Commercially Available Teas "Not Suitable For Human Consumption": Potentially Hazardous Amounts of Lead, Aluminum, Arsenic & Co in Every Cup

Would all commercially available teas have to be labeled like this?

I am usually not a fan of articles with titles like this one (see above) - they have what you call in Germany "Bildzeitungsniveau" (the German tabloid with news like "World about to disappear in a black hole, when CERN starts operating). It is however hard to resist the urge to use a headline like the one above, if the it fits the results of peer-reviewed scientific paper so well, as it is the case with the relatively recent paper from the University of Alberta and the Luleâ University of Technology in Sweden this SuppVersity article is (almost) all about.

The corresponding experiment, the results of which were published in the peer-reviewed open-access Journal of Toxicology in October 2013, already, addresses the increasing concern about contamination of foodstuffs and natural health products. With the emphasis being on foodstuff and health, it's only logical that tea, or more precisely all currently available off-the-shelf varieties of black, green, white, and oolong teas sold in tea bags were used for analysis in the said study.

So what did the researchers do?

Schwalfenberg, Genius (no joke, the 2n author is a real 'Genius by name') and Rodushkin conducted a three-step analysis in the course of which they analyzed the content of previously identified tea contaminants like aluminum, fluoride, mercury, lead, cadmium and arsenic (Fujimaki. 2004; Lung. 2008; Wang. 2008; Alvarez-Ayuso. 2011; Tan. 2012) in commercial tea preparations.

Table 1: There are not just bad, but also healthy minerals in tea!

Before we get to the "bad stuff", though, let's start with the positive findings of their investigation. The data in Table 1 is after all evidence enough that there are also "healthy" minerals in tea - the amount is not high enough to cover your RDA, but this does not mean that it could not be at least partly related to the undeniable health benefits researchers all around the world report for people who consume uncontaminated tea on a regular base. As a loyal SuppVersity readers you know most, if not all of them from previous articles on tea. The reason I still believe it's worth enumerating them again is that I don't want you to give up on your beloved (?) tea too easily - I mean, Coke is not an alternative and for coffee fungi and other stuff could make a similarly unhealthy "supplement" to your breakfast beverage:

• Cardiovascular benefits - When we are talking about health in general and heart health in particular, most people will think of green tea. That's pretty unfortunate, because there is ample research for all varieties of teas that they can lower blood lipids, provide "clean" and thus heart healthy energy, and exert antithrombotic and anti-hypertensive effects.
• Anticancer effects - Despite the fact that the anti-cancer effects have mostly observed in in-vitro studies, there is plenty of epidemiological evidence that tea drinkers have a lower cancer risk, than the average coke guzzler (not necessarily breast cancer, though ➫ SuppVersity Facebook News).
• Metabolic syndrome - While more recent studies clearly suggest that the active weight loss effects of tea, in general, and green tea, in particular, have been totally overblown, there is still a host of controlled trials, where adding tea (not necessarily green tea) improved the effects of a energy restricted diet. Compared to the rodent trials which are still fueling the myth of the potent thermogenic effects of (green) tea, the real world results in human beings are however downright disappointing.

• 

  A green tea marinade will keep your meats fresh | learn more

  Anti-infective properties - Only few people (SuppVersity readers included - of course) know that green tea can be used as a mouthwash and is currently researched as an anti-bacterial food additive by researchers all around the world. According to a paper by Steinmann et al. (2013), the anti-infective effects are mediated by the antiviral, antibacterial, and antifungal properties of Epigallocatechin gallate (EGCG). The same EGCG about which you've read only recently on the SuppVersity that it is not exactly as useful as a fat loss adjuvant, as the hype would have you believe.
• Other beneficial effects - Under "Miscellaneous Effects", Schwalfenberg et al. also list the nephropotective effects of green tea, which could come very handy if you guzzle mercury contaminated green tea, everyday (unfortunately, mercury is your least problem with tea), the anti-depressive researchers have observed in people consuming 4+ cups of tea per day and the hitherto unconfirmed hypothesis that tea drinkers are (better) protected against Alzheimer’s and neurological decline.

In view of these benefits it's only logical that the Canadian + Swedish research team chose to repeat  the dichotomous health effects of drinking tea in the title of their paper "The Benefits and Risks of Consuming Brewed Tea" (my emphasis in Schwalfenberg. 2013)

Organic is not better than regular tea

To obtain a dataset that would be as comprehensive, accurate and practically relevant as possible the authors bought 30 different organic and non-organic white, green, oolong, and black teas from the the shelves of Canadian supermarkets and analyzed (a) the "raw" tea leaves (LEAF), (b) tea that had been steeped for 3-4 minutes (3MIN), (c) tea that had been steeped for 15–17 minutes (15MIN).

Know your teas: As a SuppVersity reader you will probably know that all teas come from the same plant. It's the processing that determines if we call it "white", "green", or whatever else:

• White tea: young leaves or new growth buds, withered, uncured, baked dry 
• Green tea: steamed or dry cooking in hot pans to prevent oxidation; dried tea leaves may be separate leaves or rolled into pellets (gunpowder tea)
• Oolong tea: withering of leaves under sun and warm winds with further oxidation standard between green and black teas
• Black tea: leaves are completely oxidized, withered

Due to the processing of the leaves tea from the same camellia sinensis plant can contain different amounts of contaminants depending on whether you buy it as white, green, oolong or black tea, or shredded green tea supplement.

Still, the main determinant is and remains the soil it was grown on (see Table 4)?

All tea samples underwent the same standardized procedures before they were analyzed in their raw form (cut / shredded leaves) or as an infusion that had been prepared with only one tea bag (containing 2-3g of tea) in 250 mL of distilled water in fine bone china cups.

As you will already have expected, the scientists did not just detect the previously mentioned "good minerals" (exact values see Table 1), and a host of other beneficial trace elements, i.e.

• boron 19–115µg/L, cobalt 0.4–3.56µg/L, 
• copper 26–106µg/L, chromium 0.2–14.6µg/L, 
• iron 19–62.5µg/L, manganese 534–6351µg/L, 
• molybdenum 0.03–0.131µg/L, 
• selenium <0.1–0.34µg/L, 
• vanadium <0.01–0.151µg/L, and zinc 44.6–187µg/L,

in their samples. Schwalfenberg et al. found highly significant and, more importantly, physiologically relevant amounts of toxic elements, as well:

Table 2: Established toxicant limits in supplements (µg/day).

If you look at the value in Table 3 and compare them to the limits in Table 2, there is one thing you should keep in mind: These limits have been set by average exposure, not based on toxicity tests - that sounds very comforting, right?

"Public health warnings or industry regulation indicated" -- It sounds pretty fearmongering and I would not have used it as a subheading right beneath the introduction, if the statement "Public health warnings or industry regulation might be indicated to protect consumer safety." (Schwalfenberg. 2013) was no literal citation from the conclusion of the paper I have here right in front of me.

