The mass media and ‘rogue’ researchers are confusing the public by suggesting that exercise does not facilitate weight loss. Sensationalised, poorly researched and inaccurate media presentations have misled consumers because a thorough assessment of the evidence wasn’t undertaken. Some sports scientists and doctors have further exacerbated the problem by claiming that physical inactivity does not contribute nor is associated with becoming overweight or obese.
FitGreyStrong Advice:
Be extremely careful about making any changes to your exercise, lifestyle, dietary, supplement or medication regimens based on information produced through the media. Consult competent health care experts with recognised qualifications and good reputations, do your own research, talk to those you trust and use some good old commonsense before making any changes.
For those interested in wanting to know more on this topic please continue reading see below.
For local Townsville residents interested in FitGreyStrong’s Exercise Physiology services or exercise programs designed to achieve the above-mentioned benefits or to enhance athletic performance, contact FitGreyStrong@outlook.com or phone 0499 846 955 for a confidential discussion.
For other Australian residents or oversees readers interested in our services, please see here.
Exercise, weight loss and why it doesn’t work for everybody
The following article represents the first of a series of blogs that will explore the reasons behind why exercise may fail as a weight loss strategy. It is often assumed that when someone starts an exercise program, weight or body fat loss will happen naturally and almost by accident. However, recent research demonstrates that the magnitude of individual weight loss varies dramatically, with some losing a substantial amount of weight, others maintaining weight and a few actually gaining weight. The question is, how is this possible? What compensatory mechanisms are at play to negate the effectiveness of exercise?
In this first installment I want to discuss how the mass media and ‘rogue’ researchers have contributed to the unfortunate situation where the message about the efficacy of exercise has been obfuscated and distorted. As a result the general public have received mixed messages as to whether exercise has any role to play in weight loss at all. Some sections of the media have done a pretty good job at cherry-picking research or commentators that promote the idea that exercise is largely ineffective when it comes to weight loss. This has contributed to the public perception, then, that exercise may have limited usefulness as a method to facilitate weight loss.
One of the best examples of this occurred when the Australian Broadcasting Corporation’s (ABC) TV show, Catalyst, aired a segment called “Toxic Sugar” (see here) claiming that:
“The studies show that exercise has virtually no effect on weight loss. One thing exercise does is it makes people hungry.”
Are the media trustworthy?
Such sweeping claims – that are not based on the actual scientific evidence – are particularly worrisome given the impact that such high-rating TV shows may have on the lifestyle choices and behaviour of their viewers. Why such organisations would besmirch the value of exercise is an interesting conundrum that has no easy answers.
There are a few possible reasons why this has happened and they are by no means based on any evidence I have been able to dig up and for this I apologise. The speed of the 24/7 news cycle, nevertheless, in conjunction with the need to sensationalise stories and news segments in an effort to gain viewer attention and watchership, have more than likely played a part. Media outlets do not undergo any critical assessment from any independent body – either internally or externally – to corroborate the accuracy of their program’s content. They can therefore function with relative impunity and little accountability. Media outlets are consequently free to make – without fear or retribution – poorly researched and misleading radio or TV shows that may not be in the public’s best interests.
Another reason why the media may produce content that is inaccurate and misleading is a simple one. Basically, the research that has gone into producing a show or print article has been hasty and superficial without a thorough review of the scientific evidence. If you consider the Catalyst segment mentioned above it was so lopsided because of one key component that was missing from the show – an opposing voice. The report ended up being totally biased because it did not present – in an objective manner – robust and contradictory scientific evidence. It also failed to interview any expert commentators that hold serious doubts about many of the claims that were aired.
The public’s confusion regarding the role of exercise in facilitating weight loss was further compounded, after well respected, credentialed doctors and sports scientists suggested in the British Journal of Sports Medicine that physical inactivity and obesity was a myth. Authors Malhotra and co in their editorial titled “It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet” (see here) made one of the most contentious claims in decades by suggesting that increasing obesity rates were not related to changes in physical activity levels. To put it another way, what they were essentially saying is this:
Doing no physical activity and sitting on your arse all day does not contribute to your risk of putting weight on or becoming obese!!
Here’s an interview on ABC’s Lateline with one of the authors, Dr Aseem Malhotra, discussing this publication (see here) if you are interested in listening to some of the commentary on this.
Let’s now just take a look at exactly what was put to print, so you the reader, can judge whether or not I am justified in being perplexed by their editorial. In it they state:
“Regular physical activity reduces the risk of developing cardiovascular disease, type 2 diabetes, dementia and some cancers by at least 30%.”
Fine, that’s dandy, I’m definitely happy with that! They continue:
“However, physical activity does not promote weight loss (my emphasis). In the past 30 years, as obesity has rocketed, there has been little change in physical activity levels in the Western population” (p. 1).
Exercise and physical activity doesn’t promote weight loss?
This claim was based on one paper (see here) published in 2013 by Amy Luke and Richard S Coope (Department of Public Health Sciences, Stritch School of Medicine, Loyola University Chicago, Chicago, USA) which theorised that energy expenditure changes over the 20th century could not explain the increased obesity levels that now exist in the West and increasingly so in developing countries.
Such assertions fail to take much notice of a hefty amount of research that has shown that for many, exercise is a very effective method for assisting weight loss (see hereand here). So it is rather puzzling why a more balanced and nuanced account of our current understanding of exercise and weight loss was not undertaken by these authors. So just what did they ascribe the increasing rates of obesity to? Answer: Excessive carbohydrates and sugar. Now this is certainly an interesting hypothesis and one that will unfortunately require another blog to give this topic justice so you’ll have to wait for that one. What I will say though is that such examples truly exemplify the problems of intelligent, educated researchers entrenching themselves in a paradigm of thinking so deeply that any evidence to the contrary is either dismissed or diminished.
Anyway, following publication of this editorial the global media jumped on it. If you Google the title of their article you’ll notice the massive media coverage it received across all forms – print, broadcast and the internet. Social media like Facebook and Twitter picked up on it and the core message – that physical activity and exercise does not promote weight loss – was repeated ad nauseam. There was a harsh backlash from many corners – sports scientists, researchers, public health advocates and the like – but suffice it to say these criticisms and feedback did not generate any traction in the media nor were any corrective statements issued. The genie was out of the bottle and the message that exercise did not work for weight loss was left hanging in the air, slowly seeping and diffusing into the public’s consciousness. This just reinforces my earlier comments where the media over-sensationalise stories and news segments in an effort to gain viewer attention, watchership and market share. What seems apparent in my view, then, is that these organisations have expunged themselves of their ethical obligations to ensure that the public’s best interests are kept front and centre.
