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?

"Milk Kills," Study Says and Everyone is Afraid. Is This More Than Fearmongering Bullsh*t? Methodological Issues & Conflicting Evidence Would Suggest the Answer is "No!"

After reading this article you won't have to be afraid of milk any longer.

The editor of the British Medical Journal (BMJ) will be rubbing his / her hands. The paper by Karl Michaëlsson et al. (2014) that was published earlier this week, made it to the mainstream news in the US and Europe and did - at least at first sight - reflect well on his or her magazine. "The British Medical Journal saves you from intoxicating yourself with milk!" - That's great, right?

Well, in today's SuppVersity article, I am going to take a closer look at how "great" it actually is that studies like this hit the mainstream media, while less exciting, because beneficial studies on milk are not being mentioned at all ... unless, of course, it's the morally superior and allegedly healthier soy milk we are talking about *sarcastic laughter*

You can learn more about dairy at the SuppVersity

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Is There Sth. Like a Dairy Weight Loss Miracle?

There is Good A2 and Bad A1 Dairy, True or False?

Lactulose For Your Gut & Overall Health

Is There a "Fat Advantage" for Dairy Lovers

Dairy, Diabetes, Estrogen, IGF-1, Cancer & More

Before we get to a detailed analysis of the analysis, let's briefly remind ourselves of the type of data we are dealing with. Data from the Swedish Mammography Cohort (all female subjects) and Cohort of Swedish Men (all male subjects) that was complemented by data from food questionnaire that were send out back in the late nineteen eighties (women) and -nineties (men) along with the invitation to participate in the respective cohort studies.

Figure 1: Flow chart of the study sample (Michaëlsson. 2014).

As you can see in Figure 1 we are dealing with a hell lot of data. Data of which we still should not forget that it is based on data of which Thompson, et al. were able to show that it has an accuracy of 45-52%, specifically for dairy products (Thompson. 2002).

Now, in the study by Thompson the subjects were asked about what they ate in the last 30 days. The data in the study at hand, however, is based on what subjects said about how often they drank milk in the past 365 days! A fact that is not likely to make the data any more accurate.

Furthermore, I assume that all of you will have heard of people who change their dietary habits over time, right? Well, for Michaëlsson et al. this is obviously news. Otherwise they would not have relied exclusively data that was gathered, when the subjects were enlisted for the cohort study in the late 1980s / 1990s, when they were trying to identify the reason that 15,541 of the men and women died over the course of the 10-20 year follow-up.
Speaking of 20 years. That's the time that passed between being enlisted and speculating about their daily food intake when the 90 303 women aged 39-74 were enlisted in the Swedish Mammography Cohort and the 31st of December 2010, which was used as an end point for the analysis.

Figure 2: Mortality raters (raw data) according to milk intake in glasses / grams (Michaëlsson. 2014).

Malicious gossip would now probably have it that the additional 10 year gap, i.e. 10 more years to start eating completely differently, alone, could explain why we see a significant negative effect of drinking milk in the female, but not the male participants, for whom the interlude between the food frequency questionnaire and the end point of the study was ~50% smaller.

Figure 3: Adjusted predictions of urine 8-iso-PGF2α, a marker of oxidative stress, in 892 women (based on cross sectional data, mean age 70 years) and 700 men (Michaëlsson. 2014).

A similar criticism can be brought forward with respect to the allegedly "objective" measurements of 8-iso-PGF2α, a marker of oxidative stress, that was assessed in only 892 women (based on cross sectional data, mean age 70 years) and only 700 men, i.e. 1.4% of the female and 1.5% of the male participants, where the "trend" towards increased inflammation reached - once gain! - significance only in the female study participants (see Figure 3).

Homogenization may in fact be a problem. You find that's bogus? There is evidence that suggests that homogenization, not pasteurization is a serious problem | more.

