al. 2013]. It was proposed that this blunted serum testosterone response might reduce the anabolic response in skeletal muscle, thus attenuating the accretion of contractile protein and muscle strength gains. This may explain the attenuated increase in strength gains observed in the HP-S group in the present study (pg. 32).
However, I don’t think that the abovementioned soy-induced reduction in serum testosterone has been shown to affect muscle contractile properties in an appendicular specific manner (i.e. lower body responds differently to upper body). Moreover, in contrast to the authors proposition above, post-exercise testosterone response does not appear to correlate with, nor is it in any way indicative of subsequent strength gains following resistance training as shown, for example, by the work of Morton and colleagues (2016).
Problem #2: Assessing the results listed in table 2 for Leg Press highlights another interesting difference between the soy and dairy protein groups. The baseline strength values for the dairy and usual protein groups are significantly lower than the soy protein group (55.0 vs 77.3 vs 56.6). In fact, the 8RM baseline strength value for the soy protein group is approximately 40% higher than the other protein groups. Such a large difference would have been unexpected following randomisation with most other baseline values relatively comparable. How this difference affected the statistical analysis is difficult to say but I would have liked the authors to discuss this to put such a baseline disparity into perspective.
Given what was discussed in problem number 1, a separate statistical analysis should have been conducted on all 8RM exercises with leg press 8RM excluded. This assessment would have been able to tease out if the attenuated strength gain seen in the leg press also applied to the 4 other exercises. Based on the data for each individual exercise (excluding leg press), no differences were observed; however, there may have been insufficient power to detect any real differences. By grouping these 8RM exercises together this question could have been answered. As it stands, soy-induced strength gain attenuation can only be claimed for the 8RM leg press.
Are functional strength gains limited by machine-based training?
In relation to the training sessions, what is not particularly clear is whether the participants trained one-on-one with their instructor in solitude or whether the sessions involved small groups. It is feasible that if participants trained individually and at the same time but with different instructors, or in small mixed groups, those allocated to the dairy and usual protein experimental diets may have inadvertently or surreptitiously observed what the ‘stronger’ leg press soy participants were lifting and been incentivised to ‘push’ that bit harder in an attempt to bridge the gap.
Final comments: Based on the results of this study, I would have worded the conclusion very differently to that which was put to print by the Thomson et al. Something like the following would have probably been more apt:
Increased soy protein intake appeared to attenuate gains in leg press muscle strength only, compared with increased dairy protein or usual protein intake. With all other exercises there were no notable differences. Further research is required to explore the possibility that soy protein may specifically inhibit lower body strength gains from resistance training in older adults.
Post-script: Following further analysis and publication of part 2 of this blog, I wrote a letter to the Editor of Clinical Nutrition Journal outlining, what I believed, were some of the flaws regarding the interpretation of the results of this trial. Upon peer review this was accepted for publication and can be found here. If you are unable to access this correspondence and the authors reply to my letter, please contact me and I should be able to assist.
References
Barnes S. (2004) Soy isoflavones-phytoestrogens and what else? J Nutr 134:1225S-8S.
Cermak et al. (2012) Protein supplementaiton augments the adaptrive response of skeletal muscle to resistance-type exercise training: a meta-analysis Am J Clin Nutr 96: 1454- 64.
KraemerWJ et al. (2013) The effects of soy and whey protein supplementation on acute hormonal reponses to resistance exercise in men. J Am Coll Nutr 32:66-74.
Morton RW, Oikawa SY, Wavell CG, Mazara N, McGlory C, Quadrilatero J, et al. Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men. J Appl Physiol July 1, 2016;121:129-138.
Thomson et al. (2016) Muscle strength gains during resistance exercise training are attenuated with soy compared with dairy or usual protein intake in older adults: A randomized controlled trial. Clinical Nutrition. 35: 27-33
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
On a global scale, the number of people over 60 yr is expected to more than double from 841 million in 2012 to more than 2 billion by 2050. This change in demographics will have profound implications for many aspects of life (Thomson et al. 2016). Furthermore, Government bodies worldwide will be faced with considerable challenges related to ageing policy and how best to deal with this new reality.
Of the many things that occur during the ageing process one of the most obvious signs is the loss of skeletal muscle mass and strength, with decrements in physical function and potential predisposition to disability. In academic speak, this is known as sarcopenia. The research and interest in this area has been gradually increasing as evidenced by the below graph that shows – since the term sacropenia was first coined in 1989 – a massive increase has occurred. To enhance functional physical capacity and reduce disability into older age, it is therefore critical to develop strategies that facilitate the attenuation of skeletal muscle mass and strength. With more than 30 years of scientific evidence to show that exercise – and, more specifically, resistance training – as both very effective and safe methods to maintain skeletal lean muscle tissue mass and strength (see hereand here), current recommendations strongly advocate this form of exercise for older adults.
Interestingly, gains in skeletal lean muscle tissue and muscular strength may be potentiated through the application of appropriate nutritional strategies and in particular increased protein intake. A recent meta-analysis by Cermak and colleagues (2012) reported ~35% greater enhancement in muscle mass and strength can be achieved in older adults undertaking resistance training who consumed at least 1.2 g/kg of body weight/d of protein through supplementation or diet compared with other control groups that were either non-protein, lower protein diet or exercise training with no nutrition co-intervention. Thus, protein quality or source may further augment the effect of the resistance training stimulus by eliciting a greater stimulatory effect on muscle protein synthesis. Dairy protein compared to soy protein has been shown to be more effacacious post-exercise in stimulating increases in lean mass in young healthy males. In older adults though this response to resistance training and increased protein intake may be blunted which necessitates that higher doses of protein are required to bring about an increase.
The aim of the study under review for this article was to determine whether increased dairy or soy protein intake combined with resistance training improved strength gains in older adults.
Does Soy Protein Suppress Strength Gains?
Researchers recruited one hundred and ninety two older adults (age, 50-79 yr; BMI, 20-35 kg/m²) by public advertisement. Participation was allowed if they were physically active but not engaged in formal exercise. Those that meet the inclusion criteria undertook a resistance training program for 12 weeks. Randomisation to one of three experimental diets was performed:
High dairy protein diet (HP-D)
High non-dairy (soy) protein diet (HPeS)
Usual protein diet (UP).
