.

.
marylin monroe
Showing posts with label wheat. Show all posts
Showing posts with label wheat. Show all posts

SuppVersity Science Round Up Seconds: Wheat Gluten Hydrolysates Fail, Exposure to Air Pollutants During Workout Reduces Brain Benefits, Homocysteine, B-Vitamins, Cognitive Impairment and Mortality

Before the profound weight loss (A) you don't see any of the glucose sucking and fad burning brown fat depots (black spots in B) on the neck of the in (B) 'foermerly obese', now only 'overweight' subject (also take a look at how the visceral fat in the abdominal region in (A) is actually pushing the organs upwards; img Vijgen. 2012)
Those of you who have listened to yesterday's show will have noticed that despite its flow the number of things you can discuss in a 1h podcast is simply very limited, to say the least. This is also why these Friday posts are probably never going to be simple summaries of the SuppVersity Science Round Up of the day before. The same is true for today and still I decided not to use the allegedly lame logo I did for the first two installments, but provide you with some 'real science' evidence of the absence of brown adipose tissue on the obese and it's magical reappearance after shedding 100lbs+ subsequent to a gastric bypass operation, instead (see image on the right).

Assuming that you have no idea what this "evidence" is for, I would suspect that you missed the live show yesterday and also did not find the time to download and listen to the podcast, yet -- right? Well, you should either download and listen to the show now and digest the Seconds later, or you read the following paragraphs first and download the podcast later.

What is not an option, however, is to miss one or another - I mean you can hardly want to eat the seconds if you have not had the main dish yet... and after listening to the podcast, I cannot imagine you don't want at least some seconds. Apropos seconds, here are today's seconds...
  • Wheat gluten hydrolysate is not the new goto protein supplement - certainly not for female distance runners and probably not for anyone else, either! These are the kinds of studies that really annoy me. Studies that start out with blatant statements like "WGH [Wheat gluten hydrolysate] has been reported to suppress post-exercise rises in serum creatine kinase in male distance runners" (Hirao. 2012).

    Figure 1: CK, AST, ALT response in the "success trial" with men. In women even the miniscule beneficial effect on CK was not there. No reason to even think about buying a gluten hydrolysate as you new go-to protein supplement with only 5.6g of leucine/100g (whey has 50% more) and almost no GSH replenishing cysteine in it (0.9g vs. 3g+ in whey, which is more than +200% more).
    Sentences like that make the null-results of the study they precede look like the exception to the rule and are still nothing but a concession to a bias (let's hope not due to the grant from Nisshin Pharma Inc. which was the manufacturer of the wheat gluten hydrolysate used in this study). A bias, due to which an isolated observation as the slightly blunted increase in CK is blown up as if a slightly lower CK level was what could turn a sedentary pencil pusher into the next Hussein Bolt (Aoki. 2012).

    So, even if you are not afraid of the evil in gluten (which I believe not everyone has to), I strongly caution against making the switch from a high EAA protein with ton's of GSH boosting cysteine in it like whey to a mediocre grain protein, which is a potential allergen and contains tons of glutamine your body will readily turn into glucose, once it passes through the portal veign into the liver (I bet a large part won't even make it into systemic circulation).

    And as far as the purported "gender difference" goes the study at hand tries to blame the null result on (Hiriao. 2012), I suspect that it is rather the indisputable difference between the long-distance running at a continuous pace the women in the study at hand did, versus the totally different strains the guys in the previous study were exposed to during a soccer training + mini-match, which made the difference.
  • Working out next to a street takes away some of the beneficial cognitive effects due to ultrafine particulate matter (UFPM) exposure. "Working out in the fresh air will promote weight loss more than working out inside." You heard me state that in one of the previous installments of the SuppVersity Science Round Up on Super Human Radio. Now this is still correct and based on sientific evidence, but at least as far as the cognitive benefits are concerned, working out outside does also have its downsides - at least for those of you who live in the inner city area.

    You better watch what you breath while you run.
    During a 12-week program the researchers from the Universiteit Brussel, the Hasselt University and the Royal Military Academy measured the improvements in physical performance, changes in serum markers and corresponding ultrafine particulate matter (UFPM) concentrations in the enviromnent in which their 15 previously untrained subjects conducted their aerobic training program thrice a week (Bos. 2012). What Bos et al. found was that the UFPM levels were signfificantly higher in the urban compared to the rural environment and that the higher UFPM exposures correlated with increases in leukocyte counts (p = 0.02), neutrophil counts (p = 0.04), and eNO levels (p = 0.002) that were exclusively observed in the group that trained in the urban environment.

    With the latter being markers of inflammation which exert their effects systemically, i.e. not just in the lung or musculature of which you may be thinking now, but also in the brain, it is no wonder that
    "reaction times on the Stroop task improved in the rural group (p = 0.001), but not in the urban group" (Bos. 2012). 
    What's comforting, though, is that the physical fitness did increase to a similar extend in both arms of the study.
  • Homocysteine levels, mortality, cognitive impairment and which nutrients can offer some protection. I am not sure about what your impression is, but for whatever reason homocystein seems to be 'out of vogue' -- probably no room for it on the research agenda with all the hype surrounding vitamin D. It used to be all the rage in CVD risk research and today's news item is actually ain't about cardiovascular health, either.