Perhaps not surprisingly there is research that contradicts the central plank of their argument which hinges on the notion that activity levels have remained static over the last 30 years. Church and colleagues (2011) (see here) found that:
“since 1960 the estimated mean daily energy expenditure due to work related physical activity has dropped by more than 100 calories in both women and men. Energy balance model predicted weights based on change in occupation-related daily energy expenditure since 1960 for each NHANES (U.S. National Health and Nutrition Examination Surveys) examination period closely matched the actual change in weight for 40–50 year old men and women. For example from 1960–62 to 2003–06 we estimated that the occupation-related daily energy expenditure decreased by 142 calories in men. Given a baseline weight of 76.9 kg in 1960–02, we estimated that a 142 calories reduction would result in an increase in mean weight to 89.7 kg, which closely matched the mean NHANES weight of 91.8 kg in 2003–06. The results were similar for women.”
Based on these findings the increase in obesity levels – in the US at least – can be largely attributed to changes in energy expenditure via reductions in occupation-related physical activity rather than solely due to the over-consumption of carbohydrates and sugar as postulated by the editorial discussed above. The debate will probably continue to rage as to what the culprit is but logically it seems quite obvious that the answer lies between these two opposing explanations. So instead of it being purely diet-related or activity-related, the current obesity problem has probably come about because of simultaneous changes to both.
Do your own research
To bring this to a close I would like to conclude by saying that certain sections of the mass media and ‘rogue’ researchers have undeniably contributed to the public’s confusion regarding the role of exercise for weight loss. Until such a time that all forms of media are more closely scrutinised and held accountable for the veracity of their productions, the advice from FitGreyStrong is to be very careful about making any changes to your exercise, lifestyle, dietary, supplement or medication regimens based on information accessed via the media. Consult competent health care experts with recognised qualifications and good reputations, do your own research, talk to those you trust and use some good old commonsense before making any changes.
Disclaimer: All contents of the FitGreyStrong or FGS 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.
The results of a study conducted by Dr Kevin Hall and 10 other researchers titled “Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men” were published recently in the American Journal of Clinical Nutrition. Many interested in this area had waited patiently in anticipation wondering just what Dr Kevin Hall and co would discover given that this study attempted to answer several claims that are presently in dispute. The carbohydrate-insulin model of obesity and low carbohydrate diets have gathered greater traction in recent times. Hall’s study was designed to investigate if there was any foundation to the key tenets of this theory and ascertain whether greater increases in energy expenditure and reduction of body fat were elicited when following a low carbohydrate diet.
Dr Kevin Hall (National Institute of Diabetes & Digestive & Kidney Disease, Bethesda, MD)
A number of key claims which underpin this model are made by those advocating low carbohydrate 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, very low carbohydrate (VLC) or ketogenic diets will disproportionately increase energy expenditure compared to isoenergetically-matched low fat, 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 in a different and advantageous manner by exchanging an isoenergetic amount of dietary carbohydrate for fat.
The subsequent published findings left a lot of people with their noses seriously out of joint and Dr Hall was showered heavily with criticism. In fact, some were so dismayed with the authors interpretation of the study’s results that the rebuttals transcended professional criticism with personal attacks and slurs directed at the lead author himself. There were even suggestions made by some that there was a conspiracy amongst researchers, research agencies, government and the food industry to misconstrue the study’s findings. Essentially, these 11 researchers 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.
It is perhaps worthy to note here that those involved in this study represent some of the most well known, credentialed and respected obesity researchers worldwide. The claim therefore that these authors are misrepresenting or misconstruing the data of this study – to maintain some sort of high carbohydrate diet ‘status quo’ which is further exacerbating the obesity and growing diabetes problem – is preposterous. I don’t think they are endorsing any such thing but I will have more to say about this in a later blog (see below).
See Dr Hall’s interview below at the 2016 World Obesity Federation where he presented a poster of the authors interpretation of the study’s data and results prior to full publication of the trial.
Before I review the Hall trial in greater detail however (part 2), there is another study published in 2012 that played a pivotal role and led the way in consolidating the view that ‘a calorie is not a calorie’ after producing results that were distinctly different to the Hall study. To provide context to the criticism launched at Dr Hall, we must first understand how the results of the Ebbeling study influenced and framed up the discourse that currently exists regarding diet type and obesity. The Ebbelingtrial is perhaps one of the most influential publications of recent times within the field of nutrition and obesity management and compares the effects of 3 diets differing widely in macronutrient composition and glycaemic load on energy expenditure following weight loss. It is often referred to by those claiming the existence of a ‘metabolic advantage’ for VLC diets with weight or fat loss purported to be substantially easier and significantly greater than diets higher in carbohydrate. The abstract and summary of the study can be viewed below.
So what were the findings and what did the Ebbeling study conclude?
Results of the Ebbeling Trial
Key findings: In overweight and obese young adults that achieved 10-15% weight loss, significantly greater reductions in resting energy expenditure (REE) and total energy expenditure (TEE) were found for weight loss maintenance diets in the following order → low-fat (LF) diet > low-glycemic (LGI) diet > very low-carbohydrate (VLC) diet, when compared to pre-weightloss energy expenditure. In fact, the difference between the LF and VLC diet for TEE equated to approximately 300 kcal/d (LF diet -423 kcal/d versus VLC diet -97 kcal/d)! This is a remarkable difference and as the authors allude to, corresponds (approximately) to the amount of energy expended during 1 hour of moderate-intensity physical activity. If valid, this would constituent a very substantial ‘metabolic advantage’ in the treatment of obesity and the widespread adoption and encouragement of VLC eating practices would be justifiable. I should make it clear that it is not my intention to argue against the benefits of VLC diets given that the scientific evidence and anecdotes show them to have helped many people successfully lose weight and improve metabolic biomarkers of health. I do, nonetheless, wish to challenge the validity and generalisability of the results of the Ebbeling trial where it is claimed that a ‘metabolic advantage’ existed for the VLC diet with much higher readings for energy expenditure following weight loss.
