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Eggs or Flakes? Not 30% vs. 25% protein! A brief reminder of the fact that the stuff you eat is still food.

I am not quite sure when or why this happened, but I know that more and more people are thinking in terms of "macros" instead of foods. What I do know, though, is that the recent publication of studies from the Pennington Biomedical Research Center at the Louisiana State University System (Bayham. 2014) and an ostensibly unrelated study that was conducted by researchers from the Alimentary Pharmabiotic Centre, Biosciences Institute in Cork and scientists working at the local university and the University of Pittsburgh School of Medicine (Patterson. 2014) confirms - once again (!) - how futile this ignorant approach to nutrition actually is.

Eggs vs. cereals - not the best example, but...

In that, I am well aware that the "battle" between an egg- and a cereal-based breakfast in the Patterson study is not exactly a good model of whats currently going on in the health and fitness community. With cereals being labeled as "the devil" (its always nice to be "anti", isnt it?), no one would after all consider having ...

• One-and-a-half cup of Special K® RTE cereal, 200 ml Silk® original soymilk, one slice of Natural Grain “Wheat n’ Fiber”® bread, 13 g of butter, and 10 g of sugar-free strawberry jam (CG)

... for breakfast. In view of the fact that the same can be said for the calorie- and mocronutrient matched "high quality protein" breakfast, i.e.

• Two scrambled eggs, 120 mL skim milk, two slices of Holsum® thin white  bread, 5 g of butter, and 18 g of Smuckers® strawberry jam

... I still believe that the consequences of "breaking the fast" (learn why I am calling breakfast thus in "Breakfast or Breaking the Fast" | read more) with eggs vs. Special K are still relevant to the previously introduced context. And if you know that the acetylated form of ghrelin and PYY are "satiety hormones", it does not take a rocket scientists to interpret the data in Figure 1.

Figure 1: Level(s) of "satiety hormones" after the different breakfasts (Bayham. 2014)

What is difficult to tell, though, is whether the increased satiety after the egg breakfast would actually lead to a reduced intake at the subsequent meal.

• On an individual basis, i.e. on just one of the two eating occasions, the higher levels of acetylated ghrelin and PYY did not suppress the 20 healthy overweight or obese subjects energy intake during the subsequent lunch
• For day 1 and day 7, together, on the other hand, the 64kcal the egg eaters consumed less than the cereal eaters did reach statistical significance.

If we throw overboard all the things we (believe) we know about the fallacy of calorie counting, this would translate into a ~448kcal difference for one week and a whopping difference of 23,360kcal for a year, which should shed ~3.3kg of body fat a year.
Whether or not similar concrete weight loss vs. gain effects can be achieved with different types of fat is nothing study #2 in todays science mash-up here at the SuppVersity could answer. What it can tell you though, is that protein and obviously carbohydrates, where even Mr. Average Joe thinks in terms of "low GI" = good and "high GI" = bad carbs, these days, is by no means the only food component, where unspecifically counting macros is not going to cut it (or get you cut, if thats what you want to achieve).

This is not just about fish oil

"Of course, the bad omega-6s" ... I know that this is what youre thinking right now, but lets be honest, isnt that a bit narrow-minded?  It sure is and still, the results Ellaine Petterson and her Irish and American colleagues present in their most recent paper demonstrate quite clearly that the ingestion of fish and flax seed oil has pretty unique effects that go beyond its ability to increase the tissue concentrations of DHA to levels way beyond what youd see in low fat or high fat diets with palm, olive or safflower oil powered high fat diets.
In addition it lead to an increase in the relative abundance of bifidobacteria, a gut tenant that has been linked to all sorts of beneficial health effects, but has recently been outshadowed by various strains of lactobacilli (0.95% vs. more than 2% in all other groups), which - and this is an important information - were the lowest in the rodents who were kept on diets with 45% of the energy from fish and flaxseed oils.