Table 3: Levels of mercury (Hg), lead (Pb), aluminum (Al), arsenic (As) and cadmium (Cd) in tea infusions after 3-4 or 15-17 min of brewing; all values in µg/L (Schwalfenberg. 2013)

A brief glimpse at the data in Table 3 does moreover confirm there are plenty of toxins in the average Canadian super market tea, but it does not tell you how problematic the contamination actually is. To understand that you'd have to cimpare those values to the established toxicant limits Table 2, which do - and this is and will always be ridiculous -  obviously depend on where you live *sarcastic laughter*... but enough of the unproductive sarcasm, let's see what we've got:

"All teas contained significant amounts of aluminum. Tea  leaves contained from 568 to 3287 ng/g of tea. All brewed teas steeped for 3 or 15 minutes contained detectable levels of aluminum. The range was 1131µgm/L to 8324µgm/L steeping for 3 minute and 1413µgm/L to 11449µgm/L steeping for 15 minutes. Only 2 teas had levels above acceptable limits at 3 minutes of brewing but 6 of the teas had levels greater than the upper acceptable daily limit of 7000µgm/L. Clearly letting tea steep for longer than 3 minutes is not advisable. Two of the organic green teas had levels above 10,000µgm/L brewed for 15 minutes."

In view of the fact that tea is by far not the only aluminum source you are expose to, the high levels of this toxic metal that easily accumulates in the body should be reason enough not to brew your tea - especially not organic tea - for more than 3 minutes.

Organic tea is a worse offender than regular

If you take a look at the amount of lead in the various tea samples it becomes even more obvious that "organic" tea is not necessarily better for your organs, as well. This is particularly true for the best-sellers green and black tea, both of which contain significantly more lead in the "organic" vs. "regular" variety.

Table 4: Toxicant levels according to origin; Pb: lead, Cd: cadmium, Al: aluminum, As: arsenic (Schwalfenberg. 2013)

Probably the main factor that influences the toxicant levels of teas is the place of origin, thoug. As you can see in the overview in Table 4, the highest amount of arsenic, was detected in Chinese oolong teas (organic or regular). The total arsenic levels in all teas, which ranged from 0.06µgm to 1.12µgm/L for tea that had been steeped for 3 minutes to 0.08 to 1.27µgm/L for tea that had been steeped for 15 minutes was highest in white tea - obviously also from China. And last but not least, ...

"...[a]ll tea leaves had detectable levels of cadmium. 21 teas had detectable levels after 15 minutes brewing while only 18  teas had detectable levels after 3 minutes brewing suggesting that there is further leaching of this toxicant into the water over time. [As the overview in Table 4 already suggests] the highest level was 0.067µgm/L found in standard oolong tea from China." (Schwalfenberg. 2013)

Not listed in the tables are the levels of tin, barium, antimony and thallium, which were detected in all tea samples, but at levels of which the authors state that they don't have to be "considered to be of concern" (Schwalfenberg. 2013).

Should you stop drinking tea? You know that I don't like to tell people what to do. Unless, obviously I am 100% sure that I am convinced that there is a serious health risk involved.

In the case of green, black or white tea, the evidence that this is the case is yet insufficient. Personally, I will still make sure to check the geographic origin of the tea leaves (not where it was processed and packaged!) and avoid all products with the bad 5-letter word C-H-I-N-A on the label.

Bottom line: "Not of concern" is not exactly what I would say about the overall results of the study at hand. I mean, in the end, the high levels of toxicants in some of the commercially available tea preparations - specifically those from China - could actually explain why the real-world results with commercially available teas and tea supplements often fall short of the rodent studies, which are often conducted with highly purified green tea products from companies like Sigma Aldrich.

Ah, ... one last thing to keep in mind is that 18 out of 30 tested commercial tea preparations contained mercury in amounts that were as high as 20 ng/g, but did not make it from the leave to the tea. With your digestive tract being a much more efficient nutrient and (unfortunately) toxicant extractor than hot water, tea supplements could pose an even greater risk of heavy metal exposure than tea.

References:

• Álvarez-Ayuso, E., Giménez, A., & Ballesteros, J. C. (2011). Fluoride accumulation by plants grown in acid soils amended with flue gas desulphurisation gypsum. Journal of hazardous materials, 192(3), 1659-1666.
• Hayacibara, M. F., Queiroz, C. S., Tabchoury, C. P. M., & Cury, J. A. (2004). Fluoride and aluminum in teas and tea-based beverages. Revista de Saúde Pública, 38(1), 100-105.
• Lung, S. C. C., Cheng, H. W., & Fu, C. B. (2007). Potential exposure and risk of fluoride intakes from tea drinks produced in Taiwan. Journal of Exposure Science and Environmental Epidemiology, 18(2), 158-166.
• Steinmann, J., Buer, J., Pietschmann, T., & Steinmann, E. (2013). Anti‐infective properties of epigallocatechin‐3‐gallate (EGCG), a component of green tea. British journal of pharmacology, 168(5), 1059-1073.
• Tan, Z., & Xiao, G. (2012). Leaching characteristics of fly ash from Chinese medical waste incineration. Waste Management & Research, 30(3), 285-294.
• Schwalfenberg, G., Genuis, S. J., & Rodushkin, I. (2013). The Benefits and Risks of Consuming Brewed Tea: Beware of Toxic Element Contamination. Journal of toxicology, 2013.
• Wang, X. P., Ma, Y. J., & Xu, Y. C. (2008). [Studies on contents of arsenic, selenium, mercury and bismuth in tea samples collected from different regions by atomic fluorescence spectrometry]. Guang pu xue yu guang pu fen xi= Guang pu, 28(7), 1653-1657.

Low Fat Toddler, High Fat Adult?! Intra-Workout Carbs More 'Anabolic' Than Protein!? Iron Prevents Gastric Cancer & Insulin Resistance?! Plus: A Sixpack of Kettlebell Studies

If you want to know exactly how your neighbors or rather your county did, check out the CDC's brand new County Data Interactive Atlas (may take some time to load), select your state and click on your county. Unfortunately, it's not exactly likely that you will be pleasantly surprised after all, places with rates below 6.5% (white on the map) have become rare, while those with 11.2% or more are becoming the norm.

"100%" - In words: One hundred percent, that's the SuppVersity figure of the week and at the same time the rate at which the prevalence of diagnosed diabetes in 14 of the US states grew faster in the years between 1995 and 2000 than previous estimates had predicted. The CDC has published this figure along with more information and the link to their brand new County Data Interactive Atlas in their weekly report on November 15, 2012. The Top 5 offenders on the list that's attached to the report are (1) Oklahoma (226 percent), (2) Kentucky (158 percent), (3) Georgia (145 percent), (4) Alabama (140 percent), and (5) Washington (135 percent).

No reason to worry, though, my American friends! According to their own assessment, the CDC and its partners are working on "a variety of initiatives to prevent type 2 diabetes and to reduce complications in those already diagnosed."... you see,all is going to be good! Your well-meaning government is taking care of the problem ;-)

I guess that's enough sarcasm and useless statistics for the day. Let's get down to some serious On Short Notice business, now. And what would be more obvious than to start with something that's probably still not on the radar of the CDC or any its smart partners over at the NIH who are still promoting a high carb + low fat diet to people who can hardly tolerate the amount of carbohydrates in a TicTac. What I am talking about? The predispositioning effects of a fat-deficient toddler diet...

• Fat loving toddlers grow up to be leaner adults (Rolland-Cachera. 2012) -- To determine whether nutritional intakes in early life are associated with body composition and hormonal status at 20 years, a group of researchers from the University of Paris analyzed data from 73 subjects, who had been part of a two-decade-long prospective study (ELANCE, Etude Longitudinale Alimentation Nutrition Croissance des Enfants).
  
