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marylin monroe
Showing posts with label cardiovascular disease. Show all posts
Showing posts with label cardiovascular disease. Show all posts

Alarmingly High Levels of Lead in Calcium Supplements: Pb Content per Serving Up to 18x Over "Acceptable Levels".

Image 1: You better pick the right source of calcium: healthy milk / dairy vs. lead poisoned pills from your local pharmacy or supermarket - you still have the choice.
This, I can assure you, is a "SuppVersity News", i.e. something you will not read on the major news portals, simply because there is too much money at stake in the 3billion $ market for calcium supplements (figure according to January 2008 edition of "Heartwire") - money a huge part of which is spent by Novartis & Co to advertise their products to consumers from all age groups, regardless of the individuals' dietary calcium intake; and that despite accumulating evidence for an association of supplemental calcium intake and heart disease (for one of the latest reviews cf. Bolland. 2011)! A very recent study published in the Journal of Biological Trace Element Research (Rehman. 2011) does yet cast another, even darker shadow onto the "healthy" white chalk tabs...

What? "Pb" is not the symbol for Calcium in the Periodic Table?

Lead, that stuff nuclear physicists value, because it effectively absorbs radioactive radiation, is one of the most toxic "heavy metals" we are exposed to. And this is by no way a recent discovery. Even in ancient times, people knew about the toxic effect vessels made of this metal had on the water they contained. Back in 1990 E.K. Silberberg summarized the contemporary knowledge about the dangers of environmental lead exposure in a paper for the Environmental Defense Fund as follows (Silberberg. 1990):
[...] epidemiological studies have suggested that central nervous system (CNS) effects in children are observed at the lowest increments of lead exposure [...] Similarly, clinical studies indicate that early exposure to lead produces functionally irreversible damage to the CNS; experimental research demonstrates that this irreversibility may involve failure to remove lead from brain, permanent effects on synaptogenesis; and chelant-induced redistribution of lead from the periphery to the CNS. [...] New data on release of bone stores of lead during physiological conditions of demineralization indicate that mobilization of bone lead adds to in utero exposure of the fetus. Furthermore, postmenopausal demineralization of bone can increase blood lead levels in women by 25%; this raises concern about the potential effects of lead in an aging population and the difficulties in comprehensive exposure assessment.
As you may have guessed, time has not affected the dangers or the irreversibility of lead toxicity, so that you would assume that the results of an investigation into the lead content of 27 "commonly used" commercially available calcium supplements should be alarming enough to receive at least some public recognition. After all, it would suffice to read the abstract to be alarmed by the fact that of the calcium supplements Sohaila Rehman and her colleagues from the Pakistan Institute of Nuclear Science Technology analyzed only one out of ten "met the criteria of acceptable Pb levels (1.5µg/daily dose) in supplements / consumer products set by the United States" (Rehman. 2011).
Figure 1: Lead levels in µg in daily dose of respective calcium supplement; solid red line = acceptable Pb level for calcium supplements, dashed red line = tolerable total daily Pb intake for children <7y, dotted red line = tolerable daily Pb intake for women in childbearing age (data adapted from Rehman. 2011).
"One out of ten", well that does not sound so bad, does it? I guess you will change your mind, when you take a closer look at figure 1 - the red line at the bottom of the graph is the "acceptable Pb level" and as you can see it is met by exactly 1 out of 13 calcium chelate products (CAC 1000 by Novartis), and none of the 3 calcium chelates the researchers tested for their lead content.
Figure 2: Lead levels in µg in daily dose of respective calcium supplement; solid red line = acceptable Pb level for calcium supplements, dashed red line = tolerable total daily Pb intake for children <7y (data adapted from Rehman. 2011).
And while the lead levels of the calcium + vitamin C and calcium + vitamin D levels in figure 2 look somewhat better, there are still several outliers with Cal-C Plus from Himont Pharma, for example, providing more than 2x the tolerable daily lead intake for a child under the age 7 y (and remember these are only the official FDA figures - and you know what that means ;-) on a per serving base.
Note: The results of the study at hand may well explain a) the different outcomes of (controlled) trials and epidemiological studies on the effects of calcium supplements on cardiovascular health and b) the beneficial effects of milk and dairy intake on heart health (Soedamah-Mutuh. 2011). After all, a very recent study that was published in the Journal of Neurotoxicology and Teratology in October 2011, shows that there is a "potential for autonomic dysregulation" that manifests in "significantly greater vascular resistance and reduced stroke volume and cardiac output" in 9-11 year old children even "at levels of Pb typical for many US children" (the exact levels were 1.01µg/dL, cf. Gump. 2011).
And as if all that was not enough, the US Food and Drug Administration (FDA) and the glorious Center for Disease Control and Prevention (CDC) would have been aware of the potential of serious chronic lead intoxication from calcium supplements, if they spent more time reading scientific journals than counting the cashflow from the BigPharma companies that finance their bureaucracy. After all, Bourgoin et al. conducted a very similar study back in the 1990s, the results of which the scientists summarize in their abstract as follows (Bourgoin. 1993):
Daily lead ingestion rates revealed that about 25% of the products exceeded the US Food and Drug Administration's "provisional" total tolerable daily intake of lead for children aged 6 years and under.
In the Rehmann study it were 16 out of 27 tested calcium supplements (59%) which exceeded this limit. So  maybe the "feds" just did not act, because 1 out of 4 is not bad enough? Well, if you look at the individual results in figure 3 (usually I redo graphs, but in this case the original looks just too damn impressive), it is immediately obvious that the averages the scientist report in their abstract, do not reflect the actual potential of lead toxicity from the 70 supplemental sources Bourgoin et al. tested.
Figure 3: Results of a 1993 large-scale analysis of the lead content of 70! commercially available calcium supplements and milk (my emphasis), the safe exception (from Bourgoin. 1993)
Obviously, some of the bone based and a whole host of the "natural sources" ("natural source of calcium carbonate" according to label claim; note that coral calcium would fall into this category, as well!) are about as toxic as the worst offenders in the Rehman study. What I find do yet find particularly interesting, is that the lead content in one serving of commercial milk, which would provide the same amount of (even more bioavailable) calcium as the supplements in the study did, would provide no more than 0.71µg/day and is thusly the one and only "natural source" of dietary calcium that does not set you up for lead toxicity!

"Pah, lead!? What doesn't  kill you just makes you stronger"

Image 2: So, calcium supplement with lead are a safe source of dietary calcium, but raw milk is not? (img CounterThink)
In view of the "longstanding" history of ignorance on behalf of the governmental agencies, it sounds almost sarcastic, when Bourgoin et al. conclude their article by citing the Center for Disease Control's (CDC) statement on lead poisoning, which according to these reputable protectors of the health of the American society *cough* is "one of the most common and preventable pediatric health problems today". Notwithstanding this early insight (this is from a 1991 document from the CDC) the officials obviously have neither taken Bourgoin et al.'s advice to control calcium supplements "more rigidly" in order to "prevent unnecessary exposure in all segments of the population, particularly young children" (Bourgoin. 1993), nor have they followed the recommendation of a more recent study by Kim et al., which  estimates the mean lead intake from calcium supplements to about 5µg/day and recommends that "measures to prevent potentials of Pb toxicity from overtaking some Ca supplements should be considered" (Kim. 2010).