Do low carbohydrate diets provide a metabolic advantage?
Problems with the Ebbeling Trial
The fundamental problem with the findings of this study is that there is significant heteroscedasticity for energy expenditure and diet type. In other words, whilst the pooled data of all participants showed that the VLC diet demonstrated less reduction in REE and TEE compared to the other diets, at an individual level the effect of diet type on REE and TEE was unpredictable and lacked any reliability to predict what diet would be most suitable when, where and in whom (see graphs below).
Individual Heteroscedasticity in Energy Expenditure Response to Diet
Assessment of the pooled versus individual data indeed raises more questions than answers. There are several problems in reconciling the key findings of the study against individual data presented in the graphs above (Figure 3, pg 2632).
The magnitude of difference in TEE between the 3 diets of some participants seems highly dubious. For example, there is one participant that recorded approximately -900 kcal/d versus +400 kcal/day for TEE, on the LGI and VLC diets, respectively. A whopping difference of ∼1300 kcal/d! Such a difference is fanciful as it would exceed the energy an average person would expend following a 3 hour run. Anyone that seriously believes that a 1300 kcal/day difference can exist for an isoenergetically-matched low vs high carbohydrate diet is deluding themselves. This is simply science fiction!
There are several other participants too where the differences recorded for the LGI vs VLC diets are very large indeed (i.e. ∼ 925, 850, 725, 650). Such large disparities I would contend defy or exceed what is humanly possible – physiologically speaking – on a chronic, long-term basis. Clearly, the data for these participants are outliers and they should have been excluded.
If such differences do indeed exist, the strongest and best long-term evidence suggests that metabolic adaptation can occur over the short term – meaning REE can differ between macronutrient manipulated isoenergetic diets – but over the longer term this difference disappears. Thus if there is any ‘metabolic advantage’ to higher protein or VLC diets because of their higher thermic effect or effect on satiety, this has not translated into meaningful greater weight loss over 24 months in free-living people that are overweight or obese (see here& here).
Presumably, the striking difference recorded for the VLC diet for TEE is being driven and skewed by 5-6 participants who recorded these exceptionally large values. If we exclude these outliers from the VLC diet group, the differences between groups is substantially reduced and brought much closer together.
Inflammatory biomarkers as measured by 24-hour urinary cortisol excretion and C-reactive protein were both highest for the VLC diet compared to LF and LGI diets. It is not clear whether these differences are clinically relevant or if there are any long-term health implications. Increased inflammation is certainly not ideal so it would be prudent to monitor those that adhere to such diets; notwithstanding that other studies have shown the opposite with inflammatory biomarkers decreasing on VLC diets. Given that increased REE and TEE occurred concomitantly with raised cortisol and CRP however, it would be interesting to know if those individual’s that recorded the highest values for REE and TEE, also recorded likewise, high values for both inflammatory biomarkers. If that was the case, it would be reasonable to suggest that the propensity of some people to record substantially higher REE and TEE may be more symptomatic of some type of disordered physiological or metabolic side-effect of the VLC diet, perhaps modulated by genes. This could possibly be a negative not positive bioeffect of VLC diets.
The pattern of effect on TEE at an individual level does not concur with the overall results of the study. For example, 8 participants of 21 recorded greater reductions in TEE during the VLC diet when compared to the LGI diet. Consequently, it is problematical to suggest that VLC diets provide a novel bio-effect that is reliable and consistent in all people. It is a curiosity as to why this was not discussed and no effort was made to appropriately contextualise these findings.
A similar pattern existed for the REE data with 1 subject having higher REE for LF and LGI diets vs VLC, 2 subjects having higher REE for the LF diet vs LGI and VLC diets, 3 subjects having higher REE for the LGI diet vs LF and VLC diets and 3 subjects where there was little difference between the LGI and VLC diets. In total, 9 of 20 did not respond in a way commensurate with the pooled study REE data (data for one VLC REE has been excluded, presumably due to being identified as an outlier). Once again there were a select few of the study cohort that had very large REE measures for the VLC diet vs the LF and LGI diets.
Whilst trying not to be overly skeptical, the data of one person that was excluded from the VLC group for REE (see figure 3 with VLC diet n=20 vs LF n=21 & LGI n=21), is an interesting omission. The only reason I say this is because I find it hard to fathom why it was ok to include, for example, the participant on the VLC diet whom had a 1300 kcal/d difference in TEE data (as discussed above), but then to omit REE data for one VLC participant as an outlier (maybe on the low side?) appears rather too convenient.
Weight loss is well known for reducing energy expenditure. In the Pounds Lost study byJonge et al. (2012), for example, resting energy expenditure in men at 6 months decreased by 99.5±8.0 kcal/d and was accompanied by weight loss of 7.6±0.34 kg. There were no differences between any of the diets – that ranged from lower to higher in carbohydrates – on either REE or weight loss.
However, despite the results of this study being at odds to the Ebbeling trial, it is not this dissimilarity I am interested in; despite the fact that there are obvious questions that spring to mind as to why this would be the case. No, what I am particularly interested in is the REE values recorded during the weight loss maintenance phase. Given that a mean weight loss of 14.3 kg was achieved and this corresponded to 13.6% of baseline body weight, significant reductions in REE occurred as expected. Unfortunately we do not know what the actual pooled or individual reductions were in REE over the 12 week weight loss period as REE was only measured at baseline (before weight loss intervention) and during the final 3 days of each study diet. These data for weight loss-induced reductions in REE would have been of benefit to ascertaining what changes occurred in REE after a 12-week weight loss program and what effect, if any, the 3 test diets subsequently had on REE after each 4 week diet.
Based on the significant mean weight loss of 14.3 kg achieved over the 12 week run-in phase and on previous studies that have tracked REE in relation to weight loss, 200-300 kcal/d would be a fair estimate for mean REE reduction. It is especially impressive, then, that some participants were apparently able to offset such reductions and actually increase REE above baseline values during the weight maintenance phase (assuming all participants achieved appreciable weight loss). Five participants recorded REE values that either remained unchanged or exceeded baseline for one or more of the 3 test weight maintenance diets.