DIET: Each diet was isocaloric and low-fat (30% fat, <8% saturated fat) and aimed to maintain energy balance. The diets provided ~1 g/kg of body weight/d of dietary protein, mainly from lean meat sources. HP-D including additional dairy protein of ~27 g per day in the form of a shake (475 g Devondale Smart reduced fat milk, 200 g Nestle Soleil diet no fat yoghurt & 20 ml Bickfords vanilla milk mix syrup). The HP-S providing in the form of a shake – 300 g So Good reduced fat soy milk, 100 g Kingland soy yoghurt, 20 g Nature’s Way instant natural protein powder & 15 g poly-joule – which added an extra ~27 g of soy protein. Protein intake was distribtuted evenly across the day with the three main meals providing >20 g per feed; this is consistent with best practice for optimising muscle protein synthesis in older adults. Following resistance training sessions participants consumed the appropriate additional foods immediately after training and that represented the main meal of that day. Participants were supplied with key foods specific to their allocated diet for the duration of the study to facilitate adherence. Energy and macronutrient intakes from daily food checklists were analysed to monitor food intake and dietary compliance.
Resistance training: a key component of healthy ageing?
RESISTANCE TRAINING: All subjects participated in a whole body resistance training program three days per week on non-consecutive days for 12 weeks and the principles of progressive overload were applied. Five exercises on weight stack pin loaded machines were performed: leg press, chest press, knee extension, lat pull down and leg curl, and seated bent knee hip flexions. Trainees started with one set x 8 repetition maximum (RM; maximum weight lifted for eight repetitions), this was maintained until individuals could perform three sets of 12 repetitions and then the load was increased. This cycle was repeated again for the duration of the trial. Assessment of muscle strength, body composition, physical function and quality of life was conducted at baseline and 12 weeks. All exercise training was completed in the research gymnasium at the University of South Australia under the supervision of gymnasium staff.
Assessment of muscle strength using handgrip, isokinetic dynamometry and 8RM was completed. The leg press, chest press, knee extension, lat pull down and leg curl were tested with 8RM and a summed total 8RM for all exercises was recorded Dominant handgrip strength was measured using hydraulic handgrip dynamometer and isometric strength of the knee extensor muscles of the right leg was assessed using an isokinetic dynamometer.
You don’t have to lift weights to do resistance training
RESULTS: 83 participants completed the intervention being adherent to both diet and resistance training protocols. HP-D and HP-S had higher protein intakes compared with UP (HP-D 1.41 ± 0.14 g/kg/d, HP-S 1.42 ± 0.61 g/kg/d, UP 1.10 ± 0.10 g/kg/d; P < 0.001 treatment effect). Baseline characteristics, compliance with the intakes of the additional protein foods and adherence to the resistance training program in those that meet all relevant study protocols was not different between groups.
Increase in muscular strength as ascertained by total 8RM was significantly less in HP-S compared with HP-D and UP (HP-D 92.1 ± 40.8%, HP-S 63.0 ± 23.8%,UP 92.3 ± 35.4%; P=0.002 treatment effect). 8RM percent improvement in leg press was much greater in HP-D and UP compared with HP-S (HP-D, 136.8 ± 88.2%; HP-S, 64.8 ± 35.2%; UP, 135.0 ± 62.0%; P < 0.001). For most other exercises, 8RM was not signficantly different for each diet group. Total training volume over the 12 weeks was not different between groups.
Weight, waist circumference and total body fat decreased and lean mass and the distance covered during the 6 min walk test increased significantly increased with no difference between diets. As expected absolute protein intake (g) and relative protein intake (per kg body weight) were different with HP-D and HP-S greater than UP. Dairy protein in HP-D was significantly greater compared with both HP-S and UP with the amount of non-dairy protein in HP-S significantly greater compared with both HP-D and UP.
DISCUSSION: This study has demonstrated that 12 weeks of progressive resistance training exercise in healthy older adults did not provide any additional benefit for improvements in strength, body composition, physical function, or quality of life when additional protein from either dairy or soy is compared to usual (lower) protein intake. Perhaps of more significant interest is that results suggested that increased soy protein intake attenuated improvements in muscular strength. I am going to publish this article before it is entirely finished as I believe this is important research for those interested in this area and facilitating discussion on this topic should start now.
Stay strong and prosper
Over the next week or so I will be posting a part 2 in relation to this study as there is a lot more to explore. For example, why did the authors fail to acknowledge or discuss the fact that the attentuated strength improvement in the HP-S was confined exclusively to the leg press exercise? For all other exercises, no difference for dietary influence on strength improvement was found. Whilst not a criticism, it seems rather odd that whey protein was not included as one of the intervention dietary arms of the study. The evidence for whey protein augmenting the development of strength and facilitating the accretion of lean muscle mass from resistance training is well documented. Comparing this with the other diets would have provided some interesting insights into whether there are any further benefits of whey protein to older adults. Finally, one thing that does disappoint me about many of the studies that investigate the efficacy and safety of resistance training in older adults is the reliance on exercises that are machine-based.
CONCLUSION: Increased soy protein intake attenuated gains in muscle strength during resistance training in older adults compared with increased intake of dairy protein or usual protein intake.
Look out for part 2 (see here) titled “Does Soy Protein Really Inhibit Resistance Training Induced Strength Gains In Older Adults?” where I will discuss some of the things I mentioned above in more depth and some possible mechanisms of action as to why soy protein may or may not suppress strength gains from resistance training.
Post-script: Following further analysis and publication of part 2 of this blog, I wrote a letter to the Editor of Clinical Nutrition Journal outlining some of the, what I believed, flaws regarding the interpretation of the results of this trial. Upon peer review this was accepted for publication and can be found here. If you are unable to access this correspondence and the authors reply to my letter, please contact me and I should be able to assist.
References
Cermak et al. (2012) Protein supplementaiton augments the adaptrive response of skeletal muscle to resistance-type exercise training: a meta-analysis Am J Clin Nutr 96: 1454- 64.
Thomson et al. (2016) Muscle strength gains during resistance exercise training are attenuated with soy compared with dairy or usual protein intake in older adults: A randomized controlled trial. Clinical Nutrition. 35: 27-33
Wilson, SA (2016) Comment on: Muscle strength gains during resistance exercise training are attenuated with soy compared with dairy or usual protein intake in older adults: A randomized controlled trial. Clinical Nutrition. 35(6):1575-1576
Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
Published in the American Journal of Clinical Nutrition, researchers Dr Thomas Longland and co. showed that during marked energy deficit a diet higher in protein was more effective in promoting increases in lean body mass (muscle) and losses of fat mass when combined with a high volume of resistance training (weights) and anaerobic exercise (sprints).
