The Potato Manifesto - Part 2/2: The Sweet Potato, Is It More Than Just the "En Vogue Tuber of the Year"?

Image 1: A mixer like this would be one of the best choices to turn your healthy low-GI sweet (or regular) potato into a high GI "nightmare".

If you've read yesterday's first part of the Potato Manifesto, you should by now be aware that the common notion of the pro-diabetic high-glycemic regular potato is another of the numerous black-or-white nutrition myths that do not become right, no matter how many bloggers and forum posters reiterate them. In today's second part of the series I will try to elucidate, whether the sweet potato, of which I would venture to say that she is the "en vogue tuber of the year", is not still the "safer starch alternative". So bear with me while I am using my scientific peeling knife to check whether there is a bitter truth hidden beneath skin of the sweet potatoes ;-)

Come on sweety, show me what's beneath your skin!

Now, if we take a look at the literature, a review of the glycemic index of 33 commonly available foodstuffs from the 1990s lists sweet potatoes with a glycemic index of 49 as #17 (with #1 peanuts and a GI of 11 and #32 cornflakes and a GI of 83 as the "extremes"; Nishimune. 1991). It is "outperformed by spaghetti (GI 47) and closely followed by Buckwheat, Yam (both GI 51) and you guessed it the good old "regular" potato, to which Takahiro Nishirnune and his colleagues assign a GI of 54, which - as you should know from yesterday's installment of the Potato Manifesto is nothing but an average on a scale that ranges from 10 to 110!

Figure 1: Difference in plasma glucose concentrations (expressed as the increase due to the "high GI" normal potato vs. the "low GI" sweet potato) in response to the ingestion of 50g of carbohydrates in form of bush potato or regular potato in 7 Aborigines and 7 Caucasians (data adapted Thorburn. 1986)

A brief note on the fallacy of common arguments for "traditional diets" (=sweet potato diets): I recently started listening to archived episodes of Jimmy Moore's Living La Vida Low Carb show and encountered time and again the 99% nonsensical argumentation that the XYZ thrived on whatever diet and that by just mimicking their diet(s), we would thrive, as well. To me this is like saying: "Look, the Panda bears thrive on a 100% bamboo diet! So, the ice-bears in our zoo should get along pretty well, if we stopped feeding them meat." Now, this is obviously a provocative comparison, but if I look at myself and then look at an Aborigine, the difference may not be as significant as the one between panda and ice-bear and yet, according to the results of a 1986 study by Anne W. Thorburn et al. (Thorburn. 1986) our glucose responses to the ingestion of 50g of carbohydrates from either the sweet-potato'esque bush potato and a "normal" western potato would be completely different (cf. figure 1). While the poor Aborigine would encounter the typical blood sugar ups and downs that are so characteristic for the ingestion of "high GI" carbs, my body would probably not care whether I eat the 100% paleo bush potato or its readily available, cheap cousin. The futility of common "neo-paleolithic" reasoning aside, this example also shows that genetic individualities are another major determinant of the glycemic index.

Three yeas later, in 1994, Thomas Wolever and his colleagues from the University of Toronto tested the glucose response of diabetic patient to 102 complex carbohydrate foods (Wolever. 1994). "Complex", in this case, indicates that they tested combinations of foods like they could appear on someone's dinner table and lo and behold, the "low GI" sweet potato took a close second to the "high GI" boiled white potato, when the both were boiled and served to 16 diabetic patients along with tomatoes. The 1 GI point difference between sweet and white potato (60 vs. 59) is yet well within the statistical margin.

Identical glycemic index, but differing free sugar compositions

Although, I hope that I should by now have convinced you that the glucose response is no convincing argument in favor of the sweet potato. I am even convinced that, if people abused their sweet potatoes in similar ways as their "regular" potatoes, i.e. mashed, fried, pureed, powdered and instantized it, we would soon see the (contemporarily) sexier sister of the regular potato on the list of "foods to avoid if you want to lose wait or just live a long and healthy life". Nevertheless, taste and name of the sweet potato, leave no doubt that there must be a sugary difference between her and her white brethren.

Figure 2: Free sugar composition (in mg/g) of 16 "regular" and 3 sweet potatoes cultivars (comparison based on data from Zhu. 2011 and Dincer. 2011)

And in fact, as my juxtaposition of data from a 2010 study on the relation between amino acid and sugar content of commercially available regular potatoes and its effect on the formation of acrylamite during heating (Zhu. 2011) and data from the previously mentioned (cf. Part 1) study by Cuneyt Dincer and his (or her) colleagues from the Akdeniz University in Ankara, Turkey (Dincer. 2011) shows (cf. figure 2), there is a non-negligable difference in the amount and composition of "free sugars" (vs. sugars in the form of starch). Although I am not 100% about the exact nature of the exotic Chinese potatoes, it is quite obvious that, despite large varieties in the absolute and relative sugar content of "regular" potatoes, the "classic" potato has a lower absolute free sugar content and contains more fructose and glucose than her sweet sister, 90% of the free sugar content of which is plain table sugar (=sucrose = glucose + fructose).

Figure 3: Mean free sugar composition (in mg/g) of fresh "regular" and sweet potatoes (comparison based on data from Zhu. 2011 and Dincer. 2011)

This "sugary" pattern does yet broaden, when you expose the sweet potato to heat in the form of either boiling or baking (cf. figure 4). In that, the cultivar-dependent slight reductions in glucose and fructose carry little weight compared to the sudden appearance of significant amounts of maltose, which had been beyond the detection before the sweet potatoes were boiled or baked (cf. figure 4).

Figure 4: Free sugar content (mg/g dry weight) of fresh and cooked sweet potatoes (data adapted from Dincer. 2011)

From a chemical perspective, the latter is not really surprising and its formation in response to heat treatment has been reported as early as 1923, when H.C. Gore published a paper in the Journal of Industrial and Engineering Chemistry (Gore. 1923), in which he makes the important observation that the formation of sugars from starch takes place within the first minutes of heating:

The  raw  potatoes  contained  0.34  per cent of  reducing  sugar calculated as maltose, the  cubes  cooked for  5  minutes in boiling water contained 8.32 per cent, and the cubes cooked for 1  hour,  7.82 per  cent.  Thus,  no sugar formation  occurred  at the  boiling point.