One subject had increased REE compared to baseline for all diets, most notably for the VLC diet which was almost 200 kcal/d higher than baseline. Another subject had slight increases in REE for LGI (approx 20 kcal/d) and VLC diets (approx 50 kcal/d). An approximate 100 kcal/d increase over baseline for the VLC diet was observed in another participant. Whilst a fourth person had a slight increase on the VLC diet of approx 20 kcal/d. And finally, the fifth subject showed little change in REE for the LF diet compared to baseline REE. The fact that there were any increases at all, let alone a couple of participants that had increases of 100 to almost 200 kcal/d after substantial weight loss, is astonishing. Such results, if valid and replicable warrant serious investigation. Why these participants were able to increase or keep REE stable after significant weight loss is of great interest, as the reduction of REE in previous studies has been shown to be relatively proportional to the magnitude of weight loss.
Following each test diet it is surprising that body weight did not differ significantly following each 4-week study period given the differences, as reported above, between study diets for both REE and TEE.
I find the arguments advanced by Dr Ludwig in his response to Dr Hall’s critique of the Ebbeling trial in relation to this not particularly convincing either (see here). Body weight can fluctuate over the short term and things such as hydration and the amount of stool in the colon can influence weight. Nevertheless, after 4 weeks of each study period unless there were wild fluctuations in diet, lifestyle factors or a confounding medical condition – and there is no evidence that this was the case – these things would have been fairly stable and consistent by this stage. This explanation that all participants in the VLC diet were better hydrated and/or had not completed a bowel movement compared to the LF and LGI diets, and it is this that can explain the lack of difference in weight, is a fallacious argument, improbable and can be dismissed. In fact, in short term studies investigating VLC diets you will see larger initial decreases in body weight compared to diets higher in carbohydrates due to the reduction of muscle (water-laden) glycogen as described by Kreitzman et al (1992) (see here).
Moreover, I find the ‘substrate partitioning favouring lean tissue’ proposition a big stretch. Substrate partitioning has certainly been shown to occur during energy surplus/overfeeding (see 1, 2, 3, 4), energy deficit/underfeeding (5,6,7) and during intensive resistance training and anaerobic high-intensity exercise intervals (see 8 & 9).
These situations though are vastly different to a state of energy and macronutrient balance, as would have occurred in each 4-week diet period, where the intake of dietary carbohydrate, fat, and protein is matched by their rates of utilization (see here). Notwithstanding the results of the Pawlakstudy in rats, where a low glycaemic diet and reduced insulin secretion (versus a high glycaemic diet) showed substrate partitioning in favour of lean tissue, there exists no evidence in the short term for this occurring in humans during energy balance.
Provided sufficient protein was ingested to ensure nitrogen balance (which all 3 diets did; 104.8g/1.2g per kg BW, 105.5g/1.2g per kg BW & 151.5g/1.7g per kg BW, for the LF, LGI & VLC diets, respectively), it is implausible that a significantly greater increase in LBM and decrease in fat mass would have occurred in the VLC diet versus the LF and LGI diets during energy balance.
As the participants were not engaged in any concurrent intensive exercise or resistance training intervention, the physiological stimulus to induce the substrate partitioning like seen in reference 8 & 9 above did not exist either.
Final comments
The results of the Ebbeling study suffer from internal inconsistency and there is an inability to reconcile the data at hand. 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. The fact of the matter is that no such effect was shown in the Ebbeling trial. The notion, then, that the VLC diet was shown to provide a ‘metabolic advantage’ is repudiated.
Watch out for “The Ebbeling vs. Hall Trials: Re-visiting How Diet Affects Energy Expediture And Weight Loss – Part 2” (see here) which will discuss in more detail 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 were published recently in the American Journal of Clinical Nutrition and explore some of the reactions to this.
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.
Since the publication of the first FitGreyStrong blog ‘Sitting yourself into your grave‘ just over 2 years ago (click on the link or see the picture below), there have been a significant number of milestones and achievements that I would like to share with all of my followers.
The last 2 years have been very busy and productive. There have been several scientific critiques and analyses published as well as many blogs. These have been specifically directed at those amongst us who identify as Gen X or Baby Boomers and have primarily focused on health, fitness and nutrition-related topics or issues. The following provides a summary of the FitGreyStrong journey:
Including the globally popular 10,000 word commentary on how diet affects energy expenditure and weight loss (see hereand here)
How resistance training can affect the course of ageing (see here)
The perennial favourite “12 Reasons Why All Older Adults Need To Hit The Gym” (see here)
Nearly 1000 followers on Twitter and close to 8000 tweets
Over 800 Facebook posts
Close to 400 Instagram posts and;
110 YouTube video’s
There have been some very popular FitGreyStrong blogs/posts/tweets/videos and I have listed a short assortment of these below.
Most popular blog
The most widely read blog with readers from over 20 countries investigates how strength training can alter the trajectory of ageing and reviews the seminal work of Maria Fiatarone and colleagues back in 1990 (see here).
Most popular Facebook posts
The top 3 most popular Facebook posts were:
The sitting-rising test (SRT) that showed that the ability to sit down and stand back up again in a cross-legged position could predict the likelihood or risk of dying in the next 6 years. There have been over 100,000 views, 17 shares, 92 likes/loves and many comments (see here).
Modifying the Thomas test for one of the best stretches for the quadriceps, iliacus & psoas major (iliopsoas). A great way to improve flexibility of these muscles and improve hip extension ROM. There were over 1,000 views, 5 shares, 26 likes/loves and comments (see here).
The study was undertaken to elucidate the range of training-induced neuromuscular adaptations in elderly humans recovering from a period of disuse. It examined the effect of three types of training regimes after unilateral (one-leg) prolonged disuse and subsequent hip-replacement surgery on maximal muscle strength, rapid muscle force rate of force development, muscle activation, and muscle size. The popularity of the post was generated by the muscle scans of the thigh showing just how powerful resistance training is at inducing change in muscle structure and function. There were approximately 5000 views, 6 shares and 22 likes. It was also widely shared on other Facebook pages (see here).
Most popular Tweets
The top 3 most popular Tweets were:
Age-related dynapenia is weakly related to sarcopenia and is why we must look beyond just muscle mass (see here).
Motor effort training and low exercise intensity increases muscle strength and descending command in aging (see here).