Protein requirements are increased during intense exercise training
When attempting to decrease body fat through intense exercise and an energy deficit diet, ensure you consume high protein foods (i.e eggs, fish, meat, WPC etc) regularly across the day to maintain a steady supply of amino acids to help facilitate muscle recovery and adaptation. This study provides further confirmation of the importance of adequate protein to support muscle protein synthesis.
This is particularly important in older adults with the latest review of the evidence (discussed here) showing that maximising skeletal muscle protein synthesis rates during recovery from resistance training exercise in younger adults being different to older adults. The ingestion of ∼20 g of protein or ∼0.25 g protein/kilogram bodyweight appears to be sufficient. Older adults, on the other hand, demonstrate a blunted post-prandial muscle protein synthetic response. Older adults as opposed to younger adults therefore require higher amounts of protein during recovery from resistance training exercise to optimally stimulate muscle protein synthesis. Intakes even up to ∼40 g appear necessary. Currently, no consensus exists regarding the amount of protein required to maximally stimulate skeletal muscle protein synthesis rates during recovery from resistance training exercise in older adults.
Further comments:
Interestingly, one of the key takeouts of this study is that an energy deficit diet was utilised to elicit fat mass loss. It is very important to acknowledge that the research conducted over the last 8 decades has conclusively demonstrated that weight or fat loss will only occur if this fundamental physiological requirement is met. For an extensive discussion of this research and what the metabolic-unit based weight loss studies reveal see here.
No caloric deficit = no fat loss
Therefore, don’t believe the hype. Food quality is a an absolute must and essential to good health. However, weight or fat loss will not be realised no matter how good your diet is unless an energy deficit exists. Increased total physical activity during all waking hours and an energy-deficit diet that is wholesome, natural, minimally-processed and nutrient-dense will provide a significant opportunity for weight loss to be achieved.
Lastly, there are a number of studies and anecdotal evidence that show a significant proportion of exercisers eating an ad libitum diet – possibly as high as 50% – do not achieve the weight loss expected with as much as 15% actually gaining weight. These individuals are often referred to as ‘non–responders‘. Those on the other hand that do achieve weight loss from exercise are referred to as ‘responders‘. The question is, how is this possible and are there any practical solutions? Please see herefor more on the compensatory mechanisms that some suffer from that can thwart the success of an exercise program and some of things that can be done to combat this resistance to fat loss.
Reference: Longland, T.M. et al (2016) Higher compared with lower dietary protein during an energy deficit combined with intense exercise promotes greater lean mass gain and fat mass loss: a randomized trial. The American Journal of Clinical Nutrition (link to reference see here)
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Disclaimer: All contents of the FitGreyStrong website/blog are provided for information and education purposes only. Those interested in making changes to their exercise, lifestyle, dietary, supplement or medication regimens should consult a relevantly qualified and competent health care professional. Those who decide to apply or implement any of the information, advice, and/or recommendations on this website do so knowingly and at their own risk. The owner and any contributors to this site accept no responsibility or liability whatsoever for any harm caused, real or imagined, from the use or distribution of information found at FitGreyStrong. Please leave this site immediately if you, the reader, find any of these conditions not acceptable.
In part 1 of “The Ebbeling vs. Hall trials: Re-visiting How Diet Affect Energy Expenditure & Weight Loss” I argued that the conclusions made by authors of the Ebbeling trial – where it was purported that a very low carbohydrate diet significantly mitigated the reduction in energy expenditure subsequent to weight loss compared to diets higher in carbohydrates – were flawed. As stated previously: “The variability in the individual data for diet type and their effect on energy expenditure is discordant to that of the pooled data thus invalidating the generalisability of the results. To truly make the claim that a novel bio-effect exists for a particular diet type, a consistent, reliable pattern of response should be reproducible in a majority of people.”
In part 2 I want to take a closer look at the results of the study headed up by Dr Hall titled: “Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men” that was published in the American Journal of Clinical Nutrition. This study was designed to test the merits of the carbohydrate-insulin model of obesity. As mentioned in part 1, a number of unique claims that underpin this model are made by those advocating very low carbohydrate (VLC) diets. Firstly, that by decreasing the proportion of carbohydrate in the diet a concomitant reduction of insulinemia will ensue, and in so doing, cause increased fat mobilisation from the adipose tissue thus causing a greater oxidation of circulating free fatty acids (FFAs). Insulin is viewed in this context as the ‘gate-keeper’ of whether fat is partitioned toward storage (higher insulin) or mobilised and oxidised for energy metabolism (lower insulin). Secondly, as a consequence of reduced insulin secretion and increased availability of FFAs for use by metabolically active tissue, VLC or ketogenic diets will disproportionately increase energy expenditure compared to isoenergetically-matched higher/high carbohydrate (HC) diets. Thirdly, it is concluded that ‘a calorie is not a calorie’ therefore, because energy expenditure and body fat metabolism will be impacted differentially and advantageously by exchanging an isoenergetic amount of dietary carbohydrate for fat.
Hall and 10 of his colleagues (see page title below) essentially concluded that a VLC diet was no more effective compared to a HC diet for reducing body fat. Small increases were detected in energy expenditure for the VLC diet but this was dismissed as clinically irrelevant. The publication of these findings were greeted with an incredible range of reactions ranging from the “I-told-you-so” piece by Anthony Colpo, the excellent analysis by Stephan Guyenet, to the cringe worthy blog of Jason Fung. Indeed, many noses were put out of joint and so dismayed were some, that the rebuttals transcended professional criticism with personal attacks and slurs directed at Kevin Hall himself. What I find most perplexing about this whole thing is that the results of Hall’s trial are some of the most damaging findings to date and provide no support for the carbohydrate-insulin model of obesity.
The results of this study were presented by Kevin Hall at the 2016 World Obesity Federation meeting. He was interviewed during this conference by Yoni Freedhoff (see @YoniFreedhoff on Twitter), a Medical Practitioner and Obesity Specialist from Canada and this was uploaded to YouTube. To cut a long story short, when questioned about his study, Hall claimed that the carbohydrate-insulin theory of obesity had been debunked, with no substantial differences in fat loss between a VLC or HC diet. And whilst energy expenditure had initially increased on the VLC diet, it was a transient change that subsequently decreased linearly over time amounting to nothing clinically relevant (see the interview below).
