Creatine Non-Responder? Age+Meat Intake - Determinants of Creatine's Effect on PCr (±200%) + Probably Performance

Vegetarian strength athletes belong to the group of people who will probably benefit most from creatine supplementation. Their young, meat-eating peers, on the other hand, may well turn out to be non-responders, because they see highly individual, but overall only non-significant increases in phosphocreatine.

It has been a while since I published the last creatine article ("Dubious Effects of Creatine on Markers of CNS Adaptation and Heart Health in "Bodybuilders" - Reason to Be Afraid?" | read it); the last time that I addressed the issue of "creatine non-responders", i.e. reasons why people simply don't seem to benefit from creatine supplementation has been published in 2014, already, when I presented the results of a study suggesting that it's not a high dietary creatine intake from meat that makes the difference (learn more).

Needless to say, meat still made it on the list of possible determinants of the individual performance increases in response to creatine supplementation... I mean, it's meat - and we all know how people love to blame it for everything, these days ;-)

You can learn more about creatine at the SuppVersity

Creatine Doubles 'Ur GainZ!

Creatine Loading = Unnecessary

Creatine Pre or After Workouts?

1st Benefits of Creatine-HCL

The Real Bioavai-lability of Crea

No Ill Effect of Cre on CNS

Before we get into any further details, though, I have to point out that the soon-to-be-published study by Marina Yazigi Solis and colleagues from the Univerity of Sao Paulo did not actually test the performance effects of creatine. Rather than that the goal of the Brazilian scientists was to fill another gap in the extensive literature about creatine supplementation: the way(s) in which your creatine/phosphorylcreatine (PCr) response to creatine supplementation may be modulated by age, diet, and tissue. Or, as the scientists describe it: "[W]e aimed to determine whether the PCr responses vary as a function of age, diet, and tissue.

In their study, fifteen children, 17 omnivorous and 14 vegetarian adults, and 18 elderly were randomly assigned to consume either placebo and subsequently creatine (0.3 g/kg per day) or creatine and placebo for 7 days in a single-blind fashion.

Figure 1: Illustration of the phosphocreatine “shuttle” system (Guimarães-Ferreira 2014); as you can see PCr is - assuming you have the necessary energy in form of ATP available, automatically restored by creatine kinase - the loss in form of creatinine is, at least in healthy individuals, relatively low and may indeed be compensated for by the relatively small amount of creatine omnivores get from (esp. the red) meats in their diet.

PCr was measured via phosphorus magnetic resonance spectroscopy (31P-MRS) in muscle and brain using a whole body 3.0T MRI scanner (Achieva Intera, Philips, Best, The Netherlands) and a 14 cm diameter 31P surface coil.

The latest about "advanced creatines": A very recent review (Andres 2017) of the various currently available forms of creatine that are often advertised as "advanced creatine products" confirms previous assessments: it's all bogus. Creatine phosphate adds to the risk gastrointestinal symptoms and poses a CVD and kidney "health risk" because they will increase the already high consumption of phosphates with the Western diet. Creatine taurinate is simply unnecessary, you could as well take monohydrate and taurine. Unlike regular monohydrate, creatine ethyl ester will increase creatinine levels in serum - "probably due to the high conversion of creatine ethyl ester to creatinine in the gastrointestinal tract". Creatine orotate is a potential cancer promoter, as "orotic acid caused tumor-promoting effects in animal studies revealing a too low margin of safety in relation to the calculated human exposure". The forms of creatine (creatine pyruvate, creatine citrate, tri creatine malate, creatine pyroglutamate and creatine gluconate), Andres et al. investigated "are unlikely to pose safety concerns", but they aren't worth the extra bucks, either.

As you can see in Figure 2, the creatine supplement increased muscle PCr in children (p<0.0003) and elderly (p<0.001). What it did not do, however, was to produce significant increases in the meat-eating (=omnivorous) study subjects (the statistical significance of the changes were far from being below 0.05 | p=0.3348, a sub-group analysis for the amount and type of meat the subjects consumed was not performed and probably wouldn't have made sense in view of the relatively low number of participants).

Figure 2: Delta changes in PCr in response to creatine supplementation (i.e., creatine subtracted from placebo values) in muscle and brain (Solis 2017); with only 18 elderly subjects, it made no sense to distinguish omnivores vs. vegetarians.

What may be quite surprising is that the elderly subjects had greater PCr increases than children and omnivores (p<0.0001 for both). Less surprising, but also worth mentioning: children experienced greater PCr increases than omnivores (p=0.0022). When the scientists eventually compared vegetarians (p<0.0001) to omnivores, they found that the former were the ones with the most significant increase in PCr content and thus the subjects of whom you would expect that they'd see maximal performance gains, as well.

Chicken is not a good source of dietary creatine: Chicken has only very low levels of creatine (ca. 300-400mg/100g) and thus ~50% less than what you'd get from beef - moreover, chicken is always eaten well-done and cooking has been shown to decrease the creatine content of foods significantly, as Tarnopolsky, et al. point out in their 2010 review.

Table 1: Creatine content of some common foods (Tarnopolsky 2010).