Counter to the energy surfeit model of obesity increasing energy expenditure may be better for decreasing percentage body fat than caloric restriction (see here).
Late last year the international journal, Clinical Nutrition, published a FitGreyStrong critique of: 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 thus demonstrating that Exercise Scientists practising outside of academia have relevant and valid things to say about clinical research being conducted around the world.
Clinical Nutrition publication
The highlight of 2017, however, was being given the opportunity to present “Why the ‘strengthification’ of Gen X’ers & Baby Boomers is the greatest health challenge of the 21st century“ at the Ancestral Health Society of New Zealand conference in Queenstown in October where I postulated that muscular strength lies at the foundation of health, quality of life and functionality. The slide deck of this presentation can be viewed (by request only), so please either send me an email or use the contact form on the home page.
Presenting at the Ancestral Health Society of New Zealand
The future holds some exciting and challenging projects ahead so watch this space. Currently, FitGreyStrong is working on a journal editorial with some other researchers from around the world which will investigate and report on the importance of resistance training in older adults and the augmentative effects and safety of nutritional/drug supplementation.
Finally, I would like to express a big thank you to all those that have embraced FitGreyStrong and I hope to continue to bring quality information to all those Gen X’ers and Baby Boomers interested in advancing their health, quality of life and functionality.
Please share with those family and friends that are interested in ageing, health, exercise and wellness. The social media icons below will link it straight to your preferred platform.
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.
This before and after 6 month “transformation” was an individual experiment (n=1), which was inspired by my professional curiosity to test the validity of 5 key claims currently purported to be fundamental for improving health and body composition that I do not entirely agree with as an Exercise Scientist.
The first 3 claims are strongly and enthusiastically advanced by those that hold the view that most, if not all human beings, should severely restrict carbohydrates. This includes some carbohydrates that have traditionally been viewed as “good carbs” like, for example, sweet potato, pumpkin, parsnips, bananas, mango, apples. The fourth claim posits that saturated fat is a key driver of increased risk and incidence of cardio- and cerebrovascular disease. The fifth claim below relates to the notion that advancing age impacts the ability to alter body composition in a meaningful way – which it does – but the point is that much can still be done if the approach taken is scientifically and evidence-based.
The claims
They are, firstly, that CICO (calories in calories out) has been scientifically debunked and is not a fundamental determinant of body weight or % body fat reduction.
Secondly, that carbohydrates are metabolically toxic and bad for your health, worsening biomarkers indicative of inflammation, CVD risk and ageing such as BP, CRP, homocysteine & triglycerides-to-HDL ratio.
Thirdly, that carbohydrates sabotage and are antithetical to body fat reduction.
Fourthly, reducing saturated fat to ≤7% of total energy intake will substantially improve dyslipidemia and reduce inflammation, and hence, morbidity and mortality rates associated with vascular-related diseases.
Fifthly, that significantly increasing lean body mass or skeletal muscle tissue, and appreciably decreasing body fat in middle-aged men or women is difficult and cannot be accomplished.
Baseline-to-endpoint anthropometry & individual characteristics (25.8.16 to 17.2.17)
Age: 49
Gender: male
Height: 1.77m (5ft 10in)
Weight: 86.6 kg (191 lb) decreased to 82.4 kg (182 Ib)
Δweight = 4.2 kg (9 Ib)
BMI: 27.6 kg/m2 decreased 26.3 kg/m2
ΔBMI = 1.3 kg/m2
Waist circumference: 92.5 cm (36¼ inches) decreased to 86.0 cm (33¾ inches)
ΔWC = 6.5 cm or 2½ inches
Body fat percentage: 17.6% decreased to 10.4%
ΔBF% = 7.2%
Fat mass: 15.2 kg (33.5 Ib) to 8.7 kg (19 Ib)
Δfat mass = 6.5 kg (14.5 Ib)
Lean body mass: 71.4 kg (159 Ib) to 73.7 kg (162 Ib)
ΔLBM = 2.3 kg (5 lb)
6 month “transformation” experiment
Insights & learnings from this experiment for Gen X’ers & Baby Boomers are as follows:
1. For improvements to be seen in health and body composition, day-to-day consistency in relation to the fundamentals (what you eat and drink, regular daily exercise and good quality sleep) are paramount.
2. The NEAT effect cannot be underestimated. NEAT or non-exercise activity thermogenesis is the energy expended for everything you do that is not related to sleeping, eating and formal exercise.
Maximising NEAT – by increasing physical movement outside of formalized exercise during the waking hours (e.g. taking the stairs not the elevator, going for a walk after dinner with the family, taking regular breaks from desk-bound work etc) and decreasing time spent in sedentary activities (e.g. watching TV, playing Xbox, surfing the net, social media etc) – has a massive effect on total daily energy expenditure.
In adults, strong evidence exists of a relationship between sedentary behavior and all-cause mortality, fatal and non-fatal cardiovascular disease, type 2 diabetes and metabolic syndrome. In addition, there is moderate evidence for incidence rates of ovarian, colon and endometrial cancers.
These relationships are independent of physical activity. What this means is even if you regularly exercise, spending a lot of your other free waking time in sedentary activities is seriously harming your long-term health.
During the last 6 months I have attempted to keep moving during the day as much as I could in addition to the formal exercise sessions I was doing.
Bottomline: get up and move around for at least a few minutes for every 30-60 minutes you spend sitting or lying around.
3. Resistance training was an absolute key component of this experiment. It is essential to all Gen X’ers and Baby Boomers embarking on any lifestyle-based intervention where improved health, physical function and body composition are desired.
I could write another 10,000 words just on this point alone but I will direct you to the below links for further reading that discuss the benefits of resistance training in more detail.
Resistance training is critically important to health and body composition (Picture: pixabay)
4. Aerobic exercise remains pivotal for all exercise-based programs designed to enhance health, function and body composition. Enhanced cardiorespiratory fitness (CRF) is one of the most powerful ways to reduce the risk of subsequent disease and research demonstrates significant risk reductions for all-cause, cardiac and some cancer-related mortality. The activities I performed very regularly were cycling, walking and a little bit of rowing.
