Meal Timing, Glycemic Index & Load: Human Study Probes Whether "Hitting Your Macros" Really is All That Counts

High or low GI, carbs in the morning or in the evning, cookies and dingdongs or all bran. So many questions and way too many answers from rodent studies or studies in obese diabetics... but what are Mr. and Mrs. Healthy Average Joe supposed to do?

In a recently published paper, Linda M. Morgan, JiangWen Shi, Shelagh M. Hampton and Gary Frost take yet another look on a concept that has lost much of the momentum it had only a decade ago: The GI and / or GL paradigm (GI: glycemic index (abstract unit); GL: glycemic load, i.e. GI / actual amount of food) and combines another paradigm, which is still gathering momentum within the medical science community - the issue of nutrient timing, in order to answer the following questions:

• Will a large evening energy and carbohydrate load cause an increase in postprandial glucose that is comparable to the same amount of energy and carbohydrates in the morning?
• Will a high glycaemic excursions in the evening be ameliorated by decreasing the glycaemic index (GI) of the meal?

Or put simply: Does carbohydrate and energy timing make a difference and can this difference be mitigated by chosing the "right", i.e. low glycemic carbs (e.g. sweet potato vs. white bread)?

White bread king or all-bran pauper - is that  the question?

To answer this world-shattering question and actually prove their hypothesis that both, i.e. having carbs in the evening and having those in the form of high glycemic index foods, will have negative consequences on postprandial glycemia, the scientists picked six healthy volunteers (four females, two males; mean age 30 +/- 4.3 years, BMI 21·6 +/- 1.3 kg/m²) and randomly assigned them to a follow one of the four following dietary protocols:

• Low GI (average GI = 34), with the majority of energy load consumed in the morning (LGI-am)
• Low GI, with the majority of energy load consumed in the evening (LGI-pm)
• High GI (average GI = 84), with the majority of energy load consumed in the morning (HGI-am)
• High GI, with the majority of energy load consumed in the evening (HGI-pm)

with identical energy content of approx. 8368 kJ (2000 kcal) for the whole day on four individual intervention days with a minimum of 7 days between each of the tests. Breakfast was given at 09.30 hours, lunch at 13.30 hours and the evening meal at 20.30 hours - subjects were at the laboratory for the whole day. Blood samples were taken 2h postprandial and blood glucose levels were monitored continuously via a "MiniMed continuous glucose monitoring system" that senses interstitial glucose by electrochemical detection in subcutaneous interstitial fluid in 5 min intervals.

Figure 1: Composition of the two test diets (low GI, blue; high GI read) and individual macronutrient breakdown of the test meals the subjects consumed on two seperate occasions (based on Morgan. 2012)

It does not take a nutrition expert to see that despite the obvious differences with respect to the glycemic index and load, even the allegedly healthy low GI diet with all-bran for dinner* and a macronutrient composition 72% carbohydrates 14% protein and 14% fat is not exactly what the latest research would suggest to be a healthy, let alone a "physique enhancing" diet.

*note: The scientists probably chose similar foods for breakfast and dinner, because the study design required those to be exchangeable.

Against that background it is still astonishing how much of a difference...

• 99% higher fiber content,
• -60% lower glycemic index (GI), and
• -63% lower glycemic load (GL)

... actually make when it comes to the effect of isocaloric meals with identical macronutrient compositions (see figure 1, right):

Figure 2: Total area under the curve for interstitial glucose (0–20 h), postprandial plasma insulin, TAG (**mind the text for info a potential typo, here) and NEFA (0–2 h after each meal) in six healthy volunteers following either a high-glycaemic index (HGI) or a low-glycaemic index (LGI) diet, with most of the energy consumed either early (LGI-am, HGI-am) or late (LGI-pm, HGI-pm); all values expressed relative to respective statistical mean (data calculated based on Morgan. 2012)

I guess I don't have to tell you that the image that emerges here stands in line with the as of late largely ignored glycemic index paradigm the underlying message of which is: It is not simply the amount of sugar you eat,  but rather how fast / hard it hits your blood stream that determines it's impact of on your glucose metabolism. And with respect to the latter, the researchers remark:

"Glucose and insulin responses showed broadly similar patterns. Both meal timing and quality of carbohydrate affected postprandial glucose and insulin responses (P < 0.01). The area under the glucose and insulin response curves was greatest for the HGI-pm meal regimen. The HGI-pm meal regimen produced a significantly greater postprandial area under the glucose curve than for any of the other three meal regimens (P < 0.05). The postprandial area under the insulin curve was significantly greater than both the LGI regimens (P < 0•05). Postprandial insulin resistance measured by homeostatic model assessment was also significantly greater for the HGI-pm meal than for the two LGI meals (P < 0•05)."

However, since Morgan, Shi, Hampton and Frost also state that "[p]ostprandial TAG and NEFA levels were not affected by meal timing or carbohydrate quality", I do suspect that there is a typo in table 3 of the original study, where it says that the TAG would be 5.04 mmol/l x h (probably is 6.04) and thus more than 15% lower than the average (TAG levels and insulin resistance usually go hand in hand, so it is really very unlikely that the 5.04 mmol/l x h is correct).

So what's the take home message here?

The only question that still has to be answered would be "King or pauper? At least with regard to the former, the best thing I can to is to suggest you read both the posts on "Breaking the Fast" and the "Carbs Past 6PM Posts"  (Part 1 & Part 2). When you have done that your perspective on the importance of breakfast and the purported fallacy of having a large dinner should already have changed. The things that are still left to do is not fool yourself into the false belief that you can pound whatever junk you want (as long as it fits your macros). As the glucose curve of the high GI arms (light color) in the figure above goes to show you, your body won't be happy when you get your "carb macros" from sugary junk.

Stick to starchy (or "save carbs", if you will) and fruit. Use veggies to fill you up. Use coconut & olive oil and the fats that are already in your meats, fish and dairy products to achieve baseline fat intake of at least 40-50g (all together). Aim for a 100-120g carbohydrate basis, diverge towards the lower side, when your body fat is high, you can't train or you're dieting and towards the higher side, when you are already very lean, have a high training volume, or are trying to build muscle. Complement that with min. 20g of quality protein with each meal. Don't deprive yourself on any nutrient completely and ramp up the total amount of food (at the given ratio) to fulfill your energy requirements.

In that, avoid processed food sand rely on whole foods, whenever possible (>90%),. Use food supplements* only where it makes sense, e.g. a protein shake post workout (*creatine for example would not be a "food supplement", since you can NEVER get the amounts that are necessary to supersaturate your stores from meat alone) and don't forget to live about all that "dieting" and thinking about the best ways to eat, please!

So if we assume that my assumption with respect to the triglyceride values in the originally published study are correct and we are simply dealing with a typo here, the next questions which arise here, are...

1. What is / are the reason/s that the lipid metabolism did not suffer?
2. How reliable is the HOMA-PP, i.e. the postprandial assessment of insulin sensitivity via the homeostasis model assessment? 
3. What does all this mean for you? Does meal timing not make a difference and are macros all that counts? 

As far as (1) goes, the answer is pretty simple: With a diet that was that low in fat and not overabundant in energy (2,000kcal for both diets) any potential the negative downsides on lipid metabolism will take their time to show. The acute ingestion of three high GI meals on a single day or modifications in their distribution across the day won't have much of an effect in healthy individuals, such as the four women and two men in the study at hand (in diabetics and especially patients with NAFLD things will probably look different, though).