In view of this immediate heat-induced increase in the high GI free sugars, maltose (maltose has a ~10% higher GI than glucose), it should not surprise you that a study that was conducted by Jamaican scientists (Bahado-Singh. 2011), only a few months ago, found statistically significant increases in glycemic index and the area under the incremental glucose curve after boiling, frying, baking or roasting 10 sweet potato cultivars, which are commonly consumed in Jamaica (cf. figure 5):

Figure 5: Glycemic indices and glucose AUC of 10 common Jamaican sweet potato cultivars after boiling, frying, baking and roasting (data adapted from Bahado-Singh. 2011)

If we disregard the differences between the 10 cultivars and focus on the overall pattern, it is quite obvious that on the "less to worst thing you can do with your sweet potatoes if you are concerned about GI"-scale boiling is at the most benign end of the continuum, while baking and roasting compete for the position at the other end - a pattern, those of you who have already read Part 1 of the Potato Manifesto should be familiar with: Contrary to common believe new boiled (regular / sweet) potatoes are in fact a low GI food. In our kitchen (and even more so in the industrial processing machinery of the food industry), where the harmless tubers are mashed, pureed, dried, instantized, fried, baked, roasted etc., both, regular, as well as sweet potatoes do yet acquire at least some resemblance to the "pro-diabetic frankenfood", as which they have gotten labeled within the blogosphere, all along.

Figure 5: Comparison of regular and sweet potato glycemic indices after boiling, frying, baking and roasting.

If we now take a final look at the comparison of the average GI (figure 6 is based on data from both installments of the Potato Manifesto) of regular and sweet potatoes after boiling, frying, baking and roasting, it seems as if the main differences were that on average the regular potato has a slightly higher baseline GI (I do not need to remind you that according to Soh. 1999 boiled Desiree potatoes have a GI of 10!, do I?) and tends to be more resistant to heat-induced deteriorations in her starch / free sugar composition.

So, are boiled sweet and baked and roasted regular potatoes the way to go?

In view of the fact that probably 99% of the average and maybe 70% of the health conscious consumers don't even know the name of the potato cultivar they are using, let alone their age, storage temperature, the amount of phosphate in the soil on which it was grown, and all the other countless variables that have an impact on the "basal" GI of a potato, I honestly doubt that switching from one of the waxier, new regular potatoes (low basal GI) to a random (I mean, how many sweet potato cultivars are available at your grocery store?) sweet potato cultivar, would make you healthier, help you lose weight or offer any other GI-related benefits.

Image 2: Tapioca, another purpoted "health food" with a surprisingly high glycemic index GI of 84

Just as an aside, the Wolever study also examined the glucose response to another of the funky foods that are resurfacing on the Internet as "health foods", these days: Tapioca - also known as cassava, manioc, aipim, bitter-cassava, boba, mandioca, macaxeira, manioca, tapioca plant, yuca. With a GI of 84 it easily outperforms, corn chips (GI 76) and even waffles (GI 79).

Note: Wherever this was necessary I converted GIs that were given with white bread as a reference to the glucose as a reference.

Whether you could benefit from the (again, on average and in this case specifically referring to the white variety of the regular potato) higher beta-carotene and vitamin C content of sweet potatoes would depend on the rest of your diet. If the latter is "99% paleo" ;-), the likelihood that you would not get enough of these antioxidants is close to zero and it should thusly not really make a difference whether you go for the "paleo-" or the "neolithic" potato, as long as you don't (over-)process her into another of the innumerable frankenfoods the average member of the neolithic convenience society is so fond of.

The Potato Manifesto - Part 1/2: A (Re-)Evaluation of the Contemporary Discrimination of "the" Ordinary Potato

Image 1: The grunty regular (left) and the cute sweet potato (left), which one would you commit your health to? (img. menshealth.co.uk)

This is a blogpost, which eventually turned out to be the first part of a series, is a post with a history, a rather complex one, to be precise. It is rooted (not tubered ;-) in my amazement over the contemporary craving for sweet potatoes within the ever-growing neo-paleolithic community on the Internet and was sparked by the recent publication of a study on sweet potatoes, I stumbled upon on my daily tours of the most recent scientific literature. To make long story short, instead of immediately summarizing the data, drawing some graphs and commenting on the real-world implications of this study, I decided to use the holiday to descend into the archives and take a closer look at what science has to say on the bitter truth about the grunty regular and the starchy promises of cute sweet potato (cf. image 1 ;-)...

When wheat was devils excrement, would regular potatoes then be his horns?

According to the official obesity statistics of the European Union, British women are the fattest in Europe (Eurostat. 2011): 23.9% were classified as being obese (BMI > 30) in the year 2008 to 2009. This certainly raises the not altogether serious question, whether the British obesity problem (the obesity rate among the men was 22.1% and thusly topped only be the Maltese with 24.7%) is due to the fried fish or the fried (regular) potatoes in the unofficial British national dish, fish & chips.

Image 2: Obese British woman's rear view (img. BBC.co.uk)

A note to my dear American friends: Don't crow too soon, the obesity rate in the US tops the one in the UK by more than just a margin. According to a 2010 paper by Flegal et al. that was published in the Journal of the American Medical Association, the estimated obesity rate in the US amounts to 35.5% among the women and 32.2% among the men (Flegal. 2010). And a constantly increasing percantage (currently 4.7%) of the American population is already "extremely obese" and has a BMI > 40! Just to put that into perspective. A man or woman with a BMI beyond 40 and a height of 5 foot and 7 inches (170cm) would weigh at least (!) 254.85lbs (115.6kg) - this is already "Kig-Size Homer"-territory (cf. Intermittent Thoughts).

If we follow the current dietary paradigms and ignore the frying procedure, the answer to this question does not appear to be very difficult. I mean, when wheat was devil's excrement, then regular potatoes would be his horns or even nastier body parts, I do not want to mention here... and though a reasonable explanation for the widespread vilification of potatoes still escapes me, the contemporary nutritional paradigm within the health and nutrition blogosphere suggests that regular white potatoes have an awfully high glycemic index, will spike your blood sugar levels and have your neolithic body pump out tons of insulin - even if the rest of your diet is 99% paleo, as many of the listeners of Robb Wolf's podcast like to describe the way they are eating after having read his (widely read, yet controversial - esp. wrt to starches / carbs, fish oil and a few other topics) book ;-)

Figure 1: Names and characteristics of eight common potato cultivars in the British diet (left) and experimentally evaluated area under the glucose curve and glycemic indices (right; data based on Henry. 2005)

If we take a look at the data in figure 1, which shows both the incremental area under the glucose curve (AUC) and the GI of eight commercially available and commonly consumed British potato cultivars, it should however be quite obvious that the concept of the bad high-GI regular potato is about as misguided as the racist or religious prejudices some of our fellow human beings are still harboring against other members of the human race. With glycemic indices that range from 56 for the "waxy" Marfona to 94 for the "firm" Maris Peer, the "bad" regular potatoes cover the exact same GI range as their "healthy" sweet cousins (come back tomorrow for Part II of this series with more information on sweet potatoes).