  
  Associations of specific factors that increase the risk of being obese in the kindergarten as based on another study that's also been published ahead of print in the online version of Obesity (Flores. 2012):
  

  • born to an obese mother + 240% risk
  • gestational diabetes and gestational diabetes + 190%
  • drinking tea or coffee between meals before bedtime at 2 years old +230% and drinking sugary beverages at kindergarten age at least weekly + 130%
  • Latino or multiracial + 130% race ethnicity
  • ever-attending center-based daycare -70%
  • eating fruit at least weekly at kindergarten age -70
  • maternal history of a prior newborn birth weight greater than or equal to 4000g -90%

  If you do have or plan to have kids, you should maybe make a mental note on some of these.
  The kids, now all young adults had been examined twice, at the age of 10 months and with 2 years. During the recent followup, the  body weight, height, subscapular and triceps skinfold thicknesses, fat mass (FM), fat-free mass (FFM) and serum leptin concentration of the young adults (now twenty years of age) were recorded in order to identify associations between early nutrition and adult body weight.
  
  The adjusted linear regression models Rolland-Cachera and colleagues used to analyze the data actually showed a couple of significant associations, the first one of which, i.e. the fact thatan increase by 100 kcal in energy intake at 2 years was associated with higher subscapular skinfold thickness (β=6.4%, P=0.002) and higher FFM (0.50 kg, 0.06–0.95, P=0.03) at 20 years, seems to stand in line with the hilarious calories-in-vs-calories-out hypothesis. However, these associations could also be related to the fact that early nutrition will program our satiety response, so that those programmed to be "good eaters" by a less nurturing diet in their earliest childhood will remain "good eaters", even when they switch to the energy-laden standard American diet.
  
  Against that background, the second significant association the researchers observed, i.e. the fact that an increase by 1% energy from fat at 2 years was associated with lower subscapular skinfold thickness (−2.3% SF, −4.41 to −0.18, P=0.03), lower FM (−0.31 kg, −0.60 to −0.01, P=0.04) and lower serum leptin concentration (−0.21 μg l−1, −0.39 to −0.03, P=0.02) at 20 years appears to be even more important. After all, it looks like the Rolland-Cachera et al. had found the first relatively convincing evidence (not proof, yet) for the negative metabolic effect of early low fat diets in human beings:
  

  "Low-fat intake in early life was negatively associated with body fat (particularly at the trunk site) and serum leptin concentration at 20 years, suggesting that early low-fat intake could increase the susceptibility to develop overweight and leptin resistance at later ages. These findings substantiate current recommendations against restricting fat intake in early life and open new directions for investigating the origin of obesity." (Rolland-Cachera. 2012)

  Now let's just hope that scientists are actually tackling these "new directions" and - more importantly - that the respective results are recognized by the public and incorporated into the "dietary guidelines".
• Study suggests: If you could chose only one, your intraworkout nutrition should be a carbohydrate not a protein supplement (Kazemzadeh. 2012) -- This is at least the authors' own interpretation of the results of a recent study that was conducted by three researchers from the Azad University and the Teheran University in Iran.
  
  

  

  Figure 1: Changes in hormone levels from pre to post exercise (Kazemzadeh. 2012). If you focus solely on statistical significance you can be likewise mislead as, when you don't even check whether you findings are significant at all.

  According to the statistically significant part of the hormonal response of the 18-25-year-old subjects (university students who selected physical training course, but had no prior training experience), the consumption of an intra-workout supplement containing either 10 ml/kg of a 6% glucose solution was in fact "less catabolic" than during the same strength training routine with a 0.2 g/kg protein shake (PRO group) as an intra-workout supplement. On paper that's certainly true: The increased insulin response "enhances removal of amino acids and synthesis of proteins after the resistance exercise, on the one hand, and decreases the activity of proteolytic enzymes" (Kazemzadeh. 2012) and the non-existant increase in cortisol is in fact what scientists have long heralded as the goto indicators of anabolism.
  
  
  Note: Just as most of these studies the participants did not consume breakfast before the resistance exercise session, which comprised six selected exercises: The bench press, biceps curl with barbell, side stretch, leg press, knee stretch, knee bending. If the study had been conducted after a regular breakfast ~2-3h before the workout, the study could have yielded totally different effects with respect to both, the blunted insulin, as well as the increased cortisol response. On the other hand, the GH spike in the protein group would most certainly have been lower as well. After all, the latter is - as you may have read in the SuppVersity Facebook News earlier today - basically only a means by which your body taps into its fat reservoirs to satisfy his acute energy demands and not strictly a way to protect lean mass (Gahete. 2012).
  I do still have serious doubts about the real-world significance of the temporary blunt in cortisol. After all, the immediate post-workout response is, in contrary to sustained elevations of cortisol levels for hours or days after a workout, associated with an increase, not a decrease in skeletal muscle hypertrophy (West. 2012) and in essence nothing else, but a physiological adaptation that's necessary to maintain stable blood glucose levels during strenuous workouts and sooth the early burst of inflammation after a workout. Moreover, despite being only borderline significant, only the protein shake did increase growth hormone (p=0.057), testosterone (p=0.52) and IGF-1 (p=0.51) levels during the workout.
  
  This does not necessarily refute the benefits of carbohydrate supplementation during a workout, but if you insist on maximizing gains (not necessarily all lean I would guess) at all costs, it may be wise to consume a slow digesting protein + some fiber-laden carbs like oats 1-2h before a workout, to sip a light carbohydrate + BCCA drink intra- and wash everything down with another shake w/ whey protein and one or two bananas afterwards instead of just drinking some sugar water while you are lifting.
• Iron is a negative predictor of gastric cancer in humans and lowered hemoglobin and hematocrit levels induce insulin in rodents (Cook. 2012; Davis. 2012) -- While the alpha-tocopherol, beta-carotene cancer prevention study was a failure (at least with respect to the expected benefits of the anti-oxidants), there are still a couple of interesting side-findings.
  
  

  

   Meat-Ology: The Link Between Red Meat, Cooking Techniques & Prostate Cancer

  One of these side-findings pertains to the touted effects of increased iron intake on the etiology of gastric cancer, which is simply not existent. According to Cook et al. there were statistically significant negative associations for ferritin in the 2nd, 3rd quartile (-33% risk and -48% risk, respectively) and a borderline significant risk reduction of -31% for overall gastric cancer in the highest quartile (>241 ng/ml) and statistically nonsignificant decreases in gastric cancer risk for total iron, transferrin saturation and total dietary iron intake per 1,000kcal/day in the 2nd-4th quartiles of the respective serum parameters.
  
  That said, subsequent adjustments for H. pylori and then gastric atrophy did not materially affect a majority of the estimates ...
  

      "[...] the only exception was that the relationship  between ferritin and GNCC [Gastric noncardia cancer] was attenuated  There was little evidence for direct associations between iron metrics and H. pylori seropositivity or gastric atrophy (low pepsinogen I)—only serum ferritin appeared to share a relationship with these variables, and this relationship was stronger between ferritin and gastric atrophy." (Cook. 2012)

  So if "red meat is bad for you" it is probably not the iron content of the meat that is responsible for the observed associations of gastric cancer and high red meat intake in some previous studies (cf. WCR Fund. 2011).
  
