Foods, Not Macros: Isoenergetic Breakfast With Identical Macronutrient Content More Satieting With Eggs vs. Flakes. Plus: Omega-3 <> Microbiome <> Obesity Interactions

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 what's currently going on in the health and fitness community. With cereals being labeled as "the devil" (it's always nice to be "anti", isn't 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.

7000kcal for 1kg of body fat? I know that this is a naive miscalculation, but it should suffice to demonstrate that the protein quality (remember the amount of protein in both breakfast conditions was identical) counts and two eggs (vs. Kellog's Special K) can make the difference between slow, but continuous weight gain on the one and weight stability (or more) on the other hand.

Whether or not similar concrete weight loss vs. gain effects can be achieved with different types of fat is nothing study #2 in today's 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 that's what you want to achieve).

This is not just about fish oil

"Of course, the bad omega-6s" ... I know that this is what you're thinking right now, but let's be honest, isn't 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 you'd see in low fat or high fat diets with palm, olive or safflower oil powered high fat diets.

Increased lipid oxidation in athletes w/ low dose fish oil (Filaire. 2010)

The health benefits of omega-3s: The often-cited evidence of the benefits of high omega-3 levels in the cells is by far not so conclusive as the laypress and supplement producers would have it. Danthi et al. have shown only recently that fish consumption, but not the omega-3 content of your cells is a reliable predictor of cognitive performance in the elderly. Associations between heart health, mortality, etc. and cellular omega-3 levels could thus be mediated by the whole food source of those omega-3s, i.e. fish consumption, and not by their mere presence in the cells, as well.

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)

It's 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 who's 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 that's 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 wouldn't you agree that this oil mix looks a little too much like the mixture you'd 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... ?

Enough of the speculations, though: What I actually wanted was to remind you of the fact that you're still eating food not proteins, carbohydrates and fats and that there are physiological performance-, health- and longevity related, as well as psychological downsides, I can only hint at in the info-box to the right, to any form of "as long as it fits my macros" ignorance.

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.

Whey or Casein? Which Would be the Better "Staple" Protein Source for Your Trip to Desert Island?

Image 1: They are both sourced from cow's milk, but which is the better part? Whey, the byproduct of cheese production, or casein the cheese protein, itself? A recent study would suggest that it's the "waste product" you would have to chose if you could only have one.

"Whey is the way to go!" I suppose even I have had a headline like that in one or even several of the daily news items, here at the SuppVersity - and rightly, so! With it's high content of branched-chain amino acids (BCAAs) this fast-digesting protein source is certainly the #1 choice for anyone whose goal is to build lean muscle tissue. Whey's slow-digesting brother casein, on the other hand, is often hailed as the "muscle-preservative", the 24h-protein source that will prevent muscle catabolism, when for whatever outrageous reason (like sleep, for example) you cannot ingest your bi-hourly protein shake... well, I guess those of you who have been following the Intermittent Thoughts on Intermittent Fasting will already be "rolling on the floor laughing", but hey! Do we really know whether casein or whey would be the better "staple" protein - I mean, if you sipped it throughout the day?

Casein vs. whey - which one to chose if you cannot have both?

While I would not say that one study could provide a definite answer to this question, the results of a recently published paper by Stéphane Walrand et al. (Walrand. 2011) provides further evidence that whey, not casein would be your best choice - regardless of the diminished return that comes with sipping it.

Figure 1: Ingredients of the 6 diets the rats in the Walrand study were fed for 5 months; CAS = casein, WHEY = whey (data adapted from Walrand. 2011)

In their long-term (5 months!) feeding study, the scientists supplied 21 week old male Winstar rats (at the beginning of the study the animals were thus "middle-aged") with one out of 6 experimental diets (cf. figure 1). The composition of the diets differed not only in their total energy and protein content (ad libitum = 440kj/day; energy restricted only 60%, i.e. 264kj/day), but also with regard to the protein content and source (casein vs. whey). In that, it is particularly noteworthy is that the "energy restricted" diet was actually a "high protein" diet. After all, the protein content of the latter was identical to the one of the rats that had free access to  (the group that was "only" energy restricted received was matched to the average protein consumption of the ad-libitum fed rats.

Figure 2: Effect of 5 months of the experimental diets on muscle and fat weight of male Wistar rats (data adapted from Walrand. 2011)

Contrary, to what you may have expected, the "protein deficient" protein & energy restricted diet did yet not lead to profound losses of lean muscle tissue (cf. figure 2). On the contrary, the protein & energy restricted group that received whey protein as their exclusive protein source had 5% and 2% greater soleus and tibialis anterior mass than the ones that received the "high protein" energy restricted diet. Before you start questioning the value of "high" protein intakes when dieting, you should yet better take a look at the impact of the "high" protein content of the non-protein-restricted diet had on the diet induced reductions of the abdominal fat mass. I mean -87% reduced abdominal fat in the energy & protein reduced group is impressive, the neigh complete annihilation of the abdominal fat (-93%) in the non-protein restricted group, on the other hand, is mind-boggling.

Figure 3: Effect of 5 months of the experimental diets on muscle and fat weight of male Wistar rats (data adapted from Walrand. 2011)

If we also consider the nitrogen balance and the absolute rates of muscle protein synthesis (cf. figure 3), it also becomes evident why the rats on the protein & energy reduced diets retained slightly more lean mass (+3%), when they were fed whey protein, instead of casein. The rats who received whey as their main protein source simply had a favorable nitrogen balance and increased muscle protein synthesis.

Image 2: Sardines for diabetes prevention!?

Before you now throw away your eggs, your cheese, your beef and whatever else, I want to briefly introduce you to the results of two other recently published studies, which would indicate that rotating in some sardines or sheep meat could produce even more favorable results than living on whey alone. While Madani et al. found that sardine protein ameliorated fructose-induced hyperglycemia, insulin resistance, hyperlipidemia and inflammation (vs. casein) in a 2-months rodent study (Madani. 2011), Feng et al. report that the consumption of sheep meat instead of casein lead to increases in free T3 (thyroid hormone) and statistically significant increases in energy expenditure in Sprague-Dawley rats that were fed otherwise identical diets (Feng. 2011).

Despite these and the results of previous studies, most of which would suggest that if you had to chose just one protein source, whey or casein, whey should be the protein of choice, I hope that I do not have to tell you, as a diligent student of the SuppVersity that imbalances are the root cause of many, if not most modern diseases. So, getting all your protein from whey and nothing but whey should not be something you should even remotely take into consideration. And in case you forgot about that: Milk has both of them and a ton of other vital nutrients ;-)