Cultivar, processing, serving temperature and more have profound influences on the GI

The type  (=cultivar) of the (classic) potato, is yet neither the only, nor the most important determinant of the glycemic index of a potato meal. The processing method and, to my own surprise, even the food temperature have considerable influence on the glucose response to otherwise identical test meals, as well:

Figure 2: Incremental areas under the curve (AUC) and glycemic index values for 50 g available carbohydrate portions of white bread and seven potato meals tested in a cohort of 12 healthy subjects (data adapted from Fernandes. 2005)

On the left = "better than white bread"-side of figure 2, we have cold, boiled red potatoes (GI 56.2) and, surprise, frensh fries (GI 63.6) and roasted Californian white potatoes  (GI 72.3, but lower AUC than white bread). On the right = "worse than white bread"-side, instant mashed potatoes (GI 87.7) and the hot variety of the "low GI" red potatoes (GI 89.4) are competing for the red lantern.

With regard to the unexpected differences between cold and hot red potatoes, it is important to note that the results of a 2011 study by Kinnear et al. confirm that the latter is not an artifact of the Fernandes study. In their trial, the scientists from the University of Toronto found an average GI reduction of -37% (mean GI for the tested cultivars ~47), when the freshly boiled potatoes were refrigerated at 4°C for 24–28h before they were served to the 10 healthy study participants (Kinnear. 2011). As far as the reasons for this temperature-dependence of the glycemic index is concerned, Kinnear et al. speculate that it is an effect "due to starch retrogradation", which is a process that takes place in gelatinized starch, when the amylose and amylopectin chains realign themselves and thusly causes the liquid to gel. This is quite interesting, as it stands in line with the low GI of the Marfona potato (cf. figure 1), the texture of which is described as "waxy". The long-established relation of the phosphate content and the degree of starch gelatinization (and thusly digestibility and GI), on the other hand, could explain difference between crops and differences between identical crops grown on soil with different phosphate contents.

Figure 3: Areas under the glucose curves (AUC) in 32 healthy volunteers to 50g carbohydrates from mashed potatoes with or without 10g fructose administered 0, 30 or 60min before the meal. Measure by Accu Check finger-prick glucometer and YSI glucose oxidase analyzer (data adapted from Heacock. 2002)

Did you know that fructose, of all, is able to reduce the postprandial increase in serum glucose in nondiabetic adults (mean age: 26)? In their 2002 study, Patricia M. Heacock and her colleagues were able to show that pre-ingestion of 10g of fructose 60min and 30min before the ingestion of a 50g carbohydrate meal (from potatoes) reduced the area under the glucose curve (glucose AUC; cf. figure 3) by 25% and 27%, respectively (Heacock. 2002). The immediate co-administration of 10g of fructose with the potato meal (figure 3, 0 min), on the other, did not induce any statistically significant changes in the glucose AUC of the 13 male and 19 female study participants whose blood glucose levels were measured by finger-prick capillary blood (Accu Check) and glucose oxidase analyzers (YSI).

Furthermore, a 1999 study by Soh and Brand-Miller from the University of Sidney (Soh. 1999) shows that the real-world glucose responses of different individuals to differently processed and stored potato cultivars cover an even broader spectrum (especially on the low GI side) than the results of the previously cited studies suggested. The GI values, the Australian scientists calculated based on the glucose response to a 50g carbohydrate portion of eight different potato meals (three varieties, four cooking methods, two states of maturity) differed by as much as +/- 55pts, with canned new potatoes (GI 65) at the upper and boiled Desiree potatoes (GI 10) at the very lower end of the spectrum. And as if things were not complicated enough, already, Soh and Brand-Miller also introduce yet another variable into the equation - the size of the tuber, which showed a statistically significant correlation with the glucose response of the study 10 healthy participants (correlation between GI and tuber size: r=0.83, p < 0.05).

Black-and-white thinking and ineradicable prejudices

If we base our argumentation solely on the glycemic index, which is in fact the main argument that is brought forward against "regular" potatoes in the public debate, it is quite clear that the poor (regular) potato is another victim of the human propensity to black-and-white thinking and the public's stubborn adherence to convential nutritional wisdom. With reference to the "unjustified generalization" that "all potatoes have a high glycemic index", Anette E. Buyken and Anja Kroke, two researchers from the Research Institute of Child Nutrition in Dortmund, Germany, write in their letter to the editor of the British Journal of Nutrition (Buyken. 2005):

Figure 4: GI values (glucose reference) for potatoes by different cooking methods; the horizontal bars indicate the minimal and maximal glycemic index; the dotted vertical lines mark the conventionally accepted  "low GI" <55 (left) and "high GI" >70 (right) cut-off points (the figure was taken directly from Buyken. 2005)

[...] as with all GI data, the GI values of potatoes may depend on cooking method, processing, variety and the composition of the meal. This fact deserves attention since mashed potatoes, French fries, baked potatoes and potatoes cooked in a microwave are characterised by GI values mostly exceeding the upper limit for a high GI value of 70; whereas conventionally boiled potatoes appear to have a GI value on average below 70. The values of conventionally boiled potatoes do vary considerably though, so it may also be that some potato varieties have an inherently low GI what-ever the cooking method (Najjar. 2004; Fernandes. 2005). In this context, it should be considered that most currently available GI values are based on mature potato varieties (Ontario, Prince Edward Island, Desiree, Pontiac, Sebago). The starch of more mature potatoes is, however, easier to digest, presumably due to increased amylopectin branching and hence lower resistance to gelatinisation, which in turn results in a higher GI (Soh. 1999).

Buyken and Kroke support their argument by the means of an illustration of the broad range of the glycemic responses (and respective GI) of study participants to 46 different potato meals (cf. figure 4) and emphasize that there are significant differences in both the preferred potato cultivars, as well as the respective cooking / processing methods between European and US customers. While the former "prefer potato varieties characterised by a lower GI", the prevailing potato varieties in the US are mature and exhibit significantly higher glycemic indices. This trend toward higher glycemic indices in US potato meals is reinforced by the average American's preference to fry, bake, mash, roast or microwave his potatoes, so that it would  be "thoughtless" for any European, or American who selects less mature, low GI cultivars and refrains from frying, baking, mashing, roasting or microwaving his potatoes to follow the grossly over-generalized recommendation to eat less potatoes.

Ok, not all regular potatoes are made equal, but sweet potatoes are still king, right?

Against the background that my grand father who lived a 100% healthy, diabetes-free life into his late 90s, competed in track and fields and swam laps until about 6 months before he died, had regular potatoes with every dinner, I may be somewhat biased as far as the "bad potatoes" are concerned. This does yet not compromise the value of the rational arguments and scientific evidence against the unjust and, above all, over-generalized vilification of regular potatoes I have brought forward in this first installment of the Potato Manifesto. If you are interested in how the "holy" sweet potato which is currently hailed as the savior of the neo-paleolithic race compares, come back tomorrow for Part II of the Potato Manifesto ;-)

Sucralose, Hazardous or Innocent? A Review of the Review - Part I: Glucose, Insulin & GLP1 | Sucralose & Diabetes?