  And with respect to its effect on glucose metabolism, a recent rodent study has just shown that a reduction in hemoglobin and hematocrit due to a lack of dietary iron does actually impair, not improve glucose management in otherwise healthy rodents fed an iron-deficient diet:
  

  

  Figure 2: Blood glucose, insulin and triglyceride on iron sufficient / deficient high sugar (AIN-76) or high starch (AIN-93) died (Davis. 2012)

  "Hemoglobin and hematocrit were significantly reduced in both ID groups compared to the C  and PF groups. Similarly, animals in the both ID groups exhibited elevated steady-state levels of blood glucose and insulin [...]
  
  [Moreover, hepetic]epatic gene expression analyses revealed a ~4-  and 3-fold increase in the expression of glucokinase and pyruvate dehydrogenase kinase-4 mRNA, respectively, in the ID group on either diet compared to their respective PF [pairfed on iron sufficient diets] counterparts" (Davis. 2012)

  The accompanying negative effects on triglycerides and fatty acid synthesis and storage Davis et al. observed were yet exclusive to the animals who received a high succrose iron-deficient diet.
• Vitamin C, D & E in health not disease - Only alpha-tocopherol shows negative correlation with markers of inflammation (Garcia-Bailo. 2012)-- A very recent study that has been conducted by researchers from the University of Toronto and the University of Guelph did not find any relation between the novel and the old savior of the human race, i.e. vitamin D and C, respectively and expression of inflammatory cytokines.
  
  

  

  Suggested read: "Are Vitamin Supplements Bad For Me (1/2)? The wrong Vitamin E Supplements Increase Cancer Risk."

  Plain Vitamin E in its alpha-tocopherol form, which has almost been written off after the selenium + E (and E only) cancer trials, on the other hand, showed statistically significant correlations with interferon-gamma and RANTES, a pro-inflammatory cytokine that is also known as CCL5 and the acronym for "egulated and normal T cell expressed and secreted" plays an important role in various immune processes, such as recruitment of leukocytes to sites of inflammation and mediating T cell and monocyte traffic. In view of the fact that this cytokine has also been shown to increase angiogenesis and is generally elevated in several inflammatory conditions, including atherosclerosis, these results would suggest that keeping an eye on your E-levels is about as, if not more important for young healthy individuals than vitamin C and D.
  
  If you also consider the fact that IL-1RA (by the way not necessarily inflammatory), interferon gamma, IP-10, PDGF-bb and RANTES were the only out of 27 cytokines the researchers initially measured with high enough concentrations to be detect accurately in the 1007 subjects with a BMI of ~23 and a weekly activity level of ~7Met, these results do also provide substantial evidence that it would probably be worth spending more money on studies that investigate  what it is that makes normal people healthy, instead of spending bazillions of dollars into the 1001st study on how people with XYZ (pt your favorite disease here) have low vitamin D levels *yawn*.

• 

  Check out the Website of the Reigning Canadian Kettlebell Biathlon Champion, Ameer Rosic for some workout videos

  A sixpack of kettlebell studies to remind trainers and trainees, alike, that there are more things you can lift than just dumbbells and barbells (various authors) -- I have never gotten hooked to kettlebells myself and would never agree to exchange my barbells and dumbbells for the finest set of kettlebells for more than one week, but if you take a look at some of the studies that have been published in the past 12 months or so, there is sufficient evidence to suggest that the incorporation of kettlebell workouts into your routine, as a means to provide new muscular and metabolic stimuli, could yield highly beneficial results:
  

  Kettlebell swings restore and enhance back health and function (McGill. 2012) On the basis of electromyography, ground reaction forces (GRFs), and 3D kinematic data the researchers determined that kettlebell swings create a "hip-hinge squat pattern characterized by rapid muscle activation-relaxation cycles of substantial magnitudes (∼50% of a maximal voluntary contraction [MVC] for the low back extensors and 80% MVC for the gluteal muscles with a 16-kg kettlebell) resulting in about 3,200 N of low back compression." The way the swings activate the abs and the unique loading patterns of the posterior shear of the L4 vertebra on L5, which is opposite in polarity to a traditional lift could make it a valuable tool in re- and prehab.	Kettlebell swing training improves maximal and explosive strength (Lake 2012) 21 healthy men  were randomly assigned to either a kettlebell (KB) or jump squat (JS) training twice a week. The KB group performed 12-minute bouts of KB exercise (12 rounds of 30-second exercise, 30-second rest with 12 kg if lower than 70 kg or 16 kg if higher 70 kg). The JS group performed at least 4 sets of 3 JS with the load that maximized peak power—Training volume was altered to accommodate different training loads and ranged from 4 sets of 3 with the heaviest load (60% 1RM) to 8 sets of 6 with the lightest load (0% 1RM). The increase in maximum strength of 9.8%, as well as explosive strength (+19.8%) were identical in both groups
  Kettlebell training has "has potential for improving some components of MetS in middle-aged women." (Moreno. 2011): While the changes the author of the thesis observed in response to 10 weeks twice weekly kettlebell training did not reach statistically significance (probably due to the low subject size of N=6 physically inactive women, mean age (mean age 48.8y, BMI 31.8) the trends in " fasting glucose and body fat were encouraging and suggest that kettlebell training has potential for improving some components of MetS in middle-aged women."	Kettle bell workouts can decrease blood pressure (Douglass. 2012): Eight resistance trained pre-hypertensive and HTN males saw statistically and more importantly clinically significant declines in blood pressure (to normal levels!) in the course of a randomized cross-over designed study which included 12 minutes of continuous two-handed swings (THS), three sets of a 6 exercise circuit (CIR), and a resting control (CON).
  Kettlebell training can improve strength, power and and endurance (Mannocia. 2012):  23 subjects (age 18-72 years) were required to perform a10-week kettlebell training program that took place in a group setting two times per week. Post hoc pairwise comparisons of assessments barbell clean and jerk, barbell bench press, maximal vertical jump, and 450 back extensions performance revealed significant time x group interaction and a main effect (p < 0.05) for the bench press, a trend toward a time x group interaction and a significant main effect for clean and jerk. These observations suggest "that kettlebells may be an effective alternative tool to improve performance in weight- and powerlifting".	10 min of treadmill running may burn more more energy, than a short 10-min kettlebell drill, but pro-anabolic & strength edurance effects speak in favor of 'the bells' (McGill. 2012): Only those who still believe in santa... ah, I mean the calories in vs. out theory of weight loss, will probably care, whether they are burning 12.5 or 17.1kcal/min and therefore this "advantage" would hardly be important even if the participants had not been sprinting part of their 10min on the treadmill just to make sure to achieve the prescriped (identical) rates of perceived exertion. And as usual, there is no reason, why you could not switch back and forth from one "drill" to another.

That's it once more for this week's installment of pretty longish short news. I hope you liked one or another and will see you tomorrow for some more information on the latest and greatest from the world of exercise and nutrition sciences. And just in case you have not seen those already, I guess there are a handful of news on facebook you may be interested in:

• 

  If you just skip the hookers and the transdermal cocaine and take a regular bath, this may speed up your regeneration and propel your gains - if timepoint and temperature are spot on!