And while the CDC and the FDA could incidentally have missed those papers. They should actually be aware of Proposition 65, which is the common name for California's Safe Drinking Water and Toxic Enforcement Act of 1986 (Dietary Supplement Standard 173, Metal Contaminant Acceptance Levels. NSF International. August 19, 2003). In this paper, of which W.W. Kilgore writes in retrospective that (Kilgore. 1990)
[i]t creates a list of chemicals (including a number of agricultural chemicals) known to cause cancer or reproductive toxicity; [i]t limits discharges of listed chemicals to drinking water sources; [i]t requires prior warning before exposure to listed chemicals by anyone in the course of doing business; [i]t creates a list of chemicals requiring testing for carcinogenicity or reproductive toxicity; and [i]t requires the Governor to consult with qualified experts (a 12-member "Scientific Advisory Panel" was appointed) as necessary to carry out his duties.
the proposed Acceptable Intake Level (AIL) for inorganic lead (as extrapolated from animal studies) is 0.5µg/day and thusly 1/3 of the current Californian standards and 1/50 of the FDA allowance of 25µg/day! But hey, who cares? As long as the American citizens are protected from the dangers of raw milk, everything is all right, isn't it?

Science Round Up Seconds: 30-60% More Testosterone w/ 2.5g D-Aspartic Acid in Fertility Trial and Nicotine Amplifies Cardiotoxic Effects of ECA. Plus: Data on DHEA & Estrogen & Breast Cancer, Fermented Teas, AMPK, AKT & Co

DAA is probably not going to hurt your heart, but it's more likely to father a child than to build those abs. Ephedrine & Caffeine on the other hand, could help you get there, but esp. if you are also smoking you are increasing the risk that the kids you fathered using DAA will soon be without their begetter.
I guess most of all will have listened to the podcast of yesterday's installment of the SuppVersity Science Round Up already. If you didn't you have been missing Carl and me discuss new on the pro-carcinogenic effects of aspartame, the never-ending story of the fattening artificial sweeteners, the benefits of oat beta-glucans for weightloss, -maintenance and gut health, the way sorghum proanthocyanidins can lower the GI of carbohydrates and make them less susceptible to enzymatic breakdown in the small intestine, and more.

Actually this more, i.e. the news on DHEA, its metabolits and their proliferative effect on breast cancer cells, as well as the information about the beneficial effects of fermented teas on blood glucose management, reminded me of the fact that as how like the SuppVersity Science Round Up is a very good place discuss and explain things, but not exactly the place to present detailed data. Therefore, I decided to prelude the Seconds by adding a couple of graphs which illustrate what has been said on the last show. Thus, you can look at the figures while listening to the podcast.

Supportive material for the DHEA and fermented tea news

For this first installment of the Seconds I did, you guessed it, pick the aformentioned news on DHEA and the different fermented teas (see figure 1) that are  based on studies by Miller (2012) and Yamashita  (2012), respectively.
Effect of 7 days of oolong tea, black tea, pu-erh tea, instead of water on Δglucose AUC (left), AMPK, AKT and PI3K expression in skeletal muscle  of male mice (Yamashita. 2012)Effect of estradiol (E2), DHEA and its metabolits 7-OXO,  androstenediol, and androstenedione on breast cancer cell proliferation (based on Miller 2012)
So much for the additions to visuals for the podcast, let's get to the new stuff... or actually the seconds. Of course, the seconds ;-)

  • How to brew your own sodium d-aspartic acid The best thing about this study actually is that the scientists disclose how you can easily make your own PH stable sodium-d-aspartate from the cheap stuff you buy at your favorite bulk supplier: Take 2.66 g of D-aspartic acid neutralize it with 0.46 g of NaOH in 10 ml distilled water and you get a final pH of 6.5 - 7-0 - that's it, you are good to go.
    New study on d-aspartic acid confirms - 30-60% increase in testosterone and LH in infertile men (D’Aniello. 2012) Despite the fact that this is a non-sponsored study by researchers from the Hospital “S. Luca” in Vallo della Lucania, Italy, I am about as 'unpsyched' about the data the scientists present, as I am about the real world results of d-aspartic acid (DAA) supplementation in young weight training men.

    It's already telling that D'Aniello et al. mention the increase in testosterone and luteinizing hormone (LH) only as an aside and consider it as a "save", or I guess you better say "tolerable" side effect of a treatment  that did effectively double the amount of D-aspartic acid in the seminal plasma and did thus (at least the scientists belive in a mechanism here) increase the fertility in both, patients with reduced sperm motility and sperm count, and those who suffered only from reduced motility.

    The actual 'success rate' in terms of pregnancy rates after 2-3 months of treatment with 2.66g/day of DAA per day was however not exactly really earth-shattering, either. Of the patients with both low sperm count and sperm motility (oligo-asthenozoospermia) 4% fathered a child; of those who suffered 'only' from a low sperm motility (asthenozoospermia) 33% eventually managed to become daddy.

    Without baseline testosterone levels, of which I would not be surprised if they had been rock bottom (both oligo-asthenozoospermia and asthenozoospermia usually go hand in hand with increased oxidation and that in turn is associated with low testosterone and suppressed LH levels), this study is however about as worthless in terms of the purported ergogenic effects of DAA, as all previous human trials. That said, you could obviously mix yourself the above concussion in case you and your significant other are planning to start a new or to expand your existing family in the near future. I guess, it's unlikely that it's going to hurt.

    Suggested read: All About the Role of Androgens & Co in Building Muscle
     
  • Putting an "N" as in "nicotine" into "EC" amplifies the negative effects of ephedrine and caffeine on your heart and may well be the reason for many of the (few) deadly side effects that occurred in the day before the ban (Brown. 2012) When a group of researchers from the Arkansas State University tried to get to the bottom of the (in some cases) fatal cardiovascular side-effects, which were the main reason for the FDA to pull ephedra-containing supplements from the market, Christopher E. Brown and his colleagues observed ...
    "[...] a synergistic effect on the rat cardiac morphology [...] as a result of intera tions between nicotine, caffeine, and Ephedra. The cardiotoxicity caused by combination dosing of Ephedra and caffeine has already been shown; however, the present study revealed an enhancement of cardiotoxicity when nicotine was administered in combination with Ephedra and caffeine." (Brown. 2012)
    The scientists had exposed male Sprague-Dawley rats to (1) synthetic combinations of nicotine (0.2 mg/kg/day), ephedrine (0–30 mg/kg/day), and/or caffeine (0–24 mg/kg/day) as well as (2) an extract from a caffeine-containing Ephedra supplement (Metabolife 356). The relatively high dose treatments were administered for only 3 days either in the full or half dose and with and without nicotine pre-treatment to model the effects of different dosing regimen on smokers and non-smokers.

    Figure 1: Light micrograph of representative nuclear pro-files (background, red = atypical, green = normal nuclei; my emphasis) and volume (%) of atypical cardiac cells in anterior left ventricle of the rodents (Brown. 2012)
    As far as the results go, a a brief glance on the exemplary data in figure 1 should actually suffice to see, that a baseline "N" + "EC"  stack (as in any smoker who would take ephedrine + caffeine to lose weight or psyche himself up) could eventually pave the way to the emergency room.

    While the data from the anterior left ventricle and anterior interventricular septum (not shown) would suggest that the identically dosed synthetic versions of caffeine and ephedrine were slightly more detrimental, than the herbal supplement  in which the Ephedra came from a standardized Ma Huang extract and part of the caffeine from Guarana, this effect was not present in either the posterior left or the anterior right or posterior right ventricle (data not shown).