Whether or not, the negative effects of fish oil on the lactobacillacea count in the guts of the lab animals is also partly responsible for the more or less disappointing effects the fish and flax seed diet had on the body composition (Figure 2) of the wild-type C57BL/6J male mice (21 d old) in the study at hand is questionable.

Figure 2: Body composition analysis at the end of the study (Patterson. 2014)

Its not impossible, though. A brief glance at the insulin levels and leptin levels in Figure 3 reveals that neither of them looks anyway close to what someone whos religiously taking his fish oil caps on a daily basis would be expecting. In the end, it is thus not really that surprising that only the palm oil diet group ended up with an inferior lean-to-fat mass ratio of 1.17 (vs. 1.33 in the omega-3 group).

Figure 3: Changes (%) in relevant metabolic markers in response to the different diets (Patterson. 2014)

The results of the study at hand, i.e. the effects on body composition (Figure 2), as well as blood glucose and lipid metabolism (Figure 3) are thus clearly not in line with the ubiquitously placated message that "fish oil is good for you" - a message, the indoctrinated average supplement junkie will still discern from the abstract of the study:

"[...] Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem." (Petterson. 2014).

Neither the "loss" of lactobacilli, nor the - if anything - negative effects of the high omega-3 diet on the lean-to-fat-mass ratio and the amount of insulin thats floating around in the rodents blood are mentioned in said abstract.

Fat = Diabetes - A FAT Mistake?

If you go take a look at the actual study data, we are thus left with the question, whether the purported benefits of having high amounts of omega-3 fatty acids in our cells (see red info box a couple of paragraphs above) are real enough (or really enough - whatever you prefer) to discard the fact that the study at hand would actually suggest that olive and not fish + flaxseed oil should be your go-to source of dietary fat on a high fat diet.

Moreover, if we abandon any paradigmatic believes, we would even have to concede that - within the current context, i.e. a rodent study and a diet with protein contents of only 19.2% (low fat) and 23% (high fat), the low fat mix of 1.25% of palm, 1.25% olive, 1.25% safflower oil, 0.625% fish and 0.625% flaxseed oil the rodents in the starch and sucrose groups received is superior to any of the high fat variants.

You may say that this is "rodent shit" (and it is, because this is what the scientists analyzed to access the SFCA metabolism of the mice) and a mere coincidence, but wouldnt you agree that this oil mix looks a little too much like the mixture youd get on a low-to-moderate fat diet with olive oil as a staple for everything, where you add oils, palm and safflower oil from processed foods on your cheat days and fish oil / omega-3s from your once or twice a week serving of salmon... ?
References: 

• Bayham, Brooke E., et al. "A Randomized Trial to Manipulate the Quality Instead of Quantity of Dietary Proteins to Influence the Markers of Satiety." Journal of Diabetes and its Complications (2014).
• Filaire, Edith, et al. "Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes." International journal of sport nutrition 20.6 (2010): 496.
• Danthiir, Vanessa, et al. "Cognitive Performance in Older Adults Is Inversely Associated with Fish Consumption but Not Erythrocyte Membrane n–3 Fatty Acids." The Journal of nutrition (2014): jn-113.
• Patterson, E., et al. "Impact of dietary fatty acids on metabolic activity and host intestinal microbiota composition in C57BL/6J mice." The British journal of nutrition (2014): 1-13.

Whipped cream with strawberries - is it actually healthier with pastured cream? Is it less obesogenic, soothes inflammation and increases the oxidation while reducing the storage of body fat?

I guess I could have made two separate articles of the two recent studies from the University of Lyon (Benoit. 2014) and the INRA in Paris (Marsset-Baglieri. 2014), but in view of the fact that there are already plenty of dairy articles at the SuppVersity, I thought, Id pack them into one large "Dairy Double-Whammy Appreciation Article"; and in that I am about to start with something the average SuppVersity reader should know already: "Milk protein fractions moderately extend the duration of satiety compared with carbohydrates independently of their digestive kinetics in overweight subjects."