  Transdermal 'cocaine' in "bath salt" - 3,4-methylenedioxypyrovalerone (MDPV) in OTC "bath salt" is 10x more potent than cocaine and unquestionably hazardous
• The anti-cancer effect of 'active vitamin B6' - High levels of pyridoxal 5'-phosphate, the active form of vitamin B6 appear to have protective effects against breast cancer... or is it exactly the other way around?
• Bisphenol A is a local fat synthesizer - Study shows how Bisphenol A increases obesity: it ramps up the local cortisol production in adipose tissue and thus 'helps' you stash away more body fat

As usual there is more on facebook and further news to come, but I guess you got other things to do on a Saturday than reading SuppVersity posts all day ;-)

References:

• Cook MB, Kamangar F, Weinstein SJ, Albanes D, Virtamo J, Taylor PR, Abnet CC, Wood RJ, Petty G, Cross AJ, Dawsey SM. Iron in relation to gastric cancer in the alpha-tocopherol, Beta-carotene cancer prevention study. Cancer Epidemiol Biomarkers Prev. 2012 Nov;21(11):2033-42. 
• Davis MR, Hester KK, Shawron KM, Lucas EA, Smith BJ, Clarke SL. Comparisons of the iron deficient metabolic response in rats fed either an AIN-76 or AIN-93 based diet. Nutr Metab (Lond). 2012 Oct 30;9(1):95.
• Douglass, MJ. The blood pressure response of two popular kettlebell routines. M.S. thesis in  Kinesiology (Exercise Science). California State University, Sacramento, 2012.
• Flores G, Lin H. Factors predicting severe childhood obesity in kindergarteners. Int J Obes (Lond). 2012 Nov 13.
• Gahete MD, Córdoba-Chacón J, Luque RM, Kineman RD. The Rise in Growth Hormone during Starvation Does Not Serve to Maintain Glucose Levels or Lean Mass but Is Required for Appropriate Adipose Tissue Response in Female Mice. Endocrinology. 2012 Nov 13.
• García-Bailo B, Roke K, Mutch DM, El-Sohemy A, Badawi A.Association between circulating ascorbic acid, alpha-tocopherol, 25-hydroxyvitamin D, and plasma cytokine concentrations in young adults: a cross-sectional study. Nutrition & Metabolism 2012, 9:102. 
• Hulsey CR, Soto DT, Koch AJ, Mayhew JL. Comparison of kettlebell swings and treadmill running at equivalent rating of perceived exertion values. J Strength Cond Res. 2012 May;26(5):1203-7.
• Kazemzadeh Y, Gaeini A, Abasrashid N. Comparison of the Effect of Consuming Carbohydrate or Protein during Exercise on Hormonal Response. Zahedan Journal of Research in Medical Sciences. 2013; 15(2): 90-93. 
• Lake JP, Lauder MA. Kettlebell swing training improves maximal and explosive strength. J Strength Cond Res. 2012 Aug;26(8):2228-33.
• Moreno KIK. Effects of kettlebell training on metabolic syndrome in women. M.A. Thesis, San Jose State University, 2011, 138 pages.
• McGill SM, Marshall LW. Kettlebell swing, snatch, and bottoms-up carry: back
  and hip muscle activation, motion, and low back loads. J Strength Cond Res. 2012
  Jan;26(1):16-27. 
• Manocchia P, Spierer DK, Lufkin AK, Minichiello J, Castro J. Transference of kettlebell training to strength, power and endurance. J Strength Cond Res. 2012 May 3.
• Rolland-Cachera MF, Maillot M, Deheeger M, Souberbielle JC, Péneau S, Hercberg S. Association of nutrition in early life with body fat and serum leptin at adult age. Int J Obes (Lond). 2012 Nov 13.
• WorldCancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: a global perspective. Washington, DC: AICR; 2007.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2012 Jul;112(7):2693-702. 

Reductive Stress: An Argument Against Anti-Oxidants for Athletes & Everyone Else? Plus: AGE-Reduced Diets for Health & Weight Loss & Iron For Women in the Military

It's sort of funny that the mental fatigue is reduced, but the physical performance stagnates w/ iron supplementation.

You will probably already have seen the results of the latest study from the Norwegian School of Sport Sciences which provides additional evidence that "vitamin C and E supplementation interfere[s] with exercise-induced signalling in muscle cells after a session of strength training, by reducing the phosphorylation of p70S6K and mitogen activated protein kinases (MAPKs: p38 and ERK1/2)", two proteins with significant effect on the exercise induced increase in protein synthesis and corresponding increases in the overall adaptation to exercise, and "have the potential to adversely affect cellular adaptations to exercise in healthy individuals." (Paulsen. 2014).

To put this results into perspective I will briefly recap the main message of a corresponding review of the "sense and non-sense" of antioxidant supplementation in athletes from the University of Florida  to kick off today's installment of the Short News that will then turn towards the beneficial health and anti-obesity effects of AGE-reduced diets and the need for iron supplementation in physically active women.

Read more short news at the SuppVersity

Exercise Research Uptake Nov '14 1/2

Exercise Research Uptake Nov '14 2/2

Weight Loss Supplements Exposed

Exercise Supplementation Quickie

Skipping Break- fast & More to Control Weight

HIIT, Caffeine & Other Success Boosters

• Antioxidant supplementation in athletes, sense or non-sense? The bottom-line of the latest review of the literature appears to be clear: Non-sense! Why? Well, according to Powers & Sollanek (2014)...
• Regular bouts of endurance exercise will increase the endogenous antioxidant enzymes in the trained skeletal muscles. In view of the fact that this translates to an improved ability to protect against exercise-induced oxidative stress in skeletal muscles, supplements appear to be less useful for athletes than they are for sedentary individuals, anyways. 

• 

  Figure 1: . Illustration of the relationship between radicals (i.e., oxidants) and antioxidants in the determination of redox balance (i.e., balance between oxidants and antioxidants). Note that an increase in radicals or antioxidants results in a disturbance in redox balance. Figure from Powers & Sollanek (2014), redrawn from Powers et al. (2004)

  While there is consistent evidence of the beneficial health effects of an increased fruits and vegetables consumption, foods have two major advantages over vitamin supplements: (1) they contain a plethory of compounds with antioxidant activity, which differ in their cellular locations and radical scavenging capacity and will thus act synergistically; and (2) the amount of antioxidants is small enough to assume that ther is a limited risk of an antioxidant "overdose" and consequent i.e. "reductive stress" (see Figure 1) by consuming a diet rich in both fruits and vegetables.
• In contrast to fruits and vegetables, the ingestion of megadoses of antioxidant via dietary supplements (e.g., vitamin E) can increase the risk of toxicity and the associated possibility of negative health consequences.
Accordingly, the authors of the review conclude that "consuming megadoses of antioxidants via supplements is not recommended" (Powers. 2014).


• An AGE restricted diet reduces serum AGE and indices of body fat, study shows. In a 12 week randomized, controlled study scientists from the Universidad Guanajuato observed that the consumption of an AGE-reduced diet alone and in conjunction with exercise lead to a decrease in serum advanced glycation end product (AGE) levels and body fat - the addition of exercise provided additional benefits and lead to significant reductions in blood lipid levels.
  

  

  Figure 2: Changes in weight, waist, fasting blood glucose and blood lipids after 12 weeks on AGE reduced diet, exercise and exercise + AGE reduced diet (Macías-Cervantes. 2014)

  What is difficult to tell, though, is whether the reduction in body fat is a result of reduced AGE-levels in the diet and corresponding reductions in the blood of the participants or simply a consequence of eating a healthier diet - I mean, food products that are high in AGE are characteristic of the modern Western junk-food diet. It is thus also not surprising that the low AGE diet was both ~50% lower in AGEs and 26% lower in energy.
   