    What the researchers from China and Taiwan actually were interested in was the correlation of high and low homocysteine levels with cognitive impairment and the corresponding nutrient intakes. In that Xiu et al. paid particular attention to the "B-vitamins" and found the following correlations between the mortality, cognitive status, homocystein levels and nutrient intake of their 1412 study participants (Xiu. 2012):
    • Figure 2: Unadjusted mortality in the four quartiles of homocysteine levels (top); mortality according to homocysteine levels in subjects with different degrees of cognitive impairment (based on Xiu. 2012)
      if you go by the unadjusted data in figure 2, it's plain obvious that the all-cause mortality increases linearly from one quartile to the other 
    • this relation between plasma homocysteine levels and all mortality remained statistically significant after adjustments for age, sex, smoking status, BMI, physical function and general health were made
    • of the general foods, the scientists assessed, only regular fish intake had a statistically significant effect on homocysteine levels, with higher intakes being associated with lower homocysteine levels
    • of the b-vitamins choline was the only one with a significant association with plasma homocysteine levels (suggested read "Old School Supplement Choline Could Save Your Live and Liver!") 
    • neither betaine, nor vitamin B1, B2, B3 or B6 intakes did show statistically significant correlations with plasma homocysteine (not even "borderline significant; p > 0.15 for all, most way hither)
    • of the plasma markers, folate showed a highly significant correlation with homocysteine (14.4 nmol/L in the lowest HCY and 8.70 nnmol/L in the highest HCY group)
    • PLP, the active form of vitamin B6, came in close second with 70.3 nmol/l in the lowest HCY quantile and only 44.4 nmol / l in the highest quantile.
    Now, if you consider the fact that higher intakes of B-vitamins are probably not doing much to lower homocysteine levels int he elderly (at least not dose-dependently, when they are already getting enough) oddity #1, another look at the data in figure 2 will reveal oddity #2: The surprisingly high mortality in the lowest homocysteine quartiles in the patients with severe cognitive decline - how come? I mean, with low homocysteine they should not be at risk of having severe cognitive decline, anyway - right?

    Actually if you follow this rationale you can almost answer the question yourself. If you have low homocysteine and severe cognitive decline, the severe cognitive decline can hardly be from high homocysteine levels, so it must have another obviously pathological reason, or as the scientists have it
    "The joint effects of the 2 variables [homocysteine and cognitive decline] were most pronounced with severe cognitive impairment where mortality HRs ranged from 5- to 18-fold across a wide range of homocysteine concentrations. The findings with hypohomocysteinemia provide some insight into what might be an optimal range for this analyte in peripheral blood and tissues. The low concentrations may be seen with severe illness and malnutrition, and our study population comprises the health-vulnerable aged. For these reasons, we adjusted these associations for BMI (using the World Health Organization chronic energy deficiency category of, 18.5 kg/m 2 ), and we excluded those who died in the first year of follow-up. The findings were unchanged. Because mortality among the very old may have skewed the joint effects, these are presented for those ≤75 years and over, but again with similar findings." (
    A sarcastic person would now probably say: "We all have to go some time!" and just wave his hands at these results. True! And I am the last to advice you to become over-anxious. Yet in the mean time it would appear prudent to make sure to get your homocysteine levels checked from time to time, not to forget that choline is a b-vitamin as well and not to fall for the idea that you cannot overdose on B-vitamins - I don't have to remind you of the negative effects, specifically folic acid supplementation can have on all sorts of cancer (e.g. breast cancer, where a high folic acid intake from foods and supplements is associated with a +30% risk of cancerous growth; cf. Kim. 2006).
In case you are looking for the post on "ammonia accumulation brain-fog, toxicity, liver 'pathologies' and workout performance", yeah it was on the list, but I decided it would be a shame to tackle that within a short two paragraph seconds items. Don't worry I am not going to forget about it, after all its in my humble opinion one of the main reasons the diets and workout regimen of the many ambitious physical culturists fail. If you are still looking for more and have not listened to the podcast, yet, this would be the right moment to download the file from the Super Human Radio Network server (click here to download), otherwise the latest short news on the SuppVersity Facebook Wall may offer some diversion ;-)

      References:
      • Aoki K, Kohmura Y, Suzuki Y, Koikawa N, Yoshimura M, Aoba Y, Fukushi N, Sakuraba K, Nagaoka I, Sawaki K. Post-training consumption of wheat gluten hydrolysate suppresses the delayed onset of muscle injury in soccer players. Exp Ther Med. 2012 Jun;3(6):969-972. Epub 2012 Apr 3.
      • Bos I, De Boever P, Vanparijs J, Pattyn N, Panis LI, Meeusen R. Subclinical Effects of Aerobic Training in Urban Environment. Med Sci Sports Exerc. 2012 Oct 15.
      • Cankurtaran M, Yesil Y, Kuyumcu ME, Oztürk ZA, Yavuz BB, Halil M, Ulger Z, Cankurtaran ES, Arıoğul S. Altered Levels of Homocysteine and Serum Natural Antioxidants Links Oxidative Damage to Alzheimer's Disease. J Alzheimers Dis. 2012 Oct 29.
      • Guest PC, Urday S, Ma D, Stelzhammer V, Harris LW, Amess B, Pietsch S, Oheim C, Ozanne SE, Bahn S. Proteomic analysis of the maternal protein restriction rat model for schizophrenia: Identification of translational changes in hormonal signalling pathways and glutamate neurotransmission. Proteomics. 2012 Oct 16.
      • Hirao T, Koikawa N, Aoki K, Sakuraba K, Shimmura Y, Suzuki Y, Sawaki K. Female distance runners show a different response to post-workout consumption of wheat gluten hydrolysate compared to their male counterparts. Exp Ther Med. 2012 Apr;3(4):641-644.
      • Kim YI. Does a high folate intake increase the risk of breast cancer? Nutr Rev. 2006 Oct;64(10 Pt 1):468-75.
      • Vijgen GH, Bouvy ND, Teule GJ, Brans B, Hoeks J, Schrauwen P, van Marken Lichtenbelt WD. Increase in brown adipose tissue activity after weight loss in morbidly obese subjects. J Clin Endocrinol Metab. 2012 Jul;97(7):E1229-33. Epub 2012 Apr 24.
      • Xiu LL, Lee MS, Wahlqvist ML, Chia-Yu Chen R, Huang YC, Chen KJ, Li D. Low and high homocysteine are associated with mortality independent of B group vitamins but interactive with cognitive status in a free-living elderly cohort. Nutr Res. 2012. Ahead of print.