Unrelated to your "gainz", but probably highly health-relevant in view of the effects of creatine on the brain, e.g. its protective effect in traumatic brain injury (Sullivan 2000) and its ability to boost brain performance (Rae 2003 + Rawson 2011), is that the study at hand found no increase in Brain PCr in any group, and delta changes in brain PCr (-0.7 to +3.9%) were significantly less pronounced than the increase in muscle PCr content (+10.3 to +27.6%; p<0.0001 for all comparisons).

For the elderly individuals that seems odd, as previous studies demonstrated measurable beneficial effects on the cognitive performance of elderly subjects (Rawson 2011), for the younger subjects, on the other hand, it was to be expected that the PCr levels and thus the availability of immediate response energy wouldn't increase significantly as Rawson et al. demonstrated in 2008, already, that "creatine supplementation does not improve cognitive function in young adults" (Rawson 2008).

Guanidinoacetic Acid (GAA) 'Superior' to Creatine in Terms of Bioenergetic & Health Effects on Brain, Muscle & More? | learn more

What does this mean for you? If you're a young (red) meat lover, the chance of seeing exorbitant increases in performance (muscular and cognitive) are slim.

While we may have to take into account that exercise will temporarily deplete the PCr stores, our bodies are well-equipped to restore them by "recycling" (see Figure 1), if there's no significant increase in the phosphocreatine (PCr) pool, it is thus unlikely that your ability to lift, sprint or perform other high(er) intensity activities that tap into your muscle PCr stores will increase.

If you are a baby-boomer or who trains regularly and consumes a vegetarian (let alone vegan) diet, on the other hand, your results could be outstanding - "could be" because the study did not test the actual performance benefits, but whether and to which extent the phosphocreatine stores were increased - Plus: It is guaranteed that there's a practically relevant genetic component, as well. I mean, you do remember that the CK response to workouts is also genetically determined and in some so high that your doctor may mistakenly believe you had been run over by a truck and the crushed protein was now clocking up your kidneys, right? | Comment on Facebook!

References:

• Andres, S., et al. "Creatine and creatine forms intended for sports nutrition."  Mol. Nutr. Food Res. 61, 1600772 (2017).
• Guimarães-Ferreira, Lucas. "Role of the phosphocreatine system on energetic homeostasis in skeletal and cardiac muscles." Einstein (São Paulo) 12.1 (2014): 126-131.
• Rae, Caroline, et al. "Oral creatine monohydrate supplementation improves brain performance: a double–blind, placebo–controlled, cross–over trial." Proceedings of the Royal Society of London B: Biological Sciences 270.1529 (2003): 2147-2150.
• Rawson, Eric S., et al. "Creatine supplementation does not improve cognitive function in young adults." Physiology & behavior 95.1 (2008): 130-134.
• Rawson, Eric S., and Andrew C. Venezia. "Use of creatine in the elderly and evidence for effects on cognitive function in young and old." Amino Acids 40.5 (2011): 1349-1362.
• Sullivan, Patrick G., et al. "Dietary supplement creatine protects against traumatic brain injury." Annals of neurology 48.5 (2000): 723-729.
• Tarnopolsky, Mark A. "Caffeine and creatine use in sport." Annals of Nutrition and Metabolism 57.Suppl. 2 (2010): 1-8.

Is 'Meat' Bad for us, or Rather the Products we Call 'Meat' - A Mix of Preservatives + Colorings That's Killing Us Slowly?

Ladies and gentlemen, may I introduce: the worst offenders in the "meat" category. Foods that owe their color, their taste, their shelf-life and their tolerable bacterial count to an amount of food additives that makes me question whether these food products are still "meats".

You will probably remember from previous SuppVersity articles that the association between meat, cancer, diabetes and other ailments of the Western Diabesity Society often vanish when studies successfully adjust the odds ratios for developing one of multiple of these diseases for fresh (=unprocessed) vs. processed meat intake.

One reason for this observation unquestionably is oxidative damage to the protein and fat content of meat product during processing. Unlike these factors and the oxidation of fats that you add when you prepare the meat, there's yet another potential reason for the bad effects of processed meats on our health: many of them are only par meat, part additive.

Meat is an essential part of the "paleo diet" | Learn more about meat at the SuppVersity

You May Eat Pork, too!

You Eat What You Feed!

Meat & Prostate Cancer?

Meat - Is cooking the problem

Meat Packaging = Problem?

Grass-Fed Pork? Is it Worth it?

I know that's confusing. So let me explain: As Marco Iammarino, Rosaria Marino and Marzia Albenzio point out in their latest review, "meat products may be compromised by several admitted and not admitted procedures (i.e. addition of food additives and/or foreign proteins)" (Iammarino 2017) - to decide whether it's the meat, as in everything you get from the healthy, naturally reared animal, or the additives which are making you sick is thus impossible and accordingly beyond the scope of this article. What is within its scope, on the other hand, is to provide an overview of what exactly you may be eating on a daily basis and advise on how to reduce your exposure to pseudo-meat, significantly.

Figure 1: Colorectal cancer risk increase w/ 100g and 25g higher intake of total red meat (incl. processed meat) or all processed meats (incl. white meats), respectively (calculated in a meta-analysis by Sandhu et al. 2001), per day.