• Iron supplementation improves indicators of iron status and emotional fatigue in female offiers-in-training, study shows. Researchers who are working for the US military have recently been able to show that the exercise-induced decrease in iron-status in female officers during military training can be ameliorated by supplements with 18mg of iron that were consumed on a daily basis over the course of the 13-week study (Boot. 2014).
  

  

  Figure 3: Changes in selected markers of fatigue in iron vs. placebo supplemented women (Booth. 2014)

  As you can see in Figure 3 the provision of extra iron did not just blunt the decrease in serum ferritin in the ADFA students who participated in around 20 hours of classes (mainly lectures) and 2–7 hours of organized physical training (PT) per week, it did also have a significant effect on the emotional fatigue (-4.2 to -0.6 95% CI, P = 0.04).
  
  What is somewhat surprising, though, is that the effects on physical fatigue parameters were neither significant, nor positive.

Bottom line: There are new studies on the effects of food and supplements on our health on a daily basis. Things that we believe to be true today may be falsified tomorrow and agents that may be good for some people (like iron for athletes) and potentially bad for others are rather the rule than the exception.

D-aspartic acid: When study cherry picking turns a useless supplement into a mega-seller | learn more

Accordingly, it's important to look beyond the ostensibly obvious results like "low AGE diets promote fat and weight loss". While this may be true, even the cursory analysis of the study results in today's SuppVersity short news indicates that the obvious conclusion that reducing AGEs would mechanistically reduce body fat is probably flawed. Rather than that people who avoid high AGE foods will necessary avoid foods with high energy density, consume less energy and lose weight in response to a reduction in energy intake - not in response to the reduced intake of AGEs. Problems like these are why it is important to look beyond the conclusions in the abstracts and / or come back to the SuppVersity regularly for short and in-depth analyses of the latest studies | Comment on Facebook.

References:

• Booth, Christine K., Julia E. Carins, and Iain K. Robertson. "Randomised double-blind, placebo-controlled trial of iron supplementation attenuates fatigue and declining iron stores for female officers-in-training." RegisteR Now! 22.3 (2014).
• Paulsen, G., et al. "Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training." The Journal of Physiology (2014). 
• Powers, Scott K., et al. "Dietary antioxidants and exercise." Journal of sports sciences 22.1 (2004): 81-94.
• Powers & Sollanek. "Endurance Exercise And Antioxidant Supplementation: Sense Or Nonsense?-Part 1." Sports Science Exchange 27.137 (2014): 1-4.

Ask Dr. Andro: Are Vitamin Supplements Bad For Me (2/2)? 3+1 = 666! The Raw Data Truth about the "Vitamins Kill!" Offspring of the Iowa Women's Health Study

Image 1: "Please Dr. Andro tell me I can keep taking my essential multivitamin! I am just too busy to eat healthy..."

I must admit that I feel kind of awkward as I am about to defend one of those supplements, I consider to be the most dispensable within the dietary regimen of a physical culturist: the so-called multi-vitamin! In essence these small, and lately more often than not large pills do not even fall into the category supplement. With dose-equivalents way beyond what you would actually need, "multivitamins" are not even "replacements", they are madness or, I should say, the mad outgrowth of the prevalent "more is more" mentality that is beginning to harm us on every level of our society... but I am digressing, here. Let's take a look at the actual study which brought about such an upheaval in the supplement-addicted health community on the Internet.

Dietary Supplements and Mortality Rate in Older Women

Image 2: Is this you? No? Maybe she is "The Average American", then? No? Well, but the study says "vitamins are bad for YOU" and she could be one of the subjects (img. medscape.org)

The title alone, actually made me click the study away, back in the day when I first hit upon it, on one of my regular searches for new stories on the medical databases of the World-Wide-Web; and unless you are an old women (I would hope there were some older women reading the SuppVersity, but I guess there are none), you should have disregarded the study, as well. After all, we all know how the game changes after menopause and guess what, of those women, 98.6% were post-menopausal (in case you ever see studies done on ovariectomized rodents, remember that those are "menopausal", too ;-). Ah, and in case you are a post menopausal women with Africa-American or Hispanic background, there is likewise little reason for you to read on, because 99.2% of the women in the study were white (if you question whether or not ethnicity really matters, when it comes to the health effects of vitamins, I suggest you take a look at some reviews like Carmel. 1999).

Now, if you are still with me at this point, I guess that you either are a post-menopausal white woman, or - and I suppose that this will be the case for the majority of you - you have been agitated by the heated debate on the net (and even regular mass-media) in the last couple of days and want someone to tell you that you did not reduce your life-expectancy by -15% by religiously taking your "essential" *rofl* multi-vitamin, everyday. We will see, whether I can be this person (in case it turns out I am not, I have seen more than enough "gurus" you will tell you exactly that, if you promise to buy their "all natural" or "superior source" product in the future).

The Iowa Women's Health Study - Mrs "not so average" American

So, let's see. What we have here is an offshoot of the Iowa Women's Health Study (IWHS), which is one of those highly over-estimate surveys, the media loves, because they boast of ten-thousands of "participants". In the case of the IWHS, "41836 women aged 55 to 69 years"... well, at least that were the women the scientists send their little questionnaires to back in 1986. Interestingly, this is also where the first bias (i.e. a deviation from "objectivity") came into play:

Respondents were slightly younger, had lower body mass index (calculated as weight in kilograms divided by height in meters squared), and were more likely to live in rural areas compared with nonrespondents.

So instead of the average American "older woman", the scientists suddenly had the "slightly younger" not just as obese, better off American older women, as their study object. Moreover, the number of participants dropped to 38772 women or, in other words, the scientists "lost" 7.3% of their study population even before the study actually began. Now, of those, the Mursu et al. selected 29230, who were the "elite" which responded to both the initial 1986 and the 2nd 1997 follow-up questionnaire.

Failure 1: Not representative of "The Average American"

"Ladies, give me as little information about your supplements as possible, please!"

The latter, i.e. the questionnaire, assessed the use of 13 supplements:

• multi-vitamins; 
• vitamins A, beta-carotene, B6, folic acid, B complex, C, D, and E; 
• iron, calcium, copper, magnesium, selenium, and zinc

Now, the scientists show off their wealth of knowledge and state that "[d]ifferent forms of vitamin D, cholecalcif-erol (D3) or ergocalciferol (D2), were not distinguished". While this is obviously important, it would have been even more important to distinguish between different forms of vitamin B6 (pyridoxin vs. P5P), B complex (you can have a complete one, one with equal doses, one particularly high in one B vitamin, etc.), vitamin E (I suppose you read the first installment?), iron (heme, non-heme, chelated, etc.), copper / magnesium, selenium, and zinc (oxide, chelated, etc.), because we know that these different forms of vitamins and minerals are not only differentially absorbed, but also exhibit differential effects on our health and well-being.

Failure 2: Ignorance towards the fact that
not all vitamins / minerals with the same label are created equal

And as if this had not been enough, the scientists did not even care if the ladies popped 1 or 23 of their beta carotene (I hope you do not still believe you can take endless amounts of that orange poison), magnesium, folic acid and B-complex pills.