However, whilst in a caloric deficit state too much emphasis on aerobic activity may lead to reductions in lean body mass (skeletal muscle). I would suggest therefore that the most effective programs have a good balance of resistive and aerobic exercise (50:50). Balance training/exercises for those over 60 would also be important given that the somatosensory system suffers a similar age-related decline in function. Balance can be improved provided exercises that challenge this system are undertaken.
5. Once a sufficient baseline level of aerobic conditioning is attained, I would suggest incorporating some HIIT (short for high intensity interval training).
My favorite HIIT session was an indoor-based cycling session that consisted of: 10-15 min warm-up @ 40-60% heart rate reserve (HRR) with 1 x 30 second effort @ rating of perceived exertion (RPE) 14-16; following warm-up I would perform 3 x 30 second sprint effort @ RPE 17-19 or 85-95% HRR with 3-5 minutes rest between efforts; then 1 x 4 minute effort @ 16-18 RPE or 80-85% HRR with 4 minutes rest then; 1 x 30 seconds sprint (intensity as above) with 3-5 minutes rest; 1 x 4 minutes effort (intensity as above); cool down 10 minutes & stretch.
There is an increasing body of evidence to show that HIIT is a potent, effective, time-efficient and safe form of exercise which dramatically improves many health and fitness components including but not limited to increased cardiopulmonary fitness, reductions in cardiometabolic risk factors and some preliminary data suggesting that it can attenuate the rate at which our cells age.
Interestingly, there is little consensus on whether HIIT is effective to facilitate improvements in body composition independently of dietary changes which reduce energy intake. Several recent systematic reviews and meta-analyses came to conclusions at odds to one another thus leaving this author somewhat perplexed by these disparities.
HIIT should only be performed once there is sufficient baseline conditioning but it is now accepted and utilised in many chronic disease conditions and to great effect.
6. I would suggest that using the concepts of periodisation and polarization of physical exercise and training are beneficial to those that have a good foundation of fitness.
Periodisation is a training concept and is applied in practice by coaches of elite athletes and/or sporting teams. Whilst it can be quite elaborate and complex at the very elite level, for the purposes of this blog and those interested in applying such ideas to their exercise plan/program, it is simply the alternation of heavier or harder periods/days of exercise/training with a recovery or lighter day/week of physical activity. What should be remembered is that you can’t smash out high-intensity exercise sessions day in day out. Such an approach will spell disaster and lead to a training implosion where you’ll either get injured, sick or burnt out. It should be noted that much of the research that has explored periodisation versus no periodisation in non-elite adults tends to show that no further benefit is achieved. Providing planned periods of recovery and rest, I believe though, are critical to successful long-term adherence and fitness/health-related outcomes.
What seems to work quite well for most 40+ year old exercisers is a 3-week on/1-week off approach; meaning 3 weeks of exercise/training that is hard/challenging followed by 1 week where you back-off and reduce the volume and intensity of the sessions. This approach also seems to work well within each training week too where you could alternate more difficult or challenging training sessions with easier and lower intensity days. For example, the week may look something like this:
Monday: Resistance training workout 1 (main movement patterns: hip dominant exercise like deadlift, horizontal push/pull exercises supersetted like bench press with bent-over barbell rows)
Tuesday: HIIT (as outlined above)
Wednesday: 1 hour easy walk (20-40% HRR)
Thursday: Resistance training workout 2 (main movement patterns: quad dominant exercise like squat, vertical push/pull exercises supersetted like shoulder press with chins)
Friday: HIIT
Saturday: 1 hour easy bike ride
Sunday: Resistance training 1
Monday: HIIT
Tuesday: 1 hour easy walk
and so on.
Polarisation on the other hand is the training concept of exercise intensity either being very challenging and intense versus light and not difficult. On a subjective rating of perceived exertion (scale 6-20), very intense exercise would be anything rated over 16 compared to something light which would be 8-11. Polarising training sessions in this way tends to assist and facilitate being able to manage and cope with the psychological challenges posed by very difficult and challenging exercise.
7. Total caloric or kilojoule intake was central to achieving reductions in body weight, or more specifically, fat mass. This experiment confirmed that body fat reduction will be achieved if an energy deficit does exist.
For a more extensive discussion and a review of the research that confirms the necessity of an energy deficit to reduce adiposity see here:
8. As shown below, I used MyFitnessPal to log my various meals. This enabled some methodology to ensure that the caloric intake was appropriate (so that I could create a calorie deficit), the macronutrient breakdown assigned was optimal to maximise fat loss whilst preserving LBM, and importantly that the quality of the diet was high.
MyFitnessPal app
Critics of “counting calories” suggest that it is virtually impossible to get an accurate daily total for both energy intake and expenditure – unless you are involved in a research study with quantifiable methods such as the doubly labeled water method, for example, to determine energy expenditure. It is therefore argued that such endeavours are futile. It is easy to see why this opinion holds sway with some given the following:
* Establishing an accurate resting metabolic rate (RMR) is fraught with difficulties and there can be significant variation in RMR even between two people with comparable anthropometrics (%BF, LBM), age and sex (see hereand here).
* Assigning accurate values for energy expenditure related to exercise is likewise challenging and are more often than not, overestimated (see here).
* Trying to ascertain an activity level outside of formal exercise sessions and estimating NEAT is open to error also.
* How do you account for dietary-induced thermogenesis which accounts for about 10% of TDEE.
* There is no way of knowing that the foods and quantities that have been consumed (even if weighed) are a true representation of the calorie content of those foods and therefore reflect actual daily intake.
Whilst it may very well be true that accurately quantifying calories is a difficult task, the critics miss something that I think is fundamentally important during the process of trying to positively alter body composition. You become accountable. By attempting to measure and record daily energy intake and expenditure as accurately as possible, an acute awareness develops of how much total physical activity (including formal exercise, NEAT-type activity and sedentary behaviour) is being performed, and what and how much is being eaten.
However, even if energy intake and/or expenditure is incorrectly or inaccurately measured and recorded you now have the ability to make adjustments and tweak what is consumed or what is expended. For example, let’s assume you set an energy deficit goal of 500 kcal/day and you consistently adhere to this for period of 4 weeks but after checking your progress notice that you have not achieved any weight loss. Whether this has been caused inadvertently or not, what this basically tells you is that either total daily energy expenditure has been overestimated and/or total daily energy intake has been underestimated.