      Gluten Free, But not Suitable For Celiacs: Milk, Chocolate, Corn, Instant Coffee and 20 Other Foods & Food Ingredients That Could Cross-React With Gluten Anti-Bodies

      Unless you got the right, i.e. breast milk as a baby and have rendered your gut "gluten proof" - being breast fed, when you are first exposed (or being exposed later in life) has after all been suggested as a protective factor (Farrell. 2005)
      This is not going to be a long post; and still, at least for some of you it is going to be an important post. A post that may have the potential to change your life for the better or for the worse depending on whether you actually suffer from gluten-intolerance or have simply been bamboozeled by the "gluten is the devil" messages that are plastered all over the Internet these days.

      Actually, I would hope that you belong to neither of the groups and can thus simply ignore this post. For the unfortunate rest, I have prepared a mini-summary of the results of a recent study from the Immunosciences Lab in Los Angeles (Vojdani. 2013)

      Milk and cornflakes - a killer combo

      A couple of recent studies, as well as reports from patients all of which clearly suggested that "being gluten free" does not equal "being symptom free" had spiked the researchers interest. Was it possible that the persistent symptoms were brought about by cross-reactions between the anti-bodies that would usually attach to the gluten proteins to trigger an immune reaction and other molecules? Molecules from such innocent foods, as dairy, chocolate, and even coffee!?
      Suggested read: "Leaky Gut & Gluten Belly: Bacterial Firebugs Translocate from Your Gut to Your Ever-Growing Visceral Fat Depots" | read more
      "[W]hen histological response was assessed in celiac patients after 6 months of following a GFD [gluten free diet], complete normalization and reconstruction of villous architecture was observed only in 8% of individuals, while 65% of these patients were in remission and 27% did not respond to GFD and had no observable change in their clinical symptoms (Lanzini. 2009).

      The lack of improvement in histopathology and clinical symptomatology in a subgroup of patients on a GFD may be associated with dietary non-ad-herence or cross-reactive epitopes triggering a state of heightened immunological reactivity in gluten-sensitive individuals (Hadjivassiliou. 1997)." (Vojdani. 2013)
      The hypothesis certainly isn't totally odd. Kristjansson et al. were for example able to show that 50% of their celiac patients experienced a significant mucosal inflammatory response similar to that elicited by gluten, when they were exposed to cow’s milk protein. Of the 15 healthy controls in their study, however, not a single one showed the slightest signs of auto-immune related inflammatory processes (Kristjansson. 2007).

      So is this "real" celiac disease?

      It should be obvious though that the corresponding "cross reactive" agents do not induce celiac disease (which is per definition an auto-immune disease that's triggered by the reaction to gliadin). They are however well able to alter the intestinal barrier integrity - a symptom that is also one of the key feature of the early stages of celiac disease.
      Figure 1: Reaction of affinity-purified α-gliadin 33-mer polyclonal antibodies to gliadin and different food antigens; data in large figure relative to control, data in small inset relative to a-gliadin (Vodjdan. 2013)
      If full remission of celiac disease cannot be achieved even on gluten-free diet, the underlying reason may thus well be the presence of peptides and antigens that (cross-)react with the same anti-bodies the body of celiac patients produces against the α-gliadin 33-mer peptide aka gliadin. Scientists even speculate that the co-exposition to these agents could eventually lead to the establishment of "new" auto-immune diseases and food allergies and some argue that the ever-increasing spectrum of allergies is partly a result of untreated autoimmune reactions which are then "spreading" to other previously well-tolerated foods and food ingredients.

      Suggested read: "Beyond Celiac: Study Sheds New Light on Obesogenic Effects of Gluten - Are PPARs & Bacteria Both Involved?" | read more
      The problem seems real, if you're really gluten intolerant: With milk, all sorts of dairy products (including whey), instant coffee (but not espresso; see small inset), avenin containing oat products (unfortunately, I cannot tell you how you can recognize the "unproblematic" oats at the super market, but if you google "avenin-free oats" you will see a couple of products and stories pop up; Comino. 2011) and corn having a significant potential for cross-reactivity, it appears almost reasonable that some people come back from their visit with a mostly self-proclaimed expert in all things celiac with an endless list of items they are not supposed to eat and a tiny 5-item list of foods they are supposed to live on for the rest of their lives.