The absence of changes in lipid metabolism after one day on high vs. low GI diets w/ different meal timing patterns yields answer #1 to question (3): If you are healthy the occasional day with junk food won't hurt you as long as you keep the total amount of energy at bay and jump back on the "healthy diet" wagon the very next day.

On the other hand, if only a single day of high GI food consumption can have such a pronounced impact on the postprandial HOMA levels, this raises the question how reliable this "long term measure" of glucose sensitivity actually is. Obviously, you should not go to the doctor's office and have your HOMA measured, at a morning after a day with three SuperSize Meals from McDonalds (even if you have been fasting after supper at night before, as the participants in the study at hand did) - unless you want a prescription for meformin, of course ;-)

It would however be likewise unwise to "do everything right" for three (maybe even just one day) before you head to the doctor to get blood drawn, just to be able to rejoice over a HOMA reading that does by no means represent your "normal" insulin sensitivity. This may make your doctor happy and spare you getting ticked off, but could have you run around pre-diabetic unnoticed for months if not years - maybe so long until the first irreversible damage has already been done.

The high susceptibility of HOMA measures to acute dietary modifications yields answer #2 to question (3): If you want know where you stand, don't make last minute changes to your diet before you get blood drawn. After all, the 90:10 rule (better 95:5 rule ;-) applies both ways - the 90/95 days of consistent eating patterns will decide whether you are lean, muscular and above all healthy or fat, undermuscled and sick.


References:

• Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. Br J Nutr. 2012 Oct;108(7):1286-91.

Is Low Blood Sugar Obesogenic? Hypoglycemic Episodes Characteristic of Weight Loss Plateaus & Weight Regain - What to Do? Diet, Sleep, Exercise & Mental Work Matter

Tip: Restore your muscle and liver glycogen after workouts and before long fasts to ensure a smooth transition from glucose to fat utilization.

In view of the diabetes pandemic it sounds stupid, when J-P Chaput and A Tremblay write that low blood sugar levels could contribute to the ever-increasing obesity rates in the US and other Western countries.

Their reasoning, however, is sound: An increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect.

Chronically low levels of glucose, as well as the glucose excursions we see in the few (still) healthy people after shoveling down packages of twinkies and dingdongs, would thus precipitate overeating and eventually obesity and diabetes.

Use alternatives to sugar sweetened beverages if you want to stabilize your blood glucose!

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Artif. Sweetened Foods Good, Not Bad for Fat Loss.

Compared to the way the hypothesis was originally formulated by Jean Mayer in the 1950s, the theory Chaput & Tremblay present in a 2009 review of the literature is significantly more complex (Mayer. 1953 & 1955. Chaput. 2009) and more of a glucose homeastasis hypothesis of obesity.

In contrast to the mainstream version of the "bad blood sugar spikes", Mayer and later Chaput and Tremblay focus on the role of the blood sugar troughs, we rarely think about. It all goes back to the classic glucostatic theory of food intake which postulates that

"that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating." (Chaput. 2009)

In a state of decreased glucose utilization aka "metabolic hypoglycemia" (Mayer. 1955), there is a point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering ‘metabolizing cells’ - this, according to Mayer, is the the signal for meal
initiation.

Does this mean that fasting is counter-indicated? For most of you probably not. If your liver gylcogen levels are well-stocked at the onset of the fast and assuming that you have a decent degree of metabolic flexibility, the transition into the fast will not put you at risk of metabolic (temporary glucose shortage at the cellular level) and / or full-blown hypoglycemia (really low blood glucose levels). So, fasting is ok, if you don't turn it into "starving" by extending the fast indefinitely and/or not restocking your glycogen levels in the feeding windows.

Interestingly, Mayer argued in his previously cited 1955 paper, already that the glucostatic theory would explain the short-term control of hunger and food intake, whereas a lipostatic mechanism would control the long-term regulation of body weight and energy balance.

There is nothing static about the glucostatic theory

Today, the role of glucose in the control of food intake is thought to be dynamic: it is a satiety factor and an initiation signal that has been associated with body fat by Chaput and Tremblay in two studies, which examined the effects of low glucose concentrations on long-term energy balance and weight gain in (Boulé. 2008)

Figure 1: Surprisingly linear increase in weight and body fat regain in prospective study and experimantal trial with lower blood glucose levels after OGGT (Boulé. 2008)

• 259 participants between 20 and 67 years of age involved in the Quebec Family Study - A study which revealed a closeassociation between glucose concentrations at the end of anoral glucose challenge and changes in body mass over the course of a 6-year follow up (Boulé . 2008).

• 44 obese participants on a 15-week weight-loss programme in either a drug therapy group or a placebo group coupled with energy intake restriction - A study which showed a higher propensity for weight regain over a follow up period of 83 weeks in those who had glucose levels below fasting values at the end of the oral glucose tolerance test during the weight loss intervention (Boulé. 2008)

In view of the fact that it would be easy to over-read the significance of these results: The researchers found that (1) lower glucose concentrations at the end of an OGTT were correlated with weight gain over time, that (2) large amounts of weight loss were associated with low glycemia at the end of an OGTT, and that (3) these low glucose concentrations were strong predictors of the amount of weight regained after weight loss.

The GI does matter - but only before and after you try to lose weight

Of these findings (2) is particularly interesting as it would support the notion that low glycemia can do both: It supports weight loss, when the energy intake is restricted and it increases the risk and extend of weight (re-)gain, when there is no energy restriction.

Figure 2: When the dietary energy intake is tightly controlled, there is hardly a difference in weight loss and body fat loss with high GI, low GI and high fat dieting in obese men & women (Raatz. 2005)

These observations would support previous evidence that a high glycemic index of foods, which would obviously be connected to higher glucose excursions after meals, figures large on ad-libitum (Alfenas. 2005), but only marginally on tightly controlled diets (Raatz. 2005).

It is thus no wonder that Chaput & Tremblay write in their latest review that their results are relevant only in phases without deliberate (significant) energy restriction. In these phases, the present research clearly suggests that weight-reduced obese individuals are at particular risk of weigh (re-)gain; an observation of which the scientists say that it is brought about by a destabilization of the "body homeostasis" that occurs, whenever the weight loss exceeds 10% of the initial body weight. And indeed: Tremblay et al. have observed in 1999, already that the mean glycemia of participants who had reached the point where their weight loss stagnated had reached an all-time low of 3.3 mmol/ l, of which studies by LeBlanc show that that it is significant enough to evoke a significant counter-regulatory hormonal response (LeBlanc. 1982; Tremblay. 1999).

Hypoglycemia and depression? The reduced glycemia could also be the underlying cause of diet induced increases in symptoms of depression as they were observed by Chaput et al. in a previous trial (2005), in the course of which their male volunteers became increasingly depressed, when they had surpassed the 10% weight loss margin (Chaput. 2007a). A direct association between low glycemia and depression in weight loss was confirmed in a follow up that used a low calorie diet (700kcal/day) + aerobic exercise. (Chaput. 2007b). Intriguingly, depression peaked, when the subjects finally hit a weight loss plateau in both studies.

These "significant counter-regulatory hormonal responses", which manifest in form of blunted growth hormone and epinephrine responses and appear to be controllable by regular exercise, are of particularly interest for those of you whose weight loss efforts have plateaued. A better glucose control with a focus on avoiding low glucose levels and regular physical activity could thus help you solve this problem... switching to a ketogenic diet which guarantees 100% glucose stability since the glucose is no longer used as a substrate, would be a another option.

Exercise to the rescue!

Another and eventually probably the most promising way of increasing glucose stability, facilitating further weight loss and forestalling future weight (re-)gain would be regular workouts.