Following upload of this video to YouTube the Internet went into meltdown with Twitter specifically ablaze with discussion and fierce debate about what it was exactly that Kevin Hall’s study had actually demonstrated – here is just one example of the fascinating discussionthat occurred on Twitter following publication of this trial. There was little to go on apart from the above video, some commentary, some graphs and the poster of the study.
First off the ranks to take aim at this study was Dr Michael Eades, author of Protein Power and his blog of the same name. Eades was applauded far and wide by many on social media as debunking the debunker. After reading his blog, though, it was apparent that there were several flaws in his logic and I subsequently made these comments. My key concerns were, firstly, that there was no effort to appropriately explain why there was no relationship found between the rate of fat loss and 24-hour C-peptide levels (insulin), given that the carbohydrate-insulin model of obesity predicates that lipolysis is inversely proportionately to insulin production and therefore as insulin levels decrease, fat loss should increase. Secondly, there was no acknowledgment that total daily energy expenditure (EE) actually returned back to baseline over the duration of the VLC diet, even though insulin levels remained consistently depressed for the entire VLC diet phase. Given that insulin levels decreased and remained as such following the switch from the HC to VLC diet, it is completely reasonable to expect that EE would remain consistently elevated too if the carbohydrate-insulin model is sound. This simply did not happen and both these findings are monumentally difficult to account for as they completely contradict what would be predicted and expected to occur based on this model.
I had intended, in this blog, to explore and make further comment on some more of the reactions following full publication of this trial, but you’ll have to wait until part 3 of this series as I have decided to dedicate a whole article to that as there is a lot to comment on.
Results published
The paperwas finally published ahead of print July 6th 2016. Kevin Hall’s research group in summary took 17 overweight or obese men and confined them to metabolic wards where they consumed a HC (also high in sugar) for a 28 day run-in period followed by an isoenergetic VLC diet for an additional 28 days. All foods and beverages were provided to the participants and food outside of that on the menu plans was prohibited (this was strictly enforced). Dietary protein was clamped at approximately 16% for the entire duration of the study for both phases. The diets were structured with the intention that energy balance was achieved with sufficient energy intake to maintain participant’s body weight. Daily diet composition of the 7-day, 2400 kcal rotating menus for the VLC and HC diets is shown below.
Subjects were prescribed 90 min (3 x 30 mins blocks) of daily stationary cycling at a clamped intensity. The intensity of the cycling exercise was determined during the third screening visit. Two 30 minute bouts of stationary bicycling at a fixed speed and resistance with a HR greater than 0.3×(220-age-HRrest)+HRrest but not exceeding 0.6×(220-age-HRrest)+HRrest and no signs of arrhythmia. The initial speed and intensity was set to that of the second screening visit and adjusted to stay within target HR during the second 30 minute bout of cycling. The speed and intensity of the stationary cycling determined during the third screening visit was to be repeated on days of scheduled cycling exercise during the inpatient visit to total 90 minutes per day. Overall physical activity was quantified with small, portable, pager-type accelerometers.
Two consecutive days each week were spent residing in metabolic chambers to measure total daily energy expenditure, respiratory quotient and sleeping energy expenditure (SEE). Body composition was assessed by dual-energy X-ray absorptiometry (DXA) and the average EE during the last 2 weeks of each diet was assessed by the doubly-labeled water (DLW) technique.
Overview of Study Design
Other parameters assessed were daily respiratory quotient (24-h RQ), energy cost of cycling exercise at a clamped intensity (EEexercise), energy expenditure when not moving (EEsedentary), physical activity expenditure on days inside the chamber (PAEchamber), physical activity expenditure on days outside the chamber (PAEnonchamber), spontaneous physical activity inside the metabolic chamber (SPA). Relevant blood and urinary biomarkers measured included insulin, C-peptide, urea, ammonia, creatinine, thyroid hormones, nitrogen, ketones, adrenalin and norepinephrine. The daily diet composition is outlined below.
Primary endpoints were changes in EE (total and sleeping) and 24-hr respiratory quotient, and secondary endpoint was changes in body composition.
The key findings of this study in relation to the primary and secondary endpoints were:
EE during the VLC phase was 57 ± 13 kcal/d greater than during the HC period.
Adjusting total EE data for body composition changes resulted in the VLC diet period having 96 ± 12 kcal/d greater expenditure than the HC diet period.
SEE during the VLC phase was 89 ± 14 kcal/d greater than during the HC period.
Adjusting SEE for body composition changes resulted in the VLC diet period having 121 ± 13 kcal/d greater expenditure than the HC diet period.
There was a significant linear decrease over time in EE and SEE following the initial increases outlined above and this occurred irrespective following adjustment for changes in body weight and body composition.
The VLC diet resulted in a slowing or blunting of fat loss versus the HC diet (-0.5 kg in 28 days for VLC vs. -0.5 kg in 14 days for HC).
Following transition to the VLC diet, the loss of fat mass in the subsequent 14 days was not statistically significant.
Respiratory quotient (24-h RQ) decreased significantly from approximately 0.88 during the HC period to 0.78 at the start of the VLC period and remained approximately constant until the end of the study, indicating a rapid and persistent increase in fat oxidation.
Comments and Analysis
It is important at this juncture to state the obvious here but which ironically seems to have been missed by those that have cast aspersions on Kevin Hall. This study was intended to answer the questions as to whether the lowering of insulin levels via an isoenergetic dietary exchange from HC to VLC, translated into: 1) A disproportionate increase in EE and; 2) Greater loss of body fat. From what I can gather his recent work has aimed to uncover the perennial and mechanistic question of whether greater energy expenditure and fat loss can be achieved by altering the proportion of carbohydrates in isoenergtically macronutrient manipulated protein-clamped diets. These are important questions to answer because increased EE and body fat loss – simply induced by decreasing the proportion of carbohydrates for a given isocaloric diet – would have major implications in the treatment of obesity. As such, energy intake and protein were clamped so that the effect of dietary carbohydrate restriction could be isolated as the independent variable with EE and fat loss dependent variables.