Now, it would be unfair to say that all meat producers and processors were focusing exclusively on profit maximization. While this is, as we are about to see in this review, clearly the case, battling pathogens, reducing the growth of inert, but still unwanted bacteria and tailoring to our own demand for unperishable goods are actually the primary reasons why producers and processors use food additives such as...

• colors (cochineal, carminic acid, carmines, allura red AG and caramels),
• preservatives (sulfites, acetates),
• acidity regulators (ascorbates, lactates, citrates, and phosphates),
• polyphosphates and nitrates (sulfites, nitrites, nitrates, etc.)

Many of these ingredients are considered "GRASS" (=generally regarded safe) when consumed on their own and in small quantities. When they get together for an additive-party in the sausages you bought for tomorrow's barbecue, however, they may form a sickening cocktail of which we already know that it will, at least, increase the formation of unwanted compounds such as nitrosamines in your meats (sulphites, nitrites, and nitrates are responsible for this effect).

"For these reasons, the topic ‘food additives in meat and meat products’ has become an
emerging issue in food safety" (Iammarino 2017).

Even if we take a look only at the long list of potentially health relevant (ill) health effects of single food additives, we will find all sorts of ailments - from an allergic reaction to cancer.

• Sulphiting agents are used in the sulfuring treatment of fresh meat (but also bottled soft drinks, juice, fruit bars, dried foods, salads and fruit salads, or gelatin and coconut, as well as medications and cosmetics) and meant to avoid bacterial contamination and browning of the foods. Unfortunately, they have been implicated in asthma and other allergies (Vally 2009) and the USDA food safety documents list symptoms including chest tightness, hives, stomach cramps, diarrhea, and breathing problems (USDA^a) - according to a 1995 paper by M.R. Lester only < .05% of the population are affected, though (Lester 1995).
  

  

  Figure 1: There are also naturally sulphated foods, a greater health threat, however, seems to come w/ added sodium or potassium metabisulfite, bisulfite, sodium bisulfite/-sulfite in "meat" products (Lester 1996).

  Even though the USDA requires labeling of sulphating agents if their concentration in the finished meat or poultry food product is 10 ppm or higher, they say that "[o]verall, there is insufficient information available to set a Tolerable Upper Intake Level [often short "URTI"] for sulfate" (USDA^b). 

• 

  Table 1: Nitrate concentrations in selected meat products according to a 2009 study by Menard et al. based on representative data from 138 and 109 food items, respectively, and coming from French monitoring programs between 2000 and 2006 (Menard 2009)

  Nitrates and even more so their cousins, the nitrites, are used in meat curing due to their preservative activity have long been considered harmful food additives for humans because they may interact with secondary amines in the stomach and produce N-nitroso compounds, which are associated with gastric cancer - worst of all, the chronic (ab-)use of nitrate-/nitrite-compounds in agricultural has already raised the "natural" nitrate level to up to 40mg/kg meat, which is still less than the USDA upper limit of ~365mg/kg for nitrate from sodium nitrate and 135mg/kg for nitrite from sodium nitrite, but worrisome, nonetheless.
  
  With respect to studies investigating the de facto nitrate + nitrite content of meat products, it is interesting to note that the level of nitrate and nitrite in sausages, salami and co. is at least 2-fold higher in Australian vs. US studies (each done with products from local supermarkets) - with Australian salami reaching the USDA limit and US sausages being 50% below that limit.
  
  As data from Menard et al. (see Table 1) indicates the exact type of meat and, in that, the way it is produced does yet make so much of a difference that it doesn't make sense to compare the Frankfurter's from an Australian study fo breakfast sausages from a US study. Rather than avoiding regional products, it would thus make sense to avoid certain types of processed meat, such as coppa, in which the level of nitrate is ~400 mg/kg and thus higher than the generous USDA limit.
• Food colorings are used to make foods look the way we expect them to look - including meats; and since the latter are usually deep red, food colorings like cochineal, carminic acid, carmines (E120), Ponceau 4R, cochineal red A (E124) and allura red AG (E129) are used and mixed to achieve the same healthy pink to red tint we expect the perfect chicken breast or stake to have.
  
  

  

  Minced beef and pork are favorite targets for the abuse of food coloring.

  While the former are the only legal food colorings for meat products on the European market, the US FDA still tolerates Red Dye No.3 - a product the cousins of which, i.e. Red Dye No.1 (Ponceau 3R), Red Dye No.2 (Amaranth) and Red Dye No.4 (Scarlet GN), were banned between 1961 and 1976 due to their proven toxic effects on rats, and an agent of which many scientists highlighted its potential toxic effects that this food colouring may exhibit (significant increases in the incidence of thyroid follicular cell hypertrophy, hyperplasia and adenomas in rats | Haschek 1998).
  
  Another coloring from the same family, Ponceau 4R, on the other hand, is suspected to trigger hyperactivity in kids, prohibited in the US and still allowed in the European Union, where it is used to give chorizo sausage/salchichon and sobrasada their characteristic color - and it is difficult to tell exactly how much has been used. After all, "a complete analytical technique able to identify and simultaneously quantify all of the most important red food colorings (banned and not banned) in meat products is" as Immarino et al. point out "still not available" (Iammarino 2016).