      What is not reasonable, however, is that this is the case for more and more people who are basically asymptomatic... well, aside from their "inability to lose weight" that is obviously not related to their "inability to exercise" and their "inability to stop watching TV and browsing the Internet for easy quick-fix solutions to obesity problems", but most obviously be brought about by gluten intolerance ;-(

      References:
      • Comino I, Real A, de Lorenzo L, Cornell H, López-Casado MÁ, Barro F, Lorite P, Torres MI, Cebolla A, Sousa C. Diversity in oat potential immunogenicity: basis for the selection of oat varieties with no toxicity in coeliac disease. Gut. 2011 Jul;60(7):915-22.
      • Hadjivassiliou M, Chattopadhyay AK, Davies-Jones GA, Gibson A, Grünewald RA, Lobo AJ. Neuromuscular disorder as a presenting feature of coeliac disease. J Neurol Neurosurg Psychiatry. 1997 Dec;63(6):770-5.
      • Kristjánsson G, Venge P, Hällgren R. Mucosal reactivity to cow's milk protein in coeliac disease. Clin Exp Immunol. 2007 Mar;147(3):449-55.
      • Lanzini A, Lanzarotto F, Villanacci V, Mora A, Bertolazzi S, Turini D, Carella G, Malagoli A, Ferrante G, Cesana BM, Ricci C. Complete recovery of intestinal mucosa occurs very rarely in adult coeliac patients despite adherence to gluten-free diet. Aliment Pharmacol Ther. 2009 Jun 15;29(12):1299-308. 
      • Vojdani A, Tarash I. Cross-reaction between gliadin and different food and tissue antigens. Food and Nutrition. 2013; 4:20-32.

      Saffron, Bread & Diabetes: Rye Bread Does Not Even Have to be "Saffronized" to Help With Type II Diabetes

      Saffron-rye breads? Not necessary, if you can achieve the same beneficial effects with nothing but rye bread alone.
      The World Health Organization estimates that the diabetic population will increase from 195 to 360 million people by 2030 (4.5% of the global population; Wild. 2004; Shaw. 2010). Needless to say that it would be a real problem for a whole industry, if these prognoses did not come true. Against that background, it may not be such a problem that the results Bajerska et al. report in their recent paper in the Journal of Medicinal Food show that Saffron is not an uberpotent super-antidiabetic. What is however pretty interesting is the fact that the pharma- and the corn-industry could actually have a common interested in the world being fed wheat instead of rye bread.

      Rye + Safron is not better than rye alone

      When they were trying to come up with another (dys-)functional food, the researchers from the Poznan University of Life Sciences in Poland speculated that the addition of some expensive saffron powder that was extracted from S stigma (Crocus sativus) and contained 2% safranal as its purportedly active ingredient would exert anti-diabetic effects in streptozotocin-induced diabetic rats on a high-fat (HF) diet.
      Figure 1: Glucose management, antioxidant status and lipid management in streptozotocin-induced diabetic rats after supplementation with either saffron (S), rye bread (RB) or both (RB+S) after 5 weeks (Bajerska. 2013)
      Now what the researchers observed, when they added the saffron to the rye dough the bread that was part of the rodent chow was made of, was not exactly what they had expected. While the total phenolic content and total antioxidant value of the breads made from the dough increased linearly, the changes in lipid parameters, antioxidant capacity and leptin levels (figure 1) as well as the -50% reduction in blood glucose levels (not shown) were virtually identical with both the regular, as well as the "saffron enhanced" rye bread.
      Pasta! From a satiety perspective even white bread would be a better choice (learn more).
      "In relation to the aim of the current study, it is important to note that incorporation of S powder in the RB did not additionally improve the regeneration of damaged pancreas b-cells or the secretion of insulin, nor did it decrease blood glucose levels above that seen in the case of S powder and RB alone.

      Moreover, it should be mentioned that the amounts of S powder added to the HF diet, and of S powder contained in RB added to the HF formula were matched to the similar dose of bioactive components." (Bajerska. 2013)
      The scientists do however have a first hypothesis to explain the absence of synergistic effects in response to the saffron supplementation: The heat damage during the baking process. In the course of the latter the saffron-containing dough will be heated to temperatures way above the tolerable range of > 60 C° - a temperature at which a non-negligible fraction of the carotenoids in saffron begin to degrade. In conjunction with the low bio-accessible in the digestive tract may (in fact the latter is not much better than that of curcumin, cf. Vitaglione. 2012) being further decreased by the interactions and bindings with the processed food components of the bread (proteins and starch), this may in fact explain why the saffron didn't do the trick.

      King or Pauper, who's breaking the fast "right" (learn more)?
      Bottom line: If there was one take home message from the study at hand, it would probably read: Not all bread is created equal and not all bread is necessarily bad. In fact, the results of the study at hand are in line with previous research that supports the notion that part of a our problem with "bread" is that the assortment of E-numbers we call "bread" has little or nothing to do with what bakery has previously been all about. A classic sourdough rye bread, for example, can be consumed by celiac patients without side effects (Di Cagno. 2010) and its fiber content will have highly beneficial effects on the gut health of gluten-insensitive individuals (McIntosh. 2003).