If we accept that most people are creatures of habit then we can safely assume that the foods bought and consumed on a daily and weekly basis will be roughly the same (same supermarket, same brands, same eating patterns) so there is some internal consistency regarding the calorie content of foodstuffs consumed day-to-day and week-to-week, even if the calorie content is not a true representation. With practice, one can become very adept at making the appropriate adjustments to ensure that continued progress is made.
Keeping tabs on intake is effective for many
Notwithstanding that reductions in adiposity can occur in the presence of little or no change in body mass, and increases in LBM can obscure body composition changes, the fact remains that the capacity to increase LBM is finite and if a substantial amount of body fat is shifted this will be reflected on the scales. In other words, you rarely see someone reduce body fat mass by 20 kilograms and increase LBM by 20 kilograms; it can happen, but I have rarely seen this occur “naturally”. Therefore the use of good scales to track weight lost is a reasonable approach to take when larger amounts of fat loss are needed.
It is important to realise also that both RMR and energy expenditure for physical movement decreases commensurately with reductions in body weight so such changes need to be factored in as fat loss is achieved. As body mass decreases so to do energy requirements. If a large amount of weight loss is achieved, the caloric deficit will eventually disappear with no further weight loss realised.
For example, a 120 kg man who reduces his body mass to 100 kg will potentially reduce his resting energy requirements by almost 500 kcal and in some individuals this can be even larger and persist following weight regain (see here). These are important considerations during the weight maintenance phase given that a significant majority of people experience weight and body fat rebound.
Research does however demonstrate that those that keep tabs on their daily diet and physical acitivity levels are more successful in achieving the desired changes in body composition, and perhaps more importantly, maintaining these changes.
Finally, the claim that “counting calories” is a futile endeavour and does not lead to real changes in body composition is most strongly disputed by the ability of body builders and physique models to dramatically reduce body fat levels when readying themselves for competitions, shows or photo shoots.
It is generally well accepted that the magnitude of change in the myriad of bodily processes that regulate and “fight against” continued adipose fat mass reduction are directly proportional to body fat percentage and the amount of actual body fat lost. In theory then, further body fat reduction – when percentage body fat is already quite low – should be extremely difficult.
What this example shows is that recording energy expenditure and energy intake as accurately as possible and creating an energy imbalance aimed at influencing and enhancing adipose tissue lipolysis is possible and extremely effective. The greatest challenge nevertheless is avoiding weight and body fat rebound following any intervention designed to alter body composition. Certainly the evidence suggests that regular physical activity plays a fundamental role in successful maintenance of changes in body composition.
A special mention of whey protein is warranted. It is an excellent source of leucine. This amino acid is instrumental and has been identified as key in stimulating muscle protein synthesis (MPS) rates in the post-prandial state and following resistive exercise.
Older adults need higher levels of protein/leucine to maximally stimulate muscle protein synthesis (MPS) both at rest and following resistance exercise. Whey protein (WP) has been scientifically shown in clinical trials to significantly increase LBM and improve body composition. Recently, WP was shown to benefit diabetes by reducing postprandial glycemia and HbA1c, weight loss and satiety versus other protein sources.
FitGreyStrong now provide a high quality, leucine-rich (4 grams per serve) whey protein supplement that will help facilitate your strength, functionality, muscle gain or weight loss goals.
For more information or for purchasing options of the FGS whey protein blend see here.
There is abundant evidenceto show that when in a caloric deficit state, a diet higher in protein helps preserve skeletal muscle tissue (lean body mass). This is critical because the loss of muscle tissue negatively affects strength, physical function and will reduce basal or resting energy expenditure.
It is the long-term implications, however, that reduced skeletal muscle has on health, strength, mobility and functionality that are of a real concern. Researchers with expertise in this area now concur that for older adults 0.4-0.5 grams of protein per kilogram of body weight per main meal is required to ensure that post-prandial muscle protein synthesis (MPS) is maximised thus attenuating the loss of skeletal muscle with ageing over time.
See more here:
See Professor Stuart Phillips discuss the importance of protein here.
High-quality protein is essential for preserving skeletal muscle tissue
10. For carbohydrates I aimed to consume 2-3 grams per kilogram body weight per day. In absolute terms, this varied from around 170 to 240 grams/day with consumption of simple sugars from whole foods varying from 40-80 grams/day.
These primarily consisted of cellular carbohydrates and acellular carbs, whilst not excluded, were minimised. Examples of cellular carbs were sweet potato, pumpkin, kale, zucchini, carrot, apple, berries, banana whilst examples of acellular carbs are bread, bagels and rice.
I continued to eat honey (10 grams/day) in my morning smoothie (frozen berry, whole milk, whey protein, peanut butter, LSA) after my exercise sessions. I also didn’t completely eliminate added sugar indulging in 1-2 teaspoons of raw sugar in the occasional bowl of porridge. Nonetheless, added sugar from table sugar or derived from foods more highly processed were kept to a minimum.
The question is, of course, are carbs ‘toxic’ to health and do they thwart attempts to alter body composition? I very much doubt it but I need to caveat this statement with some comments.
Some believe these foods are fattening and toxic to health
Many factors modulate individual tolerability in response to dietary carbohydrates and the propensity to induce adverse health outcomes and worsening adipose-related body composition. Whilst not a finite list, chronic overnutrition and an energy surplus state, the amount of carbs, the type or source, when they are consumed in a meal, sleep patterns, stress, physical activity levels, the FITT makeup of weekly exercise sessions, sedentary behaviour patterns, age, metabolic and skeletal muscle/mitochrondrial health and genetics all interact and play a role in relation to individual tolerability. What may suit one person, may be metabolically problematic for someone else. Whilst it is not my intention to explore all these factors in depth there are a few key points worth acknowledging.
Research investigating the affect of genes to different macronutrient-based diets suggests that individual response varies substanitally so the idea that there is a particular diet template that suits everyone is therefore a myth. It is clear that genes interact with diet which necessitates individual experimentation, and trial and error to establish what is most suitable regarding the proportionate breakdown of macronutrients.
Manipulating the sequence of fat and protein ingested before carbohydrate can potentially reduce postprandial hyperglycemia. In type-2 diabetes patients, altering the sequence whereby carbs are consumed before or only after after high-protein and high-fat foods at each main meal (lunch & dinner), elicited the same weight loss but very difference effects on HbA1c, fasting plasma glucose, postprandial glucose excursions and other indices of glucose variability.