Sweet, low and unhealthy? Is sucralose as bad as a recent review would suggest?

I guess I could say "I've written more than enough about artificial sweeteners!" and simply ignore the sensational press release about the "bioactivity" of this increasingly common artificial sweetener you've read on the SuppVersity Facebook News, yesterday (check it out). In view of the fact that most of my previous artificial sweetener articles revolved around a possible impact on body weight / insulin sensitivity, ca. 90% of the claims in the press release are actually "news" - even for SuppVersity readers. Ample reason to take another, closer look at the study outcome and analyze both the "real" results, what the press release made of it and whether or not the panic that's already spreading on the Internet is warranted.

First things first: What are we talking about?

As the press release informs us, an "extensive review published by Taylor & Francis"... stop, so here is our first hint. The authors of the press release are people from Taylor & Francis and have a vested interest in writing it in a way that will have people share the text and their name on the Internet (that worked pretty well, as you can see - even I am talking about it ;-)

This is part I of a multi-part series:

Sucralose, insulin, glucose, GLP-1

Appetite, Obesity & Gut Health

Cancer, Drug & Hormone Interact.

I know that Mark Sisson likes to says this, but this website is not written by a machine, but by a man who has the same "short" 24h days you have... basically, what I am trying to say is that I had to split this review of the review into a "trilogy" - and be honest, you wouldn't want an article thrice as long as this one, would you?

Next on the list is some information about the "extensive review" and the hint that it was authored by Susan S. Schiffman, PhD, "an internationally known sweetener researcher" and Kristina I. Rother, MD, MHSc, "of the National Institutes of Health (NIH)". So, now it stands out of question that what's in this review is the truth and nothing but the truth. I mean, what else would it be if these experts, one working for the almighty and benevolent NIH "summarize[d] the biological properties of sucralose based on hundreds of archival, peer-reviewed scientific journal publications" (my emphasis).

Based on hundreds of [...] publications?

While it is true that the review has 476 references, not all of them deal with sucralose and only few of them provide data that would by any means be relevant to the most important question of all: "Can sucralose consumption harm us". The statement "based on hundreds of [...] publications" is thus misleading, because when it's used in conjunction with the word "review" people will interpret it as the number of relevant papers - or, even worse, of studies the data of which has been used in a systematic review. The paper at hand is yet everything but a systematic review - it's a narrative one.

Next on the list of our "review with your critical thinking cap on the head" list are the following claims about the health / environmental effects of sucralose:

• Please note: I will address all the issues within this trilogy, but for today I will focus on the one with the asterisk (*). As you can see from the headlines in my preliminary outline above, the rest of the issues are going to follow, asap.
  

  The best thing you can do if you want to make sure you're not going to miss a single article is to register for the SuppVersity Newsletter at the bottom of the page or - even better - like the SuppVersity Facebook Page and you'll always be in the know.
  alterations in insulin, blood glucose, and glucagon-like peptide 1 (GLP-1) levels,
• metabolism of sucralose in the gastrointestinal tract to metabolites whose identity and safety profile are unknown,
• induction of cyctochrome P450 and P-glycoprotein in the gastrointestinal tract to levels that may limit the bioavailability of therapeutic drugs,
• reduction in the number and balance of beneficial bacteria in the gastrointestinal tract,
• histopathological findings in gastrointestinal tract including lymphocytic infiltrates into epithelium, epithelial scarring, mild depletion of goblet cells and glandular disorganization in the,
• decomposition and generation of chloropropanols (a potentially toxic class of compounds) during baking, and
• mutagenic alterations using several types of biological assays

What I am going to do now, is to track each and every of them back to the review and take a brief look at the research that's out there to make sure that we are actually dealing with "the truth", here ;-)

Claim I: Sucralose messes w/ blood glucose management

I have to admit I was very curious to see the evidence on which Schiffman & Rother base this claim and was pretty disappointed, when I saw an extensive list of rodent and cell model studies, like those by Jang et al. and Margolskee et al., in which human NCI-H716 cells (Jang. 2007) and mouse enteroendocrine cells (GLUTag; Margolskee. 2007) were used to support the claim that sucralose would lead to an increase in GLP-1 - which is, by the way you usually won't hear as an argument against artificial sweeter use ... anyways, we are going to see why later, for now it should suffice to say that this intrigued me.

In view of the physiological role of GLP-1 it's by no means clear whether the mentioned increase is actually something to be afraid of (see "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!? Roux-en-y Bypass Study Sheds a Whole New Light on Satiety(Hormone)-Induced Weight Loss" | learn more)

After taking a closer look at the two studies and realizing that I had no way to tell whether it's realistic to assume that our cells are exposed to 1nM or 5nM of sucralose, which is what Jang et al. observed was the dosage they needed to elicit the desired increase in GLP-1 (Jang. 2007). And even if it would - would increases in GLP-1 actually be such a bad thing? I mean, you've read about the use of GLP-1 and its synthetic analogues to treat diabetes I & II (Pettus. 2013; Schwartz. 2013), protect you from NAFLD (Panjwani. 2013), reduce the oxidative damage to the heart during hypoglycemic episodes in type I diabetics (Ceriello. 2013), etc. both right here at www.suppversity.com, as well as over on the SuppVersity Facebook Wall.

The thing we'd have to fear is thus not the release of GLP-1 (for a large majority of the increasingly overweight population this could actually be beneficial), but a "dysregulation" GLP-1, GIP, C-peptide, insulin, glucose, and so on and so forth....

I don't say that it's impossible that this is going to happen, but by no we have no convincing evidence that it will and in view of the fact that a scarcity of glucose is not exactly something to be afraid of in this day and age, an increase in GLP-1 could actually be an advantage for the majority of SAD-dieters. Unfortunately, the real-world (=non-petri dish) evidence from a 2009 study by Ma et al. tells us that this is not going to happen in humans.

Figure 1: GLP 1 (left) + insulin (right) response in healthy individuals to sucrose, saline (control) or 80mg and 800mg sucralose (theoretically this would be as sweet as 48g and 480g of pure sugar; Ma. 2009).

In face of the data in Figure 1, which leaves little doubt that only sugar (sucrose), but neither 80mg, nor 800mg of sucrose will have any effect on the critical hormones / peptides GLP-1, GIP, and insulin, Schiffman & Rother's argumentation breaks down. And if you take into account that the corresponding (theoretical) sweetness equivalents of 80mg and 800mg of sucralose are 48g and 480g of pure sugar, I seriously doubt that we'd have to test higher dosages to make sure that nobody "intoxicates" himself ;-)

Granted: Even the authors cite evidence against the GLP-1 hyothesis

I know, not everyone is willing to briefly type "GLP1 subjects sucralose" into a search engine, wait for the results to pop up and follow the link to the previously cited study by Ma et al. I understand that, but if that was you, you would actually just have to scroll down to the bottom of sensationalist press release, I cited on Facebook and click on the link (or enter the doi) to the (free) full-text, to find the following line on page 402:

"Oral consumption of sucralose without co-administration of glucose (Brown et al.,
2011) produced no significant effect on blood glucose levels. Sucralose delivered by intraduodenal infusion in combination with glucose also exerted no marked effect on blood glucose or plasma GLP-1 (Ma et al., 2010)."