    Apropos interventricular septum (IVS), with increases in atypical cardiac cell volume of up to 1.5% in the anterior IVS even without nicotine pre-treatment, the stout wall that separates the lower chambers was most susceptible to the effects of caffeine and ephedrine:
    "In the anterior section of this region, both caffeine + ephedrine combination as well as the multicomponent supplement Metabolife 356 resulted in larger numbers of atypical cells compared to water controls, in both saline- and nicotine-pretreated rats. However, only rats pretreated with nicotine responded negatively to supplements in the posterior region of the IVS. " (Brown. 2012)
    If you consider the high-pressure forces it must sustain for proper ejection volume to the arterial vasculature it should be obvious that "these changes to the ventricular tissue could be particularly detrimental to overall cardiovascular health" (Brown. 2012). Bad news? Why? At least you do now have another good reason to stop smoking... what, oh yeah, I forgot: This is irrelevant because Ephedra has been banned anyway ;-)
While I do have a couple of other Seconds I am a bit pressed on time, today. Don't worry sooner or later they will appear ither on the SuppVersity Facebook Wall, where I am posting at least half a dozen of exclusive links and mini-items, comments and more you won't find on www.suppversity.com. So, I'd suggest you do now first listen to the podcast (if you have not already done so), then check out the latest SuppVersity Facebook News and when you are done with that wait till tomorrow for this weeks installment of On Short Notice.  

    References
    • Brown CE, Trauth SE, Grippo RS, Gurley BJ, Grippo AA. Combined Effects of Ephedrine-Containing Dietary Supplements, Caffeine, and Nicotine on Morphology and Ultrastructure of Rat Hearts. Journal of Caffeine Research. 2012; 2(3).
    • D’Aniello G, Ronsini S, Notari T, et al. D-Aspartate, a Key Element for the Improvement of Sperm Quality. Advances in Sexual Medicine, 2012, 2, 47-53.
    • Miller KKM, Al-Rayyan N, Ivanova MM, Mattingly KA, Ripp SL, Klinge CM, Prough RA. DHEA metabolites activate estrogen receptors alpha and beta. Sterespectivelyroids. November 01, 2012. Ahead of print.
    • Yamashita Y, Wang L, Tinshun Z, Nakamura T, Ashida H. Fermented Tea Improves Glucose Intolerance in Mice by Enhancing Translocation of Glucose Transporter 4 in Skeletal Muscle. J Agric Food Chem. 2012 Nov 5.

    Cardio, Fat and IGF-1: Study Investigates Modulatory Effect of Endurance Exercise and High Fat Meals on IGF1 Binding Protein Levels in Obese Human Subjects

    Image 2: 3D structural model of the IGF1 protein (rendered by Emw)
    It's probably less than 24h ago, that you read about growth hormone (GH) here, at the SuppVersity. Its increase during fasts was one of the points, I addressed in yesterday's installment of the Intermittent Thoughts on Intermittent Fasting series. In fact it has been known for quite some time now, that fasting does increase the release of the 191-amino acid, single-chain polypeptide from the anterior pituitary gland, which in turn facilitates the (mostly) desirable switch to non protein-catabolic metabolic state, where fat becomes the major energy substrate. GH's growth promoting magic, on the other hand is believed to be largely mediated by the growth hormone induced production and release of insulin like growth factor 1 (IGF-1) in the liver, as well as directly at the level of target tissues. Apart from the sheer amount of IGF that is produced, its binding to respective carrier proteins, so called insulin like growth factor binding proteins, or IGFBPs, is yet another major determinant of the half-life and more importantly the mode of interaction of the IGF peptides with their target receptors at the cell surfaces.

    From previous studies into the effects of exercise on IGF-1 levels activity, we already know that trained endurance athletes exhibit higher levels of IGFBP-1 (insulin like growth factor binding protein 1) than their sedentary counterparts (Manetta. 2003). Other studies have shown that after acute (vs. chronic) bouts of aerobic exercise the levels of IGFBP-1 return to baseline within 12-24h (Nindl. 2009; Berg. 2008; Koistinen. 1996) In that, the IGF-binding effect of exercise appears to be restricted to endurance type of exercises, as a more recent study by Nindl et al.found no increase in IGFBP-1 levels in young lean women after 8 weeks of strength training (Nindl. 2010).
    Image 2: Ronny Coleman's belly is recurrent topic on various bulletin boards. This image was part of a discussion on the muscular development forum. Is it s imply fat or the results of the false(?) belief in "the muscle building magic" of IGF-1? (photo by Dan Ray for MuscularDevelopment.com)
    The results from the Nindl study are also important in view of the interpretation of "increased" or "reduced" endogenous (i.e. produced by the body) IGF-1 levels in terms of their purported anabolic effect on muscle tissue, as Nindl. et al. point out...
    [...] increased lean mass, aerobic fitness, and upper and lower body strength resulting from an 8-wk exercise training programs can occur without concomitant increases in either circulating bioactive or immunoreactive IGF-I, as well as associated IGFBPs. In terms of reflecting positive anabolic neuromuscular outcomes, these data do not support a role for endocrine-derived IGF-I. (Nindl. 2010)
    All horror stories about GH-guts aside, you may want to keep that in mind before you condemn all aerobic exercise as being anti-anabolic and pay a shitload of money for supplements that "have been shown in clinical trials" (why are you laughing? ;-) to increase IGF-1 levels.
    From epidemiological studies (Heald. 2003; 2005), we also "know" (you are probably familiar with my antipathy against epidemiology) that high fat diets are associated with lower levels of IGFBP-1. It has also been implicated as more or less reliable predictor of cardiometabolic diseases in longitudinal studies (Heald. 2001). Reason enough for Prior et al. to probe the combined effect, or I should say, the interference of 6 months of potentially IGFBP-1 lowering aerobic exercise ("3 weekly sessions of 20 minutes at 50% of heart rate reserve and gradually increased to 3 weekly sessions of 40 minutes at 70% of heart rate reserve"), on the one hand, and IGFBP-1 suppressing high fat meals (84% was derived from fat, 13.7% from carbohydrates, and 2.7% from protein), on the other hand, in a group of 10 overweight (bodymass index = 28.7 ± 0.9 kg/m²), older (61± 2 years) men and women.
    Figure 1: Effect of 6 month of aerobic exercise on serum free glucose, free insulin, HOMA-IR and IGFBP-1 levels in obese subjects (data calculated based on Prior. 2011).
    As the data in figure 1 goes to show, the exercise regimen had profound beneficial effects on insulin sensitivity - evidenced by the increase in serum free insulin levels and HOMA-IR (considered a "reliable" long-term marker of insulin resistance). As previous research had suggested, these changes were accompanied by a major increase in IGFBP-1 (and thus presumably a decrease in IGF-1 receptor activity). The increase in IGFBP-1 was however (almost completely, cf. figure 2) 4h after the study participants consumed a single high fat meal.
    Figure 2: Effect of high fat meal (84% fat, 13.7% carbohydrates, and 2.7% protein) on IGFBP-1 levels (data calculated based on Prior. 2011)
    This negative effect of high fat feeding on IGFBP-1, as can be seen in figure 2, was almost identical before and after the 6-month exercise intervention, which led the scientists to conclude that despite the fact that ...
    [...] aerobic exercise training has a potentially beneficial effect to increase fasting plasma IGFBP-1 concentrations in previously sedentary middle-aged to older adults  [..., a]erobic exercise training did not attenuate the adverse effect of a high-fat meal on plasma IGFBP-1 concentrations
    Image 3: Germany's former foreign minister Joschka Fischer is a famous "victim" of the "low-fat-marathon-style-endurance-training" fat loss myth with built in YoYo-effect - I guess you will have your own celebrities with similar impressive "transformations" ;-)
    and (you probably expected this) use this as a welcome opportunity for repeating the good (I should rather say "bad") old mantra of the benefits of chronic endurance exercise and low fat dieting.... I mean, come on. Look at our (Germany's) former foreign minister, Joschka Fischer (cf. image 3) - don't we all know that low-fat cereals and marathon running are no solution.