      Moreover, epidemiological data suggests that the consumption of rye could protect against cancers of the upper digestive tract and entails significant reductions in myocardial infarction, diabetes and ischaemic stroke risk ( Hallmans. 2003). So, if you don't want to join the current hysteria about bread being (yet another) root cause of all disease, and keep eating bread on a regular basis, it may not be the worst idea to switch from "W" as in wheat to "R" as in rye. And by the way, if you are into porridge, having some whole grain rye porridge for breakfast has been shown to have an 8h satiety effect (Isaksso. 2008) - certainly not bad, if you are one of those people who are having a hard time not to snack in between meals, right?

      Reference:
      • Bajerska J, Mildner-Szkudlarz S, Podgórski T, Oszmatek-Pruszyńska E. Saffron (Crocus sativus L.) Powder as an Ingredient of Rye Bread: An Anti-Diabetic Evaluation. J Med Food. 2013 Aug 3. [Epub ahead of print]
      • Di Cagno R, Barbato M, Di Camillo C, Rizzello CG, De Angelis M, Giuliani G, De Vincenzi M, Gobbetti M, Cucchiara S. Gluten-free sourdough wheat baked goods appear safe for young celiac patients: a pilot study. J Pediatr Gastroenterol Nutr. 2010 Dec;51(6):777-83.
      • Hallmans G, Zhang JX, Lundin E, Stattin P, Johansson A, Johansson I, Hultén K, Winkvist A, Aman P, Lenner P, Adlercreutz H. Rye, lignans and human health. Proc Nutr Soc. 2003 Feb;62(1):193-9. Review.
      • Isaksson H, Sundberg B, Aman P, Fredriksson H, Olsson J. Whole grain rye porridge breakfast improves satiety compared to refined wheat bread breakfast. Food Nutr Res. 2008;52.
      • Shaw JE, Sicree RA, Zimmet PZ: Global estimates of the prevalence of diabetes for 2010 and 2030.Diabetes Res Clin Pract. 2010;87:4–14.
      • Vitaglione P, Barone Lumaga R, Ferracane R,et al.: Curcumin bioavailability from enriched bread: the effect of microencapsulated ingredients.J Agric Food Chem. 2012;60:3357–3366.
      • Wild S, Roglic G, Green A, Sicree R, King H: Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diabetes Care. 2004;27:1047–1053

      Study Says: Wheat Belly is All in Australians' Head. And in Fact, the Peer-Reviewed Scientific Evidence for Non-Celiac Gluten-Sensitivity is Scarce, But Probably Not Non-Existent

      From a paper in the Journal of Cereal Science: Histological structure of wheat grain showing bioactive components which are related to the fiber fraction of wheat and are present in whole meal but absent in refined flour. (Brouns. 2013).
      A recent study from the CSIRO Food Futures National Research Flagship and the University of Adelaide says: The data indicate that many adult Australians are consciously avoiding consumption of wheat foods, predominantly without any formal diagnosis. Reported symptoms suggest a physiological but not allergenic basis to this behavior.

      Can this be? Can your "gluten intolerance" really be in your head? Certainly it can, it's what scientists call a nocebo effect: A situation, where a harmless substance taken by a patient is associated with harmful effects due to negative expectations or the psychological condition of the patient.

      But wheat is no harmless substance, right?

      Certainly not. At least not for those people who suffer from celiac disease. As far as the ever-spreading gluten-intolerance is concerned, though, more and more scientists voice concerns over the ever-increasing number of self-diagnosed gluten-intolerant individuals strike one food item after the other from their already short list of "gluten kosher" foods.
      Social influences on Australian "wheat avoiders" (Golley. 2014)
      Surprisingly, it's not the Internet that makes people go gluten-free. That's at least what the "wheat avoiders" in Sinead Golley's study claim. For them individuals in their surrounding had a much greater impact on their decision to go gluten free. It's their naturopath, their alternative medicine practicioner, friends, family and, surprisingly, even the doctor. And that in spite of the fact real illnesses (from asthma to IBS) were rare among the "wheat avoiders". Non-wheat food intolerances and allergies, on the other hand, were significantly more prevalent among the wheat avoiders than among their wheat eating (generally healthies) peers.
      In an enlightening paper with the telling title "But we're not hypochondriacs: The changing shape of gluten-free dieting and the contested illness experience" in Social Science & Medicine, Lauren Renée Moore wrote only a couple of months ago:
      "[T]his research suggests that self-ascriptive looping results in a greatly expanded illness prototype, and that gluten-free individuals promote a broadened illness prototype and self-diagnosis to their friends and families. Some work to promote the diet further. As a result, self-ascriptive looping can function as one vector in the diet's growing popularity." (Moore. 2014).
      The so-called looping effect describes how categories are continually redefined as the people within them change. The group of "gluten intolerant" individuals, once only celiacs, has thus over time transformed into an amalgam with celiac patients on the one end and real hypochondriacs on the other end of the extreme. And they all have one thing in common. For each of them, his or hear gluten intolerance is absolutely real.