In other words, contrary to the author(s) of the press release, Schiffman and Rother are well aware that their evidence is far from being conclusive. What I am not so certain about, though, is whether they are also aware that their reference to a study by Brown et al. from 2009, where the coningestion of sucralose with acesulfame-K in 240 ml of caffeine-free diet soda (Diet Rite cola) produced an increase in the GLP-1, but not insulin or glucose (see figure 2), could actually be interpreted as a highly beneficial result.

Figure 2: Glucose, insulin and GLP1 response to oral glucose tolerance test conducted 10min after the ingestion of 240 ml of caffeine-free diet soda (Diet Rite cola; boxes) or carbonated water (circles; Brown. 2009)

If glucose is around, an increased GLP-1 response is after all not necessarily a bad thing. In 2002, for example, Zander et al. reported in The Lancet that 6 weeks "on GLP-1" ...

• 

  The WM-HDP ↔ GLP-1 ↔ fatty oxidation connection | reread "Waxy Maize Reloaded" read more

  reduced the fasting and 8h post-meal free fatty acid levels of type II diabetics by -25% and 30%,
• improved the 8h blood glucose levels,
• decreased the HbA1c value from 9.2% to 7.9%,
• normalized the levels of cell-toxic fructosamine, 
• slowed down gastric emptying 
• decreased their ravenous appetite,
• improved insulin sensitivity and β-cell function, and
• induced a -3% reduction in total body fat.

Not much of a surprise, if you are familiar wit the effects of GLP-1 I discussed in the "Waxy Maize Reloaded" article (learn more), right? As far as the physiologically measurable mechanisms for derangements of the blood glucose management go, this leaves us with a potentially centrally mediated dysregulation of glucose sensing for which we do as of yet only have in-vitro "evidence" from a 2009 study by Ren et al. The researchers observed (obviously in the petri dish) that the normal expression of one out of three hypothalamic sweet taste receptors (Tas1R2) in cells from the hypothalamus is reduced in the presence of 0.5mM of sucralose. Up to now we do yet neither know if orally ingested sucrose can actually make it into the brain, whether the corresponding changes in Tas1R2 expression would be physiologically relevant, or what its consequences would be.

"Science Round-Up Seconds: The Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | more

Preliminary bottom line: As far as a potential dysregulation of the glucose metabolism is concerned, I still believe that there is currently not enough evidence to support the claims from the press release or implications of the biased listing of "significant findings" in the conclusion of the full text, where the authors discard all previously cited counter-evidence from human studies and focus on a study by Pepino et al., the questionable implications of which I already discussed in the Science Round-Up on May 21, 2013 (more). In the absence of controlled long term human studies this bottom line must however not be misunderstood as a full acquittal. In other words, the only thing this study demonstrates is how little we actually now.

As far as centrally mediated effects are concerned, the upcoming installments of what began as a comment and became a series of articles on sucralose may provide at least some insights into potential long(er) term effects on blood glucose management. Derangements that occur in response to changes in the gut microbiome, endocrine system or toxic effects of sucralose or its byproducts would after all only become visible after weeks or months of chronic (high dose?) ingestion of this globally approved artificial sweetener.

References:

• Brown, R. J., Walter, M., & Rother, K. I. (2009). Ingestion of diet soda before a glucose load augments glucagon-like peptide-1 secretion. Diabetes Care, 32(12), 2184-2186.
• Ceriello, A., Novials, A., Ortega, E., Canivell, S., La Sala, L., Pujadas, G., ... & Genovese, S. (2013). Vitamin C Further Improves the Protective Effect of Glucagon-Like Peptide-1 on Acute Hypoglycemia-Induced Oxidative Stress, Inflammation, and Endothelial Dysfunction in Type 1 Diabetes. Diabetes care, 36(12), 4104-4108. 
• Fujita, Y., Wideman, R. D., Speck, M., Asadi, A., King, D. S., Webber, T. D., ... & Kieffer, T. J. (2009). Incretin release from gut is acutely enhanced by sugar but not by sweeteners in vivo. American Journal of Physiology-Endocrinology and Metabolism, 296(3), E473-E479.
• Jang, H. J., Kokrashvili, Z., Theodorakis, M. J., Carlson, O. D., Kim, B. J., Zhou, J., ... & Egan, J. M. (2007). Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1. Proceedings of the National Academy of Sciences, 104(38), 15069-15074. 
• Ma, J., Bellon, M., Wishart, J. M., Young, R., Blackshaw, L. A., Jones, K. L., ... & Rayner, C. K. (2009). Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. American Journal of Physiology-Gastrointestinal and Liver Physiology, 296(4), G735-G739.
• Margolskee, R. F., Dyer, J., Kokrashvili, Z., Salmon, K. S., Ilegems, E., Daly, K., ... & Shirazi-Beechey, S. P. (2007). T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1. Proceedings of the National Academy of Sciences, 104(38), 15075-15080.
• Panjwani, N., Mulvihill, E. E., Longuet, C., Yusta, B., Campbell, J. E., Brown, T. J., ... & Drucker, D. J. (2013). GLP-1 receptor activation indirectly reduces hepatic lipid accumulation but does not attenuate development of atherosclerosis in diabetic male ApoE−/− mice. Endocrinology, 154(1), 127-139.
• Pettus, J., Hirsch, I., & Edelman, S. (2013). GLP-1 Agonists in Type 1 Diabetes. Clinical Immunology. 
• Ren, X., Zhou, L., Terwilliger, R., Newton, S. S., & De Araujo, I. E. (2009). Sweet taste signaling functions as a hypothalamic glucose sensor. Frontiers in integrative neuroscience, 3. 
• Schiffman, S. S., & Rother, K. I. (2013). Sucralose, A Synthetic Organochlorine Sweetener: Overview Of Biological Issues. Journal of Toxicology and Environmental Health, Part B, 16(7), 399-451.
• Schwartz, S., & DeFronzo, R. A. (2013). Is Incretin-Based Therapy Ready for the Care of Hospitalized Patients With Type 2 Diabetes? The time has come for GLP-1 receptor agonists!. Diabetes care, 36(7), 2107-2111.