    It would be nice to see some scientists going beyond this illusive paradigm, in order to gain insights into the underlying mechanisms or, even more fundamentally, to answer the question whether high(er) levels of free IGF-1 are causative or just corollary to cardiovascular disease, cancer and all the other maladies IGF-1 is currently held responsible for and which role all the healthy low-fat grains we are supposed to eat play in the etiology of these diseases... in case that is going to happen within my life-time, you can be dead-certain (pun intended) that the SuppVersity is the place, where you will read about it first.

    Calcium, Magnesium, Potassium & Co in Food, Water & Supps - Getting Enough is Easy, Knowing How Much Is Not!

    Image 1: "Minerals? Yeah that's the stuff you need to avoid cramping" While this is certainly true, the mineral loss during "normal" workouts is largely overblown, the most important and actually only necessary ingredients in respective drinks, even for Ironman Triathletes, are salt, water and sugar and what's worse this prejudice conceals the importance of electrolytes for our general health.
    While it is Thursday, it is plain to see that this is not Adelfo Cerame's weekly SuppVersity post. There have been a couple of issues with the promised workout videos and neither I nor Adelfo wanted to postpone them yet another week so that we decided to rather publish videos + Adelfo's weekly update tomorrow instead of a reduced snippet today. To make sure you have more than enough food for thought to bridge the time, I applied a coupe of tweaks to a longer snipped from the next installment of On Short News that dealt with the protective effects of high(er) intakes of calcium, magnesium and potassium on the incidence of vascular dementia (=dementia in response to low blood flow to / oxygenation of the brain) and Alzheimer's dementia (=dementia due to the build up of plaque in the brain). As you may already have seen, the result got somewhat epic, so let's not waste anymore time and get straight into the original data before it's too late and we have already become demented ;-)

    Don't forget your minerals or they'll soon be just one of the many things you tend to forget

    While the studies and reviews on the effects of minerals, especially calcium (and as of late also magnesium), on cardiovascular health is about as abundant as the assessments of their individual and joint benefits and / or pitfalls, their role in the etiology of another, quieter, but not less prevalent pandemic is still insufficiently studied. Against that background, the results Ozawa et al. present in a recently published paper in the Journal of the American Geriatric Society could well provide some novel insights on whether or not forgetting to keep an eye on your mineral intake now will make you forget more than just a couple of minerals in the more or less distant future - and that even if none of the 1081 community dwelling elderly (>60y) Japanese the scientists followed up for 17 years is even remotely related to you ;-)
    Figure 1: Hazard ratios for all-cause, vascular and Alzheimer's dementia for patients in the lowest to highest quartiles of potassium (≤1,856 / 1,857–2,149 / 2,150–2,559 / ≥2,560), calcium (≤431 / 432–531 / 532–638 / ≥638) and magnesium (≤147 / 148–169 / 170–195 / ≥196) intake in mg/day (top) and difference in intake of selected foods in the highest vs. lowest quantile of overall mineral intake (bottom; all calculated based on Ozawa. 2012)
    Aside from the general association of higher potassium, calcium, and magnesium intake with lower incidence of dementia, which was - given the overall low median intake - more or less to be expected, there are a couple of other very noteworthy things I want you to take note of (see figure 1; data adjusted for age; sex; low education; history of stroke; hypertension; diabetes mellitus; total cholesterol; body mass index; smoking; alcohol intake; regular exercise; and energy, vitamin C, cholesterol, saturated fatty acid, monounsaturated fatty acid, and polyunsaturated fatty acid intake):
    • a higher mineral intake was had a more pronounced beneficial impact on vascular compared to Alzheimer's dementia (-77% vs. -46% max. reduction)
    • for potassium and calcium the general rule of thumb is "the more, the better" (the deviation from that rule in the individual analysis for Alzheimer's is statistically nonsignificant), but I don't this is mediated by the overall low intake of both and thus only valid within the given range of ~700-900mg of calcium and ~2600-3000mg of potassium - intakes you can by the way easily get from your diets alone
    • aside from the usual suspects, i.e. (green) vegetables, fruits and fish, dairy is among the most important source of minerals and high dairy eaters tend to be high mineral consumers, while low / no dairy eaters tend to be in the lowest quartiles of overall mineral intake
    as well as a couple of things you cannot read off the graphs, e.g.:
    • women had  significantly higher mineral intakes than men, i.e. 68.3% of the persons in Q4 for overall mineral intake were women
    • age had no effect whatsoever on the overall intake of potassium, calcium and magnesium
    • a low(er) education (<6 years of schooling) was a good predictor of low total mineral intakes, just as it is by the way in view of an overall worse diet quality (this is however less pronounced than conventional wisdom would suggest)
    • intriguingly, people with diabetes had on average higher mineral intakes than people without diabetes, almost certainly a non-causative relationship that is probably mediated by supplements and nutritional counseling the diabetics received
    • contrary to the US, there was no association between high salt and low Ca, Mg, or K intakes, this is also surprising because the "average" middle aged Japanese consumes way more than 5g of salt (Nagata. 2004) and thus 2x more than the US "tolerable upper intake level" of 2300 mg (Cogswell. 2012)
    Apropos US, in view of a couple of other studies that have only recently provided support for the widely held, but in fact rarely scrutinized believe that, the lack of adequate amounts of potassium and magnesium, in particular, is associated not only with the age-related cognitive decline and even dementia, but also with such profane things as "simple" obesity, e.g. ...
    • Donfrancesco et al. report higher potassium and magnesium intakes were associated with lower BMIs in 1168 men and 1112 women aged 35-79 yrs from 12 Italian regions (Donfrancesco. 2012)
    • almost identical results in a study by Shay et al. that found associations with lower BMIs for potassium and magnesium 1794 men and women (ages 40-59 y) from 8 US population samples (Shay. 2012)
    ... it would unquestionably make sense to eventually stop bashing on sodium and start promoting the consumption of magnesium- and potassium-rich foods, instead.
    Figure 2: Percentage of the population mineral intakes below the EAR for individuals aged ≥2y (data from NHANES 2003–2006; n = 16,110; Fulgoni. 2011).
    Did you know that according to latest data from the CDC (Cogswell. 2012) less than 2% of US adults meet the dietary recommendations for potassium (≥4700 mg K/d) and that the lack of potassium was even more pronounced in the elderly (0.5% of the >72y-old US citizens meet the dietary requirements) and obese (0.7% meet the recommendations. With two out of five Americans also failing to meet even the required amount of magnesium in the diet, it appears more than questionable why the good-meaning (I don't doubt they are but too often they are mislead of have the good of the wrong people in mind) policy makers don't put magnesium and potassium into the water supply instead of toxic junk such as chlorine and fluoride...

    I mean, you will probably remember from "On Short News on July 28, 2012" that each milligram of magnesium per liter drinking water could decrease the heart disease risk of people with an unbalanced mineral intake by 5%! But, alas, who am I to make such bold suggestions?
    Now, while the importance of watching your dietary magnesium and potassium are pretty obvious and probably nothing you have not heard before, there is still one question left to be answered - a question that will point us away from RDAs and EARs and back to foods, which never contain only one of the aforementioned minerals in isolation. So here is the question: What do we make of calcium? In the Ozawa study it appeared to be clearly useful, but that was with intakes of >638mg/day in the highest quintile of the study population! The average European citizen, on the other hand, consumes roughly 1g = 1,000mg, i.e. 36% more than the Japanese and still we (us Europeans) are about as sick, if not sicker than the average Japanese? How come?  

    Potassium, check; magnesium, check; calcium, ... wait a minute! What about phosphorus? 