Paleo Goes "Real Science" - First Meta-Analysis of Available RCTs Shows Improvements in Health + Body Composition - Paleo is not just effective, it also allows for a broad range of foods to be consumed - not exclusively fresh meats | more

So what's the take-home message, then? While it is too early to make specific recommendations in form of "avoid" salami from the US and chorizo sausages from Spain, it is quite clear that the best way for meat eaters to make it past their own "best before date" is to avoid processed meats altogether. This will limit your the exposure to added nitrates and sulphites, of which Immarino et al. write in their previously referenced review that they are often used at high concentrations in meats [and may thus] represents a food safety risk" (Immarino 2016), and it will reduce the risk that you consume high amounts of potentially carcinogenic and/or ADHD promoting food colorings from processed meats (note: all these agents can also be used in "fresh" meat that's actually not fresh at all to make it look as if it came right from the butcher) | Comment!

References:

• González, Carlos A., et al. "Meat intake and risk of stomach and esophageal adenocarcinoma within the European Prospective Investigation Into Cancer and Nutrition (EPIC)." Journal of the National Cancer Institute 98.5 (2006): 345-354.
• Haschek, Wanda M., Colin G. Rousseaux, and Matthew A. Wallig, eds. Fundamentals of toxicologic pathology. Academic Press, 2009.
• Iammarino, Marco, Rosaria Marino, and Marzia Albenzio. "How meaty? Detection and quantification of adulterants, foreign proteins and food additives in meat products." International Journal of Food Science & Technology 52.4 (2017): 851-863.
• Lester, Mitchell R. "Sulfite sensitivity: significance in human health." Journal of the American College of Nutrition 14.3 (1995): 229-232.
• Menard, Céline, et al. "Assessment of dietary exposure of nitrate and nitrite in France." Food Additives and Contaminants 25.8 (2008): 971-988.
• Sandhu, Manjinder S., Ian R. White, and Klim McPherson. "Systematic review of the prospective cohort studies on meat consumption and colorectal cancer risk." Cancer Epidemiology and Prevention Biomarkers 10.5 (2001): 439-446.
• Vally, Hassan, Neil LA Misso, and V. Madan. "Clinical effects of sulphite additives." Clinical & Experimental Allergy 39.11 (2009): 1643-1651.

BCAAs Mess W/ Vegan Glucose Management, Human Study Says - Do You Have to Stay Away From BCAAs, Now?

Are vegan athletes who supplement their low BCAA baseline diet with amino acid powders making an unhealthy mistake? At first sight a recent study from Poland suggests just that. Upon closer scrutiny, however, the practical relevance of the results appear less and less convincing.

It seems (and I have to admit that I fell for that logic, too) only logical that vegans, unlike omnivores and lactovegetarians run the risk of not getting enough BCAAs from their diet. After all, their diets allow the neither the consumption of dairy nor many of the other wonderful high BCAA protein sources.

Against that background, I would venture the guess that many vegan athletes spike their diets with copious amounts of the ubiquitous BCAA supplements, supplement vendors all around the globe are pushing on unsuspecting customers who have no clue that a new study claims that these supplements may ruin one of the often-heard benefits of vegan diets: improved glucose management and reduced diabetes risk (eg. -62% in Tonstad et al. 2013).

You can learn more about BCAAs & other amino acids at the SuppVersity

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Taurine and the Microbiome

Based on the observation that BCAAs will reduce the glucose clearance rates in healthy human beings, in some (Tremblay 2005 | glucose uptake ↓ by 33%; Robinson 2015 | glucose uptake ↓ by 40% and 23% at low and high insulin levels, respectively), but not all (Everman 2015) pertinent studies and in view of the fact that

Bad news for BCAA-junkies | more

"[d]ata on the effect of a chronic supplementation with BCAA in humans are still limited making it impossible to clarify whether increased dietary BCAA themselves are sufficient to trigger IR-related diseases or whether the perturbations in BCAA levels only reflect an already developed insulin resistant state [here, the authors refer to the observation that people with metabolic syndrome have, across the board, significantly elevated BCAA levels in the blood]" (Gojda. 2017)

the authors speculated that supplementing healthy subjects with 20g of BCAAs (female subjects received only 15g to make up for their lower body weight) and comparing the results of vegan (=low BCAA intake) and omnivore (=high BCAA intake) subjects would yield valuable insights into the 'true' effects of BCAAs on human glucose metabolism.

Don't rejoice too early, omnivores: If you're an omnivore you may still be concerned about the literally 'depressing' effects of BCAAs - a supplement of which most research shows that it is useless if you have a high intake of quality protein, anyway.

Now, while I cannot tell in how far a single 12-week study can do that, i.e. contribute valuable insights into the 'true' effects of BCAAs on human glucose metabolism, I can tell you that the results Gojda et al. present in the European Journal of Clinical Nutrition will make at least the vegans in the SuppVersity audience sit up and question their use of BCAA supplements... at least for as long as they didn't read the rest of the article ;-)

Figure 1: At first sight, the changes in the subjects' basal glucose levels and their ability to clear glucose during the hyperinsulinemic euglycemic clamp test clearly suggest that 20g/15g/day BCAAs are bad for vegans (Gojda 2017).