Post-Workout Chlorogenic Acid / Caffeine Supplementation - For Good or For Worse? Plus: Glycogen Synthesis & Why A Post-Workout May Be a Better Idea Than You'd Think

"Done,... where is my post-workout coffee?" - Post workout caffeine / chlorogenic acid - good or bad idea?

I know it's kind of late to post an article like this months after the ISSN conference, but I recently hit on an overview of the poster presentations and noticed that I did actually miss a couple of interesting studies. Don't worry, I won't be addressing a couple of them in the weeks to come in some detail.

Not all are really news-worthy, but aside from today's item on caffeine and chlorogenic acid, there were also posters on nutrient timing, different forms of protein, commercially available supplements and other stuff that's all classic "SuppVersity fodder"?

Chlorogenic acid? Isn't that Ozzy's green coffee bean stuff? You are correct, but could actually read about it here at the SuppVersityway before it was on Dr. Oz. Plus, I still believe that there is something wrong with the corresponding study and do still have to meet someone who has successfully lost weight by just adding some GCB to the diet, which is effectively what Ozzy and the study promised | learn more

Caffeine and chlorogenic acid? Right, that sounds like green coffee bean extract, but in the case of Jason R Beam et al.'s study, we are dealing with an artificial stack of

• 5mg/kg body weight of caffeine plus 75 g of dextrose (CAF), 
• 5 mg/kg body weight of chlorogenic acid plus 75 g of dextrose (CGA), or 
• 5 mg/body weight of dextrose plus 75 g dextrose (PLA)

the 10 moderately to highly trained study participants consumed after 30-minutes of  high intensity cycling at 60% of peak power output (~90% HR max).

Figure 1:

As you can see in Figure 1, we do see quite extra-ordinary effects of the administration of both caffeine and chlorogenic acid on post-workout glucose metabolism. The changes in the area under the cure (2h AUC) do yet overestimate the real-world difference between the glucose curves (not shown), which have a slightly higher spike immediately after the ingestion.

"Ok, no caffeine after a workout - right!?"

In the case of caffeine that was to be expected, it has after all been shown to decrease the insulin-induced glucose uptake (Graham. 2001). The fact that the glycemic response was - within the statistically probable margins - still identical, is simply the result that the stimulation of glucose uptake and hepatic, as well as muscular glucose storage is not really necessary as long at the glycogen stores are low. Accordingly, a 2004 study by Battram et al. was unable to show any effect of caffeine ingestion on proglycogen and macroglycogen resynthesis after a workout (Battram. 2004).

Figure 2: Skeletal muscle glycogen content (mmol/kg dw) immediately after exercise 0. 1, 4h after cycling to volitional fatigue (70% Vo2Peak) w/ or w/out coingestion of 8mg/kg BW (+ 1g/kg glucose) after the workout - left; corresponding levels of pCAMK and p-Akt (arbitrary units) 1h and 4h after the workout, right (Pederson. 2009).

As you can see in Figure 2 the net amount of glucose that ends up in the musculature after exhaustive (if you don't deplete the stores this effect won't be there) exercise was in fact favorably affected by the congestion of 8mg/kg caffeine and 1g/kg glucose in with caffeine in the 7 endurance-trained cyclists and triathletes in a study by Pedersen et al. from 2009. The exact underlying mechanisms of this beneficial effects, as well as dose response relationships do yet still have to be determined, but Pederson et al. speculate that it may a result of the increased activation of p-AKT:

You think you've heard about p-Akt before, but are not sure where? Well, chances are it was here at the SuppVersity, yet probably in a different context, i.e. as part of the Intermittent Thoughts on Building Muscle | read more

"The increase [in p-AKT] tended to be higher after the ingestion of caffeine with CHO after both 1 and4hof recovery, but failed to reach statistical significance. Akt seems to regulate glucose uptake by phosphorylating and inhibiting the Rab-GTPase-activating protein AS160. Thus it is tempting to speculate on the role of Akt in glucose transport given that the Akt substrate AS160 has been identified as an important regulator of GLUT4 traffic.

We have recently shown that AS160 is phosphorylated in human skeletal muscle after endurance exercise with concomitant phosphorylation of Akt (7), providing correlative evidence to suggest AS160 is an exercise-responsive protein with a role in glucose uptake." (Pederson. 2009)

If we discard potential negative effects of the caffeine-induced CNS activation on post-exercise nervous system recovery, and take into account that the elevated glucose + insulin AUC Beam observed in the experiments for his dissertation and ISSN conference poster are negligible, the preliminary bottom line for post-workout caffeine intake would be: "If glycogen resynthesis is what you are looking for, do it!"

"What about the effects of chlorogenic acid. Shouldn't the exact opposite happen?"

Now that we've searched for explanations of the effects of caffeine on post-workout glycemia we are still left with the astonishing increase in the two-hour glucose area under the curve, i.e. total glycemia, Beam observed in the glucose + chlorogenic arm of his study.

Figure 3: Insulin (AUC) for each subject during the placebo, caffeine, and chlorogenic acid trials (Beam. 2013)

If you take a closer look at the data to the right, you won't get a mechanistic explanation of the underyling reasons, but you will at least get an idea of what statistical significance means and why we are talking about it in almost every study analysis, even if it does not equate physiological significance.

In this particular case the 2 outliers, subject 1 and subject 6 do not simply "ruin" the statistical significance, they are actually the (almost) only reason that insulin response is not virtually identical to the placebo trial.

As far as potential negative consequences of the post-workout consumption of cholorgenic acid goes, you do thus not have to be worried, whether it is actually a good idea to use a supplement that's meant to increase the activity of AMPK in a phase, when the latter is already maximized, is however questionable. In the best case, the additional benefits will be minimal, in the worst case it  CGA will ruin the glucose repartitioning effects of the workout by increasing AMPK and thus glucose uptake in the fat cells (Alonso-Castro. 2008).

If you actually have problems with insulin resistance / glucose uptake (which is not the case for 90%+ of the people who buy corresponding supps), I suggest you check out this list of useful anti-diabetes agents.

Bottom line: I would assume that you will not have expected that, but based on the results of the study at hand and the review of previous literature the effects of caffeine and chlorogenic acid on post-workout glycemia are most likely negligible.

If you still insist on supplementing with one or the other immediately after a workout, though, there would be a rationale to use caffeine. The use of chlorogenic acid, green coffee bean extracts or any other highly advertised and for physical culturist 100% useless "nutrient repartitioning agents", would be at least non-sensical, in view of the potential negative effect on the true nutrient repartitioning effects, even potentially downright counterproductive.