    Aside from the mere possibility that we could already be consuming way too much calcium (which is not supported by science as long as those 1,000mg come from your diet and not from supplements; cf. "Higher Calcium Intake Greater Fatty Acid Oxidation"), the most straight forward explanation would be an imbalanced intake of phosphorus. For the average European the latter is at about 1,675mg/day (mostly from dairy, cereals and meats - 27.9, 23.4, 17.4.% of daily intake, respectively) and thus clearly twice the amount our (the European) version of the well-meaning policy makers are telling us each and every one of us should be consuming on a daily basis.
    Figure 4: Relative potassium intake in European countries according to source; note: with 4,110mg/day the average potassium intake in the Euopean Union is much higher than in the US, highest intakes were observed in Spain, lowest in Germany (Welch. 2009)
    Did you know that the average magnesium intake in Europe (409mg/day) is much higher than in the US? And guess what, the usual suspects, i.e. dairy and cereals aside, non-alcoholic beverages are the #2 source (19% of total mg intake) of dietary magnesium in Europe! I would, an observation Welch et al. attribute just like the almost "optimal" (wrt to the US recommendations) average potassium intake of 4,110mg/day to the high quality tap and bottled mineral water, and other non-alcoholic beverages (and certainly not to reverse osmosis or the consumption of mineral-free distilled water, which is something you can use to satisfy the water requirements of your radiator or  iron, but not those of your body ;-).
    Figure 3: Hazard risk analysis based on the Cholesterol and Recurrent Events (CARE) study (n = 4127; Tonelli. 2005)
    In fact, we have broached on another of these imbalances in the context of the effects that were observed with higher magnesium : calcium ratios in drinking water (cf. red box above + "On Short News on July 28, 2012"), before. With phosphor we have yet another "antagonistic partner" of calcium, of which Ritz et al. have only recently argued that its increasing use as a food additive (check out the label of whatever processed food you buy, chances you find a XZY-phosphate on it are >50%) poses a serious health risk. To support their argument, the researchers cite data from a 2005 study by Tonelli et al. that indicates that even serum phosphor levels that are well within the normal range (2.0-4.0mg/dl) were associated with significantly increased CVD risks (cf. figure 3; suggested read: "Does Low Vitamin D Protect Us From Dietary Phoshporus Overload?").

    These are only two selected examples of the available evidence that suggests that we are still totally underestimating the effects of "electrolytes", in general, and their ratios, in particular, on our neurological and metabolic health - and, even worse, doctors, policy makers, experts and gurus keep making mostly unwarranted recommendations to increase our intake of one and decrease the intake of another mineral, when in fact the lack of synergists (e.g. normal amounts of dietary magnesium to complement calcium) and absence or abundance of antagonists (e.g. potassium and magnesium for salt and calcium, magnesium and potassium for phosphorus) are the actual problems we are dealing with.
    Figure 5: Don't forget that there are personal, regional and historical difference in total and relative mineral intakes and never supplement, high amounts of isolated minerals simply because Mr or Mrs average would benefit, without checking how "average" you actually are in terms of your solid, fluid and supplemental mineral intake (data for image based on Crawford. 1971; data on US water hardness according to the Water Research Center)
    Implications: I guess based on all the information on the allegedly complicated interactions between the different minerals, you will by now have realized that statements like "everybody will benefit from taking 300mg of supplemental magnesium" let alone "everybody must take at least 300mg of supplemental magnesium" are about as useful as the constant advice to cut your salt, cut your fat and cut your calories people are confronted with on a daily basis. The chances that person X may benefit are probably high, but they are certainly much lower than the chances that you will survive the sting of a bee - and even that will still kill 53 US citizens per year.

    Individualization, evaluation are therefore obligatory steps which must necessarily come before supplementation, which would - as some of the data in the figure 4 did already suggest - rarely be necessary, if the average inhabitant of the Western hemisphere did not top his sugary, salty and phosphate-laden fast-food diet with beverages that are either devoid of any minerals or will simply exasperate the existing imbalances.

    Too many people (and I believe this is particularly true for the US) seem to have forgotten that we have not always been forced to filter all the minerals out of our water just to make the chlorinate, fluorinated, and "estrogenated" sludge that streams out of the faucet suitable for human consumption. Think of that and the data in figure 5, the next time the as of late often second-guessed recommendation that you got to have "at least X cups of water per day" resurfaces and of how little use each of them is, when it does not contain any of the electrolytes your body needs to handle the water appropriately.
    References:
    • Cogswell ME, Zhang Z, Carriquiry AL, Gunn JP, Kuklina EV, Saydah SH, Yang Q, Moshfegh AJ. Sodium and potassium intakes among US adults: NHANES 2003-2008. Am J Clin Nutr. 2012 Aug 1. 
    • Crawford MD, Gardner MJ, Morris JN. Cardiovascular Disease and the Mineral Content of Drinking Water. Br. Med, Bull. 1971; 27,1: 21-24.
    • Donfrancesco C, Ippolito R, Lo Noce C, Palmieri L, Iacone R, Russo O, Vanuzzo D, Galletti F, Galeone D, Giampaoli S, Strazzullo P. Excess dietary sodium and inadequate potassium intake in Italy: Results of the MINISAL study. Nutr Metab Cardiovasc Dis. 2012 Jul 24.
    • Fulgoni VL 3rd, Keast DR, Bailey RL, Dwyer J. Foods, fortificants, and supplements: Where do Americans get their nutrients? J Nutr. 2011 Oct;141(10):1847-54.
    • Ozawa M, Ninomiya T, Ohara T, Hirakawa Y, Doi Y, Hata J, Uchida K, Shirota T, Kitazono T, Kiyohara Y. Self-Reported Dietary Intake of Potassium, Calcium, and Magnesium and Risk of Dementia in the Japanese: The Hisayama Study. J Am Geriatr Soc. 2012 Aug 2. 
    • Ritz E, Hahn K, Ketteler M, Kuhlmann MK, Mann J. Phosphate additives in food--a health risk. Dtsch Arztebl Int. 2012 Jan;109(4):49-55. Epub 2012 Jan 27. 
    • Shay CM, Van Horn L, Stamler J, Dyer AR, Brown IJ, Chan Q, Miura K, Zhao L, Okuda N, Daviglus ML, Elliott P; for the INTERMAP Research Group. Food and nutrient intakes and their associations with lower BMI in middle-aged US adults:  the International Study of Macro-/Micronutrients and Blood Pressure (INTERMAP). Am J Clin Nutr. 2012 Aug 1. 
    • Tonelli M, Sacks F, Pfeffer M, Gao Z, Curhan G; Cholesterol And Recurrent  Events Trial Investigators. Relation between serum phosphate level and cardiovascular event rate in people with coronary disease. Circulation. 2005 Oct 25;112(17):2627-33. 
    • Water Research Center. Hard Water  Hardness Calcium Magnesium - Water Corrosion Mineral Scale. < http://www.water-research.net/hardness.htm > retrieved Aug 16, 2012.
    • Welch AA, Fransen H, Jenab M, Boutron-Ruault MC, Tumino R, Agnoli C, Ericson U, Johansson I, Ferrari P, Engeset D, Lund E, Lentjes M, Key T, Touvier M, Niravong M, Larrañaga N, Rodríguez L, Ocké MC, Peeters PH, Tjønneland A, Bjerregaard L, Vasilopoulou E, Dilis V, Linseisen J, Nöthlings U, Riboli E, Slimani N, Bingham S. Variation in intakes of calcium, phosphorus, magnesium, iron and potassium in 10 countries in the European Prospective Investigation into Cancer and Nutrition study. Eur J Clin Nutr. 2009 Nov;63 Suppl 4:S101-21.