What do commenters say? If you take a closer look at the hitherto published comments (retrieved on October 31, 2015) on the BMJ website, you will find commenters mentioning (1) the obvious association between having too little calcium <> fractures and the desire to increase ones calcium intake by drinking more milk (Kerr, J. Prof. of Epidemiology in Columbia), (2) the absence (or as Rom R. Hill from the Newcastle University says "significant omission") of a clear distinction between raw and pasteurized milk and low fat and full fat milk that makes the study, in Kerr's eyes, more or less meaningless, (3) last but not least, an unknown commenter mentions the issue of hormone, antibiotics and analgesic abuse in modern milk production and highlights that somatotropin (rBST) was still allowed in the EU, when the data from the study was collected. In view of the fact that rBST can affect hormonal and metabolic growth factors including human serum insulin-like growth factors (IGF), this could be another reason specifically for an increase in cancer related mortality (Allen. 2002; WHO. 2006).

Learn more about dairy from Liz in a previous SuppVersity article, i.e. "Dairy - The Good, Bad or Ugly?"

Moreover, the hazard ratios you read of in the news may have been adjusted, but the question remains, whether the adjustment could correctly make up for the fact that men and/or women who consumed more milk, ...

1. consumed significantly more energy on a daily basis (39% more in women, 24% more in men),
2. consumed significantly more saturated (36% more in women) and total fat, and
3. were significantly less likely to use bone building calcium supplements (15 % less in women).

Of these three factors (1) + (2) could explain the increased mortality and cancer risk in women and (3) could explain why women, but not men have a higher risk of hip, but not general bone fracture (hypothetically!).

My recommendation: Don't overrate the results of the study at hand. It has truckloads of methodological shortcomings, a tinge of the hysterical attention grabbing sensationalism and, most importantly, it stand in stark contrast to previous results which indicate that...

Figure 4: If you look at all the evidence, you will see that milk is more likely to protect than to kill you (Elwood. 2008; Bonthuis. 2010; Goldbohm. 2011)

• a high intake of milk is associated with a 16% reduced risk of cardiovascular disease and an 8% reduced risk of diabetes, two of the most important health issues that will have you pass away years, if not decades before your time (Elwood. 2008 | meta-analysis of 15 pertinent studies),
• Australians with a high fat milk intake of of 339g/day or more have a 69% reduced risk of dying from cardiovascular disease than their peers (Bonthuis. 2010),
• Dutch full-fat dairy connoisseurs have a 1% reduced all-cause mortality risk for each 10g of full fat dairy consumption per day (Goldbohm. 2011).

And in spite of the fact that several other studies find no beneficial effects of milk consumption of CVD or all-cause mortality (e.g. non-significant -23% in partly adjusted model in the Whitehall II study), it appears very unlikely that "milk kills". That this statement makes appalling headlines and will get a lot of clicks on the Internet, on the other hand, stands out of question | Read the whole paper for free @ the BMJ Website make up your mind and tell me on Facebook what you think.

References:

• Allen, Naomi E., et al. "The associations of diet with serum insulin-like growth factor I and its main binding proteins in 292 women meat-eaters, vegetarians, and vegans." Cancer Epidemiology Biomarkers & Prevention 11.11 (2002): 1441-1448.
• Bonthuis, M., et al. "Dairy consumption and patterns of mortality of Australian adults." European journal of clinical nutrition 64.6 (2010): 569-577.
• Elwood, Peter C., et al. "The survival advantage of milk and dairy consumption: an overview of evidence from cohort studies of vascular diseases, diabetes and cancer." Journal of the American College of Nutrition 27.6 (2008): 723S-734S.
• Goldbohm, R. Alexandra, et al. "Dairy consumption and 10-y total and cardiovascular mortality: a prospective cohort study in the Netherlands." The American journal of clinical nutrition (2011): ajcn-000430.
• Michaëlsson, Karl, et al. "Milk intake and risk of mortality and fractures in women and men: cohort studies." BMJ 349 (2014): g6015.
• Thompson, Frances E., et al. "Cognitive research enhances accuracy of food frequency questionnaire reports: results of an experimental validation study." Journal of the American Dietetic Association 102.2 (2002): 212-225.
• WHO Expert Committee on Food Additives. "Toxicological evaluation of certain veterinary drug residues in food/prepared by the sixty-sixth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JEFCA)." (2006).

1g of Vitamin K2 (MK-4) Could Boost Your Testosterone Levels by More Than +50% - At Least, This is What the Results of a Recent Rodent Study Would Suggest.

Image 1: Who would have thought that this piece of goose liver pate contains a natural test-booster? Unfortunately even this SuperFood won't give you your 1g /day.