Well, at least the first part shouldnt be news. The fact that this happens independent of their digestive kinetics, on the other hand, may come as a surprise.
Why? Well, "independent of their digestive kinetics", that means that the satiety effect does not depend on whether were talking about fast- or slow-digesting dairy proteins. Or, practically speaking, it did not matter, if the subjects consumed

• 30g of casein (digested in 6h)
• 30g of whey protein (digested in 2.5h), or
• 30g of whey + casein protein (digested in 4h)

in conjunction with 30g of carbohydrates, the effect, i.e. the effects on  pancreatic and gastrointestinal hormones and the 17min increase in the time it took the subjects to ask for launch.

Figure 1: .Effects of the protein snackv. the control carbohydrate snack on the time period elapsing before the request for lunch in all subjects (n82) (a) and in early eaters (n=41) (b). The satiating effect of the protein snack is represented whatever the type of protein snack as well as in each protein group (Marsset-Baglieri. 2014).

In that, the effect on the size of a subsequent ad-libitum meal depended non-linearly on the proximity between the subjects regular launch-time and the time the snack was ingested. With 32min (vs. only 17min), the satiating effect of  the liquid protein meal was thus significantly more pronounced in the "early eater" who could have consumed their regular lunch within less than 2h after the ingestion of the test "snack".
Now that we know that dairy proteins can help you keep your weight in check, its about time to have a look at the macronutrient, Marsset-Baglieri, et al. simply forgot in their previously discussed study: Dietary fats!

From dairy protein to dairy fat - this is where pasture may matter

The question whether pasture (grass-fed) dairy is healthier, better or what-not is a topic of ongoing discussion among the members of the health and fitness community. While some people believe that the slightly higher amounts of CLA and omega-3 fatty acids, doesnt make a difference, others pretend as if eating conventional dairy would cost you 10 years of your maximal life experience.

Figure 2: Effect of feeding a control (CT), a standard dairy cream (SDC) or a pasture dairy cream (PDC) diet for 12 weeks on the gene expression of different markers of inflammation in the epididymal adipose tissue: (a)IL-6, (b) Toll-like receptor 4 (TLR4), (c) cluster of differentiation 68 (CD68), (d)CD11c, (e) monocyte chemoattractant protein 1 (MCP-1) and (f) TNF-alpha normalised to hypo-xanthine-guanine phosphoribosyl-transferase (HPRT; Benoit. 2014).

If we take a look at results of a recent study from the University of Lyon (Benoit. 2014), you will realize: The truth lies - as usual - somewhere in-between.

The markers of inflammation, for example, were significantly reduced in rodents who were fed a 20% pasture (PDC) vs. 20% standard dairy cream diet (SDC; see Figure 2). The levels of PPAR-alpha & carnitine palmitoyltransferase in the liver and the levels of UCP2 in the adipose tissue, all three indicative of increased fatty acid oxidation in the liver and fat cells, respectively, increased (not shown in Figure 2).

And although the effects on the tight junctions of the gut (important for "leaky gut" prevention) were non-significant, the increase in the percentage of crypts with Paneth cells, the number of goblet cells per crypt and the expression of MUC-2 in the colon indicate that the pastured dairy had beneficial effects on the intestinal health of the rodents, as well.

Overall, the scientists attest that the replacement of a standard dairy cream with a pasture
dairy cream, albeit as part of a generally unhealthy "high-fat" (=hypercaloric) diet...