    Mutant Milk!? New Research Fuels the Flames on Hushed Up Concerns About Ill Health Effects of Homogenized Milk

    Image 1: Wolverine could be the only face of the "Got Milk" campaign who does not have to care about potential negative health effects of homogenized milk.
    In view of the fact that even the Wikipedia article on milk mentions the long-touted hypothesis that the release of the  membrane bound (bovine) xanthine oxidase during the homogenization process and it's potential to generate reactive oxygen specimen could pose a serious health risk, it's quite funny that none of the multitude of papers on the pro- or anti-atheriogenic effects of milk ever mentions mentions the issue of homogenization.

    Now even if we discard the potential negative effects of BXO, the results of a recently published paper from the Center of Specialized Nutrition in the Netherlands would still suggest that milk does at least lose some of it's beneficial health effects in the course of the homogenization process (Oosting. 2012).

    Large and fluffy or small? That does ring a bell, doesn't it? 

    In their experiments the Dutch scientists fed mice infant formulas with either small or large phospholipid coated lipid droplets. Probably to the utmost satisfaction of Danone, the producer of the large lipid droplet formula (Nuturis) and sponsor of the study, the mice who received the regular formula with small lipid droplets were fatter and had compromised lipid and blood glucose levels (see figure 1), as well as pathologically increased leptin levels (not shown in figure 1).

    Figure 1: It may remind you of comparing apples and oranges, but let's be honest, if it were not for the disruption of the large fat globules during the homogenization process, similarly large phospholipids as those Danone plans to unleash onto our children would be present in milk, anyway.
    Irrespective of the funding and product pimping, the results of this study could have major implications that reach way beyond infant formulas and parenteral nutrition. After all, homogenized milk is common used in all sorts of milk based or milk-containing products. It's shelf stable and above all highly standardized and easily processable by the dairy and food industry, who are still spending truckloads of money to find means to further reduce the unwanted clumping that's so characteristic for the naturally occurring large fat molecules most of the end-consumer don't want to float on top of their heated milk either.

    So, if the bovine xanthine oxidase that's released during the homogenization process does not, as Ho & Clifford and other researchers argued in the late 1970s (Ho. 1977), pose a risk for heart disease, what about the structural changes in the lipid fraction of milk? Do we know anything about these at all and could they be the underlying cause of the increase in allergies, diabetes risk that have never been convincingly attributed to milk consumption in general or whole milk consumption in particular? Did we focus to much on the quantity and type of fat in the milk and overlooked its structural organization?

    Though shalt not fix something that ain't broken!

    In a 2007 review of the literature on the potential impact homogenized milk could have on our health, Mikalski discusses exactly this question: What's the physiological consequence of the physical "rupture of fat globules" which occurs during the heating and homogenization process and "creates a new interface" on the membrane of the fat globules so that "other surface active components" (Mikalski. 2007) will more or less randomly adsorb to the remnants and form a new structurally different membrane.
    Figure 2: After the homogenization process took place none of the original functional large fat globules is left, smaller ruptured globules have taken their place and are used by other molecules as a "Trojan horse" (left), distribution of milk fat globule sizes in different types of whole milk - open circles - raw whole milk, full circles - whole milk homogenized at 5MPa, open squares - whole milk homogenized at 10 MPa, full squares - whole milk homogenized at 50MPa (partly adapted from Mikalski. 2007)
    Unfortunately, the #1 compound that will bind to the now the disrupted surface structures of the molecules in the homogenized monster milk are casein micelles (Zahar. 1996). Yep, exactly those molecules, of which some scientists, though most of them discard the hypothesis that homogenized milk is not at least as good for you as regular milk, still speculate that they could be responsible for many if not all of the aforementioned negative health effects of milk (Kohno. 1994; Laugesen. 2003; Tailford. 2003).

    Homogenized, fat reduced zombie milk?

    Figure 3: Distribution of milk lipids in globule core, membrane and skim phase (top, based on Michalski. 2007) and electron micrographs at 15× and 100× augmentations of (A) raw, (B) pasteurised, (C) homogenised–pasteurised, and ultra-high-pressure homogenised milk samples at (D) 100 MPa (Zamora. 2012)
    That the process of homogenization will also affect the normal distribution of tri- and diacylglycerols, which are necessarily released from the core of the ruptured fat molecules (figure 3, top - blue) and modify the intricate phospholipid structure of the membrane (figure 3, top - red) should be as obvious as the fact that those tri- and diacylglycerols, phospholipids, cerebrosides and gangliosides are suddenly part of the skim fraction are easily lost during further processing (such as the removal of fat) and will have different physical attributes, physiological effects, digestive properties and absorption kinetics (cf. Berton. 2012).

    The degree of homogenization increases according to the pressure that's used to force the the hot milk between valve needle and seat of the homogenization machine, so that  the aforementioned effects are particularly pronounced in the high-pressure homogenized milk (also "ultra-homogenized" milk). Accordingly even the last few "unwanted" (by the food industry) larger, intact fat globules that are left in the regular homogenized milk (figure 3, C) break apart.

    What used to be a huge container-like fat molecule in the raw milk (figure 3, A), survived the pasteurization process relatively unharmed (figure 3, B) is now, after it has been pressed with 100MPa through the valve of the homogenization machine, nothing but a heap of very shelf-stable and non-clumping, highly convenient debris (figure 3, D) - awesome, right?
    Bottom line: Aside from the disgusting taste of what we here in Germany call "H-Milch" ("h" as in "haltbar", which denotes the longer shelf-life) the structural changes and the potentially problematic downstream effects of the homogenization process, such as
    Image 2: Assuming that the plastic canister the girl on the right holds in her hands contains homogenized milk, it may in fact be better for the girl on the left, if it was fat free :-o After all, when the homogenized whole milk is further processed into 0.2% = no fat milk ~95% of the previously created mutant fat molecules will be removed ;-)
    • a rise in potentially artherosclerotic free bovine xanthine oxidase, which would otherwise be "locked" in the the intact milk fat globule membrane (MFGM),
    • the formation of new lipid layers from casein and other milk components and milk fat globule membrane fragments with potentially allergenic, and inflammatory properties,
    • a decrease in curd formation / stability, an increase proteolysis and lipolysis (=digestion of the proteins and fats) and the subsequent increase in nutrient absorption and speed in the gastrointestinal tract with its potentially detrimental downstream effects on blood lipids, and
    • the increased absorption of casein molecules and the loss of the beneficial health affects such as the anti-viral, antimicrobial, anabolic and gut protective effects that have been ascribed to the natural MFGM structure of milk
    should be reason enough not to make the most convenient, but the most natural choice - and that irrespective of whether the milk is for a toddler, a child, a teen or an adult... and by the way, the changes the fat molecules in the milk are undergoing and the subsequent "mutant" protein + fat fragment structures they are forming make the otherwise nonsensical advice to use "low" or better "no-fat dairy" actually appear quite sensible.
    Apropos "high fat dairy", did I mention that the "bad high fat cheese" is not just almost always made from regular, non-homogenized milk (which is hard to get, these days, as even the cooled milk is routinely homogenized, so make sure to check the label), but that its consumption is also associated with a decreased risk of developing metabolic syndrome (Høstmark. 2011)? No... well, than that's even more food for thought ;-)
    References
    • Berton A,Rouvellaca S, Robertd B, Rousseaud F, Lopez C. Effect of the size and interface composition of milkfatglobules on their in vitro digestion by the human pancreatic lipase: Native versus homogenized milk fat globules. Food Hydrocolloids. 2012; 29:1, 123–134. 
    • Ho C, Clifford A Bovine milk xanthine oxidase, blood lipids and coronary plaques in rabbits.J Nutr. 1977; 107, 758–766
    • Høstmark AT, Tomten SE. The Oslo health study: cheese intake was negatively associated with the metabolic syndrome. J Am Coll Nutr. 2011 Jun;30(3):182-90.
    • Kohno Y, Honma K, Saito K, Shimojo N, Tsunoo H, Kaminogawa S, Niimi H. Preferential recognition of primary protein structures of alpha-casein by IgG and IgE antibodies of patients with milk allergy. Ann Allergy. 1994 Nov;73(5):419-22.
    • Laugesen M, Elliott R. Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein. N Z Med J. 2003 Jan 24;116(1168):U295.
    • Michalski MC. On the supposed influence of milk homogenization on the risk of CVD, diabetes and allergy. Br J Nutr. 2007 Apr;97(4):598-610.
    • Oosting A, Kegler D, Wopereis HJ, Teller IC, van de Heijning BJ, Verkade HJ, van der Beek EM. Size and Phospholipid Coating of Lipid Droplets in the Diet of Young Mice Modify Body Fat Accumulation in Adulthood. Pediatr Res. 2012 Jul 31.
    • Tailford KA, Berry CL, Thomas AC, Campbell JH. A casein variant in cow's milk is atherogenic. Atherosclerosis. 2003 Sep;170(1):13-9.
    • Zahar M, Smith D- Adsorption of proteins at the lipid-serum interface in milk systems with various lipids. Int Dairy J. 1996: 6, 697–708.
    • Zamora A, Ferragut V, Guamis B, Trujillo AJ. Corresponding author contact informationChanges in the surface protein of the fat globules during ultra-high pressure homogenisation and conventional treatments of milk. Food Hydrocolloids. 2012; 21:1, 135–143.