Can you imagine how it must feel to be the shrinking violet in a family of nutritional saviours? Where your brothers C, E, not to mention the rising superstar D, get all the attention and you are treated just like another letter in the vitamin ABC? Well, I guess you don't ... but if vitamins had feelings, menaquinone, also known as Vitamin K2, certainly would ;-) After all, even many supplement junkies know it only as "that strange co-factor of vitamin D. In part this may even be my fault. After all, I have discarded all the previous studies on its beneficial effects on heart health (Galeijnse. 2004), bone formation (Yamaguchi. 2001) and resorption (Yamaguchi. 2003) and so-on and so-forth, as not "sexy" enough to make it into the SuppVersity news. The results of a recent study, by Asagi Ito et al. (Asagi. 2011), on the other hand, are sexy, there is no doubt about it ;-)

Image 2: Don't be fooled by the soy industry - there is exactly ZERO MK4 in Natto! You will have to resort to "real" foods if you want some MK-4 in your diet - cf. figure 4, below; unfortunately even goose liver, the dietary source with the greatest amount of menaquinone (MK4) won't give you enough to see results.

Did you know that there are thousands of forms of "vitamin K"? The major ones are yet phylloquinone, also known as vitamin K1, which is abundant in all sorts of green vegetables (>200g/100g), has a pretty low bioavailability of <10% and is important for normal blood coagulation aside, and a certain form of menaquinone that has been labeled MK-4. Only recently have scientists discovered that the latter is  synthesized from phylloquinone or menanquinones with longer side-chains in certain mammalian tissues (Suttie. 2011). This ability to produce MK-4 from dietary substrates and the high MK-4 content in human brains and reproductive organs speaks for the importance of this hitherto largely overlooked "vitamin" (in the strict sense it is no vitamin if your body can produce it on its own).

The Japanese scientists treated a group of Male Wistar rats on a standard diet with 75mg/kg body weight of vitamin K2 (menaquinone-4; human equivalent 12mg/kg, 972mg for an 80kg adult) for 5 weeks and measured their plasma and testes levels of testosterone... and the results, were "sexy", as you can see in figure 1 ;-)

Figure 1: Serum testosterone levels (in ng/dl) in male Wistar rats in the course of five weeks on 75mg/kg MK4 vs. control (data adapted from Asagi. 2011)

As the data goes to show there was - despite the usual diurnal ups-and-downs a clear trend towards increased serum testosterone levels in the MK-4 group - on average, +56% more testosterone from weeks 1-5 in the MK4 group. And a whopping +70% at the end of the study period. An even greater increase of +88% was seen in the tissue concentration of testosterone within the testes. The latter went hand in hand with a profound enrichment in vitamin K2 content in the reproductive organs, as well as in the livers of the MK4-supplemented animals (no, I did not make a mistake, there really was almost no MK4 in the livers of unsupplemented animals, cf. figure 2).

Figure 2: MK4 levels (pmol/g tissue) in liver and testes of rats after 5 weeks on 75mg/kg supplemental menaquinone-4 (data adapted from Asagi. 2011)

Interestingly, these profound increases in testosterone production were not mediated by changes in luteinizing hormone concentration.

From the rat model to the petri-dish: Exploring the underlying mechanism

In in-vitro studies, the scientists also found that vitamin K1 was without effect on testicular I-10 cells, and that Warfarine, a pharmacological anticoagulant did not suppress the dose-depend (cf. figure 3) testosterone boosting effects of MK4 on a cellular level.

Figure 3: Relative increase in testosterone production of testicular I-10 cells after 24h of incubation with different amounts of MK4 (data calculated based on Asagi. 2011)

The most likely explanation, according to Asagi et al., for the profound effects MK4 has on the output (its like an after-burner for your testes ;-) of testosterone would be c-AMP mediated, as

treatment of I-10 cells with MK-4 in the presence of db-cAMP was found to significantly enhance testosterone secretion into the cul-ture medium, and the maximum enhancement of secretion was observed when 30μM MK-4 was present in the medium.

That being said, I bet your next question is "where can I get that stuff"? Well, the most obvious answer would be: At the supplement vendor of your choice, which is basically where the scientists got their MK-4 (Nisshin Pharma Inc.), as well.