This study was not, however, designed to answer the questions as to whether dietary carbohydrate restriction decreases ad libitum energy intake through enhanced appetite satiety – which could account for the efficacy of VLC diets in altering body composition – or whether such restriction generates greater improvements in metabolic health in those suffering from obesity or disorders such as type-2 diabetes. Those claiming, then, that Hall and co are misrepresenting, misconstruing or ‘spinning’ the data of this study – to either “protect one’s reputation”, or perpetuate some sort of “government and industry conspiracy” to maintain the “high carbohydrate diet status quo” and thereby place “people’s health and wellbeing at risk” – are preposterous and offensive. I see no evidence whatsoever that Hall et al. are advocating high sugar, high carbohydrate diets for those suffering from obesity and other metabolic disorders or conditions.
Energy Expenditure
At face value and in support of the argument that VLC diets provide a “metabolic advantage”, adjusting total EE data for body composition changes resulted in the VLC diet period having 96±12 kcal/d greater expenditure than the HC diet period. If we base our conclusions on this figure alone, we should be able to say that this study supports the existence of a “metabolic advantage” that could potentially be harnessed to facilitate obesity treatment. And this is precisely what was latched on to by the VLC diet advocates. In my opinion, however, this does not adequately contextualise the temporality of the EE data and, as such, obfuscates a more nuanced interpretation of what the results show. Let’s take a look at figure 3A and 3B from the trial that track both EE and SEE.
Changes In Total Daily EE and SEE
If you eyeball and track EE/day over time in figure 3A, the trajectory of decline from ∼day 10 to endpoint, is ∼100 kcal/day to ∼20 kcal/day, respectively. For figure 3B, the decline is even greater. SEE peaks at ∼200 kcal/day around day 4 and tanks, decreasing to ∼20 kcal/day by endpoint. Therefore, in support of the argument against any sort of “metabolic advantage” of VLC diets, this waning of total EE clearly shows that no clinical difference exists given that:
By ∼day 12 and thereafter EE and SEE for the VLC diet are not statistically significant versus the HC diet.
95% confidence interval for the VLC diet by ∼day 18 contains zero with no statistically significant difference for EE or SEE.
Thus, we should accept the null hypothesis as there is no difference between the HC and VLC diets.
The trajectory of EE and SEE in the VLC diet and waning and return back to baseline demonstrates that these metabolic changes were acute and transient. Whilst I do not want to speculate as to the reasons why, it is fascinating that these findings – that are as clear as the light of day – were either ignored, dismissed or not understood by those endorsing the idea that VLC diets provide a “metabolic advantage”. Interestingly, Hall’s is not the only study to show the phenomena of “adaptive” thermogenesis, as discussed by the POUNDS lost study, where resting energy expenditure (REE) is indeed adaptive over time. Both body weight and REE decreased by 6 months, but were unaffected by diet composition.
Lastly, body composition-adjusted EE would have been overestimated given that such adjustment was not able to discern that much of the weight reduction following transition to the VLC diet came from water losses and not metabolically active tissues. In short term studies investigating VLC diets you will see larger initial decreases in body weight compared to diets higher in carbohydrates due to potassium deficits and the reduction of muscle (water-laden) glycogen as described by Kreitzman et al (1992). The additional data below showing an initial increase in protein utilisation and metabolism, and concomitant blunting in fat loss provides further support for this.
Hall’s data, therefore, strongly indicates that there is no chronic, persistent and clinically relevant elevation of EE and SEE with VLC diets when compared to isocaloric HC diets. As discussed by Hall and co, other controlled, inpatient isocaloric feeding studieswhere dietary protein is held steady, demonstrate that varying carbohydrates from 20% to 75% of total calories found either small decreases in EE or no significant differences with carbohydrate restriction. Taken together, it would appear that dietary carbohydrate restriction as low as 20% fails to elicit any noteworthy changes in EE, but further restriction to a level where carbohydrates supply 5% of total calories results in slight but transient increases in EE and SEE. It should be acknowledged that the study authors anticipated this slight (initial) increase and the results confirm their mathematical model simulations. Such increases seem to be part of an “adaptive” thermogenic response where an increased shift toward ketogenesis is required, but which probably subsides once gluconeogenesis declines following the brain’s shift away from glucose toward ketone oxidation.
Body Weight Changes Over The Study Period
Body Composition
Unintentional weight and fat loss occurred throughout the study and indicated an overall state of negative energy balance. Negative energy balance during the last 2 weeks of the HC and VLC diet periods were not significantly different whether assessed by the measured DXA body composition changes or by calculating energy intake minus expenditure as measured by DLW. However, following transition to the VLC diet, fat loss actually slowed (see below). Moreover, 95% confidence intervals (day 28 of the VLC diet) lends support to this, with the lower range of the interval for body fat loss encroaching upon zero.
Fat Mass Change Over The Study Period
Even if we grant that most of this slowing in fat loss was confined to the first 15 days following transition to the VLC diet, the rate of loss from days 15-30 remained constrained in comparison to that seen in the HC diet (VLC -0.3 kg vs HC -0.5 kg). This occurred despite daily fat oxidation adapting completely within the first week of the VLC diet, as shown by the rapid and sustained maximal drop in respiratory quotient seen by day 4 (depicted in figure 3C below). Such data illustrates that daily fat oxidation adapts very quickly and completely when dietary carbohydrates are dramatically reduced. Indeed, this challenges the argument that many weeks are required to become “fat adapted”. Furthermore, it dispels any notion that fat loss was reduced due to partial fat adaptation. At least from a metabolic perspective, maximal fat oxidation and adaptation occurs quite rapidly. At this stage, I have seen no evidence either to support the idea that if a longer period of time (on a VLC diet) was provided, fat oxidation efficiency would have been further augmented with increased body fat loss.
Respiratory Quotient
Based on the data at hand one could argue the opposite to that proposed by the carbohydrate-insulin model of obesity, with very low insulin levels actually blunting the rate of fat loss. Certainly in the short term at least, the rate of proteolysis was up-regulated as demonstrated by the increase in nitrogen excretion following transition to the VLC diet. Consequently, energy metabolism of participants on the VLC diet required an increased reliance and utilisation of protein from lean body mass to meet energy needs. Over the long-term, negative nitrogen balance and increased catabolism of lean body mass is undesirable but fortunately this change only subsisted until day 11. In spite of this, the blunted rate of fat loss persisted from this point to the end of the study as demonstrated by the DXA results. The nitrogen excretion, RQ, 24-hr C-peptide and DXA data support that the rate of fat loss observed was as good as things were going to get.