    Up To 180% Increase in Testosterone w/ Taurine? Androgen Boost Just One of the "Side Effects" of Cysteine Derivative That Won't Benefit (Pre-)Diabetic Baby-Boomers, Only

    Image 1: No, taurine is not made from the sperm of Belgian Blues and no it won't make you look like one overnight, either ;-)
    After yesterday's allegedly pretty complicated post on the fallacious ups and downs in body weight from repetitive dieting and episodes of overeating, I decided it was about time to readdress one of your all-time favorites: supplemental testosterone boosting. Instead of the next best herb from the Brazilian jungle that has a "history as a potent aphrodisiac in traditional medice" or the shrub that can be found "only in a specific region of the remote [... insert whatever your marketing guy believes would increase sales here]", I decided to take another look at one of the established readily available and dirt cheap ways to give your natural androgen production, fertility, fatty acid and glucose metabolism a leg - taurine, or 2-aminoethanesulfonic acid (which is, by the way, not produced from bull semen, although its name, which has the greek word "tavros", or ταύρος for the wanna-be intellectuals out there, would suggest ;-)

    Taurine doubles testosterone production in diabetic rats

    The reason I am addressing this again is the recent publication of a study on the beneficial effects of supplemental taurine, administered at a dose of 500mg/kg (human equivalent: 80mg/kg, or 3-4g /day) on the following diabetes related ailments:
    What's up with intraperitoneal administered drugs? When something is injected into the peritoneal cavity the cannot vomit whatever scientists would otherwise have to stuff down their pieholes or inject into their tiny veins back up. Unfortunately the bioavailability is usually higher than via the oral route with the differences varying profoundly between compounds. Melatonin, for example, has a bioavailability of 54% when administered orally and 74% for i.p. injections (based on 10mg/kg dose; cf. Yeleswaram. 1997).

    • wasting (loss of body weight),
    • testicular damage,
    • defect spermatogenesis,
    • systemic oxidative damage,
    • DNA damage,
    • loss of natural antioxidant defense,
    • low testosterone
    in six-week-old male wistar rats. As the data in figure 1 goes to show, the non-essential amino acid, both humans and rodents (not so cats) can produce from dietary cysteine, was administered (as it is common practice in rodent studies) not orally, but via the peritoneal cavity had profound effects specially with regard to the oxidative damage and restoration of the natural antioxidant defense system.
    Figure 1: Relative Body, testicular and epididymal weight (left); relative testicular & serum MDA, testicular catalase, serum testosterone and DNA damage (middle) and testicular damage (tissue samples) and Johnson score for spermatogenesis (right); all data except Johnson scores expressed relative to control (calculated based on Tsounapi. 2012)
    Yet despite the fact that the serum malondialdehyde (CH2(CHO)2, marker of oxidative damage) decreased from 185% in the streptozotocin treated and consequently diabetic animals to 92% in the animals who received 500mg/kg of taurine for 4 weeks after the streptozotocin injection (50mg/kg intraperitoneally) and were thus lower than in the healthy control animals, the 7.5x increas in blood glucose which was not ameliorated by taurine was obviously too much for the testosterone levels to return into the normal range.

    The average American is likely to benefit, as well

    Figure 2 (Shin. 2012): Adjusted mean values of total testosterone according to fasting plasma glucose (FPG) - Q1 (65 - 88 mg/dL), Q2 (88 - 94 mg/dL), Q3 (94 mg/dL - 100 mg/dL), and Q4 (100 - 126 mg/dL; prediabetic according to American Diabetes Association)
    With a 2x increase over the diabetic group the testosterone boosting effect in the Tsounapi study was yet still highly significant and could, in view of the results of Shin et al. who found that even high-normal (fasting blood-glucose levels ≥ 88 mg/dL) were associated with a decrease in testosterone levels in prediabetic and non-diabetic men (Shin. 2012; ,cf. figure 2), help one or another of the men among the estimated >79,000,000 American adults aged 20 years who are prediabetic (CDC. 2010) to bump their -25% reduced testosterone levels back into the normal range.

    Adequate dosages are probably higher for diabetics

    That would obviously require adequate dosing schemes which would, according to the Tsounapi study range from ~3-5g and are thus more than twice as high as the 1.5g /day Brøns et al. administered to overweight men with a genetic predisposition for type II diabetes mellitus without seeing the expected outcomes in terms of increased insulin sensitivity and glucose tolerance (Brøns. 2004). Especially in diabetics, whose ability to absorb taurine is decreased (-32%), while the amount of taurine they excrete is increased (+35%; cf. Merheb. 2007), dosages in the 5g+ range (like 3x2g per day with meals) could be very well indicated - not least because the previously calculated human equivalent dose did not account for the increased bioavailability from intraperitoneally injected vs. orally ingested taurine.

    Taurine, women, pregnancy and healthy children

    Likewise, low(-ered) serum levels of taurine have been identified as a correlate of gestational diabetes by Seghieri et al. According the researchers from Italy,
    [...] plasma taurine was inversely related to previous gestational area-under-curve of glucose and directly related to post-gestational CP/glucose [CP: C-reactive protein, important marker of inflammation and correlate of cardiovascular disease and other ailments], as well to CP/glucose measured during pregnancy (p<0.05 for both). [Moreover, the] relative risk of altered glucose metabolism during previous pregnancies [impaired glucose tolerance and gestational diabetes] was higher as plasma taurine decreased, even after adjusting for age, time-lag from pregnancy, body mass index and family history of diabetes (OR: 0.980; CI 95%: 0.963-0.999, p=0.003)
    Thus taurine is by no means a "man's amino acid" - despite the fact that its concentration is particularly high in "manly" foods, such as fish and meat. In this context, the results of Kim et al. appear noteworthy, as well.