"Physical exercise can be described as a stimulus contributing to optimal body functioning. This is discretely expressed at many levels of regulatory processes, be it by stimulating the effect of key enzymes, by increasing the sensitivity to hormones, by facilitating substrate transport through the membranes, by influencing cell receptors in a tissue-specific manner and probably many others.  The participation in regular physical activity has also been shown to prevent both hyperglycemia and hypoglycemia, which is concordant with the idea that exercise enhances the accuracy of substrate balance regulation." (Chaput. 2008)

It's thus not best to sit around all day to avoid your blood glucose levels from plummeting. On the contrary, individuals who are physically engaged in their daily schedule may expect a better control of both high and low glucose levels and better overall glucose homeostasis. And in fact, previous research also suggests that physically fit individuals are less likely to experience feelings of hunger associated with declines in blood glucose (Chaput. 2008).

The unbeatable benefits of exercise include both improved glucose control in the traditional sense of avoiding hyperglycemia and improved glucose control in the more comprehensive sense of avoiding both high and low glucose levels.

Chaput and Tremblay do yet add another factor to the discussion: Mental exercise! The glucose demands of our brain during cognitive activity are a commonly overlooked factor, when it comes to both glucose and energy control and that in spite of the fact that we all know that (with the exception of full ketosis) carbohydrate represents a critical energy substrate for the brain. Against that background,...

"the low capacity of the body to store carbohydrate might be perceived as a paradox of nature, particularly when cognitive activities are dominant in the daily activity schedule. This limitation is exacerbated by the inability of the body to synthesize glucose from free fatty acids." (Chaput. 2009)

It is thus not surprising that Cognitively and thus energetically demanding tasks will influence the ad-libitum meal intake, even if the measured energy expenditure during sitting at the desk doing nothing and performing a reading–writing task for 45 min is practically the same (13kj difference in Chaput. 2007c).

The brain may be your hungriest muscle

Figure 3: In contrast to both high (HIE) and low intensity exercise (LIE) 45 minutes of knowledge-based work will increase energy intake at a subsequent buffet (McCann. 1990)

In that the results presented in Figure 3 are not a statistical artifact. They agree with the results with the results of a study involving scientists from the University of Washington who increased their energy and fat intake at the time of the preparation of NIH grant applications (the additional influence of stress should be considered, here, as well | McCann. 1990)

In conjunction with the increase in the variability of glycemia, Chaput et al. observed in a 2008 follow up (Chaput. 2008), this may well explain the increased food intake the researchers observed in response to "cognitive work" in the broadest sense in all three studies.

Unquestionably, Chaput & Tremblay are right, when they warn that these observations raise the question as to whether other sedentary leisure activities (for example, video game playing, television viewing, chatting on internet) are also hyperphagic stimuli. In other words, whether they will make you overeat similar toknowledge-based work; and whether associations with glucose instability, as they were observed by Chaput et al. in 2008 exist for "texting", as well.  And even if that wasn't the case, the mere fact that knowledgebased work represents the main working modality in the current way of living, alone, would warrant further research in this direction.

Apropos "modern lifestyle", sleep or rather a lack thereof figures, as well

If you take a look at the data in Figure 4, you will realize that another feature of the modern way of living, i.e. a lack of sleep quantity and quality is associated with glucose excursions into hypoglycemia as well.

Figure 4: Mean glucose area below fasting glucose concentrations (GABF | higher values increase more severe / longer episodes of hypoglycemia) in men and women according to their habitual sleep duration (Chaput. 2007d)

The mean glucose area below fasting glucose concentrations (GABF) Chaput et al. measured in a yet another study they conducted in 2007 (Chaput. 2007d) clearly indicate that border line hypoglycemia is much less pronounced in long vs. short sleepers.

In that, it is interesting to see that the differences in mean glucose area below fasting glucose concentrations reflect the contemporary evidence of associations between sleep duration, obesity and type II diabetes - both sleeping too short (Xi. 2013) and too long is associated with increased risk of metabolic syndrome and/or type II diabetes (Ohkuma. 2014).

Bottom line: I doubt that hypoglycemia is the ultimate weight loss tool, but I hope you will agree that the previously presented evidence is significant enough to argue that you better keep an eye on both overtly high and overtly low glucose levels.

Table 1: Overview of factors that are believed to directly influence glucose homeostasis (Chaput. 2009)

As I've pointed out before, the latter damaging effects of low glucose levels are particularly pronounced, when you're not dieting. Yet even if you're calorically restricted, it's certainly a wise advise to keep the number and duration of episodes with borderline low glucose levels to a minimum to (a) reduce cravings, specifically for sweets, (b) minimize the negative long(er) term effects on the production of catecholamine and thyroid hormone (Leung. 1975), testosterone (Oltmanns. 2001) and the rest of the hormones the production of which depends on an intact hypothalamic signalling that is disrupted as a consequence of low glucose availability in the brain | Comment on Facebook!

References:

• Alfenas, Rita CG, and Richard D. Mattes. "Influence of glycemic index/load on glycemic response, appetite, and food intake in healthy humans." Diabetes Care 28.9 (2005): 2123-2129.
• Boulé NG, Chaput JP, Doucet E, Richard D, Despre´s JP, Bouchard Cet al. Glucose homeostasis predicts weight gain: prospective and clinical evidence.Diabetes Metab Res Rev 2008;24: 123–129. 
• Chaput, Jean-Philippe, et al. "Psychobiological impact of a progressive weight loss program in obese men." Physiology & behavior 86.1 (2005): 224-232.
• Chaput, Jean‐Philippe, et al. "Psychobiological effects observed in obese men experiencing body weight loss plateau." Depression and anxiety 24.7 (2007a): 518-521.
• Chaput, Jean-Philippe, et al. "Increase in depression symptoms with weight loss: association with glucose homeostasis and thyroid function." Applied Physiology, Nutrition, and Metabolism 33.1 (2007b): 86-92.
• Chaput, Jean-Philippe, and Angelo Tremblay. "Acute effects of knowledge-based work on feeding behavior and energy intake." Physiology & behavior 90.1 (2007c): 66-72. 
• Chaput, J-P., et al. "Association of sleep duration with type 2 diabetes and impaired glucose tolerance." Diabetologia 50.11 (2007d): 2298-2304.
• Chaput, Jean-Philippe, et al. "Glycemic instability and spontaneous energy intake: association with knowledge-based work." Psychosomatic medicine 70.7 (2008): 797-804. 
• Chaput, J. P., and A. Tremblay. "The glucostatic theory of appetite control and the risk of obesity and diabetes." International journal of obesity 33.1 (2008): 46-53.
• LeBlanc, J., et al. "Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects." Metabolism 31.5 (1982): 453-456.
• Leung, Yan, et al. "The effect of hypoglycemia on hypothalamic thyrotropin-releasing hormone (TRH) in the rat." Endocrinology 97.2 (1975): 380-384.
• Mayer J. Glucostatic mechanism of regulation of food intake. N Engl J Med1953;249: 13–16.
• Mayer J. Regulation of energy intake and the body weight, the glucostatic theory and the lipostatic hypothesis.Ann NY Acad Sci 1955;63: 15–43.
• McCann, Barbara S., G. Russell Warnick, and Robert H. Knopp. "Changes in plasma lipids and dietary intake accompanying shifts in perceived workload and stress." Psychosomatic medicine 52.1 (1990): 97-108. 
• Ohkuma, Toshiaki, et al. "U-shaped association of sleep duration with metabolic syndrome and insulin resistance in patients with type 2 diabetes: The Fukuoka Diabetes Registry." Metabolism 63.4 (2014): 484-491.
• Oltmanns, Kerstin M., et al. "Hypoglycemia, but not insulin, acutely decreases LH and T secretion in men." The Journal of Clinical Endocrinology & Metabolism 86.10 (2001): 4913-4919.
• Raatz, Susan K., et al. "Reduced glycemic index and glycemic load diets do not increase the effects of energy restriction on weight loss and insulin sensitivity in obese men and women." The Journal of nutrition 135.10 (2005): 2387-2391. 
• Tremblay, Angelo, et al. "Metabolic Fitness in Active Reduced‐Obese Individuals." Obesity research 7.6 (1999): 556-563. 
• Xi, Bo, et al. "Short sleep duration predicts risk of metabolic syndrome: A systematic review and meta-analysis." Sleep medicine reviews (2013).