Notwithstanding the recent publication and thought provoking work of Professor James Johnson and co (using rodent models and experiments) that proposes a direct causal role for hyperinsulinemia in obesity, results of human studies are less convincing and not conclusive. The current study under review is a case in point, given that the dietary modulation and significant/persistent reduction of insulin did not translate into greater fat loss as would be anticipated if causality was prominent. This is a particularly incongruous outcome that contradicts and questions the fundamental underpinning of the carbohydrate-insulin model of obesity, given that insulin levels did not apparently affect, or were correlated to, the rate of fat loss.
Adipose cell size changes and regional fat deposition as predictors of metabolic response to overfeeding in insulin-resistant and insulin-sensitive overweight/obese human subjects in the McLaughlin et al. (2016) study, also reported results which were opposite to that expected by the researchers. Interestingly, insulin-resistant subjects showed, as would be expected, significantly greater hyperinsulinemia at baseline and at peak weight following the intervention, but surprisingly tolerated and responded better to overfeeding than did insulin-sensitive subjects. The authors state:
In contrast to our hypothesis that IS subjects would demonstrate adaptive adipose tissue and metabolic responses to weight gain, we found the opposite: IS subjects exhibited maladaptive adipose tissue responses and developed clinically significant insulin resistance. Adipose mass expanded in the visceral and intrahepatic depots, and adipose cell hypertrophy was evident. FFA concentrations under steady-state insulin conditions increased by 133%, indicating resistance to insulin suppression of lipolysis, whereas AUC FFA concentrations after a standardized test meal were not increased, likely due to concomitant increases in the insulin AUC. Muscle insulin resistance, as measured by SSPG, worsened by 45% in the IS group compared with 8% in the IR group with similar weight gain. Interestingly, the magnitude of change in all of these variables, including VAT, IHL, adipose cell peak diameter, and insulin suppression of lipolysis, significantly predicted the degree to which SSPG worsened. Further, these associations were independent of weight gain per se, implying that differential cellular and regional fat distribution patterns of adipose tissue may contribute to the metabolic heterogeneity of obesity.
The results of the abovementioned studies and other human trials show, as stated by Hall and co in their study, that “it is clear that regulation of adipose tissue fat storage is multifaceted and that insulin does not always play a predominant role.” Results like these raise another very pertinent question. Just how relevant are experiments in rodents and their related models of disease, when the results of human research is discordant to their postulations?
24-hr C-peptide
Now to the crux of the matter.
The body composition results of the Hall study confirm and add to over 80 years of scientific research that conclusively demonstrates that when it comes to weight or fat loss, the laws of energy balance hold true. Since the early 20th century at least 30 tightly controlled metabolic ward studies have been conducted and they resoundingly find the same thing. Regardless of one’s age, race or gender, for an increase or decrease in body fat to occur, a commensurate positive or negative energy imbalance, respectively, must exist. Whilst there may be some advantage of higher protein diets preserving or increasing LBM (see here, hereand herefor example) and insulin resistance status possibly influencing response to different diets (see hereand herefor example), fat loss achieved by manipulating the proportion of energy derived from carbohydrates and fat in isocaloric diets, is not significantly different.
An assessment of the research where study participants are confined to an in-patient metabolic unit/ward/chamber are the most accurate way to scientifically determine the specific energy requirements needed for weight change. Such studies are expensive because they are very resource and equipment intensive. However, what they allow researchers to do is measure what is being consumed (energy in) and what is being expended (energy out) quite precisely – or at least, a lot more precisely than studies that involve free-living subjects.
The methodology of such studies looks something like this. For the duration of these trials subjects’ have to remain in the hospital or unit and in some cases, spend time in metabolic chambers. Participants are allocated and given all consumables (food and drink) for the duration of the intervention. The caloric content of what is consumed is a known entity and has been prepared and accurately measured. The macronutrient percentages of the diet for protein, carbohydrates and fat has been determined. Physical activity is closely monitored, measured and accounted for. Resting EE and total daily EE is measured as accurately as possible based on the equipment available and methods employed in the study.
With energy intake (EI) and energy expenditure (EE) measured as close to actual as possible, investigators can now establish whether firstly, the prerequisite for weight or fat loss is an energy deficit, and secondly, if macronutrient composition exerts differential effects on such loss. Evaluation of such research has shown that no major differences have been found for weight or fat loss when macronutrient diverse isoenergetic diets are compared. Results from these studies show beyond dispute that the fundamental determinant for decreased weight is a caloric or energy deficit, not diet composition. To look at the evidence another way, not one of these trials – not even one – has ever been able to demonstrate a decrease in weight (excluding loss of water weight) or body fat when daily EE is less than daily EI. This remains so irrespective of the macronutrient breakdown. If a “metabolic advantage” of VLC diets truly existed, researchers should be able to show under tightly-controlled metabolic unit/chamber conditions, decreases in fat mass when changing from a isocaloric HC weight maintenance diet to a isocaloric-matched VLC diet (Hall’s study attempted to do this but the unintentional weight and fat loss slightly altered the course of the study). Obviously, such a dietary change will yield decreases in weight due to changes in water balance as described above (see Kreitzman et al (1992) & Yang and Van Itallie (1976)), but there has never been any methodologically sound and robust published research (under ward conditions) to show that greater fat loss is facilitated by isoenergetically swapping out carbohydrate for dietary fat.
Below is a small selection of these metabolic ward-based studies and their key findings to illustrate the aforementioned.
Keeton & Bone (1935) – No difference in weight loss diets low in calories containing varying amounts of protein.
Werner et al. (1955) – No difference in weight loss for the low-carbohydrate, high fat diet versus high-carbohydrate diet.
Yang and Van Itallie (1976) – No difference in fat loss for an 800 kcal/day ketogenic versus non-ketogenic diet. The authors state: “Rate of fat loss was a function of degree of energy deficit.”
Leibel et al. (1992) – No difference in body weight or stability during very wide variations in the fat-to-carbohydrate ratio (fat energy varied from 0% to 70% of total intake) with no significant variation in energy need. Sixteen human subjects were confined to a metabolic ward for an average of 33 days and fed precisely known liquid diets with protein derived from milk, carbohydrate as cerelose and fat from corn oil.