      In view of the way this illness prototype or rather its contemporary realization is constantly changing it's no wonder that it has lost all resemblance to what doctors call "gluten intolerance". The logical consequence: Patients feel misunderstood and blame their "doctors for their failure to correctly diagnose the problem." (Moore. 2014)

      The illness is real, and so are the risks

      In the end, it's thus not a question of who's wrong and who's right. For the "patients" who have now become their own doctors their illness is absolutely real. The previously asked question, whether wheat is a harmless substance or not is thus no longer practically relevant for them and they are willing to pay the price - literally that is by paying significantly more money for (oftentimes) nutritiously inferior foods from the "gluten-free" industry (Hallert. 1998; Long. 2010).
      Figure 1: 0.548% of the US citizens are "gluten-free" spec. middle-aged + older women are jumping aboard - for what? Well the only potentially health-relevant differences between wheat eaters and non-wheat eaters are lower TSH (thyroid gaspadel) and higher HDL values - and no one knows if those weren't present before going gluten-free (DiGiacomo. 2013)
      Money is yet not the only concern researchers have with the increased trend towards gluten-free "elimination diets". Many of them warn that this trend entails a significant risk for the self-diagnosed gluten intolerant individual, who may not just be risking his health by consuming unnecessarily restrictive diets with potentially serious dietary imbalances, but could also be overlooking a much more serious health issue that's the actual cause of their symptoms (Monsbakken. 2006; Teufel. 2007) - or as Golley apptly puts it: The most serious risk is the delay in diagnosis and treatment of potentially serious underlying medical condition, due to self-diagnosis of symptoms as due to a food intolerance.

      What about the physiological side?

      As the previous remarks have shown, there is little doubt that the contemporary trend towards "gluten-free" diets is a socio-psychological phenomonen that's not (yet?) rooted in conclusive scientific evidence that would point towards general detrimental effects of wheat consumption on non-celiac human beings (Brouns. 2013).
      Table 1: Trends in publication on celiac disease (CD) and non-celiac gluten sensitivity (NCGS) during the last decades (Catassi. 2013). It's not as if researchers were not interested in non-celiac-gluten-sensitivity (NCGS).
      And still, there is a significant difference between the absence of conclusive evidence and the claim that "no data justifies a negative opinion about whole-wheat products in a healthy population" you will find in Brouns', Buuls' & Shewry's unquestionable not exactly impartial review of the literature in the Journal of Cereal Science (Brouns. 2013). If you look closely and without the wheat-colored glasses the National Association of Wheat Growers may have sponsored, you will find a handful of studies which do suggest that the consumption of high amounts of wheat and gluten has general detrimental effects on our health:
      • Wheat amylase trypsin inhibitors may drive intestinal inflammation via activation of toll-like receptor 4 -- Yvonne Junker et al. report in a 2012 paper that the natural α-amylase/trypsin inhibitors in wheat "may fuel inflammation and immune reactions in other intestinal and non-intestinal immune disorders." (Junker. 2012).
      • Auto-immune reactions could be triggered without the expression of T-cell specific antigens -- Using recent evidence from celiac patients as an example, Ludvig M. Sollid & Bana Jabri argue that the constant exposure to certain immuno-modulating substances such as gluten, could be exogenous factors which "might be identified as drivers of autoimmune processes, in particular when evidence for T cells with specificity for self antigens driving the disease is lacking." (Sollid. 2013)
      • Low-fermentable, poorly-absorbed, short-chain carbohydrates could contribute to symptoms (at least those related to IBS) experienced by non-celiac-gluten-sensitivity patients -- With the low-fermentable, poorly-absorbed, short-chain carbohydrates, i.e. fermentable oligo-, di-, and mono-saccharides and polyols, aka FODMAPs an international group of scientists suspects another of the blogosphere's usual suspects may be to blame.

        Figure 2: A low FODMAP diet will progressively reduce the symptoms of NCGS (Biesiekierski. 2013)
        The data from a 7-day low FODMAP study does actually appear to support a relevant interaction of FODMAPs and gluten sensitivity (Biesiekierski. 2013).