Macro Ratios & Glucose Management: Eating Lower GI Carbs and Higher Protein Alone is Less Effective in Blood Sugar Normalization Than You May Have Thought

Macronutrient ratios matters, but food quality does, too. And so do exercise, laziness, sleep, .... the list is endless, so can we be surprised that modulating GI and protein is not helping much?

We all "know" that going low(er) carb is good for your blood glucose management, right? Nice! So, we probably don't need studies like the Marleen A. van Baak's conducted only recently, right? I mean, carbs are bad! So why would we even be interested to hear how much the subjects of the Diogenes Study lost on one of four different diets with varying protein content and glycemic index? Or who would want to know what the subjects' 24-h glucose profiles on one out of four diets differing in carbohydrate content by 10 energy % and glycemic index by 20 units during three days. No one would like to know that, right!?

In view of the fact that you're still there, I suppose that I was wrong and you are interested in the effects of different marconutrient ratios and types of carbohydrates (low vs. high glycemic index) on weight loss and glucose management. Let's take a closer look at the design of the Diogenes Trial (learn more), then.

Use alternatives to sugar sweetened beverages if you want to improve your blood glucose!

Unsatiating Truth About Sweeteners?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Sweeter Than Your Tongue Allows!

Stevia, Much More Than Sweet?

Artif. Sweetened Foods Good, Not Bad for Fat Loss.

The Diogenes Study was a field study, in the course of which subjects were randomized into 5 different diets: lower protein (LP)/lower GI(LGI), higher protein (HP)/LGI, LP/higher GI (HGI),HP/HGI and a control diet according to national recommendations for a healthy diets.

• The intended difference in protein content of the LP and HP diets was 10%–12% of energy intake.
• The intended difference in glycemic index between the LGI and HGI diets was 15. 

All diets were reduced in fat (<30 energy%) to make room for significant differences in the CHO to PRO ratios. All subjects had to keep food diaries and monitor their glucose levels continuously.

Table 1: Examplary diet composition in the Diogenes Trial (van Baak. 2014)

As some of you will probably remember (I've written about the Diogenes Study and its results in the Facebook News, previously), the total amount of weight the subjects lost from the start of the Diogenes Study was 8.8 ± 8.4 kg. The subsequent weight regain since the start of the randomized diet intervention was 1.6 ± 7.3 kg, with no significant differences between the diet groups (in spite of a marginal advantage for those who kept eating a high(er) protein diet).

Lifestyle changes are more powerful than supplements: So don't forget that it's imperative to realize the lifestyle changes described in the first installment of the "Improve Your Glucose Sensitivity"-series. Otherwise the best you can hope to achieve with supplements (and drugs) is to slow the progression from insulin resistance to full-blown diabetes.

The analysis of the three-day dietary records showed the expected differences in carbohydrate content and glycemic index between the diet groups, but the differences were smaller than intended (a bummer in view of the fact that they were not large to begin with). Much in contrast to what our initially phrased prejudice would say, there were no significant differences in mean 24-h, daytime or nighttime glucose concentrations between the diet groups.

Table 2: Self-reported dietary macronutrient composition in the field study (a) and macronutrient
composition of the diet in the lab study (b) (van Baak. 2014)

Moreover, the absence of at least a deviation in standard deviations (SD) signifies that the lack of statistical significance is not due to extreme outliers who may not have adhered to their dietary prescription (macronutrient make-up / reported / see Table 2).

"Post hoctesting did not reveal differences between the LP/HGI diet and any of the other diets for the glucose parameters studied. Adjustment for BMI, HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) index, minutes of exercise performed by the subjects, total weight loss or weight regain did  not change this outcome (data not shown)." (Van Baak. 2014)

Still, in a relatively uncontrolled scenario like the one in the Diogenes Study it's always possible that someone cheated twice, i.e. he deviated from the diet and reported to have stuck to it to the literal "T". Against that background, the results of van Baak's three-day follow up in a very controlled scenario is all-the-more interesting.

Figure 1: Parameters of glucose homeostasis means (left) and standard deviations (right)
on the different diets in the lab study (van Baak. 2014)

It's a study in which we see the same non-significant effects of the macronutrient ratio on ability of the study participants to keep their glucose in check. With goodwill you could say that protein seems to buffer the glucose excursions, but with p-values of p >> 0.05, this effect is everything but statistically significant.

To find an effect that is statistical significant we do thus have to take a look at the continuous overlapping net glycemic action over 1 h periods (CONGA1) values over 24 h on the different diets in the lab study, where the high protein + low GI group finally shows the statistically significant advantage we've been waiting for all along (see Figure 2). Still, as the scientists point out, overall their data does not support the hypothesis that "glucose concentrations would be highest on the reference diet (LP/HGI) compared to all other diets and especially compared to the HP/LGI diet." (van Baak. 2014). As the author points out, the study did yet provide support for the hypothesis regarding glucose variability was found, since both 24-h and daytime variability of glucose concentrations were lower on the HP/LGI diet than on the LP/HGI diet.

Learn how to improve and maintain your insulin sensitivity in a previous article and the corresponding series about ways to improve your insulin sensitivity, naturally.

Bottom line: I am not sure what to make of this study, but I guess that the fact that the macronutrient manipulation had a relatively minor impact on the glucose levels of the overweight subjects confirms that "hitting your macros" is by far not all you've got to do if you want to get away from the road to diabesity | What's your take on this study - comment on Facebook!

That being said, there is no doubt that a high(er) protein, low(er) GI will make it much easier to return to the realms of the few non-pre-diabetics. In that, the effects will probably be even more profound if you increase the protein intake by more than 10% over the reference value of 0.8g/kg.

Doubling the protein intake, for example, would necessarily require a reduction in carbohydrate and fat intake of 3.2kcal/body weight. For a person who weighs 100kg that would be 320kcal and 80g of carbs or 40g of fat - with the former usually being the better idea for anyone who's still significantly overweight and not already eating less than 180g of carbs per day.