Golay et al. (1996) – No difference after 6 weeks for weight loss, fat loss or waist-to-hip circumference. This study compared diets equally low in energy (1000 kcal) but widely different in relative amounts of fat and carbohydrates on body weight reduction in 43 obese adults during a 6-week period of hospitalisation. The diets were composed of 32% protein, 15% carbohydrate and 53% fat versus 29% protein, 45% carbohydrate and 26% fat.
Stimson et al. (2007) – No difference in fat loss for the isocaloric phase of the study period.
Graves et al. (2013) – No difference in BMI or weight reduction for the 3-week inpatient period for each diet (or for the 48-week outpatient treatment).
Hall et al. (2016) – No difference for body fat loss for the VLC versus HC diet.
There are many other such studies but the overall findings tell the same story, which is that the fundamental arbiter of weight or fat loss is the existence of an energy imbalance where total daily EE exceeds EI. One of the largest meta-analyses and systematic reviews available, the massive 2014 review by Naude and colleagues titled “Low Carbohydrate versus Isoenergetic Balanced Diets for Reducing Weight and Cardiovascular Risk: A Systematic Review and Meta-Analysis”, assessed as many as 228 studies including those with free-living subjects. The authors reached the same conclusion and stated:
The similar reported mean energy intakes in the low CHO and balanced diet groups and the corresponding similar average weight loss in the diet groups supports the fundamental physiologic principle of energy balance, namely that a sustained energy deficit results in weight loss regardless of macronutrient composition of the diet.
So let me put some social media context on this. The next time someone makes the claim that “calories don’t matter” or “the concept of energy balance has been debunked” or “has no scientific basis”, ask them why the most controlled, rigorous and accurate methods used by researchers has repeatedly proven the concept to be valid and hold true over the last 80 years or so.
Before I finish up this section I need to make some clarifying comments.
There will be those that read this and conclude that what I am suggesting or all that I think matters is calories, with diet quality just a cursory concern. I can hear some of you saying right now “….but surely 2500 calories of jelly beans or junk food is different to 2500 calories of atlantic salmon, walnuts, broccoli and berries.” Really? Well, yes, of course it is, thanks for pointing that out. A diet consisting of wholesome, natural, minimally processed and nutrient-dense foods is paramount to ensuring good health. I should state now that I am not suggesting for one moment that the quality of the diet is not important. Irrespective of how good a diet is, the fact remains nonetheless that it is still possible to gain weight eating a wholesome, natural, minimally processed and nutrient-dense diet. It is probably much more difficult to do so, but regardless, you cannot escape the fact that you have to be in a consistent calorie deficit to lose fat or a chronic caloric surplus to gain fat.
With all of the above being said I remain of the firm belief that further research is warranted. Among many issues that remain outstanding and require elucidation, I am particularly interested in seeing more research on such things as:
Does altering the macronutrient composition of the diet (fat for carbs) elicit an inequivalent effect on appetite satiety with an inadvertent spontaneous reduction in food intake? There is certainly some evidence to support this.
Does swapping out carbohydrate for increased dietary fat provide benefit to those with metabolic abnormalities such as insulin resistance and type-II diabetes? Once again, there is evidence to support this also.
The only thing I will say about these questions is that the published research is somewhat mixed. Three meta-analyses and systematic reviews do not concur on whether metabolic outcomes are affected by manipulating the macronutrient composition of the diet. Naude et al. (2014) and Boaz et al. (2015)concluded that there were no differences on metabolic outcomes when the protein, carbohydrate and fat composition of the diet was varied. In contrast, Schwingshackl and Hoffman (2014) suggested the opposite stating that dietary manipulation in favour of increased fat did alter metabolic outcomes. More work is obviously required but I suspect that diet quality is going to have a significant role to play based on the findings of Veum et al. (2016) where consuming energy primarily as carbohydrate or fat for 3 months did not differentially influence visceral fat and metabolic syndrome in a low-processed, lower-glycemic dietary context.
Finally, I would like to suggest that what we cannot and should not invest anymore time or money researching or debating, is whether or not the energy balance model holds true. Based on our best science suggesting otherwise is moot. The jury is in. We can debate, argue and disagree about the ‘why’ in relation to the growing rates of obesity but not the ‘how’. In the words of Stephan Guyenet, “….the evidence suggests a simpler and more compelling explanation: We eat too much food that is obviously unhealthy, and it’s not because researchers or the government told us to, but because we like it.”
Spontaneous Physical Activity
The inclusion of the low intensity cycling was an interesting component of the Hall study which was prescribed, as explained in correspondence to me, to prevent the usual decrease in physical activity that occurs when people spend many days as inpatients on a metabolic ward. The data supports that this was achieved. In fact the physical activity levels and energy expenditure recorded for this metabolic ward study (inside and outside the chamber) are quite impressive. The total daily EE measured during chamber stays (EEchamber) was over 2600 kcal/day for both diets. Physical activity expenditure on days outside the chamber (PAEnonchamber) and total daily EE certainly suggest that the participants were far from sedentary and in fact quite physically active. Assuming sedentary energy expenditure (EEsedentary = SEE + AFT) was consistent and similar inside and outside the chamber – and there is no reason why this wouldn’t be the case – the total daily EE when outside the chamber exceeded 3100 kcal/day and 3300 kcal/day for the HC and VLC diets, respectively.
For the HC diet for example, total daily EE when outside the chamber would approximately equate to:
EEsedentary + PAEnonchamber
(1.34 kcal/min x 60 x 24) + (1221 kcal/day) = 3151 kcal/day (See table 2 below).
In my mind, total daily EE and physical activity of this level in similar free-living adults is not representative of sedentary levels of activity. It would therefore surprise me if total daily physical activity EE of these participants, prior to this study, was this high. This may go some way in explaining the unintentional weight loss that occurred during this study. The combination of the daily clamped cycling exercise (∼300 kcal/day) and the increased SPA outside the chamber (>500 kcal/day) appears to have contributed to the overall state of negative energy balance and concomitant body composition changes.
Physical activity EE outside the chamber (PAEnonchamber) was found to be 126 kcal/day higher but was statistically nonsignificant at the end of the 2 month inpatient stay. This was a sum total of: 1) energy expenditure for 90 minutes cycling at a clamped intensity (EEexercise) and; 2) spontaneous physical activity (SPA) energy expenditure.
