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.

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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.

+87% Increase in Testosterone Within 21 Days from a 100% Natural Supplement? Study Shows: Soy Bean Extract Can Do Just That While Wreaking Havoc on Your Testes. Plus: Corn Oil Reduces Testosterone to Estrogen Ratio by -50%!

Image 1: I guess the feed of those boars does not contain any corn oil and is spiked with both bisphenol A and soy bean extract - I mean, how else could you possibly explain those balls? (img dirtybutton.com)

Let me start today's post with a few questions: Would you buy a 100% natural product that can lower your estrogen levels by up to -98%, increase the weight of your testes by ~30% and, above all, boost your testosterone levels by a whopping +87%? I guess, at least all those of you who either have not read or not understood the Intermittent Thoughts episode on estrogen's role in skeletal muscle hypertrophy are just sitting there, nodding their heads... I would yet also venture the guess that this nodding will end pretty abruptly, now that I am about to tell you that this all natural testosterone booster is derived from the powder of 2kg of Glycine max soy beans via methanol extraction, subsequently freeze dried and capped into 600mg caps of which the average adult (~80kg body weight) is supposed to ingest two per day.

Chose your poison: BPA, soy, or maybe just some governmentally subsidized corn oil?

The preceding paragraph was an ironic, yet as far as the underlying facts and figures are concerned 100% accurate introduction to today's post which revolves around a study Evanski from the Mind&Muscle forum has brought to my attention (Norazit. 2012). The authors, a group of scientists from the University of Malaya in Kuala Lumpur, Malaysia, had set out to investigate the purportedly negative effects of what they call "soya bean extract" (interestingly this spelling of "soy", which is identical to the German version is probably the reason the study did not appear on my "interesting stuff for the SuppVersity radar", before ;-), bisphenol A, 17β-estradiol and "harmless" corn oil on the testis and endocrine system of juvenile rats.

Figure 1: Phytoestrogen content (µg/g dry weight; mind the logarithmic scale!) of soy bean extract an standard rat chow measured by LCMS (data adapted from Norazit. 2012)

To this ends, the scientists divided thirty 21-day old juvenile male Sprague-dawley rats (=the standard lab rat) into five groups, receiving either a standard diet (which contained an insignificant amount of soy, cf. figure 1) + 100mg/kg Tween 80 (a standard food emulsifier with derived from polyethoxylated sorbitan and oleic acid; this group served as control for the soy and the bisphenol group) or standard diet +100mg/kg of corn oil (Mazola; this group served as a control for the estradiol group because the 17b-e did not dissolve in the Tween 80), soy extract, bisphenol A (Aldrich Chemical Co.) and 17b-estradiol (the most active form of estrogen, which binds to both the alpha- and beta-receptor) for three weeks.

Note: It is (at least in my view) a lucky coincidence that contrary to the soy extract and the bisphenol, the estradiol did not solve in the Tween 80, so that the scientists had to come up with Mazola corn oil as a "positive control". I mean, if you take a look at the effects this supposedly neutral "solvent" had on the endocrine milieu of the peripubertal rats, it is no wonder that with the average testosterone levels of the male inhabitants of the #1 corn producer of the world, the Unites States of America, is on a constant decline.

At the end of the study period the rats were sacrificed, the testis were excised and their testosterone and estrogen levels were assessed using standardized enzyme immunoessay (EIA) kits from Caymen Chemical.

Figure 2: Section of seminiferous tubules from control Tween 80 group, BPA group and soy bean extract group; (1) maturing spermatids, (2) lumen filled with cellular debris, (3) vacuaolation, (4) interruption of spermatogenesis (data adapted from Norazit. 2012)

Even a layman can see that both the bisphenol A, as well as the soy bean extract treatments induced profound changes in the cell-morphology of the testes (cf. figure 2). Vacualation (3), i.e. formation of vacuoles in cellular tissue, was present in both, only the bisphenol A group showed the characteristic lumen filled with cellular debris (2). Visible signs of spermatogenesis (1) were visible in neither of the groups, a clear interruption of the latter (4), was yet observed only in the soy and the estrogen group (latter not shown in figure 2). Moreover, the estrogen treated animals were the only ones where the testis showed clear signs of apoptosis (cell death).