Failure 3: Careless ignorance towards dosages

Raw foods are dangerous and so is raw data

Hence, the scientists got a set of data that was full of holes from a group of women who are by no means representative of "The Average American" (let alone every human being) - what did they do next? Well, obviously "raw data" is as dangerous as raw meat (or even raw milk), that is why the next step for every good scientists is data processing. In that Mursu et al. were particularly skilful as far as not revealing what they actually did was concerned:

In the minimally adjusted model, we adjusted the association for age and energy intake; in multivariable adjusted model, version 1, we additionally adjusted for educational level, place of residence, diabetes mellitus, high blood pressure, body mass index, waist to hip ratio, hormone replacement therapy, physical activity, and smoking status. For multivariable adjusted model, version 2, we added intake of alcohol, saturated fatty acids, whole grain products, fruits, and vegetables.

Even, or I should say, especially for a physicist, who is a 75% mathematician, the idea that by some sort of mathematical magic you could reliable subtract out all those influence, so that you get the "real picture" of what is going on, with an average human being is so hilarious that I avoid any further comment. Everything that goes beyond the "minimal adjustment" is so full of speculative hypothesis and mainstream paradigms (like "Whole grains are good for you! The more, the better!") that I will simply ignore this data... unfortunately these results of "3+3 = 666" mathematical manipulation were what the scientists (in their press releases) highlighted as their main results and what was accordingly taken up by the laymen (initially I wanted to write idiots, but that would be unfair, because laymen they are) in the editorial offices of the mass media.

Failure 4: Over-"analysis" of the data

Let's get to the raw truth

This would not be the SuppVersity, if I did not have something to offer that goes beyond the angry rants and criticism (see above) you probably have read elsewhere, anyways. So, I went through the pains of compiling and comparing the "real", i.e. the N=X data and not the calculated hazard ratios for you.

Figure 1: Raw data and minimally adjusted (age and caloric intake) data on the effect of taking vitamin A, beta carotene, vitamin C, vitamin D, vitamin E, and finally the multivitamins on overall mortality (data calculated based on Mursu. 2011)

Now, I want you to take a close look at the data for vitamin A, beta carotene, vitamin C, vitamin D, vitamin E, and finally the multivitamins. I don't know what you see, but I see only vitamin A and beta carotene scratching at the increased mortality margin of 1.0 (cf. dotted red line in figure 1). And, just for a better understand, two examples:

• the 1.04 as for vitamin A (minimally adjusted) in 2004-08 indicates a +4% higher risk and 0.80,
• the 0.80 for vitamin E (raw data) in 2004-08 indicates a -20% decrease in mortality risk

So, what would you say, how "dangerous" is taking vitamin pills if you do not process the data to death? Interestingly, things get really nasty, from here. And moreover, they get nasty, where you probably would not have expected it unless you are a very diligent student of the SuppVersity and are thus aware that messing with the methylation cycle via B6 or folic acid supplementation for no reason is not a good idea.

Figure 2: Raw data and minimally adjusted (age and caloric intake) data on the effect of taking vitamin B6, folic acid, B-complex, calcium, and magnesium on overall mortality (data calculated based on Mursu. 2011)

Given the fact that an increasing amount of "old" people are taking magnesium supplementation, I would say that in this case the age-adjustment is probably necessary - if you also consider that back in the 1980s this bias was smaller, since people were not told that taking mg supplements would be necessary for older folks, the respective adjustment will be "too small" and thus I would simply ignore the fact that the 1996 value still signifies a +2% greater risk of dying when you take a magnesium supplement (add to that that the study participants could have taken magnesium in the 10x recommended dosage and the scientists would not know that /see comment on dosage, above). What really surprises me, though is the enormous benefit that is (even in the raw data) associated with calcium supplements - 22% reduced risk according to raw data and 21% reduced risk with age/energy adjustment - impressive!

Figure 2: Raw data and minimally adjusted (age and caloric intake) data on the effect of taking iron, copper, zinc, and selenium on overall mortality (data calculated based on Mursu. 2011)

Last but not least - the worst offenders, the dreaded "heavy metals" ;-) Ok, I guess iron really is a bad guy (at least for post-menopausal women), but even copper, which has gotten such a bad rep, lately turns out to come pretty handy in the female part of the aging American population, ... interestingly only in the early to late 2000s - how come? I'll leave it up to you to make up your mind on this and other questions, but I assume that now, that you know the raw truth, you will not blindly follow Bjelakovic's campaign to "wake up [regulatory authorities] to their responsibility to allow only safe products on the market" (Bjelakovic. 2011), but rather scrutinize his "invited comment" to the Mursu study, which was published in the same issue of the Archives of Internal Medicine and has caused such an upheaval among the increasingly health conscious American and International public.

Are Elevated Iron and Uric Acid Levels Too Much of a Price to Pay for a Creatine-Induced 11% Performance Increase?

Video 1 (GSSI): Notre Dame's Michael Floyd goes all out on the Wingate test (click to watch)

I guess you could say that these are the "classic days", here at the SuppVersity, contrary to my previous post on choline, which is - judged by the few people who still use it today, an "old school supplement" (cf. "Choline: Stronger, Faster, Leaner & More Muscular, or Just Another Dumb-and-Barbell Story?") - yesterday's post on caffeine highlighted the efficacy of a potent ergogenic aid and metabolic activator, with the effects of which most of us are so familiar that we are alway tempted to turn to useless crap like raspberry ketones, when what we are already doing is not only tried and proven, but based on respectable scientific data even more effective than the latest "innovation" from the snake oil industry. And let's be honest, haven't we all been tempted by one or another "new creatine", as well?

+11% peak performance in one week, solely from 5x4g of creatine per day!

A a matter of fact, creatine monhydrate does in fact share the same fate of being proven, but "boring" staple supplement and although that alone should be incentive enough to address the unquestionably outstanding +11% in anaerobic peak performance, +5% in continuous anaerobic performance and a +6% increase in total workload in a classic wingate anaerobic performance test speak, Barros et al. observed in a group of trained male subjects in response to a 7-day creatine loading protocol (20g creatine monohydrate, in 5 doses spread across the day, not glucose / sugar added; cf. Barros. 2012) After all, my gut tells me that the contemporary changes in the concentration of iron in the blood of the subjects in the the creatine arm of the study could revoke the mainstream-media fearmongerish hoopla over the purported dangers of the #1 natural ergogenic.

Figure 1: Basal iron, FRAP, malondialdehyde (MDA) and uric acid levels before and after 7-day supplementation with 5x4g of creatine monohydrate per day (based on Barros. 2012)

I mean, there is no debating, the level of iron in the blood of the creatine supplemented undergraduate students (age, 23.1 ± 5.8 years; height, 175.4 ± 2.3 cm; weight, 81.1 ± 9.3 kg) all of whom had been avid trainees for at least 6 months did increase by no less than 94.3%, while the subjects in the placebo group experienced a -21% reduction of these highly reactive molecules (Just as an aside, the decline in serum iron in the placebo group and the significant difference in baseline levels between the random groups, alone, render any implications at least questionable; I mean, wouldn't you expect the serum parameters to stay the same, when you do nothing extraordinary, aside from popping some sugar pills?).

Figure 2: Changes in wingate anaerobic performance (left) and exercise induced changes iron, FRAP, malondialdehyde (MDA) levels during the wingate test at the end of the supplementation period (based on Barros. 2012)

In conjunction with the likewise highly significant increase in uric acid levels, conventional (blogosphere-)wisdom, which constantly ignores the antioxidative nature of uric acid, which acts as efficient antioxidant and chelating agent for iron ions (Karlsson. 1997), limits the oxidation of polyunsaturated fatty acid in the erythrocyte membrane and prevents hemolysis (= the rupture of red blood cells) in vitro (Einsele. 1987), would suggest that taking creatine takes a close second to fructose on the list of the villains of the bad, bad "neolithic" century.