References:

• Alonso-Castro, A. J., Miranda-Torres, A. C., González-Chávez, M. M., & Salazar-Olivo, L. A. (2008). Cecropia obtusifolia Bertol and its active compound, chlorogenic acid, stimulate 2-NBD glucose uptake in both insulin-sensitive and insulin-resistant 3T3 adipocytes. Journal of ethnopharmacology, 120(3), 458-464. 
• Beam, J. (2013). The effect of post-exercise caffeine and chlorogenic acid supplementation on blood glucose disposal and insulin sensitivity.
• Battram, D. S., Shearer, J., Robinson, D., & Graham, T. E. (2004). Caffeine ingestion does not impede the resynthesis of proglycogen and macroglycogen after prolonged exercise and carbohydrate supplementation in humans. Journal of Applied Physiology, 96(3), 943-950.
• Pedersen, D. J., Lessard, S. J., Coffey, V. G., Churchley, E. G., Wootton, A. M., Ng, T., ... & Hawley, J. A. (2008). High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine. Journal of Applied Physiology, 105(1), 7-13.

3.8g/Day CLA as Anti-Diabetic Glucose Repartitioner - Two Recent Study Show Interesting Benefits from Conjugated Linoleic Acid Supplementation in Mouse & Man

CLA - A muscle specific glucose repartitioner for lean & athletic individuals?

In their latest article in the scientific journal Nutrition Research scientists from the Universidad Nacional del Litoral report that dietary CLA increases the glucose utilization under basal conditions and prevents the palmitate-induced inhibition of glucose uptake and incorporation that is stimulated by insulin.

Interestingly, Farina et al. also found that the beneficial effects of CLA were significantly more pronounced and without significant side effects in rodents who had been deprived of all omega-6 fatty acids - including CLA - before.

You can learn more about CLA at the SuppVersity

Natural CLA Sources Prevent Weight Gain

DHA Blunts CLA's Ill Health Effects on the Liver

Microencapsulated CLA for Fat Loss?

Fish Oil & CLA as Natural Anabolics?

Cis-9,11 o trans-10,12 Which to Take?

CLA as Natty Testosterone Booster?

Unfortunately, the provision of conjugated linoleic acid did also have negative effects on some aspects of glucose control. For example, Farina et al. observed a significant reduction in insulin response capacity that may - in the long run - compromise their ability to handle glucose.

Figure 1: CLA increases basal glucose intake and glycogen synthesis - the latter yet only when the rodent diet does not contain any linoleic acid (-LA), if it's not there is also a significant negative effect on insulin stimulated glucose uptake in the soleus muscle of the rodents (Farina. 2014)

Now, rodent studies are one thing, human studies are - at least according to some experts - something totally different. Against that background you will probably be more interested in the results of a recent study from the National Taichung University of Education in Korea. The authors, Jung-Piao Tsao, Su-Fen Liao, Mallikarjuna Korivi, Chien-Wen Hou, Chia-Hua Kuo, Hsueh-Fang Wang & I-Shiung Cheng, were able to show that the provision of a standard CLA supplement containing a 50:50 mixture of trans-10 cis-12 and cis-9 trans-11 isomers at a dosage of 3.8 g CLA per day for 8 week lead to significant can enhance the glycogen resynthesis rate in exercised human skeletal muscle.

Figure 2: Glycogen levels (a) and differences (b) in vastus lateralis of human skeletal muscle after a single bout of exercise in CLA and placebo trials (Tsao. 2014)

As you can see in Figure 2 this advantage was not just statistically significant, but appears to be high enough to be physiologically relevant. What is not clear, though, is whether the increased glycogen uptake of the vastus lateralis is a direct or indirect benefit - after all, previous studies indicate that CLA can decrease the glucose uptake in adipocytes (=fat cells | Perez-Matute. 2007). The increase in glycogen synthesis in the muscle of the 12 male young college students (aged 22.56 ± 0.45 years, body mass index 23.35 ± 0.79 and VO2 max 49.4 ± 1.67 ml/kg/min) who participated in the study may be a simple results of an increased relative glucose availability - or, as a supplement producer would call it to sell their supplements: "Glucose repartitioning"!

Figure 3: GLUT4 protein level (a) and P-Akt/Akt ratio (b) in vastus lateralis of human skeletal muscle after a single bout of exercise in CLA and placebo trials (Tsao. 2014).

A claim that is supported by the data in Figure 3, which indicate that the increased glucose uptake and subsequent increase in glycogen synthesis is a result of a CLA-induced increase in GLUT-4 glucose transporter expression, of which the data in Figure 2 also tells us that it occurred before the regular exercise-induced increase in GLUT-3 expression.

4g of Conjugated Linoleic Acid Promote CYP17A1 + Leydig Cell Testosterone Production and Increase Cardio-Mediated Muscle, Strength and Endurance Gains | more

Bottom line: Even if we take into consideration that this "study has limitation with lack of maintenance of the dietary recall or training diary for all participants," the result are an impressive argument in favor of CLA supplementation in athletes in whom the previously mentioned negative effects on insulin response capacity may not be physiologically relevant - if it occurs at all.

And still, Tsao et al. are right: "These findings suggest that CLA could consider as an effective ergogenic aid to improve the muscle glycogen levels and endurance capacity. However, it is necessary to monitor the whole-body glucose homeostasis to avoid possible adverse effects of CLA [..] on glucose metabolism" (Tsao. 2014) | Comment on Facebook!

References:

• Fariña, Ana C., et al. "Conjugated linoleic acid improves glucose utilization in the soleus muscle of rats fed linoleic acid–enriched and linoleic acid–deprived diets." Nutrition Research (2014).
• Perez-Matute, P., et al. "Conjugated linoleic acid inhibits glucose metabolism, leptin and adiponectin secretion in primary cultured rat adipocytes." Molecular and cellular endocrinology 268.1 (2007): 50-58.
• Ritsche, Kevin, et al. "Acute Exercise-Induced Growth Hormone is Attenuated in Response to Short-Term, High-Intensity Exercise Training." (2014).
• Tsao, Jung-Piao, et al. "Oral conjugated linoleic acid supplementation enhanced glycogen resynthesis in exercised human skeletal muscle." Journal of sports sciences ahead-of-print (2014): 1-9.

Reduced Exertion High Intensity Training - A Minimalist 2x20s HIIT Protocol For The Male Convenience Generation.

Image 1: Looks like humans are not the only lazy creatures, in these days of unhealthy convenience.

Laziness, it seems, is utterly human. If you look around, these days, it appears as if we were genetically programmed to be bone idle. And, from an evolutionary perspective, we may actually be. After all, moving around, hunting and gathering was an obligatory part of our lives in 99% of the human history. It was thus only consistent that our genes would tell us to sit down at the fireplace and relax, once we had found enough to eat on a given day... (un-)fortunately things have changed since those early days. Not only have we moved out of our caves, we have also found ways to radically reverse the ratio of activity to inactivity in our lives.

"Convenience" is the buzzword of the modern western civilization and the obesity epidemic is its unwanted consequence.