It stands out of question, a -28% decrease in glucose clearance during the scientists' two-hour hyperinsulinemic euglycemic clamp test is quite a significant negative effect (the effect size, here, is d = 0.99; anything >0.8 is considered a "large" effect size). Before you freak out, however, it must be said that the metabolic rate of glucose clearance per unit of insulin, which is what I would consider a much better measure of insulin sensitivity, was decreased by a statistically highly non-significant, practically (check out the standard deviation in Figure 2) irrelevant 3%, only (addendum: I calculated the effect size, which is d = 0.08 and would thus confirm the lack of practical relevance of this finding, after all, anything < 0.2 is already considered a "small" effect size - 0.08 is thus quasi no effect).

Figure 2: Unlike the absolute glucose infusion rates during the hyperinsulinemic euglycemic clamp, the rates per unit of insulin were not affected by 3 months on 20/15g of BCAAs per day (Gojda 2017).

Nevertheless, the scientists are still confident to conclude that "[a] chronic increase in BCAA intake led to a decrease of IS only in vegans" (Gojda 2017) - and that despite the fact that they did not observe the typical increases in serum BCAAs seen in obese / metabolically diseased subjects during the supplementation period (only the levels of leucine increased from the 20g of BCAAs that contained leucine, valine, and isoleucine at a ratio of 4:1:1) and admit that previous studies in metabolically deranged people show "an improvement of glucose uptake after a long term high-BCAA protein supplementation" (Gojda 2017).

Obviously, the last mentioned real-world (i.e. meals vs. insulin clamp + glucose infusion as in the study at hand) effects may obviously be a mere result of an increased release of insulin in the otherwise insulin resistant subjects when they were fed cod and whey protein, the "high-BCAA protein sources" in Ouellet, et al. (2007) and Jakubowicz, et al. (2013), the two studies Godja et al. are referring to in the previously cited statement. With nothing but eventually elusive evidence from a single lab test with conditions that hardly resemble our everyday dietary glucose exposure, I would still be hesitant to jump on the 'BCAAs mess with your glucose metabolism'-train - and that's despite the fact that I have been very critical in previous articles about BCAA supplementation.

What's the message for the omnivores? There are two things omnivores should take away from the study: (a) the increased clearance of glu-cose in the hyperinsulinemic euglycemic clamp test the scientists observed in the omnivores is as misleading as the decrease in the vegan subjects, because it was likewise not complemented by an increased rate of glucose disposal per unit of insulin; and the former was (b) probably a mere result of an increased production of insulin (+63% in the omnivore subjects of the study at hand; p < 0.05) and thus the insulinotropic effect of BCAAs that has been pre-viously observed in both, healthy and (pre-)diabetic subjects, whose glucose levels improve with the consumption of high BCAA proteins merely due to an increase in insulin production. In conjunction with the hitherto not discussed omnivore-exclusive increase in the ex-pression of lipogenic genes FASN and DGAT-2, as well as corresponding increases in two additional lipogenic genes, PPARγ and SCD-1, the increased insulinemia with extra BCAAs in omnivores is in fact the only substantially 'bad news' of a study that, initially, appears to hold bad news only for vegans.

So what's the verdict, then? The practical significance of the study at hand is much lower than headlines like "BCAAs mess with vegans' glucose metabolism" would suggest - and that's despite its relatively long intervention period and the inclusion of a follow-up.

So why is it too early to freak out? Well, for one, the scientists "conclusion that BCAA could have a direct negative impact on IS in healthy humans" is based on a test the practical relevance of which remains questionable: the hyperinsulinemic euglycemic clamp test has little to nothing to do with the metabolic response to a complex meal; and even if we accept its results as reliable indicators of real-world changes in glucose sensitivity, there's still the lack of changes in the metabolic clearance rates for glucose on a per unit of insulin base. And while the scientists address the non-significance of this data in the limitations section of their paper, where they declare that the "statistical power of our study to show differences of MCR/I after the intervention was therefore only 7%", that doesn't explain that the MCR/I dropped by only 3% and thus 50% of the standard deviation.

Furthermore, the scientists did not observe the 'classic' changes in BCAA metabolism gene expression that have been observed in the previously hinted at studies that link a high serum BCAA level to insulin resistance (Newgard 2012). And it's not just genes that are involved in BCAA metabolism that didn't change in the vegans: the same goes for all other genes the scientists tested, as well.

No effect on MCR/I, no effect on the expression of metabolically relevant genes (including insulin receptor and glucose transporter expression), this leaves us with the 4% increase in serum glucose of which even a layman can see that it's very unlikely a result of the BCAA supplementation... if it was, the glucose level should not increase by another 8% after the three months supplementation period, should it? No, it shouldn't and you shouldn't freak out if you read elsewhere that "a recent study shows that BCAAs decrease your insulin sensitivity" | Comment!