        The results do yet require experimental verification and further research should try to reveal the underlying mechanism which could explain the reduction in gluten sensitivity in response to the low FODMAP diet, will yet have to be elucidated - an involvement of the gut microbiome, by the way, is not impossible.
      The interaction with non-fermentable short-chain carbohydrates and the influence of the gut microbiome are also two key points in Aziz' and Sanders' recent editorial "Patients Who Avoid Wheat and Gluten: Is That Health or Lifestyle?", in which they emphasize the role of excessive fermentation from small intestinal bacterial overgrowth in the etiology of what many people think was "gluten intolerance". Whether "SIBO" (small intestinal bacterial overgrowth) and "gluten intolerance" are co-incidental or whether one is actually responsible for the other will yet have to be determined in future studies. Studies of which the data in Table 1 suggests that they will be done, as the relative research interest in non-celiac gluten sensitivity is continuously growing.
      Bottom line: In the end, it may not even be important if non-celiac gluten sensitivity is a real or a social-psychological epidemic. If you are "infected" and avoiding gluten-containing foods and or non-fermentable short-chain carbohydrates helps you, do it! As long as you keep an eye on your micronutrient intake and don't live off ready-made processed gluten-free junk, it's probably not going to harm you - physiologically that is.
      It's not always easy to be "gluten-free", even for animals (Gulls Comic)
      As far as to the psychological side effects are concerned, I am yet not sure, whether the constant (perceived) need to double check each and every product level is not going to drive one or another of the mostly already OCD-ridden anti-wheat-warriors to insanity.
      Reference:
      • Biesiekierski, Jessica R., et al. "No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates." Gastroenterology 145.2 (2013): 320-328.
      • Brouns, Fred JPH, Vincent J. van Buul, and Peter R. Shewry. "Does wheat make us fat and sick?." Journal of Cereal Science 58.2 (2013): 209-215.
      • Catassi, Carlo, et al. "Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders." Nutrients 5.10 (2013): 3839-3853.
      • DiGiacomo, Daniel V., et al. "Prevalence of gluten-free diet adherence among individuals without celiac disease in the USA: results from the Continuous National Health and Nutrition Examination Survey 2009-2010." Scandinavian journal of gastroenterology 48.8 (2013): 921-925.
      • Golley,  Sinéad  et al. "Motivations for avoiding wheat consumption in Australia: results from a population survey." Public Health Nutrition (2014). First view available on CJO2014. 
      • Hallert, C., et al. "Quality of life of adult coeliac patients treated for 10 years." Scandinavian journal of gastroenterology 33.9 (1998): 933-938. 
      • Junker, Yvonne, et al. "Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4." The Journal of experimental medicine 209.13 (2012): 2395-2408.
      • Long, K. H., et al. "The economics of coeliac disease: a population‐based study." Alimentary pharmacology & therapeutics 32.2 (2010): 261-269.
      • Moore, Lauren Renée. "“But We’re Not Hypochondriacs”: The Changing Shape of Gluten-Free Dieting and the Contested Illness Experience." Social Science & Medicine (2014).
      • Monsbakken, K. W., P. O. Vandvik, and P. G. Farup. "Perceived food intolerance in subjects with irritable bowel syndrome–etiology, prevalence and consequences." European journal of clinical nutrition 60.5 (2006): 667-672. 
      • Sollid, Ludvig M., and Bana Jabri. "Triggers and drivers of autoimmunity: lessons from coeliac disease." Nature Reviews Immunology 13.4 (2013): 294-302.
      • Teufel, Martin, et al. "Psychological burden of food allergy." World Journal of Gastroenterology 13.25 (2007): 3456.

      New Insights Into the Difference Between Whey, Casein, Cod & Wheat Proteins: Increased Dopamine, Decreased Gastric Emptying, Unknown Hydroxy-Fatty Acids & More

      This is not your average protein shoot-out - the amount of leucine and the mTOR and protein synthetic response were not even measured.
      It's actually rare to read the phrease "in contrast to previous studies" in a study about whey protein. There have been dozens,... ah, what do I see, hundreds of studies that have investigated almost all aspects of the biochemical, digestive, and health properties of whey proteins and still, there it is: The sentence-starter "in contrast to previous studies" in a paper that's about to be published in one of the upcoming issues of the Journal of Proteome Research.

      The proteome, by the way, is the entire set of proteins expressed by a genome, cell, tissue or organism at a certain time and a study that compares the acute differential effects between whey isolate, cod and gluten (=wheat) protein on postprandial amino acid, and lipid levels, as well as other metabolites is not what I would be looking for in this journal.
      You can learn more about protein intake at the SuppVersity

      Are You Protein Wheysting?

      Cod protein for recovery

      Protein requ. of athletes

      High EAA protein for fat loss

      Fast vs. slow protein

      Too much ado about protein?
      But alas! I am happy that the research by Jan Stanstrup, Simon Stubbe Schou, Jens Holmer-Jensen, Kjeld Hermansen, and Lars O. Dragsted got published at all; I mean "in contrast to previous studies" - that certainly sounds promising, doesn't it?

      So what was in contrast to previous studies, then?

      Quite a good question, well... ok, I am not going to keep you on the tenderhooks any longer. The surprise finding the researchers made, when they conducted this randomized, single-blinded, crossover meal study with 11 obese non-diabetics, aged 40 – 68 years with BMI 30.3 – 42.0, is after all mentioned in the title of the paper, as well:
      "Whey protein delays gastric emptying and suppresses plasma fatty acids and their metabolites compared to casein, gluten and fish protein." (Stanstrup. 2014).
      As a regular at the SuppVersity it should be easy for you to identify what is odd here: The digestion speed of the isocaloric test meals which consisted of an energy-free soup with 100 g of good Danish butter, 25 g of raw leek and 45 g of either whey isolate (WI), casein (CAS), cod protein isolate (COD), or a wheat protein (GLUT) and was served with white bread (total carbohydrate content 45 g) was different from what it should have been.
      Figure 1: Amino acid composition of the 4 protein sources used in the study (Stanstrup. 2014)
      As a well-versed student of the SuppVersity you do of course know that one of the characteristic qualities of whey isolate is that it passes through the gut at lightning speed - so fast, in fact, that some people develop diarrhea, but that's a topic for a different SuppVersity article. Accordingly, it's not surprising that Stanstrup et al. state that the delayed gastric emptying for whey isolate was
      "[...] surprising since β-lactoglobulin (the major whey protein) was found to be highly soluble in the gastric juices and rapidly emptied from the stomach when compared to other protein sources such as casein, which coagulates in acidic environments and is therefore retained in the stomach." (Stanstrup. 2014)
      On the other hand, others have reported similar rates of gastric emptying for whey and casein (Calbet. 2005), before - albeit in a scenario, where they were administered alone and not in combination with a meal.
      "When Whey & Casein Unite in the Spirit of True Physique Improvements, BCAAs & Glutamine Better Shut the F*** Up" | learn more
      Delayed gastric emptying w/ whey? In contrast to previous studies, we are dealing with the time it takes to evacuate a whole meal, not a shake. In view of the well-known amino acid kinetics (=fast appearance w/ whey vs. slow appearance w/ casein) which were confirmed in the study at hand, there is no reason to question the established benefits of whey protein.
      In other words: It still makes sense to combine whey + casein to create the perferct "anabolic" as I outlined it in "When Whey & Casein Unite in the Spirit of True Physique Improvements, BCAAs & Glutamine Better Shut the F*** Up" | learn more.
      Figure 2: The digestion process (Stanstrup. 2014)
      If you take a closer look at the graphical illustration in Figure 2 you will see that what appears to be counter-intuitive at first, is eventually only logical. The slow(er) transit of the whey protein through the gastrointestinal tract does after all leave more time for the complete assimilation of the amino acid content, which - and this is something you knew already - is particularly fast, because whey is easier to disassemble than casein for example.