• lowers metabolic inflammation - for some markers even below the levels of the "healthy" standard (low fat) rodent diet
• prevents fat mass accumulation, despite increased energy intake - possibly due to an inxrease in lipid beta-oxidation, the pasture cream fed rodents could eat 0.8g/day more of the isocaloric chow and still presented lower body fat stores
• improves the protective function of the intestine - the increase in mucus coat thickness in the colon of the PDC mice might actually also have contributed to the reduced inflammation by decreasing the proportion of lipopolysaccharide crossing from the gut lumen to the systemic circulation

Their study is yet not without limitation, such as the lack of a detailed identification of the CLA isomers, which does not allow a causal analysis of the contribution of differences in the conjugated linoleic acid make-up to the reduction in body fat Benoi et al. observed. Similarly, the amount of beta-sitosterol and desmosterol, polyphenols and flavonoids which varied between the creams, could have figured in, sa well.
Reference:

• Benoit B, Plaisancié P, Géloën A, Estienne M, Debard C, Meugnier E, Loizon E, Daira P, Bodennec J, Cousin O, Vidal H, Laugerette F, Michalski MC. Pasture v. standard dairy cream in high-fat diet-fed mice: improved metabolic outcomes and stronger intestinal barrier. Br J Nutr. 2014 Aug;112(4):520-35.
• Marsset-Baglieri A, Fromentin G, Airinei G, Pedersen C, Léonil J, Piedcoq J, Rémond D, Benamouzig R, Tomé D, Gaudichon C. Milk protein fractions moderately extend the duration of satiety compared with carbohydrates independently of their digestive kinetics in overweight subjects. Br J Nutr. 2014 Aug;112(4):557-64.

What now? Wait 3 minutes or off to the bench for an alternate set of bench presses or pulls ?

Traditional strength training with 80% of one-repetition maximum (1RM) utilizes 2- to 5-minute rest periods between sets. These long rest periods minimize decreases in volume and intensity, but result in long workouts. Performing upper-body exercises during lower-body rest intervals may decrease workout duration, but may affect workout performance.

The above is how Anthony B. Ciccone, Lee E. Brown, Jared W. Coburn, Andrew J. Galpin kick off their latest paper in the venerable Journal of Strength and Conditioning Research (Publish Ahead of Print).
The purpose of the corresponding study was to compare the effects of traditional to those of alternating whole body strength training on squat performance. To this ends, Ciccone et al. recruites 20 youn men, who had to perform two workouts:

• The traditional set workout (TS) consisted of four sets of squats at 80% of 1RM on a force plate with 3-minutes rest between sets. 
• The alternating set workout (AS) also consisted of four sets of squats at 80% of 1RM but with bench press, and bench pull exercises performed between squat sets 1, 2 & 3 with between-exercise rest of 50 seconds, resulting in approximately 3-minutes rest between squat sets. 

For both workouts, sets 1-3 were performed for four repetitions, while set four was performed to concentric failure. The total number of completed repetitions, the peak ground reaction force (GRF), peak power, (PP), and average power (AP) of every squat repetition were recorded and averaged for each set.

Figure 1: Maximal # of reps on last set and average power in the classic vs. alternating condition (Ciccone. 2014)

Interestingly, there was no significant interaction for GRF, PP, or AP. Only, the volume-equated AP was ca. 5% greater during the TS condition (989 ± 183) than the AS condition (937 ± 176). A more pronounced difference which was yet still within the margin of one standard deviation (in this case 2.2. reps) was observed for the fourth squat set to failure, where the TS condition resulted in 15% more reps to failure (7.5 ± 2.2) than the AS condition (6.5 ± 2.2). Reason enough for Ciccone et al. to suggest that:

1. Individuals who aim to optimize squat AP should refrain from performing more than three AS sets per exercise.
2. Those who aim to maximize squat repetitions to failure should refrain from performing upper body multi-joint exercises during squat rest intervals.

Certainly a sound advice, but in the end, we all live in a world where time is a precious gem and some people give a fuck about average power and the number of reps until they fail.
References:

• Ahtianen, Juha P., et al. "Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men." The Journal of Strength & Conditioning Research 19.3 (2005): 572-582.
• Ciccone AB, et al. "Effects of Traditional Versus Alternating Whole-body Strength Training on Squat Performance." J Strength Cond Res. (2014) Jun 17. Ahead of print.
• de Salles, Belmiro Freitas, et al. "Rest interval between sets in strength training." Sports Medicine 39.9 (2009): 765-777.