References:

• Everman, Sarah, et al. "Effects of acute exposure to increased plasma branched-chain amino acid concentrations on insulin-mediated plasma glucose turnover in healthy young subjects." PloS one 10.3 (2015): e0120049.
• Gojda, J., et al. "Chronic dietary exposure to branched chain amino acids impairs glucose disposal in vegans but not in omnivores." European Journal of Clinical Nutrition (2017).
• Jakubowicz, Daniela, et al. "Incretin, insulinotropic and glucose-lowering effects of whey protein pre-load in type 2 diabetes: a randomised clinical trial." Diabetologia 57.9 (2014): 1807-1811.
• Newgard, Christopher B. "Interplay between lipids and branched-chain amino acids in development of insulin resistance." Cell metabolism 15.5 (2012): 606-614.
• Robinson, Matthew M., et al. "High insulin combined with essential amino acids stimulates skeletal muscle mitochondrial protein synthesis while decreasing insulin sensitivity in healthy humans." The Journal of Clinical Endocrinology & Metabolism 99.12 (2014): E2574-E2583.
• Tonstad, S., et al. "Vegetarian diets and incidence of diabetes in the Adventist Health Study-2." Nutrition, Metabolism and Cardiovascular Diseases 23.4 (2013): 292-299.
• Tremblay, Frédéric, et al. "Overactivation of S6 kinase 1 as a cause of human insulin resistance during increased amino acid availability." Diabetes 54.9 (2005): 2674-2684.
• Ouellet, Véronique, et al. "Dietary cod protein improves insulin sensitivity in insulin-resistant men and women." Diabetes Care 30.11 (2007): 2816-2821.

Your Meat Consumption is Probably Not the Reason You're a Creatine Non-Responder: 5% Faster 50m-Sprint Time in 6 Days W/ 20g/day of Creatine for Vegetarians & Omnivores

It's hard to be a non-responder andno way to change it.

In some people the ingestion of creatine appears to be ineffective. Aside from minor diarrhea, when they increase the dosage to the 20g+ range per day in a desperate effort to reap the benefits of one of the, if not the only tried and proven natural ergogenic with significant (real world!) effects, these creatine non-responders don't get any results from either creatine monohydrate or any of the fancier, but mostly inferior "advanced creatines" you can buy at you local, national and international supplement vendor.

One of the commonest and eventually most reasonable explanation for "non-responding", I've heard is the hypothesis that non-responders have a high enough creatine intake from meat that would reduce any additional benefit from supplemental creatine to unmeasurable levels.

You can learn more about creatine at the SuppVersity

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ALA + Creatine = Max Uptake?

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Build 'Ur Own Buffered Creatine

And in fact, with beef and co being your best dietary creatine sources, it seems legit that meat-eaters would benefit less from supplemental creatine than vegetarians whose plant-based diets are more or less devoid of creatine.

By now you should yet be used to the fact that there are billions of things in the realm of nutrition, health and fitness that make perfect sense and still don't exist... and yes, the aforementioned hypothesis that omnivores won't benefit from creatine is one of them.

Figure 1: Higher increase in the previously low creatinine levels, but identical increase in 50m spring performance in vegetarians ans omnivores in response to 6 days on 20g of creatine (Seyedjalali. 2014)

If you take a look at the data in Figure 1, data from a recent study from the Chandrashekar Agashe  College  of  Physical Education in India, you will see that the omnivores had higher blood creatine (=used creatine) levels, but an identical increases in 50m sprinting performance.

The study at hand does therefore the findings of this study support the usefulness of short-term creatine supplementation at 20 grams  per  day  for  6  days, but it does not support the hypothesis that the corresponding increases in 4x 50 m dash run performance would be more pronounced in the vegetarian subjects, whose baseline creatine intake borders zero.

Are you like one of three subjects in Greenhaff's 1994 study?

Bottom line: If you belong to the small group of creatine non-responders you will obviously have to wait until someone identifies another hopefully non-genetic determinant of your non-existing response to the provision of creatine monohydrate or any other form of creatine. Until then, a highly efficient creatine recycling / endogenous production and / or the inability to use exogenous creatine remain the most likely and eventually the only realistic explanation for a phenomenon of which only the second one, i.e. the inability to use supplemental creatine as a means to increase muscular the creatine stores has scientific backup from one of the early studies on creatine (Greenhaff. 1994)

Reference:

• Greenhaff, P. L., et al. "Effect of oral creatine supplementation on skeletal muscle phosphocreatine resynthesis." American Journal of Physiology-Endocrinology and Metabolism 29.5 (1994): E725.
• Nimkar, Nayana, and Ph D. Physical Education. "Comparative Effect of Creatine Supplementation Blood Lactate and Intermittent Running Performance on Vegetarian and Non-Vegetarian Active Males." Heg©< e Òeew {veeieefjkeÀeb® ³ee jkeÌleoeye Je ceOegcesneJej efveJe [keÀ ÒeeCee³eece Je Deemeveeb® ee nesCeeN³ee HeefjCeeceeb® es DeO³e³eve-mebefoHejepe Me. Deewlee [s: 30.

Grass-Fed Pork? Not Really. Still the Difference in Fatty Acid Composition & Micronutrient Content Are Profound & Not Accounted for by Food Databases - Let Alone Epidemiology

You often hear that pigs are pretty closely related to us humans, but "are all pigs created equal"? Or what may be a more appropriate question for the SuppVersity: Is all pork really created equal?