Reference:

• van Baak, Marleen. "24-Hour Glucose Profiles on Diets Varying in Protein Content and Glycemic Index." Nutrients 6 (2014):3050-3061

700% Increase in Insulin, Elevated Blood Glucose + Identical Cortisol & CK Levels Challenge Usefulness of Intra-Workout High GI Carb Ingestion in Advanced Strength Trainees

Image 1 (IndiaToday): If you insist on ingesting 3x cans (=sugar equivalent of the maltodextrin supplement in the study at hand) of a not-to-be-named energy drink during your workouts and don't die from caffeine poisoning, you may gain more, but I suspect not in those areas, where you ant it ;-)

Whether you should or should not supplement with carbohydrates is a matter of constant debate among strength trainees. While some swear that they cannot perform if they aren’t guzzling a glucose-laden “intra-workout” supplement or energy drink from the supermarket, others prefer to get the lion's share of their carbs from whole foods, settle for BCAAs or plain water as their workout beverage of choice and wash down a sweet ripe banana with a tasty protein shake after their workouts. And while a previous paper by Bird et al. suggested that the former practice, i.e. the ingestion of a carbohydrate supplement (6%, preferably with 6g of EAAs) during your workouts, could significantly blunt the exercise induced cortisol spike (CHO alone -116%, CHO + EAA -112% vs. placebo), a very recent study, which was conducted by a group of scientists from the University Federal of Paraíba in Brazil, yielded very different results (de Oliveira Quirino. 2012)

To carb-guzzle or not that is the question!

Contrary to Bird et al., who had recruited previously untrained subjects for their study, de Oliveira Quirino's team picked 7 healthy young men (BMI 25.4kg/m²; age 27.3y) who had been training for at least 6 months with a minimum 3 resistance training sessions per week – this is important to note, because it should, for most of you, increase the real-world significance of the data, as I assume that many of you will have been following a similar protocol for probably longer than 6 month, already. What may be less in line with your own exercise regimen, though, is the exact training protocol, which comprised ten exercises for the upper limbs, i.e.

bench press, inclined press, dumbbell pullover, back lat pulldown, back lat push-down,

front press, bar-bell curl, pushdown, preacher curl, and lying triceps extension

which were performed for 3 sets of 12-15 reps to voluntary failure (60% RM) and at a cadence of 2-0-2-0 (2s concentric, 2s eccentric; no transition time between phases). Obviously all participants performed this protocol twice (in random order) and with a 96h interval in-between the supplemented (1,080ml of an 8% carbohydrate solution =86.4g of maltodextrine, ingested at regular intervals every two exercises) and the placebo (sucralose) trial.

Figure 1: Plasma glucose levels (in mg/dl) at rest, after the first, second, third, fourth and fifth pair of exercises (left) and increases in insulin and cortisol from pre to post exercise (de Oliveira Quirino. 2012)

As you can see in figure 1 the ingestion of  ~350kcal of readily available energy was more or less unnecessary, as it did not blunt, but rather augment the cortisol response (effect was not statistically significant, though); and that in the presence of profound elevations in blood glucose and insulin levels, and without any effect on circulating creatine kinase levels (a marker of muscle damage, not shown in figure 1).

A "substantial" increase in "anabolic hormone activity"?

Now in the absence of concrete data on protein synthesis / degradation, mTOR activity & co and without any information on confounding factors such as an increased training intensity during the carbohydrate trial, it is difficult to provide a conclusive answer to the initially raised question, whether the provision of fast acting carbohydrates during a strength training session would, as the scientists conclude, provide an "additional [benefit] for those engaged in this type of exercise with the aim of hypertrophy”. After all, it may be correct that the findings of the study …

[…] show that carbohydrate ingestion during the course of a training session comprising resistance exercises does not affect catabolic activity, but does increase substantially anabolic hormone activity. (De Oliveira Quirino. 2012)

but the „anabolic hormone“ the Brazilian scientists are talking about is insulin, which is beyond doubt among the most "anabolic” hormones in our body, but unfortunately, not exactly muscle specific, as it is simply a matter of fact that skeletal muscle is not the only tissue that’s going to benefit from insulin’s facilitative effects on nutrient uptake (Timmerman. 2010). It thus appears more than reasonable to assume that two other major players in the complex orchestrate of our metabolism will avail themselves of the superfluous amount of glucose that would be floating around in our bloodstream if we mimicked the supplementation protocol in the de Oliveira Quirino study. Their names? Your liver and your body fat stores!

So what are the implications?

Image 2: Another recently published study by Wax et al. suggest that slow digesting starches can help to maximize workout intensity and volume (read more in my article for Physique Magazine)

If you are not training fasted (the participants worked out on 11am on both occasions) and/or low-carbing without regular re-feeds, so that you have adequate muscle and liver glycogen stores, when you hit the gym, and you are no rookie anymore (cf. Bird. 2008), so that working out is no longer a totally novel stressor for your body, my personal interpretation of the study data is that you simply don’t need the additional fast acting carbohydrates! Neither to stabilize your blood sugar, nor to ward off any exorbitant increases in cortisol.

And as far as the increase in insulin is concerned, it appears more than questionable whether the latter would actually exert significant additive effects on muscle protein synthesis or could not even negate the nutrient repartitioning effects of your workouts (Poehlman. 2000; Hawley. 2008) by diverting the obviously superfluous energy to places where you’d rather not have them stored ;-)

A note on the "importance" of insulin to build muscle: One of the most comprehensive reviews on the role of insulin in skeletal muscle anabolism states it quite aptly "the full response of translation initiation and protein synthesis to either effector is not observed in the absence of a minimal concentration of insulin", but - and this is important - "the amount of insulin required for the effects is low, and a concentration of the hormone that approximates that observed in fasting animals is sufficient for maximal stimulation." (Kimball. 2002)

Bottom line: Avoid the unnecessary insulin spike from the ingestion of high GI carbs before and/or during a workout, but make sure that you have an ample amount of muscle glycogen before you hit the gym via an adequate total and post-workout carbohydrate intake (the lion's share in form of low GI carbs) and planned carbohydrate re-feeds (esp. for low carbers). This practice will not necessarily augment post-exercise protein synthesis (cf. "Glycogen-Free Muscle Growth"), but it is certainly going to help you to increase or at least maintain your workout intensity and overall training volume (Wax. 2012).

References:

1. Bird SP, Tarpenning KM, Marino FE. Liquid carbohydrate/essential amino acid ingestion during a short-term bout of resistance exercise suppresses myofibrillar protein degradation. Metabolism. 2006 May;55(5):570-7.
2. de Oliveira Quirino EL, da Conceição Rodrigues Gonçalves M, de Oliveira CVC, Porto dos Santos E, Silva AS. Influence of carbohydrate supplementation during resistance training on concentrations of the hormones cortisol and insulin. Sport Sci Health (2012) 7:93–97
3. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf). 2008 Jan;192(1):127-35. Review. 
4. Kimball SR, Farrell PA, Jefferson LS. Invited Review: Role of insulin in translational control of protein synthesis in skeletal muscle by amino acids or exercise. J Appl Physiol. 2002 Sep;93(3):1168-80.
5. Poehlman ET, Dvorak RV, DeNino WF, Brochu M, Ades PA. Effects of resistance training and endurance training on insulin sensitivity in nonobese, young women: a controlled randomized trial. J Clin Endocrinol Metab. 2000 Jul;85(7):2463-8.
6. Timmerman KL, Lee JL, Dreyer HC, Dhanani S, Glynn EL, Fry CS, Drummond MJ, Sheffield-Moore M, Rasmussen BB, Volpi E. Insulin stimulates human skeletal muscle protein synthesis via an indirect mechanism involving endothelial-dependent vasodilation and mammalian target of rapamycin complex 1 signaling. J Clin Endocrinol Metab. 2010 Aug;95(8):3848-57.
7. Wax B, Brown SP, Webb HE, Kavazis AN. Effects of carbohydrate supplementation on force output and time to exhaustion during static leg contractions superimposed with electromyostimulation. J Strength Cond Res. 2012 Jun;26(6):1717-23. 

Sex-Dependent Low GI Advantage(s) & Vasodilating Effects of Insulin. Diet-Dependant Effects of Active Vitamin D on Glucose Metabolism. Plus: Supplemental Flaxseed Oil?