The deadlift probably wont benefit from blocked periodization either... at least if you do it only once a week anyway.

I hope you all remember my recent article about the beneficial effects of block periodization on the training outcome of trained cyclists (if you dont Id suggest you read up on it: "Block Periodization - Impressive Performance Gains in Pro-Athletes") and the hypothesis that the mechanism behind the beneficial effects Rønnestad et al. report in the corresponding paper are not actually a consequence of this specific periodization scheme. Rather than that, the benefits the researchers have observed may well have been a mere consequences of the "change", of "breaking out of the rut" and the provision of a new challenge thats absolutely essential to induce what everyone, from housewife to Olympian athlete is training for: adaptation.

Lets discard the mechanism for a moment, though and lets rather focus on the hard facts - hard facts that are complemented by the results of a soon-to-be-published paper by researchers from the University of Bologna and the University of Central Florida.

Whats so interesting about this paper is ...

....that it looks at the effects of block periodization in trained strength athletes and could thus help us answer a question that may have been preying on your mind, ever since I published the previously cited article about the beneficial effects of block periodization in endurance athletes: "Do Different Rules Apply for Strength vs. Endurance Athletes?" Or, put simply: Would a weight lifter benefit to a similar extend from block periodizing his training regimen as a cyclist - irrespective of what the underlying mechanisms may be?

Figure 1: The subjects trained 4x per week - identical training plans in both groups (Bartolomei. 2014)

The answer is "yes and no" - Yes, if we are talking about the upper body, no - and thats interesting because cycling obviously involves the same muscle groups - when we are looking at the lower body performance gains in Figure 2:

Figure 2: Changes in max. strength (1RM in kg), mean power (in % of baseline) and jump height (in cm) in the 24 study particpants in response to traditional linear or block periodization (Bartolomei. 2014)

As you can see, the gains in lower body power was identical - irrespective of the type of periodization (see overview in Figure 1). For the upper body, on the other hand, the subjects who did not simply ramp up the intensity continuously from 5 sets of 8-10 reps at 65-75% of  1RM  with  less  than  2  minutes  of  recovery  between  sets to 5 sets of 3 - 4 reps at 85 -95% of 1RM with 3 minutes of recovery from week 1 to week 12 (TP group), the ...

"[p]articipants  in  BP  were  more  likely  (79.8%)  to increase the area under the force-power curve than TP. Participants in BP also demonstrated a likely positive (92.76%) decrease in the load corresponding to maximal power at the bench  press compared to TP group, and a possible improvement (~ 60%) in maximal strength and power in the bench press." (Bartolomei. 2014)

Whether thats muscle-specific reaction to the three 5-week mesocycles, instead of one 15-week mesocycle is yet highly questionable - or do you think the legs respond less to the periodization program thats depicted in Figure 3, than chest, back, arms & co?

Figure 3: Illustration of the interplay between intensity and volume of the n=14 24-year-old male, resistance trained (>3 years, >3 sessions per week) subjects in the block periodization group (Bartolomei. 2014)

Personally, I would rather come back to the "novelty approach". It goes without saying that we can assume that the abrupt changes on a blocked periodization regimen favor "growth promoting overloads". In the case of the musculature of the lower body, the simple fact that it was trained just once a week may yet have provided a similarly "novel" or at least less accustomed stimulus on every leg-day.
References

• Bartolomei, Sandro, et al. "A Comparison of Traditional And Block Periodized Strength Training Programs in Trained Athletes." Journal of Strength and Conditioning Research (2014). [ahead of print]
• Rønnestad, B. R., J. Hansen, and S. Ellefsen. "Block periodization of high?intensity aerobic intervals provides superior training effects in trained cyclists." Scand J Med Sci Sports 24 (2014): 34–42.