Increasing protein and swapping out carbohydrate for increased dietary fat should be considered and warranted in prediabetes and diabetes. For example, a recent studyshowed that after 6 months on a high-protein (HP) diet, 100% of the subjects involved had remission of their prediabetes to normal glucose tolerance, whereas only 33.3% of subjects on the high carbohydrate (HC) diet achieved remission. The HP diet group exhibited significant improvement in (1) insulin sensitivity (2) cardiovascular risk factors (3) inflammatory cytokines (4) oxidative stress and (5) increased percent lean body mass compared with the HC diet at 6 months.
This is the first dietary intervention feeding study, to the authors knowledge, to report 100% remission of pre-diabetes with a HP diet and significant improvement in metabolic parameters and anti-inflammatory effects compared with a HC diet at 6 months. It should be noted that the HP diet was also lower in carbs compared to the HC diet so the superiority of the HP diet inducing remission of pre-diabetes in participants cannot be solely ascribed to increasing dietary protein. What these results suggest is that prediabetes is most effectively treated (with respect to the diet component of the intervention) by concomitantly as a percentage of total energy intake, increasing dietary protein to ≥30%, whilst simultaneously reducing carbohydrates to ≤40%.
Could more of this be a boon for health?
Diets that reduce carbohydrate and increase dietary protein and fat generally elicit improvements in those suffering impaired glucose regulation and diabetes, including but not limited to, glucose tolerance, FBG, HbA1c, insulin resistance, insulin sensitivity, dyslipidemia, HDL-to-triglyceride ratio and hyperinsulinemia. It is therefore a case in point that when I ask the question – are carbs toxic? – the answer is going to depend on many factors as I alluded to above and needs to be considered in context.
Indeed for those that have serious metabolic impairment (i.e. type-2 diabetes) and significantly reduced capacity to dispose of glucose post-prandially plus an inability to adequately stabilize blood glucose to acceptable concentrations across the day, cellular carbs may even present tolerance problems for some. As such, this may necessitate a need to reduce and minimise all types of carbs to ensure maximal improvements in blood glucose regulation.
If carbohydrate reduction – in those with pre-diabetes and diabetes – yields the most favourable changes in metabolic biomarkers, does this therefore mean that everyone should be reducing carbohydrates to very low levels?
This raises one of the central questions that I was trying to explore with this n=1 experiment.
That is, would a primarily high quality carbohydrate intake 35-40% of energy intake (170-240 g/d) impair my health and stall changes to body composition?
Lastly, it is important to point out (see here) that total energy intake will modulate, to some degree, carbohydrate tolerability. An energy deficit or energy surplus state will have a profound effect on metabolism and glycaemia.
11. For dietary fat, I aimed for 1-1.5 grams per kilogram body weight per day. This was derived from nuts, seeds, pepitas, avocado, peanut butter, olive oil, coconut oil, LSA. Fat (mainly saturated fat) from full fat dairy foods (milk, cheese, yoghurt) was also consumed. Saturated fat from some of the protein sources (meat and eggs) was also not minimised. Saturated fat consumption as a percentage of total energy intake per day was around 15%, which is at least double and well above the recommended ≤7% per day. Fatty fish (salmon, sardines, mackerel) was consumed 2-3 times/week to ensure a decent intake of omega-3 long-chain fatty acids, EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid).
For those that have known me for a while, I have held the view for over 20 years now that saturated fat is not a primary instigator of atherosclerosis, coronary heart and cerebrovascular diseases. After a careful and continued assessment of the evidence over this time, my opinion has not shifted.
There is no convincing evidence that reducing saturated fat to ≤7% of total energy intake – from say double or even triple that – has any meaningful effect on all-cause mortality rates. I continue to remain unimpressed by the evidence used to justify the position that saturated fat is atherogenic. Interventional research, where the intake of saturated fat is modified and decreased, results in little change to future morbidity or mortality. In some cases, such reduction has in fact been counterproductive and manifested in higher rates of morbidity and mortality.
A recent interventional studyshowed that consuming energy primarily as carbohydrate or fat (34% of energy from saturated fat or nearly 5 times the recommended limit) for 3 months did not differentially influence visceral fat and metabolic syndrome provided the diets were low-processed and lower-glycaemic based. Furthermore, in recent years, scientific evidencehas increased concerning the ability of lipids, in particular omega-3 polyunsaturated fatty acids (n-3 PUFAs), to positively influence muscle and overall physical function in older patients.
Bottomline: quality counts!!
12. My daily macronutrient breakdown based on caloric energy intake (EI) was approximately 25-30% protein, 35-40% carbohydrate, 30-35% fat. The percentages for the carb-to-fat ratio would vary day-to-day, some days higher in carbs, other days higher in fat, but protein would come in close to the 2 grams/kg body weight (∼30% of EI) each day. Simple sugars consumed per day varied from 40-80 grams.
I would describe this type of nutritional approach as an energy deficit, high-protein, moderate carb, moderate fat diet based on non-processed foods.
13. The picture below is a snapshot of my blood tests and is provided as evidence to demonstrate that for my physiology, the lifestyle-based intervention was very effective. All biomarkers were excellent and those indicative of inflammation were very low. Blood pressure measured 122/70 and was normal for the duration of the intervention.
Blood test health biomarkers
Summary
In summary, this n=1 experiment confirmed that improvements in health and body composition, with decreased body fat and increased lean body mass, can be achieved in a 49 yo middle-aged male. Consuming 35-40% of the diet as carbohydrates (170-240 grams/day) containing 40-80 grams/day of simple sugars, 2g/kg/d of protein or 25-30% (160-200 grams/day) and 30-35% fat (with 15% of energy intake derived from saturated fat), was effective and safe with no ill effects. Biomarkers measured through blood tests corroborated this.
Physical activity – both formal exercise sessions and increased NEAT – was an integral component of this experiment. Finally, I would like to finish by saying to all those that read this blog to continue partaking in resistive exercise 2-3 times/week or for those not doing any such exercise to seriously consider adding this to your weekly routine. The benefits over the long-term go well beyond any words I can write.
Disclaimer: All contents of the FitGreyStrong or FGS 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 blog or the FGS 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.