It seems as if the glycemic index of her diet during puberty could determine on which side of this photoshopped divide a will end, when she's a young woman. Intriguingly, the association between high GI diets and high waist circumferences and obesity risk was not observed in the boys whose 5-year follow up data the researchers analyzed.

"145mm" that's the SuppVersity figure of the Week and the number of additional millimeters the waist circumference of a 12-year old girl is going to increase until she's 17 for each 1-SD increase in dietary GL. In conjunction with the observation that each 1-SD increase in dietary fiber intake was associated with a concurrent 0.44 kg/m² decrease in mean BMI, in girls and a 145mm lower increase in waist circumference, in boys, these results from a soon-to-be-published paper clearly support the notion of the fattening high GI carbs for girls (Gopinath. 2013).

The data does yet also raise the question, whether a higher activity level, a greater muscle mass or whatever something totally different is responsible for the non-significant effect the consumption of a high GI diet appears to have on the "strong sex". After all, even the devilish sugar sweetened soft-drinks which were associated with 4.45% higher body fat levels in girls who consumed one or more servings of the sugary glue per day, did not make a difference for the "young men" (suggested read: "Women Have a Much Higher Time Losing Body Fat Than Men")... ok, so let's see what else we've got "in the news today".

The vasodilatory effects of insulin could be life saving 

 (Hornstra. 2013) -- As a SuppVersity reader you are way beyond the stage of bro-science and thus fully aware that insulin not the villain everybody believes it was. Aside from the fact that it prevents catabolism, which is probably the only thing the average bro knows about, it helps nourish your cells, it keeps your blood from turning into a sweet slurry and has potent vasodilatory effects (ever wondered why you cannot get a decent pump ever since you went low carb?)

You don't still believe in the urban myth that adding fat to a high carb meal would blunt, the subsequent insulin spike, do you? Oh, you do? Well, in that case I recommend you take a look at one of the more recent installments of True or False (learn more)!

There is just one downside to it: Insulin does these and all the other good things only to people like yourself. People who work out, eat clean and remain insulin sensitive. In that, you do however have overweight company, that's at least what the results of a recent study from the Department of Internal Medicine at the VU University Medical Center in Amsterdam clearly suggest. In order to elucidate the hitherto only partially understood local microvascular vasoactive effects of insulin and their impact on systemic vascular resistance. J.M. Hornstra and colleagues conducted a cross-sectional studied in 37 healthy, overweight subjects (age 25 – 55 years, BMI 25 - 30 kg/m²), in whom they measured the local insulin-mediated vasodilation in response and transcutaneous iontophoresis of insulin and compared them to the local effects of acetylcholine and sodium nitroprusside, a potent pharmacological vasodilator.

What the researchers found was a clearcut inverse relationship between insulin-mediated vasodilation (r=-0.50; p<0.01) and the subjects' vascular resistance - a finding that was maintained after adjustment for age, sex, blood pressure and smoking and was not associated with local microvascular effects of acetylcholine.

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Bottom line: The results of the study at hand do thus corroborate to the notion... or I should better write "the proven fact" that insulin is not solely the fattening villain the current mainstream Internet paradigm says it was. It is a powerful hormone with physiological importance well beyond it's role in glucose management and the increased risk of cardiovascular diseases in type II diabetics and the average non-insulin sensitive overweight Westerner is not due to having too much insulin floating around in the system, but due to the non-responsiveness of the cells of the ever-increasing number of pre-diabetics.

Low GI diets helps to shed >10% more during three months exercise intervention 

(Solomon. 2003) -- In a way, you could say that the results of a soon-to-be-published study from the Department of Pathobiology at the Cleveleand Medical Clinic stands in line with both the SuppVersity Figure of the Week and the previous post on insulin's role in peripheral and systemic vascular resistance.

In the study at hand, the ingestion of a low glycemic index diet, as it was prescribed to the 20 older, obese individuals who participated in a 3-months fully-supervised aerobic exercise program will did (a) improve the weight loss success of the subjects in the low GI (LoGIX) vs. high GI (HiGIX) groups by +10.5%, (b) improved their insulin sensitivity and should (this was not measured) thus have have had a beneficial impact on the vascular resistance of the overweight individuals and (c) promoted a lower respiratory exchange ratio (a low RER which is the ratio of glucose / fat oxidation is an indicator of in creased fatty acid and/or lowered glucose oxidation) during exercise and did thus help them to decrease the amounts of lipids floating around in their system.

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Study probes whether "Hitting Your Macros" is all that counts (read more)

Bottom line: In the end, the results of the study at hand are not new, they only confirm what you will probably have known all along: The modulatory effects of low GI diets on the substrate utilization during exercise is highly relevant for the overweight and/or insulin resistant individual (skinny fat people included). With it's ability to improve and conserver insulin sensitivity, it is yet likewise important for the active individual and/or athlete trying to maintain his insulin naturally high insulin sensitivity without having to compromise his/her performance and endocrine health by running around glycogen depleted 24/7.

All of you who did not see the discussion revolving around the necessity of high GI carbs and thus insulin spikes for glycogen repletion after a workout, I suggest you take a peak at the corresponding graph on I posted on Facebook earlier this week (go to the SuppVersity Facebook Wall). One thing you should keep in mind though, is the fact that "high GI diets" are not characterized by the occasional ingestion of "fast carbs" in the postworkout window - this alone is thus unlikely to cause the same ill health effects as a dietary protocol that does not even give your body the chance to clear the steady and rapid influx of glucose from the bloodstream (the "GL", i.e. the glycemic load may in fact be a better measure here, learn more)

Diet- and tissue-specific effects on transcriptional regulation of glucose metabolism 

(Alharfy. 2013) -- In what is unfortunately yet another rodent study on vitamin D, researchers from the College of Pharmacy at the , King Saud University in Riyadh, Saudi Arabia, took a closer look at the differential effect vitamin D (1,25-(OH)2D3, Rocaltrol(R)) supplementation exerts on the transcriptional regulation of insulin-sensitive in liver, muscle and adipose tissue in Male C57BL/6J mice on regular low fat or obesogenic high fat (+high carb) chow.

Figure 1: Effect of vitamin D treatment on transcript levels of insulin sensitive genes in low-fat diet (LFD)- and high-fat diet (HFD)-fed mice (Alharfy. 2013)

If you take a closer look at the data in figure 1, you see that in muscle tissue of LFD-fed mice, vitamin D treatment increased vitamin D receptor (VDR, not shown) to 2.03-fold and insulin receptor substrate (IRS-1) to 1.5-fold. An even more pronounced increase in IRS-1 (+140%; IRS proteins play a key role in transmitting signals from  insulin receptors to the intracellular pathways, as well as growth promotion) expression occurred in the mice that were fed the obesogenic high fat diet - in this case, the increase was yet accompanied by a -50% reduction in VDR expression (not shown) without having downstream effects on GLUT4 expression.

Maybe some of you remember that I covered a study in which vitamin D3 lead to increased obesity levels in rodents back in October 2011 (learn more)

In the liver of the mice receiving the species-appropriate low-fat diet, the provision of supplemental 150 IU/kg calcitriol (the active form of vitamin D!) did not induce any statistically significant trancriptional changes, whereas the -85% decrease in exogenous IRS-1 level in the HFD group and the concomittant upregulation of the hepatic vitamin D receptor expression (+260%) show that the liver could be a major target for the previously observed anti-obesity effects of active vitamin D (see "Active vitamin D does what vitamin D3 doesn't do"; read more). In lean mice, on the other hand, similar effects were absent and the expression of glucose transporters /GLUT-4) decreased by -30%.