The "harmless" corn oil shifts the testosterone to estrogen ratio from ~1/1 to 1/2pg/ng

Reckless, as I am I decided to discard Norazit et al.'s distinction into the BPA and soy groups with the Tween 80 group as a control and the estradiol group with their corn oil control and just plotted the total body and total and relative testis weight gain, estrogen and testosterone levels relative to the Tween 80 group. In other words, I treated the corn oil group as if it was just another treatment group. This is obviously somewhat fishy, but if no scientist appears to be willing to investigate the potential negative effects of corn oil on the endocrine system of adolescent rodents (let alone humans), this is the only way for us to get respective data ;-)

Figure 3: Body weight gain, total and relative right testis weight, estradiol and testosterone levels in peri-pubertal rats after 21 days on diets containing 100mg/kg bisphenol A, soy bean extract, corn oil or 17b-estradiol (in soy bean oil); data expressed relative to Tweenn 80 (polysorbate + oleic acid) control (data calculated based on Norazit. 2012)

And if you take a look at the data in figure 3 (the vertical axis of which is by the way discontinuous!) it becomes clear that you better feed your boys a food solvent such as Polysorbate 80 (=Tween 80) than the "healthy" corn oil the US government is trying to con you into. After all, the administration of 100mg/kg corn oil (human equivalent ~16mg/kg) during puberty decreased the testis weight of the rats by -23% it reduced the amount of estradiol by -35% and the amount of testosterone by -66% and thusly shifted the testosterone / estrogen ratio in the peri-pubertal rodents from 1.11pg/ng to 0.57pg/ng!

BPA and soy compete for the title of "most potent endocrine disruptor"

Following the bro-scientific "the more the better" type of reasoning, bisphenol A and soy bean extract are two potential candidates for the "testosterone booster of the year"-award. After all both, the organic solvent bisphenol A, as well as the "natural toxin" (sorry, I just had to write that ;-) soy, exert potent (8x) and ueber-potent (100x) effects on the testosterone to estrogen ratio, which is 8.2pg/ng for BPA and 100.1pg/ng for soy!

Note: Neither I, nor the scientists have any clue as to why the results of this study are diametrically opposed to those of previous studies in which extracts from soy products reduced, not increased, testosterone levels in male rodents and monkeys(!), across-the-board (eg. Sharpe. 2002; Cline. 2004) - and that although Sharpe et al. observed an increase in the testosterone producing Leydig cells in their soy-formula fed monkeys. Whether the rats in the study at hand were in a state where similar effects temporarily increase testosterone output until the Leydig cells literally "burn out", or whether other effects were responsible for the temporary increase in testosterone, would have to be elucidated in future studies, the results of which you will obviously read here at the SuppVersity, first ;-)

So, even if we assume that the data is correct and there were no cross-reactions between components in the soy bean extract and the testosterone anti-body test, I would strongly caution against the use of either of this compounds to boost your testosterone levels - I mean what's the use of a wickedly skewed testosterone to estrogen ratio (which in and out of itself will probably mess up your health and can potentially hinder your gains, cf. "Are You Serming Away Your Gains?"), when, at the same time, your testicles turn into dysfunctional balloons?

Devil in the Feeding Trough: PGE-Response to "Bad" Red Meat from Grass-Fed Cattle Could Prevent not Cause Cancer, Stroke and a Whole Host of Autoimmune Diseases.

Image 1: You do not need to hunt your red meat like a paleolithic human being, just make sure it comes from grass-fed animals and you will have a "health food" that modulate the your prostaglandin response to inflammatory assaults and thusly reduce your risk of cancer, stroke and autoimmune disesases in a way no fat-free chicken breast will ever do.