Components of Total Daily Energy Expenditure
Given that the low intensity cycling was performed at a clamped intensity and based on the data that no difference existed for EEexercise for both diets during chamber stays (see table below), it is reasonable to assume that EEexercise when outside the chamber would be similar for both diets too. The 126 kcal/d difference between the HC and VLC diets in PAEnonchamber can only be accounted for, then, by increased SPA. The authors of this study allude to this in their discussion (pg. 332) saying: “Despite slight positive energy balance during the chamber days, the overall negative energy balance amounted to ∼300 kcal/day and was likely due to greater spontaneous physical activity on nonchamber days.” However, the exact increases in SPA outside the chamber were not directly reported in this paper. Obviously, it is important to recognize and indeed be reminded before exploring the possibilities that could explain this increased nonchamber SPA, that there was no statistical significant difference shown for PAEnonchamber. As such, the discussion below is largely speculative and purely an exercise in intellectual curiosity.
Notwithstanding, the difference may be related to:
The time spent on the metabolic ward caused behavioural-induced SPA alterations.
The VLC diet had a direct modulating effect on SPA.
Increased SPA was influenced by increased fitness and/or fat loss over the course of the study.
Time spent on the metabolic ward led to behavioural-induced SPA alterations
The first explanation posits “that the subjects’ behaviour was affected by the time spent on the metabolic wards” with subjects anxious to finish the inpatient study. However, this explanation whilst appearing sound in theory is not supported by the results of the study. For this behavioural-induced increased PAEnonchamber explanation to be consistent and valid, you would expect to see by the end of the study as well, the same type of relative change in PAEchamber. That is, both SPA inside and outside the metabolic chamber would change in a comparable way, both in direction and relative magnitude. This was not the case though with SPA inside the chamber being lower, albeit minimally, in the VLC phase of the trial compared to the HC diet (0.1963 vs 0.2241 kcal/min; p=0.0102). This corresponds to ∼40 kcal difference over 24 hours – a statistically yet arguably clinically irrelevant difference. In contrast, SPA outside the chamber was non-statistically higher for the VLC vs HC diet. It is this discordance for chamber vs nonchamber SPA and diet type that makes it unlikely that behavioural change drove the increased PAEnonchamber by the end of the study.
SPA was directly impacted and increased by the VLC diet
Supporters of the “metabolic advantage” theory would interpret the higher PAEnonchamber (due to increased SPA) as suggestive that the VLC diet had a direct impact on physical activity levels. But how precisely or by what mechanism(s) decreasing dietary carbohydrates translates into increased physical activity EE is anyone’s guess. I am yet to be convinced and have found no compelling research that altering the macronutrient composition of the diet alters SPA in any significant way. Furthermore and as discussed above, SPA for both diets differed for PAEchamber versus PAEnonchamber. The question then is why would SPA increase when outside the chamber and decrease when inside the chamber when the VLC diet is compared to the HC diet? If diet truly changed this parameter of energy expenditure, a consistent effect would be expected irrespective of setting.
Increased fitness and/or fat loss led to increased SPA
Another possible explanation for the increased PAEnonchamber is that a training effect of the low-intensity cycling and accompanying weight loss affected SPA levels. As such, my proposition is that this is not directly related to the dietary intervention at all. Let me explain. Not knowing how active or inactive the participants were prior to entering this study (I’m assuming given the description that they were not doing much physical activity at all in the lead up to the study), it is plausible that the 90 minute cycling performed each day during the study was over and above what they were doing beforehand.
If that is the case, logic would suggest that it is probable that participants would have increased their cardiovascular fitness over the duration of the study despite the clamping of exercise intensity, being confined as an inpatient to a metabolic ward and spending 16 days over 2 months in a metabolic chamber. As mentioned above the low intensity cycling was included in an attempt to offset the usual decrease in physical activity that occurs during metabolic ward studies. Whilst sedentary-like behaviour can mitigate the positive effects of aerobic exercise, the data for PAEnonchamber and total daily EE suggest that such behaviour was largely curtailed. This supports the possibility that the combination of the cycling exercise and high levels of SPA facilitated increased cardiovascular fitness.
This improvement in fitness and concomitant fat loss may have, then, inadvertently affected SPA with increased expenditure during the 2nd month of the trial. There is some evidence that exercise, improved fitness and fat loss lead to increased SPA in some people. In a study by Manthou et al (2010) which explored the behavioural compensatory adjustments to exercise training in overweight women, the loss of weight/fat mass or lack thereof, was attributable to an increase or decrease in SPA, respectively. Physical function and peak oxygen consumption has also been shown to improve significantly more in older obese men randomized to an exercise-diet intervention (with accompanying weight loss) compared to a diet-only group (with accompanying weight loss) or exercise-only group (with no weight loss), with improved functionality and fitness correlated to increased levels of SPA. This explanation has one major caveat however with an underlying assumption that SPAchamber remained unaffected by improved fitness and fat loss due to a curbing effect of confinement. This is a big assumption which thereby leaves us with our last explanation and basically brings us full circle to what the results originally showed.
That no real difference existed as suggested by the statistical analysis
The final explanation is that PAEnonchamber and SPA did not differ between diets. The most compelling evidence to support this is that no meaningful difference was found between diets for fat loss or body composition. If such a difference in SPA actually existed, a difference in body composition should have been detectable.
Final remarks
The recent study conducted by Kevin Hall, Kong Chen, Juen Guo, Yan Lam, Rudolph Leibel, Laurel Mayer, Marc Reitman, Michael Rosenbaum, Steven Smith, B Timothy Walsh and Eric Ravussin demonstrated that a VLC diet was no more effective compared to a HC diet for reducing body fat. Increases were detected in EE for the VLC diet but the clinical relevancy is of dubious value given that this was a transient phenomena, significantly decreasing linearly over time with EE returning to baseline by the end of the study. The results provide further confirmation of the fundamental physiologic principle of energy balance and reinforce that a sustained energy deficit results in weight loss regardless of macronutrient composition of the diet. Despite insulin secretion and respiratory quotient being dramatically reduced during the VLC diet, no enhancement of fat loss was evident. This provides compelling evidence that the regulation and storage of fat in the adipose tissue is far more complex and nuanced in humans, with insulin not always playing a predominant role. Further investigation and research is warranted to elucidate any appetite attenuating and metabolic benefits of higher-fat diets.
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