The decrease in hepatic GLUT-4 was yet still small compared to the rapid decline in GLUT-4 expression in the adipose tissue of the LFD group. Whether this could precipitate high blood glucose levels is yet about as uncertain as the implications of the highly elevated GLUT-4 expression in the HFD group. Theoretically the latter would help reduce blood glucose levels, but at an expense of profound increases in adipose tissue - that this is not very unlikely, is something you have read about here at the SuppVersity in October 2011, already (go back)

So what do the scientists say?

In view of the necessity to convert supplemental vitamin D3 to it's active form, it is questionable, whether the provision of the former would induce any of the changes Alharfy observed in the study at hand - learn more in a previous installment of the short news!

As Alharfy et al. point out the absence of significant changes in GLUT-4 expression in response to the adminstration of physiologically highly significant amounts of the active form of vitamin D provides further evidence that the "insulin action in mammalian tissue is not a direct one" but are brought about by "intracellular mechanisms of insulin action mediated by IRS-1 and VDR" in the absence of any immediate effects on "glucose transport across major insulin-sensitive tissues, including adipose and liver in mice under LFD and HFD conditions". Consequently, the...

"[...] antidiabetic effect of vitamin D may be directed through its anti-inflammatory action in obese conditions. Reduction in inflammatory cytokines production by vitamin D may play a role in decreasing insulin  resistance." (Alharfy. 2013)

The scientists' conclusion does therefore stand in line with the observations of Waldron et al. about which you've probably read on the SuppVersity Facebook Wall about a month ago (Waldron. 2013).

Based on the 25OHD response (remember: 25OHD is the precursor to calcitriol and will thus be lowered, when more calcitriol is produced from this 'storage form') the researchers from the New Cross Hospital, in Wolverhampton in the UK observed in response to inflammatory assaults, they were among the first to propose that "serum 25-(OH)D is a negative acute phase reactant [... and h]ypovitaminosis D may be the consequence rather than cause of chronic inflammatory diseases" (Waldron. 2013)

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Bottom line: While we are still far away from a proper understanding of the exact mechanisms which underly the observed correlations between low vitamin D levels and all sorts of (eventually) inflammatory diseases, the results of the study at hand corroborate the notion that D3 levels (=passive storage) have little to no direct effects on the etiology of the diabetes, cancer, and what not.

Figure 2: Reductions (!) in all risk mortality calculated on the basis of NHANES data for each 10ng/ml increase in vitamin D up to the "magic" 21ng/ml margin from the Amer study (Amer. 2013)

This would also explain why the vitamin D deficient ballet dancers from yesterday's SuppVersity Facebook news did benefit from supplementation, while the 10,000 participants in the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2004 in another recent study by Amer et al. did not have lower risks of all cause mortality, once their 25OHD levels were just above lowest margin of the normal range (see figure 2 + today's SuppVersity Facebook news; Amer. 2013). What it does not explain, though, is the fact that we see similarly increased risk of all-cause mortality among women with low (20 ng/mL) as well as high (50 ng/mL) levels of serum 25(OH)D (Melamed. 2008) or the 50% increase in mortality Michaëlsson et al. observed in 1194 elderly men (mean age at baseline, 71 years) with vitamin D levels below 18.5ng/mL and above 39.4 ng/mL during a median follow-up of 12.7 years (Michaelsson. 2010).

In the end, studies such as the one at hand, would have to be conducted over long enough periods in human beings to finally identify the mechanism behind the non-linear effects of vitamin D on mortality and metabolic health in the these and other studies. Personally, I would hope that studies like the one by Amer et al. get some more mainstream attention and raise people's awareness of the simple paradigm "test first, supplement second".

Flaxseed oil does not offer metabolic advantages over olive oil  

If you don't like the feminine look and the size of certain body parts of this Greek statuette, you just found another reason to avoid flaxseed - at least if you are and want to stay male (learn more)

(Kontogianni. 2013) -- With all the hype around fish oil, flaxseed oil has more or less been forgotten. If you ask the average Joe or Jane, about whether you should rather use olive or flaxseed oil if you wanted to improve your lipid metabolism and reduce inflammation, many of them will probably still answer: "Flaxseed, of course!"

According to a recent study from the Harokopio University in Greece this is yet nothing but another urban myth. In their randomized cross-over study (2x6 weeks + 6 weeks washout in-between), the scientists found that it did not make a physiologically significant difference whether the 37 normal weight young subjects (age: 22 years) consumed 15 mL/day of either flaxseed oil or extra virgin olive oil.

When it comes to the differences the scientists observed in response to the olive oil vs. flaxseed oil supplemented diet, you better have a magnifying glass ready, as the only highly visible change was allegedly not significant:

Figure 3: Relative levels of inflammatory and biochemical parameters before and after the interventions; all data expressed relative to baseline / after washout = pre-crossover values (Kontagianni. 2013)

Even the fatty acid composition in the cell membranes differed only in terms of the amount of alpha linoleic acid (short-chain omega-3), while the amount of what people often falsely label as "fish oil", namely the long-chain omega-3 fatty acids, DHA and EPA, did not change in either group.

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Oleuropein in olive oil is a natural testosterone booster (learn more)

Bottom line: Aside from statistically non-significant decreases in total and LDL cholesterol in the flaxseed oil group and a physiologically irrelevant increase in the ALA content of the in the erythrocyte membranes,  there were surprisingly little differences between the two study arms.

Now, you can certainly argue that the changes and potential benefits would have been more evident if the amount of flaxseed oil in the diet had been higher. On the other hand, you all should be aware that flaxseed oil goes rancid in no time, cannot be heated and tastes like a$$... this limits it's use as a regular part of your diet. What's more, if you take close look at the levels of hs-CRP in figure 3, you will have to admit that more flaxseed oil could also equal an increase in inflammation.

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That's it for today: Why? Well, I simply had no time to write more earlier today and other than briefly posting this no additional time to spend writing up additional short-news... but judged by the visitor counts on the last weekends, you are probably busy enjoying the weekend, as well. Enjoy your weekend, everyone!

References:

• Amer M, Qayyum R. Relationship between 25-Hydroxyvitamin D and All-cause and Cardiovascular Disease Mortality. Am J Med. 2013 Apr 17. 
• Brown LJ, Midgley AW, Vince RV, Madden LA, McNaughton LR. High versus low glycemic index 3-h recovery diets following glycogen-depleting exercise has no effect on subsequent 5-km cycling time trial performance. J Sci Med Sport. 2012 Nov 12.  
• Gopinath B, Flood VM, Rochtchina E, Baur LA, Louie JC, Smith W, Mitchell P. Carbohydrate nutrition and development of adiposity during adolescence. Obesity (Silver Spring). 2013 Mar 21.
• Hornstra JM, Serné EH, Eringa EC, Wijnker MC, de Boer MP, Yudkin JS, Smulders YM. Insulin's microvascular vasodilatory effects are inversely related to peripheral vascular resistance in overweight, but insulin-sensitive subjects. Obesity (Silver Spring). 2013 Mar 20.
• Kontogianni MD, Vlassopoulos A, Gatzieva A, Farmaki AE, Katsiougiannis S, Panagiotakos DB, Kalogeropoulos N, Skopouli FN. Flaxseed oil does not affect inflammatory markers and lipid profile compared to olive oil, in young, healthy, normal weight adults. Metabolism. 2013 May;62(5):686-93.
• Melamed ML, Michos ED, Post W, Astor B. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008;168(15):1629-1637. 
• Michaëlsson K, Baron JA, Snellman G, et al. Plasma vitamin D and mortality in older men: a community-based prospective cohort study. Am J Clin Nutr. 2010;92(4):841-848.
• Solomon TP, Haus JM, Cook MA, Flask CA, Kirwan JP. A low glycemic diet lifestyle intervention improves fat utilization during exercise in older obese humans. Obesity (Silver Spring). 2013 Mar 20. 
• Waldron JL, Ashby HL, Cornes MP, Bechervaise J, Razavi C, Thomas OL, Chugh S, Deshpande S, Ford C, Gama R. Vitamin D: a negative acute phase reactant. J Clin Pathol. 2013 Mar 1.