I have had this in the news before, in the context of the purported health benefits of CLA, with respect to the modulation of the n3/n6 ratio in your diet and in various other context, you heard me saying, or, I should say, read me writing that rather than popping tons of fish oil caps, you should rather focus on decreasing your overall omega-6 intake by making healthy food choices at the supermarket. In this regard, choosing grass-fed over commercially raised beef (and other meat) products could turn out to be one of the most far-reaching choices you can make. While that alone will help you to concomitantly reduce the n-6 overload, as well as the overall PUFA-burden that is so characteristic of the "Western diet", a recent study shows that eating red meat, even instead of the "healthy" white fat-free chicken breasts, everyone is pounding these days, could actually have profoundly beneficial effects on your (auto-)immune health, protect you from cardivascular disease and (this is important for the ladies) get your menstrual periods and related issues back in order.

How grass-fed beef can help and why it outperforms bison, elk and chicken

In their study, the results of which were published in issue 31 of the journal Nutrition Research, K. Shane Broughton, Daniel C. Rule and Eldon Handrich did what scientists have been doing for decades now. They took mice (your usual carnivorous animal) and put them on one of those grain-based diets that was then enriched with "bad" red meat to make the animals sick. Well, ... while the design was in fact the same, the good news is that the intention was by way of exception not to show "prove" (as if mainstream dietary advice would be interested in "proof", anyway) how bad those nasty red meats are, but to evaluate whether the

[...] consumption of meat from range-fed bison vs range-fed and grain-finished cattle and grain-finished bison would lead to reductions in PGE-2 [prostaglandin E2] release without altering PGI-2 [prostacyclin] release after an infl ammatory stimulus in a mouse model.

Or put simply, the scienists wanted to check whether there was any truth to the superiority of bison compared to the "bad" red meat, when it comes to balancing out the ratio of PGE-2 and PGI-2.

Image 2: Bayer probably won't like it if everyone would start eating grass-fed beef. After all, that would probably reduce the sales of their COX-inhibitor Aspirin protect.

For those of you wondering about a) what those prostaglandins are and / or b) why you would want to modulate their ratio and not eradicate them completely, here is is brief rundown on one of my favorite topics, the Yin&Yang of life and, on a related note, the fallacy of common black-or-white thinking. As with almost everything there are also two sides (in fact there are many more ;-) to the inflammatory coin and PGE-2 and PGI-2, two acronyms that differ by only a single letter, are situated on those opposing sides. If they are expressed at the right ratio, everything is fine. The (relative) over-expression of PGE-2 that is commonly observed in people following the "Western diet", on the other hand, is associated with a host of pathologies, such as elevated risk for color ectal cancer, suppression of ovulation, and increased problems with rheumatoid arthritis and headaches. (Relative) underexperssion of PGI-2, the other hallmark result of the "food" people are poisoning themselves with on a daily basis, in turn, increases the risk of thrombosis and stroke. If any of that does ring a bell, but you do not know which one, you may want to check out the label of your Aspirin tablets - as a cyclooxygenase inhibitor Aspirin also blocks the production of PGE-2... but before you do now pop another of those tabs, I suggest you read on and learn that by paying a few extra bucks for "real meat", you will probably never have to take your daily dose of Aspirin protect.

And while the scientists were right, grass-fed bison is in fact better than grain-fed beef, a closer analysis of their results will show that the often-heard and widely believed statement that "bison is the best form of red meat you can possibly find" is nothing but another of the 1001 dietary fairy-tales of the bloggosphere.

Figure 1: Fatty acid content of the diet (in g per 100g of the whole chow) - saturated, mono- and polyunsaturated fatty acids (n3, n6), left; CLA content, right (data adapted from Broughton. 2011)

But let's first take a look at the experimental diets, the male CD-1 mice were fed for 14 days. What is interesting about these, is that, due to the inclusion of standard rodent chow, the differences in fatty acid composition between the grass-fed vs. corn-fed bison and beef diets and the diets that were based on (wild-type) elk and commercial chicken breast meat were actually not very pronounced (cf. figure 1). And while the inclusion of corn oil in every diet may sound blasphemic in the ears of the hard-core anti-grain croud (I know you are out there ;-), the addition of grass-fed meat to an otherwise standardized (and probably suboptimal) diet is actually a strength of the study. Thusly, the study does reflect pretty well, what could happen, if the average Joe or Jane did nothing else, but replace the corn-fed meat in his/her diet with meat from range-fed animals - and wouldn't you agree that this is a much more realistic scenario than living on nothing but grass-fed beef or bison?