This add is a perfect example of how saturated fat, in this case lard has always been blamed for the "lard" on ones hips.

Any hypothesis that tries to blame for our "fat misery" on a single nutrient is short-sighted. After years of fat-bashing, carbophobia and fructose hating in the course of which the situation progressively, we are now seeing the first studies which investigate what the Polish researchers, Adam Jurgo?ski, Jerzy Ju?kiewicz and Zenon Zdu?czyk from the Institute of Animal Reproduction and Food Research at the Polish Academy of  Sciences call the "biological interactions among these dietary factors" in their latest paper in the peer-reviewed open-source journal Nutrients (Jurgo?ski. 2014).

With the publication of the data of a their latest rodent study, the scientists have already taken the first step to a new, an "interactionist" perspective on the obesogenic effects of saturated vs.unsaturated and simple vs.complex carbohydrates and their interaction with another previously overlooked factor that has gotten quite some attention in the past months: The gut and its inhabitants.

Goodbye! Nutritional scapegoatism 

It goes without saying that this model study is nothing but a first step on a long road we still have to travel, but the differential effects the four diets (see Table 1)...

• Table 1: Composition of the diets.

  the soybean powered high cornstarch diet (OS),
• the lard-laden high cornstarch diet (LS), 
• the soybean-powered high fructose diet (OF), and
• the lard-laden high fructose diet (LF)

...had on the health, caecal short-chain fatty acid concentrations, cholesterol and triglyceride levels are revealing, to say the least.
If you take a closer look at the actual study outcomes, you will see that the answer(s) the study provides are about as complex as its design.

In contrast to the dietary fat which had no independent effect on any of the measured markers of gut function, the carbohydrate source, i.e. cornstarch vs. fructose lead to significant differences in total small intestinal mass, mean pH of the ileal digesta and the mucosal activity of sucrase, all of which were increase on the high fructose diet.

Figure 1: Serum lipid levels of the rodents after 4 weeks on obesogenic diets containing different forms of dietary fat and carbohydrate (Jurgo?ski. 2014)

Interactive effects were observed for the mass of the cecum itself (the tissue) and the digesta with opposing effects of fructose on when it was administered in conjunction with lard (reductions) vs. soybean oil (increases in cecum mass). Slightly different effects were observed for the short-chain fatty acid composition (SCFA):

"Both the dietary fats and carbohydrates contributed to changes in the total SCFA concentration in the caecal digesta of rats (p < 0.05 and < 0 0.001, respectively). The highest total SCFA concentration was in group LS, while group OS had a significantly lower concentration (p ?0.05). Similarly, the acetate concentration in the caecal digesta was influenced both by dietary fats and carbohydrates (p < 0.05 and p < 0.001, respectively) with a similar span of differences among particular groups (p ?0.05). The type of dietary carbohydrate had significant influence on the propionate and isobutyrate concentrations in the caecal digesta (p < 0.001 and p < 0.05, respectively); however, both dietary factors had an interactive effect on their concentrations (p < 0.05). The highest propionate concentration was observed in the LS and OS group, whereas significantly lower concentration was found in the OF group. The lowest isobutyrate concentration was in group OF and it was significantly higher in group OS (p ?0.05)." (Jurgo?ski. 2014)

The serum lipid profiles were influenced by both, the types of fats and carbohydrates as shown in Figure 1. Whats particularly striking, here, is the nasty effects of a combined lard + fructose feeding on the triglyceride levels.

A similar fat-dependence as for the fructose induced triglyceride boost can be observed for the levels of total and HDL cholesterol, which were increased only by the combination of fructose + saturated fat. In the rodents that received soybean oil with their coke, ... ah, I mean with their fructose, the researchers observed the exact opposite trend and a 5x lower yet similarly increased artherosclerosis risk (as evidenced by the 5x higher atherogenic index).
References:

• Gajda, Angela M. "High fat diets for diet-induced obesity models." A Report for Open Source Diets (2008).