A consequence, which is yet by no means inevitable. After all, we all know that getting our behinds off our couches and into the gym, and setting the dietary recommendations of the (fast-)food industry, ahh... pardon, the government at naught would solve the problem, if ... yeah, if there was not this aforementioned genetically programmed laziness that makes the couch so much more appealing to us than the hard benches in the gym...

Sacrifice 30min per week of your TV-time and live to see your grandchildren graduate

A recent study from scientists from the United Kingdom does yet show that you could still spend more than enough time in front of your beloved television set, if you just performed what what Richard S. Metcalfe and his colleagues from the United Kingdom call the "minimal amount of exercise for improving metabolic health" (Metcalfe. 2011) - a 3x per week 10min exercise regimen with no more than two (yes, only 2x!) all-out sprints.

Figure 1: Outline of the training protocol, the black bars indicate all-out sprints at a breaking force equivalent to 7.5% of the individuals body weight (directly adapted from Metcalfe. 2011. Fig. 1)

As you can see in the outline of the experimental protocol, the 29 healthy and normal-weight, but sedentary young (~23y) men (n=13) and women (n=16) did not even have to start with 2x20s sprints. They rather built up to it, by starting out with a single 10s all-out cycle-ergometer sprint at a braking force equivalent to 7.5% of their body weight in the first week of the 6-week study period and built their exercise capacity from there.

Image 2: "Cardio" does not have to be steady state.

Note: If you have not read my previous blogposts on HIIT, you may have missed the information that interval training (not necessarily at the maximal intensity, though) is suitable for everyone - even heart disease patients (cf. Interval, not Steady State Aerobics is the Way to Go - Even for Patients with Myocardial Infarctions!). This has been confirmed only recently by Neil A. Smart et al. who found that "[i]ntermittent exercise may improve functional capacity [of congestive heart failure patients] to a greater extent than continuous exercise" (Smart. 2011) - and that despite the fact that both continuous (30min), as well as interval training (60min, 1 min cycling, 1 min rest) were performed at the same low intensity.

The rest of the 10-min exercise sessions, the subjects were pedaling along at 60W, which is about as much as it takes so that you do not fall off the bike, because of the lack of resistance that is required to stabilize yourself on the bike. The latter would have been tragic, at least if you are a man, because that would have counteracted the surprisingly (not for who has read about the magic of HIIT here at the SuppVersity before) profound effects this regimen, for which the scientists coined the name "reduced exertion high intensity training" (REHIT), had on the glucose homeostasis of the male subjects.

Figure 2: Changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test in men and women after 6 week of "reduced exertion high intensity training" (data calculated based on Metcalfe. 2011)

As the data in figure 2 shows, the statistically more than significant decreases in the area under the glucose (-12%) and insulin (-39%) curve (AUC) measured during an oral glucose tolerance test was exclusive to the 13 male participants - and that despite the fact that both, male as well as female study participants exhibited similar improvements in their individual VO2Max (+15% in men; +12% in women).

(RE)HIIT only for men?

As far as the underlying reasons for these gender differences are concerned, the scientists are pretty much at a loss, stating that this could be due to "the low statistical power of our study, with only eight female subjects performing the REHIT", " differences in metabolic perturbations during the brief high-intensity cycle sprints",  and the 3-day delay after the last HIIT session before the glucose tolerance test was done (as a SuppVersity reader you will be familiar with the notion that the "anabolic barn door" is wide open for 24-48h), so that "insulin sensitivity was improved in female subjects at an earlier time-point". Now, I do not want to sound like a himbo, but I would say that another observation the scientists made, provides a much better explanation:

[...] we observed that some of the female volunteers struggled with the transition from 60 W to the all-out sprints, and were unable to substantially increase their pedal frequency, and thus their power output during the sprints. This may have increased the aerobic contribution to energy supply and reduced glycogen depletion.

In other words, what was supposed to be a sprint turned out to be a sluggish ordeal. The slightly, but statistically significantly higher rates of perceived exertion (+10%) in the female study participants corroborates the assumption that the women simply did not burn enough glycogen. If we do now also consider the results of a 2008 study by Hagobia et al. who report that

[...] in women, exercise altered energy-regulating hormones in a direction expected to stimulate energy intake, regardless of energy status. In men, the response to exercise was abolished when energy balance was maintained.

It appears obvious that an increase in pedaling frequency by adapting the resistance to the individual fitness levels and dietary controls may be necessary to render this minimalist "REHIT" protocol productive for the fairer sex.

Figure 2: Comparison of changes in VO2Max, glucose and insulin area under the cure in response to oral glucose tolerance test subsequent to 6 weeks of REHIT, or 10 months of "classic cardio" exercise, or dietary intervention (data calculated based on Metcalfe. 2011 and Dengel. 1996)

The comparison of this 6 week exercise program with the results of a 10 months intervention program in likewise healthy sedentary, but older men (45y) who exercised 3x a week for 40min (steady state) at 75-85% of their maximal heart rate, goes to show that it would well be worth making the REHIT protocol work for women, as well (Dengel. 1996). After all, the steady state endurance protocol in the Dengel study was not only four times more time-consuming (plus, the intervention period was 6.6x longer) than the modified HIIT protocol in the Metcalfe study, it also failed to improve the glucose response to the oral glucose tolerance test and produced less pronounced improvements in insulin sensitivity (cf. insulin AUC in figure 3). The mild caloric reduction (-300-500kcal/day) that was imposed on another group of the study participants, on the other hand, yielded similar reductions in glucose and insulin AUCs as the REHIT protocol in the Metcalfe study that was accompanied by a body weight reduction of ~10%, a reduction in body-fat of -5.8% and essentially no loss in fat free mass!

Note: Unfortunately, Metcalfe et al. did not measure the body composition of the study participants. In view of the results of the Whyte study (Whyte. 2010), I cited in the Intermittent Thoughts on Healthy Weight Loss, where the participants lost -2.4cm of their allegedly obese bellies within no more than 2 weeks of doing HIIT, as well as the well-established correlation between insulin resistance and the size of your beer-belly, it is very well possible that the male participants in the Metcalfe study will have lost some body fat doing no more than 8.67 minutes of all out cycling spread across 18 training sessions in 6 weeks... and if they didn't their diet probably was still too convenient ;-)

The (in-)convenient truth about your future

Taken together the results of these studies suggest that a) steady state aerobic exercise is pretty pointless, b) even a minimalist HIIT regimen goes a long way, as long as c) you really hit it hard and d) adhere to your regular (hopefully non-convenient) diet, or even better e) introduce a slight calorie deficit. In other words, without at least some "inconveniences" as far as nutrition and exercise are concerned, chances are that YOU will either remain or become one of the 34,004,946 obese human beings that are now populating a planet where the US alone spend 1,550,566$ per day on the detrimental health consequences of the"convenience" of its citizens (data from Obesity Statistics).