Figure 2: Modulatory effect of 2 weeks on prostaglandin expression of mice after two weeks on diets enriched with range-fed, or feedlot fed meat of different sources (data adapted from adapted from Broughton. 2011)

And, if we focus solely on the PGE-2 to PGI-2 ratio (you can read up on its importance in the red box above), it is obvious that a small dietary change from grain- to grass-fed meets could actually have pretty profound effects on your (auto-)immune health. The data also shows that the "healthy" lean chicken breast your nutritionist has probably told you to eat actually should not be your first choice, when it comes to establishing a healthier prostaglandin milieu - and if you don't believe me, maybe you want to trust Broughton et al.'s judgement:

[...] chicken is promoted for its health benefits, yet in our study, it was no better for possible prevention of PGE 2-associated immune pathophysiology. Furthermore, chicken would not be as beneficial as grain-fed beef and elk consumption in reducing thrombos is and stroke potential.

So, while eating (commercially raised) chicken won't harm you, it will not help you steer your inflammatory response into either the PGE or the PGI direction. Broughton, Rule and Handrich are thusly right, when they conclude that

Based on results of the present study, consumption of any of the range-fed meat sources examined would be better at reducing the possibility of immune-related pathophysiologies than meat from grain-fed cattle. [...] Although range-fed beef and bison consumption would be equivalent for their immune-based role, consumption of range-fed beef would be better for the prevention of thrombosis and stroke.

Now, isn't that surprising? Chicken not the best thing you can eat? The "healthy alternative to beef" that has been pimped in the mass media lately only on par with plain beef and superior as far as reduction in the risk of stroke and thrombosis are concerned?

Could it really be possible that the "bad red meat" is not so bad, after all? Is there the remote possibility that it's not red meat per se, but sick meat, or I should say the meat of animals we have been making sick by feeding them the same "healthy whole grains" with which we have been poisoning... ah, I mean nurturing *rofl* ourselves over all these years that is giving us migraines, arthritic joints, cancer, strokes and a whole host of nasty autoimmune diseases? I guess, I will leave it up to you to find and answer to that question ... and I am confident that you are smart to one and one, or rather grain-fed meat and (auto-)immune disease together ;-)

Xylitol, a Low-Calorie Sweetener With Unknown Fat-Burning Side-Effects!? Replacing Cornstarch With the Five-Carbon Sugar, Xylitol, Ramps Up Fat Burning Enzymes in Rodent Model of Diet Induced Obesity.

Image 1: Xylitol christals under the micro-
scope (photo taken by Anders
Østergaard Madsen, Denmark 2001)

From a health perspective, the five-carbon sugar alcohol Xylitol has hitherto principally been known for its beneficial effects on dental health. With a caloric value of 3kcal/g the naturally occurring ingredient of a wide variety of plants, citrus fruits (plums, strawberries, raspberries) and vegetables (cauliflower) does have less calories than sugar, nevertheless, according to the fundamentally flawed, but still widely held paradigm that "a calorie is a calorie, no matter where it comes from", the idea of replacing sugar with xylitol to reduce the overall caloric load would make little sense even on a diet that was relatively high in carbohydrates. So, if it were not for the highly marketable statement "sugar free" on chewing gums and candies, xylitol would probably not even have made it to the consumer market. A cursory glance at the abstract of a study (Ama. 2011) that is about to be published in the July issue of the Journal of Clinical Biochemestry and Nutrition (Vol. 49, No. 1) does yet suggest that these research results could renew the interest in a compound many of you may have considered to be nothing but another marketing scam from the (diet-)food industry - and, before this new data came out, you were 100% spot-on with your assessment ;o)