    Taurine an essential component of breast milk

    Taurine has a whole host of additional beneficial effects related to the prevention of comorbidities of diabetes (Ito. 2012):
    • diabetic nephropathy
    • diabetic retinopathy
    • diabetic neuropathy
    • diabetic cardiomyopathy
    The Korean researchers found that the taurine content (obviously a vitally important nutrient for infants, as well) is profoundly decreased in the breast milk even of lacto-ovovegetarian mothers, compared to their non-vegetarian counterparts (31.0-54.4 mg/L vs. 19.1-52.3 mg/L; Kim. 1996). That this could be a substantial risk factor for
    • diabetes, insulitis and pancreatic dysfunction (Arany. 2004)
    • cardiovascular disease (Kulthinee. 2010)
    • distortions of the renin-angiotensin system (Thaeomor. 2010)
    • high blood pressure (Roysommuti. 2009)
    • kidney problems (Roysommuti. 2010)
    and all sorts of downstream complications, regardless of the obesity / glucose tolerance of the mother, is supported by a whole host of studies (see references above); and novel papers on related benefits appear on an almost monthly basis.

    You don't have to be (pre-)diabetic, on the SAD diet or pregnant to benefit

    Despite the fact that (pre-)diabetics, women in childbearing age and the notorious "average American" on his "standard American diet" (mostly this is identical to being prediabetic, as the previously cited data from the CDC goes to show; cf. CFC. 2010) already cover the majority of average Joes and Janes in the Westernized (or should I say super-sized?) world, this would not be the SuppVersity if today's post would not also have some merit for physical culturists.
    Image 2: Those of you who listened to my dissertations in Episode III of the Amino Acids for Super Humans series on Super Human Radio, back in the day, will remember: Taurine ain't for obese pre-diabetics, only ;-)
    Now, those of you who have been around for a while will probably remember the series of shows I did with my friend Carl Lanore, host, head, heart and soul of the Super Human Radio Network, on "Amino Acids for Super Humans" - and maybe, some of you have even read all the shownotes and will thus remember a study I mentioned both on the air, as well as in detailed notes on Episode III of the Amino Acids for Super Humans series.

    T for T: Taurine for testosterone for athletes and beyond

    The study I am talking about was conducted by Yang et al. in 2009 and compared the effects of taurine supplementation on male reproduction in rats of different ages. With ~1% taurine at a water the rodents received, which would be (assuming an average weight & water consumption) be equivalent to ~15g for an adult human being - or 3x5g per day (Note: I am emphasizing the split dosages for two reasons: (1) I think it is a mistake not to consider the intricacies of supplementation and chronic low dose vs. bolus does make a huge difference with other supplements, e.g. "Never(!) Sip Your Whey, If You Want to Kickstart Protein Synthesis", and (2) taurine is somewhat harsh on the stomach and taking 15g in one sitting is almost guaranteed to make you sprint to the toilette within no time ;-)
    Figure 3: Serum testosterone levels (in mIU/ml) after 22 (baby) and 30 days (adult and aged rats) treatment with or without 1% taurine in drinking water (adapted from Yang. 2009)
    As the data I have compiled in figure 3 goes to show, the chronic taurine administration lead to statistically significant increases in serum testosterone levels in rodents from all three age groups, i.e. baby rats (born to mothers who consumed the taurine enriched / control water during pregnancy), 10-week old adult rats, and 72-week old aged. Notwithstanding, the +46% increase in testosterone in the old rats, is probably still the most significant change as it would effectively restore the "old agers" testosterone levels to youthful heights, a change, the real-world significance of which cannot be underestimated in view of the effects "low" (as in "low" in lab standards, not as in low in bro-standards!) testosterone levels can have on your body composition as discussed in one of the installments of the "Intermittent Thoughts on Building Muscle" (specifically "Quantifying the Big T" > figure 2).

    Image 3: Believe it or not, eggs contain sulfur and the raw materials to make taurine, but no taurine (cf. Zhao. 1998)
    In conjunction with the improved antioxidant activity (SOD, ACP, GSH were all elevated), reduced oxidative damage and markers of muscle and liver damage, AST and ALT, as well as lipid oxidation, MDA, were all significantly reduced) and the increased expression of nitric oxide synthase and subsequent raise in nitric oxide production - by the way, the only parameter with statistical significance p<0.05 only in aged rats- it stands to reason that even people who have already found their way to physical culture are very likely to benefit from one or another gram of supplemental taurine. This is all the more true in view of the fact that even high taurine foods such as crustaceans and mollusks (300-800mg/kg), Albacore tuna (176mg/100g), lamb (110mg/100g), cod (108mg/100g), mackerel (78mg/100g), beef (77mg/100g), wild salmon (60mg/100g) and pork (40mg/100g) contain too little to get anywhere close to where the magic happens.
    Implications: I guess based on the previous discussion it should be clear that of the numerous supplements that are marketed to gymrats and health-enthusiasts, alike, taurine unquestionably is one of the most promising ones (suggested dose non-diabetics start with 3x2g or 2x3g /day). Moreover, with the focus of today's post being on testosterone and glucose metabolism, I did not even mention all the proven and purported benefits of taurine, such as its ability to...
    • keep exercise induced oxidative stress at bay (Zhang. 2004; Silva. 2011)
    • prevent fructose induced hypertension (Rahman. 2011)
    • facilitate cell hydration (Lang. 2012)
    • increase skeletal muscle force production (EMS test, Goodman. 2009)
    • preserve function and exercise capacity in skeletal and heart muscle (Ito. 2010)
    • enhance the anorexic effects of insulin in the hyptohalamus (Solon .2012)
    • maintain the lipolytic activity in fat cells (Piña-Zentella. 2012)
    • increase fat oxidation while cycling (Rutherford. 2012; dosage 1.5g pre)
    • counter the obesogenic effects of MSG (Nardelli. 2012 + more on MSG & obesity)
    • increase stomach acid (Huang. 2011)
    ... and the list goes on and on and should theoretically be extended to all the benefits of TUDCA, I have written about only recently (cf. "Tauroursodeoxycholic Acid (TUDCA) - Research Overview"), because unless you don't have enough taurine all the cholesterol and bile in the world won't help your body to conjugate UDCA to taurine and make TUDCA from it ;-)

    A word of caution
    :
    Since I know that you are just about to order a couple of bounds of taurine from your favorite bulk supplier, let me briefly mention a not-yet fully elucidated potential downside to excessive taurine supplementation (5g/day in divided doses does not seem to be a problem, though), which relates to its ability to act as a neurotransmitter in the brain: While Louzuda et al. point out that this can be an advantage and would render taurine a potential candidate for the treatment of Alzheimer's and other neurological disorders (Louzada. 2004), it's interactions with the GABA receptor in the brain and peripheral tissues (Hanretta. 1987; Albrecht. 2005; Jia. 2008) may be a problem for people with anxiety issues - whether it exerts anti- or pro-anxiety effects, is yet still a matter of constant debate and I am not even sure how reliable the rodent models are, by the means of which Chen et al., Kong et al. and Zhang et al. (Chen. 2004; Kong. 2006; Zhang. 2007) demonstrated anti-anxiety effects, El Idrissi et al. observed anti-anxiety effects after injection and pro-anxiety effect after chronic supplementation (El Idrissi. 2009), and Whirley et al. observed only "subtle" if not non-existant effects (Whirley. 2008).
    References:
    • Albrecht J, Schousboe A. Taurine interaction with neurotransmitter receptors in the CNS: an update. Neurochem Res. 2005 Dec;30(12):1615-21. Review. 
    • Arany E, Strutt B, Romanus P, Remacle C, Reusens B, Hill DJ. Taurine supplement in early life altered islet morphology, decreased insulitis and delayed the onset of diabetes in non-obese diabetic mice. Diabetologia. 2004
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