If you like databases like nutritiondata.com or the USDA's very own detailed nutrient database in order to evaluate whether your diet is actually delivering all the nutrients you need you are probably missing half of the picture. At least as far as the more sophisticated details go, a recent paper from the Instituto de Ingeniería de Alimentos para el Desarrollo at the Universidad Politécnica de Valencia clearly indicates that you would at least have to consider what the animals, in this case pork, were fed and from which muscle of the animal the piece of meat you are eating has been cut, in order to get an approximate idea of how much of unquestionably health relevant micronutrients, such as coQ10, carnosine, anserine, taurine, creatine glutamine or haem you get - and in some cases the differences can be way larger than 100%!

If pizza salami equals pork...

... in epidemiological studies, how can these studies on the fallacies and advantages of eating red meat, which usually get a hell lo of media attention, be accurate, given the fact that the amount of unquestionably beneficial coQ10, for example, would differ by 60 percent, even if you would only ignore the difference between loin that was cut from the trapezius (= high coQ10 content) and the longissimus dorsi (=low coQ10 content)?

Figure 1: Content of selected amino acids and micronutrients in cuts from different muscle; data expressed relative to respective mean (total value is given in mg/100g above the bars) of all tested muscle samples (data based on previous studies by the co-authors that have been compiled for Reig. 2012).

Moreover, if you take a look at the complete data in figure 1 it should be clear that coQ10 is only one of several micro-nutrients / amino acids that are highly dependent on which muscle your particular steak or whatever you are about to eat was cut from. Let's take taurine as yet another example. A prolonged low dietary intake of taurine has been observed to be linked to a number of disorders including retinal degeneration, retardation of growth and development, cardiovascular dysfunctions, CNS abnormalities, immune impairment and hepatic disorders (Abebe. 2011). If you eat meat (fish & other animal products) only occasionally and are therefore at risk of not getting adequate taurine in your diet, eating sausages from a butcher you trust would be a better choice than a piece of ham, since the former do include the high taurine meat from the masseter (cheeks) of the animals, while ham does not.

Let's get to the obvious: Grass-fed is... ah, wait a minute

"Grass fed is best" as you will people say about beef obviously won't be the case for pork, because pigs, just like humans, by the way, are omnivores. The simple formula, grass-fed = most beneficial fatty acid and micronutrient profile that may (in general) be valid for beef doesn't apply and we will have to take a closer look at the actual data first to decide what would be the "best" feed for pigs, if the goal was not a maximal yield of lean meat (in that case adding some clenbuterol, like the Chinese like to do it would be the least you should do; cf. The China Post. 2011), but rather to produce the meat with the most beneficial fatty acid  composition.

Figure 2: Fatty acid composition (primary axis) and omega-6 to omega-3 ratio of pork from pigs fed different diets (corrected version of data Reig et al. re-pupublished based on previous studies; spec. the figure for the n6:n3 ratio in the "standard feed" group that's based on Enser et al. was off - a ratio of 1.54 is obviously unrealistic)

I we define "most healthy" as having the lowest omega-6 to omega-3 ratio - a practice that seems appropriate given that 95% of the inhabitants of the so-called 'Westernized World' consumes way too much of the former and (comparably) way too little of the latter type of polyunsaturated fatty acids, the data in figure 2 clearly argues in favor of *surprise* the standard feed - at least if you define that by the feed the animals the meat of which (50 samples) Enser et al. bought in British supermarkets in 1996 (note: these values are still higher than for the conventional beef samples from the same study, which had a n-6:n-3 ratio of ~2.2; cf. Enser. 1996). There are however more intricate patterns that are not evident from the overview in figure 2, but could have implications as far as the direction into which "pork production" could or should head to in the future is concerned (summarized based on Reig. 2012):

Do you notice a pattern? I guess even based on the data in figure 2 you will already have noticed that the "grainier" the diet, or in other words, the more corn and soy there is in the diet of the swine the less favorable is the fatty acid composition of their meats going to be. Now, I am asking an outrageous question: If swine are such a good model for human metabolism, what do you believe your belly was going to be made of, if you copied the pigs' diets and lived on "healthy grains", their oils and the uber-healthy soy beans for the (probably pretty short) rest of your life?
• more food (yet no excess) can produce overall leaner muscle meat in the type II fibers, while the total body fat is increasing
• aside from local desaturation and elongination effects, the overall muscular fatty acid pattern does (much like in humans, by the way) mirror the dietary intake
• canola or linseed oils produce a substantial increase in the content of linolenic acid (C 18:3), and slightly increase the eicosapentaenoic (EPA, C 22:5) and docosahexaenoic (DHA, C 22:6) acid contents in pork mea
• soy, peanut, corn, and sunflower increase the content of linoleic acid (C 18:2; omega-6), increase the n-6:n-3 ratio and reduce the content of mono-unsaturated fats (MUFAs)
• fish oils or algae added to the feed substantially increases the content of EPA and DHA and thus reduce the n-6:n-3 ratio
• a high saturated fat content as in tallow (see figure 2) increases the levels of palmitic, palmitoleic, stearic and oleic acids in pork meat and reduces the PUFA:SFA ratio 
• CLA supplementation can increase the CLA content of the fatty portion of the meats (1% CLA results in 5.5 mg CLA/100g) and the adipose tissue (2% CLA yields 1,490mg CLA/100g fatty acids).