In the course of an 8-week feeding period, Kikoko Amu and his collegues from the University of Tokoshima Graduate School, the University of Shizuoka and the Food and Science Institute in Kanagawa, Japan, fed a group of 18 male Sprague-Dawley rats (initial body weight 290-310g) a high fat diet containing 312.3 g/kg cornstarch (control group), of which, in the experimental groups, X1 and X2, 16% (X1) or 29% (X2) were replaced with 1.0g/100kcal (X1) and 2.0g/100kcal (X2) of xylitol for group X1 and group X2, respectively. At the end of this period the scientists found that

long-term intake of xylitol supressed the accumulation of visceral fat [cf. figure 1, below] and the increase in plasma insulin and lipids concentrations in rats fed a high-fat diet.

Interestingly, at least part of the effects were mediated by xylitol-stimulated "expression of fatty acid oxidation genes in the liver, and lipid degradation and adiponectin genes in the adipose tissue." Furthermore, Amo et al.

found for the first time that xylitol ingestion lowered postprandial hyperglycemia [if administered at] a none-effective dose in causing diarrhea, and within the limits of orally administered physiological amounts (1-4g/kg body weight daily).

The human equivalent dose for this "non-effective dose in causing diarrhea" (nice, how these Japanese try to paraphrase that the dose they used did not cause "the runs", isn't it?) is 0.16-0.65g/kg per day, which would amount to somewhere between 13g and 52g of xylitol for a man who weighs 80kg. A pretty large dose considering the fact that some low-carbers out survive on hardly more than 40g of carbs a day.

Figure 1: Weight [in g/kg body weight] of retroperitoneal, epididymal and mesenteric part of visceral fat in high-fat (HFD) and high-fat xylitol-substituted (X1, X2) fed rats after 8 weeks of treatment (data adapted from Ama. 2011)

Despite being on a high-fat diet (I hope the readers of this blog have already gotten the message that low carb wont work in the absence of fat) its highly questionable, especially for "low-carbers", whether and to which extent healthy human beings would benefit from xylitol substitution. After all, the "high-fat" chow the rats were fat contained a whopping amount of 362.3g carbohydrates from corn and only 200g of fat from lard (75%) and soybean oil (25%). In view of the dietary 'quality' (I hardly dare to use this word in the context of what those poor critters were fed) of the grub the rats were given, it should not come as a surprise that despite having smaller visceral fat pads, the rats from the experimental groups (X1, X2) were just as overweight (X1: 525.1 +/- 9.6g; X2: 540.4 +/- 9,9g) as their mates (HFD: 543.2 +/- 10.2) who were crammed with what I would like to call a "high-fat corn diet". Furthermore, there were no significant differences in the amount of energie the rats from the different groups consumed and the lean mass of the soleus muscle, the only muscle variable measure in the study, was almost identical. Against that background the improvements in glucose management (cf. figure 2), the scientists observed, could simply be related to the decreased carbohydrate intake. 

Figure 1: Serum markers of glucose and lipid metabolism in high-fat (HFD) and high-fat xylitol-substituted (X1, X2) fed rats after 8 weeks of treatment (data adapted from Ama. 2011)

So, if it were not for the statistically significant increases in adipose gene expression of PPAR-gamma (key regulator of adipocyte differentiation) and the insulin sensitizing hormone adiponectin, as well as the increased lipolytic enzyme-activity (hormone sensitive lipase, HSL; adipose triglyceride lipase, ATGL) within the adipose tissue of the xylitol fed animals, all of you, who have already gotten off the westernized fast-food diet, the scientists were emulating in this study, could easily discard their results as meaningless. Until now, however you will have to wait for future studies on the effects of xylitol on metabolic health and body composition in animals (or humans) who are not fed a diet the detrimental health effects of which cannot be fought off by any supplement or drug on the market. And remember: As always, the SuppVersity is where you will hear about those studies first ;-)