      You also know that the increased influx of amino acids goes hand in hand with an insulin spike that's more pronounced than it would be for white bread (learn more).

      Many of you will probably also know (some by experience) that this spike in insulin leads to an increase in glucose uptake that leaves many low carbers notoriously hypoglycemic and makes them feel tired, shaky and miserable. What you probably didn't know, though, is that the increased glucose clearance goes hand in hand with a decrease in the amount of various fatty acids in the blood, while the cheap (see Table 1) wheat gluten meal caused elevated levels of a number of unidentified hydroxy fatty acids and dicarboxylic fatty acids, which is somewhat scary, since increases in linolic acid derived hydroxy fatty acids in human low density lipoproteins have also been observed in atherosclerotic patients (Jira. 1998; note: it's not clear whether the HCFs Stanstrup et al. observed were identical to the ones Jira et al. associated with atherosclerosis).

      You can tell me whatever you want: Wheat gluten is not "kosher"

      In the results section of their paper, the researchers from the University of Copenhagen and the University Hospital in Aarhus, also point out that dopamine-3-O-sulfate (the predominant form of dopamine in plasma) levels increase above baseline at 2 h for the GLU meal. In spite of the fact that the plasma levels returned to baseline again at 4 h, this appears to be in contrast to previous findings that a gluten-free diet increased major serotonin and dopamine metabolite concentrations in brain (Hallert. 1983). What Stanstrup et al. forget to mention, though, is that Hallert et al. observed this effect in patients with celiac disease; and unlike the average Internet guru tries to make you believe, we don't all suffer from gluten intolerance, let alone full-blown celiac disease.
      Table 1: Wheat gluten is the cheapest form of protein - no wonder it's so popular among food manufacturers (Day. 2006)
      It's still not impossible that "these findings suggest that gluten causesdecreased uptake of dopamine into the brain with concomitant increase in plasma dopamine" (Stanstrup. 2014), on the other hand there are a dozen of other possible mechanisms to explain the appearance of increased levels of dopamine-3-O-sulfate in response to the ingestion of the wheat protein isolate. This, as well as the effects of the Dicarboxylic and hydroxy fatty acids elevation after the wheat (=gluten) protein meal certainly need further investigation, though.
      Bottom line: Irrespective of the initially counter-intuitive increase in gastric emptying time in response to the whey protein-laden meal, the study at hand provides additional evidence for the various metabolic benefits of whey protein (increased glucose clearance, reduced fatty acid levels, superior amino acid delivery, etc.).

      Seitan looks like meat, but is actually "bread" - Due to its incredibly cheap price and its convenient processing properties gluten has become extremely popular among "food" manufacturers.
      As far as wheat proteins are concerned, the effects the systemic levels of dopamine, as well as the sudden increase in certain Dicarboxylic and hydroxy fatty acids in response to the wheat protein meal require immediate follow-up studies. After all gluten proteins are "finding increasing use as a food ingredient to provide a range of functional properties at a more modest price than competitors such as milk and soy proteins" (Day. 2006) - if it turned out that this stuff has negative side effects that go way beyond the contemporary gluten scare (i.e. the tummy), the ever-increasing number of vegetarians and vegans who resort to seitan products as their main protein sources may be paying for the industry's decision to use cheap, convenient wheat protein instead of expensive soy or dairy proteins dearly in the years to come.
      References:
      • Calbet, Jose AL, and Jens J. Holst. "Gastric emptying, gastric secretion and enterogastrone response after administration of milk proteins or their peptide hydrolysates in humans." European journal of nutrition 43.3 (2004): 127-139.
      • Day, Li, et al. "Wheat-gluten uses and industry needs." Trends in Food Science & Technology 17.2 (2006): 82-90.
      • Hallert, Claes, and Göran Sedvall. "Improvement in central monoamine metabolism in adult coeliac patients starting a gluten-free diet." Psychol Med 13.2 (1983): 267-71.
      • Jira, Wolfgang, et al. "Strong increase in hydroxy fatty acids derived from linoleic acid in human low density lipoproteins of atherosclerotic patients." Chemistry and physics of lipids 91.1 (1998): 1-11.
      • Stanstrup, Jan, et al. "Whey protein delays gastric emptying and suppresses plasma fatty acids and their metabolites compared to casein, gluten and fish protein." Journal of Proteome Research (2014).