As you can see, the same rule applies for humans, pigs and, as you know from a previous SuppVersity post, mice who are fed inferior, since soy-fed salmon, as well: You are what you eat, folks!

Wallowing, roaming, routing: Work out like a pig

Since pigs make a pretty decent model of human metabolism and in view of the fact that - aside from our diets - the amount of exercise we get is one of the fundamental determinants of the total and relative levels of body fat, it should not be forgotten that "exercise" or rather the ability to range freely and be as active as any swine should be, is another determinant of the quality of the meat you are buying at the supermarket, grocery store, butcher or your local farmer. In this context, Reig et al. point out that

If you have no idea of the different cuts and location of the individual muscle, I suggest you download the "Meat Cuts Manual" from the website of the Canadian Food Agency. It's free and bilingual.

"[i]t has been reported that pigs maintained in free-range conditions in the Mediterranean forest had subcutaneous and intramuscular fats with higher monounsaturated fatty acids and lower saturated fatty acids than those pigs housed individually and receiving acorns as feed. The subcutaneous fat depth increases with exercise being 15.9 mm for exercised pigs in comparison to 11.5 mm depth for those kept in confinement. The same applies for the intramuscular fat content where 3.36% for extensive vs 1.44% for intensive raised pigs have been reported in the semimembranosus muscle." (Reig. 2012)

And if you really intend to overcomplicate things, you would also have to ask your butcher, whether the sausages you are about to buy were made of the meat of male of female pigs. After all, meat from barrows typically contain more fat and marbling and a thicker subcutaneous fat layer than meat from gilts (Armero. 1999). But let's face it: If you start stressing about things like this, the quality of your meat is probably your least problem.

If you want to know read more about epidemiological overgeneralization andthe effects of "pork" and red meat on your health (spec. the prostate) I suggest you go back to the Meat-Ology post.

So what's the bottom line, then: I guess the bottom line of the above insides is twofold. As far as you as an individual are concerned, it would be yet another argument for getting your meats (pork or whatever else) from a farm nearby, where you know what you are getting. It is yet also evidence of the fact that meticulous nutrient counting as I often see it in former calorie counters who have nor grasped the notion that "a calorie is not a calorie" is of little avail - at least if you expect to be able to calculate them as precisely as you can read them on the nutrition labels of the 90% artificial and 100% standardized convenient foods that's probably much more the answer to the question "Why are we fat?" than the non-descript statement "insulin".

In fact, the real significance of these results lies elsewhere. It concerns the way epidemiological studies are conducted (I may remind you of the metaphorical pizza salami being red meat or pork), their over-generalizing interpretations and the conclusions on what the optimal human diet should look like. So, once the next study is telling you "red meat" or "pork" is bad for you - you may want to remind yourself of some of the things you have learned in today's blogpost and ask yourself (and if you incidentally have the chance, the researchers as well): What kind of "pork" are we talking about?

References:

• Abebe W, Mozaffari MS. Role of taurine in the vasculature: an overview of experimental and human studies. Am J Cardiovasc Dis. 2011;1(3):293-311.
• Armero E,  Flores M,  Toldrá F,  Barbosa JA,  Olivet J,  Pla M,  Baselga M.Effects of pig sire types and sex on carcass traits, meat quality and sensory quality of dry-cured ham.  Journal of the  Science of  Food  and  Agriculture. 1999; 79:1147-1154.
• Enser M, Hallett K, Hewitt B, Fursey GA, Wood JD. Fatty acid content and composition of english beef, lamb and pork at retail. Meat Sci. 1996 Apr;42(4):443-56.
• Reig M, Aristoy MC, Toldra.Variability in the contents of pork meat nutrients and how it may affect food composition databases. Food Chemistry. 2012 [ahead of print]
• The China Post. Clenbuterol-tainted pork latest China food scandal. March 18, 2011. < http://www.chinapost.com.tw/china/national-news/2011/03/18/295146/Clenbuterol-tainted-pork.htm > retrieved Dec 06, 2012.

Going Vegan? Better Get Some B-12 Lozenges

While my personal credo is: "Man is made for eating meat." I respect everyone who - for ethical or whatever reasons - refuses to do so. In spite of that, a recent study by Gilsing et.al. (Gilsing. 2010) found that vegetarians and vegans even more so, have a high risk of being vitamin B12 deficient. In their conclusion on the evaluation of the EPIC-Oxford cohort study, the scientists write:

the results from this study show that vegetarians and vegans have much lower concentrations of
serum vitamin B12 but higher concentrations of folate in comparison with omnivores. Mean serum vitamin B12 was not associated with the duration of adherence to a vegetarian
or vegan diet, which may indicate that mechanisms that maintain circulating concentrations of vitamin B12 are upregulated in vegetarians and vegans. Further research into the health effects of vitamin B12 deficiency and depletion in vegans and vegetarians is warranted , and vegetarians and vegans should ensure a regular intake of sufficient vitamin B12 from fortified foods and/or supplements. (Gilsing. 2010)

Especially if you are an athlete or gymrat, this is another reason to include either a reliable high dosed B-vitamin complex or another source of  source of additional B12 in your supplement. In case you are already taking a multi covering all your needs, don't bother taking additional B-vitamins - although it is often stated otherwise some of them can produce negative side effects not only in susceptible individuals.