Breaking the Fast, Cardio & Your Brain: Cardio on Empty is Fatiguing. Fasting Without Exercise, However, is Nootropic

Boking: Every endurance athletes knows and fears it, so wouldn't just that happen when you do your cardio on empty in the morning? And what about the effects on your brain power? Will your gray matter bonk, as well? And if so, what can be done about it?

Today's SuppVersity post is a little different from the usual "Training on empty? Yes / No / Maybe!" debate that flares up every now and then on almost every fitness related bulletin board of the World Wide Web. And in as much as I would like to say that this was all the credits belong to me, the fact that the the following dissertation may actually make a practically relevant contribution is due to the experimental design of the latest study from the Northumbria University in Newcastle, Tyne and Wear, in the UK (Veasey. 2013).

Why is that? Well, contrary to the majority of breakfast "yes or no" studies this one has both an exercise and and a cognitive performance aspect. Since I suppose that most of you are not living to train, but training to live, this is practically highly relevant. I mean, what's the use of "looking good naked" due to the purported benefits of working out "on empty" first thing in the morning if that reduces your cognitive performance in a way that you risk being fired?

Now that I've got everyone's attention, let's look at what exactly R.C Veasey and her colleagues did to find out whether having / not having breakfast before morning cardio or rest will impact cognitive performance and mood later in the morning. To this ends, the researchers recruited 12 healthy, active men in their early 20s with an average BMI of 24.5 ± 2.0 kg/m², who had to abstain from rigorous exercise and alcohol consumption prior to the exercise trials before they reported back to the lab after a 12h fast.

Do the online stroop test to get an idea of what the subjects in the study had to do and why it may in fact not be ideal to have breakfast when you are not exercising. After all, the results of the study at hand clearly suggest that the the accuracy in the stroop performance test decreases significantly in the "no exercise, but breakfast" condition.

"After confirming compliance to the study restrictions, a baseline completion of the cognitive tasks and mood scales was then undertaken, before participants were administered the test breakfast or remained fasted. During the 2 h rest period which followed, cognitive performance and mood were measured at 60 and 120 min. In between these periods, participants were allowed to read, write or watch a DVD. In the exercise trials (NB E and B E), participants then completed a treadmill run at 60% of their VO2, until 2.9MJ had been expended with heart rate and rate of perceived exertion (RPE) measured at 10 min intervals throughout. [...] On rest days (NB NE and B NE), participants rested for the equivalent amount of time. Cognitive performance and mood were reassessed before participants were administered a test drink, followed by a 90 min rest period where cognitive performance and mood was assessed at 30 and 75 min. This was followed by an ad libitum lunch where participants were asked to consume enough food to feel satisfied to a normal level. After lunch, they completed the cognitive tasks and mood scales for a final time and were then free to leave the laboratory." (Veasey. 2013)

"Hah?" Yeah, that was my initial reaction to the overcomplicated study protocol, but don't worry, after you've taken a peak at the following overview I guess, you will be able to identify how this corresponds to getting up, driving to the gym, working out and head to your working place with or without breakfast.

Illustration 1: Outline of the allegedly somewhat difficult to understand study protocol (Veasey. 2013)

You see? It's not so complicated as the scientists description of the protocol made it appear. Four conditions, total, two conditions with and two without 72g syrup flavor porridge oats with 360ml milk, each repeated twice with or without exercise after the initial rest period - that's all.

"Ok, whatever... what were the results? "

As the scientists had expected, the consuming breakfast prior to exercise did in fact elicit the most beneficial cognitive performance and mood effects following in the exercise conditions.

Figure 1: Cognitive performance, mental fatigue and tension in the four trials (Veasey. 2013)

The data in figure 1 does yet also reveal that having breakfast before rest had detrimental effects on the ability of the study participants' ability to rapidly process visual information and omitting breakfast improved their performance on Four Choice Reaction Time test.

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Whey and carbs as cognition booster and stress buffer for breakfast: In view of the results of a soon-to-be-published paper from the University of Helsinki clearly shows that a combination of whey and carbs for breakfast improves coping with mental tasks in healthy subjects compared to the "breakfast" used in the study at hand (Sihvola . 2013), it would appear prudent to remember that, when you rise and shine and decide to have breakfast - regardless of whether you intend to work out, or not (the increased protein intake may even help with the performance decline in the "breakfast, no exercise" condition - emphasis on may and assuming you don't ingest it in isolation just to end up hypoglycemic). Apropops, don't forget: Low GI carbs are your brain's friends (e.g. Micha. 2010; Cooper. 2012)

Bottom line: According to the results of the study at hand, you do have two options to maintain / optimize your "desk performance" (cognitive performance at the job) in the morning hours:

• either you fast and refrain from working out or
• you have breakfast and work out

It goes without saying that even minor changes in the protocol, e.g. the omission of the 120min rest period (I gather you don't need that long in the bathroom before you either leave the house and go for a jog, sit on your cycle ergometer or drive to the gym), for example could skew the results in a favorable way for the "non-breakfast condition", if  you don't stick to a meager 250ml of chocolate milk after your workout but indulge a real breakfast (see box on the right for a scientifically warranted suggestion)...

The latter is by the way a practice that has always worked pretty well for me. I did however have to realize that this does only work if you really eat and don't just down a protein, let alone whey shake that will only spike your insulin and send you down into the abyss of borderline hypoglycemia. A state which is certainly nothing your cognitive performance can benefit from (Lindgren. 1996).

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Highly suggested read: "Circadian Rhythmicity - "Breakfast" or "Breaking the Fast"? Fasting as Zeitgeber & All About King, Prince & Pauper" (read more)


References:

• Cooper SB, Bandelow S, Nute ML, Morris JG, Nevill ME. Breakfast glycaemic index and cognitive function in adolescent school children. Br J Nutr. 2012 Jun;107(12):1823-32. 
• Lindgren M, Eckert B, Stenberg G, Agardh CD. Restitution of neurophysiological functions, performance, and subjective symptoms after moderate insulin-induced hypoglycaemia in non-diabetic men. Diabet Med. 1996 Mar;13(3):218-25. 
• Micha R, Rogers PJ, Nelson M. The glycaemic potency of breakfast and cognitive function in school children. Eur J Clin Nutr. 2010 Sep;64(9):948-57.
• Sihvola N, Korpela R, Henelius A, Holm A, Huotilainen M, Müller K, Poussa T, Pettersson K, Turpeinen A, Peuhkuri K. Breakfast high in whey protein or carbohydrates improves coping with workload in healthy subjects. Br J Nutr. 2013 Apr 16:1-10.
• Veasey RC, Gonzalez JT, Kennedy DO, Haskell CF, Stevenson EJ. Breakfast consumption and exercise interact to affect cognitive performance and mood later in the day: a randomized controlled trial. Appetite. 2013 Apr 19.