How dangerous is the creatine induced increase in iron?

Image 1 (Paramount Pictures): I guess, it must have been creatine monohydrate, then, that turned Robert Downey Jr. into Ironman ;-)

Now, despite the as of late publicly propagated concerns about increased iron levels and their potential causative role in the etiology of insulin resistance and diabesity (obesity + diabetes), recent scientific evidence suggests that "high iron", such as all previous scapegoats people like to hold liable, just to make sure not to admit that it is the sickening combination of laziness, convenience and unsound dietary advice that is at the heart of the current obesity epidemic.

Huang et al., for example, did observe a direct effect of iron overload on diabetes risk - the latter was however a result of hereditary hemochromatosis (a genetic defect in iron metabolism) in their 2011 rodent trial (Huang. 2011). Results from two more recent studies by Silva et al. also indicate that the metabolic disturbances lead to differential expressions of the proteins involved in the metabolism of iron and thus substantiate the associative (and not causative) nature of the relation between high iron / ferritin and the metabolic syndrome (Silva. 2011; Silva. 2012).

Iron not causative? So why does phlebotomy help, then? If you read my post on the recently published data from the first controlled human trial that investigated the effects of phlebotomy on markers of blood glucose management, you will be aware that the measures they took, e.g. the HOMA-IR, are not really appropriate to assess the effects of this particular treatment (cf. "Phlebotomy: Can You Bleed Yourself Healthy and Lean?"). Furthermore, it is only logical that the removal of some of this "highly inflammable stuff" from an inflamed body will provide health benefits, even if the latter was totally benign for someone who has a lot less inflammation going on.

What is even more important, though, is that the difference between exercise-induced increases in serum iron and diet and diabesity-related increases in the storage form of iron, ferritin, in the liver. This is particularly true in view of the fact that our understanding of the former, i.e. the exercise induced release of iron into the blood stream is more than limited (Roberts. 1989; Smith. 1994). What we do see in the Barros study, however, is that the overall effect of creatine is rather anti- than pro-oxidative, since the increase in overall antioxidative capacity (as indicated by the changes in the iron-specific FRAP essay; cf. figure 1) did not just...

• negate the potential negative effects of increased basal iron levels (see lowered baseline MDA levels post supplementation in figure 1), it also 
• countered the exercise-induced lipid oxidation during the 2nd wingate test (as indicated by lower MDA levels; cf. figure 2). 

Eventually, the scientists say, the increase in antioxidant activity that is brought about by the ingestion of 20g/day creatine irrespective of whether you exercise or not could actually yield "general health benefits" (Barrios. 2012); and I would like to add that evidence for Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, recovery from ischemia and, guess what, diabetes already exists (Tarnopolsky. 2000;"Creatine Ameliorates Type II Diabetes")! Certainly not bad for one of those bodybuilding supplements, "anabolics" or "gateway drugs", as creatine is often mislabeled , when a 100% clueless "journalist" tries to get the attention of his editor-in-chief, wouldn't you agree?

Suggested readings (some also mentioned in the text):

• The Pharmacology of Creatine (Part 1 and Part 2) 
• Supercharging Creatine With Baking Soda (click here to read)
• 5g/day Creatine for Type II Diabetics? (click here to read)
• All posts tagged with "creatine" (click here to read)
• Phlebotomy: Can You Bleed Yourself Healthy and Lean? (click here to read)

References:

1. Barros MP, Ganini D, Lorenço-Lima L, Soares CO, Pereira B, Bechara EJ, Silveira LR, Curi R, Souza-Junior TP. Effects of acute creatine supplementation on iron homeostasis and uric acid-based antioxidant capacity of plasma after wingate test. J Int Soc Sports Nutr. 2012 Jun 12;9(1):25. 
2. Huang J, Jones D, Luo B, Sanderson M, Soto J, Abel ED, Cooksey RC, McClain DA. Iron overload and diabetes risk: a shift from glucose to Fatty Acid oxidation and increased hepatic glucose production in a mouse model of hereditary hemochromatosis. Diabetes. 2011 Jan;60(1):80-7.
3. Orozco MN, Solomons NW, Schümann K, Friel JK. Response of urinary biomarkers of systemic oxidation to oral iron supplementation in healthy men. Food Nutr Bull. 2012 Mar;33(1):53-62. 
4. Roberts D, Smith DJ. Effects of high-intensity exercise on serum iron and α1-antitrypsin in trained and untrained men. Clin Sports Med 1989, 1:63–71.
5. Silva M, Bonomo Lde F, Oliveira Rde P, Geraldo de Lima W, Silva ME, Pedrosa ML. Effects of the interaction of diabetes and iron supplementation on hepatic and pancreatic tissues, oxidative stress markers, and liver peroxisome proliferator-activated receptor-α expression. J Clin Biochem Nutr. 2011 Sep;49(2):102-8.
6. Silva M, de Brito Magalhães CL, de Paula Oliveira R, Silva ME, Pedrosa ML. Differential expression of iron metabolism proteins in diabetic and diabetic iron-supplemented rat liver. J Biochem Mol Toxicol. 2012 Mar;26(3):123-9. 
7. Smith DJ, Roberts D. Effects of high volume and/or intense exercise on selected blood chemistry parameters. Clin Biochem 1994, 27:435–440.
8. Tarnopolsky MA. Potential benefits of creatine monohydrate supplementation in the elderly. Curr Opin Clin Nutr Metab Care. 2000 Nov;3(6):497-502.

Ironclad Liver Hampers Insulin Sensitivity: Association Between Hepatic Iron Load and Insulin Resistance Discovered

"Insulin resistance", "insulin sensitivity", etc. Type in these key words and find 4.000.000 +1 results on Google. I want to focus on the +1 here and briefly report the results of a study (Haap. 2011) coming from the University of Thübingen, Germany.

Via magnetic resonance gradient echo imaging technique Michael Haap and his colleges assessed the iron load in the livers of of 113 healthy nondiabetic subjects [69 females, 44 males; age 47 ± 1 yr; body mass index (BMI) = 28.9 ± 0.5 kg/m2], who were "at increased risk for type 2 diabetes". Various statistical analysis of their data revealed that:

[Hepatic iron levels] adjusted for age negatively associated with serum ferritin levels (P < 0.0001) and positively associated with IS [insulin resistance] (P = 0.009). In addition, T2* values [indicator of hepatic iron load] associated with LF [liver fat] (P = 0.008) but not with BMI (P = 0.6). In a multivariate model, IS adjusted for gender, age, and BMI was associated with T2* values (P = 0.015). IS adjusted for gender and age was independently associated with LF (P = 0.033) and T2* values (P = 0.004). In a stepwise regression analysis, LF explained 13.5% (P < 0.01) of the variation in IS, and HIL [hepatic iron load] explained an additional 4.1% (P = 0.03).

With 4.1% the contribution of iron to the development of type II diabetes is certainly only one out of a multitude of factors. I would yet still be interested in further information on the interplay of iron, insulin and blood glucose, also because low ferritin levels, which, according to the study, go hand in hand with high hepatic iron loads, have also been implicated in other metabolic disorders such as hypothyroidism, which in and out of itself would further aggravate existing blood sugar and weight issues within the pre-diabetic study population.