Figure 4: MK4-content (µg/100g) of the only significant (~10µg/100g or more) dietary sources of MK4 (data based on Schurgers. 2000)

If you look at the only "reasonable" (i.e. foodstuff with 10µg or more MK-4 per 100g) dietary MK-4 sources I have compiled for you in figure 4, you will probably also understand, why the rats had almost ZERO MK-4 in their livers and MK-4 was not even detectable in the serum of the 6 healthy male volunteers whose serum Schurgers and Vermeers as part of their analysis of the plasma vitamin K response to different foodstuff (Schurgers. 2000). Since the scientists focused on K1 and MK-7 (the "Natto-K2") the rest of their results, i.e. everything but their analysis of 13 types of meat, 6 types of fish, 9 types of fruits and vegetables, 10 types of dairy, egg products, oils, breads, and beverages (the only relevant sources are listed in figure 4) are unfortunately useless for us.... anyway, if you want to build some muscle, you better go now and enjoy a few kilo of the good old goose liver paste, although even that would not give you the 1g "human equivalent" of the 75mg/kg the rats in the study received.

Mercury, From Fish to Toenail; Less Testosterone Needed W/ TRT + Tongkat Ali; R,R-Monatin the Next Stevia From South Africa! Plus: Magnesium Protects Mitochondria from LPS & Caffeine Arteries from HIIT Induced Platelet Activity!

Image 1: Looks like the Terminator was concerned about "bone" health, maybe he should consider Tonkgat ali as an addition to his TRT... or whatever regimen;-)

If you want to, you can call today's news a special installment of "On Short Notice", I have already had a couple of interesting news and before I am piling up another truckload, I thought I could make at least some of you happy and put a handful of them out before the Super Human Radio & SuppVersity Science Round-Up on Thursday (you better make time to listen live, Thursday, 12PM/EST and download the first installment if you haven't done so, already ;-) and the "official" Saturdaily installment of "On Short Notice", here at the SuppVersity.

So let's see what we have here: Contrary to the order in the headline we will check out your toenails later, after all, I don't know what they look like and don't want to kill your appetite so that you cannot fully appreciate the findings of Fry et al. who discuss the potential application of an extract from the bark of Sclerochiton ilicifolius A.Meeuse as an all natural sweetener that's probably at least as, if not sweeter than stevia and - you guessed it - 100% calorie free! The same, i.e. being calorie free is obviously true for magnesium aspartate... whatever, in view of its potent protective effects against lipopolysaccharide induced mitochondrial damage and decay, you should not care about that, anyways.  And despite the fact that I would hope that the same goes for the minor pro-thrombotic effects of interval training, there may be one or another of the SuppVersity readers who's having issues with platelet activity already and will therefore be relieved to hear that a cup of coffee before your workout will not increase, but rather decrease the risk of thrombosis in response to the post-exercise increase in platelet activity.

You don't want to miss this week's installment of the joint Super Human Radio + SuppVersity
Science News Roundup - the show airs each Thursday, 12PM/EST (tune in live!)

The latter, i.e. the risk of thrombosis would by the way be even higher, if you were one of Xun et al.'s study participants who consumes one or more servings of fish per day. This would place you at greater risk of having high toenail mercury levels and with those being representative of whole body and tissue mercury levels you would already have higher baseline platelet activity than Mr. or Mrs. Healthy Average Joe, which would probably be a reason for your doctor to tell you that he cannot, by any means, put you on TRT (testosterone replacement therapy) - and that even if you were about as hypogonadal as the castrated rats in the Saadiah Abdul Razak study from the latest issue of Evidence Based Complementary Medicine. A study by the way you could print, show it to your doctor and say: "Look, I don't want to lose my muscle and break my bone, so let's do this you give me a script for low dose TRT and I get myself some quality Eurycoma longifolia extract and we will see how my values look like in 6 weeks from now." 

You see, as usual, even doctors can learn something, here at the SuppVersity so let's not put them on the rack for another paragraph or two and start right with our first item for today:

• 

  Image 2: Could the bark of these twigs from a spiny-leafed, hardwood shrub from South Africa hold a likewise natural stevia alternative?

  Is R,R-Monatin the new stevia? I know you all love your stevia, but there are people who simply hate the taste and still don't want to resort to any of the dubious sugar alcohols let alone the 100% artificial sweeteners, who may be interested that John C. Fry and a couple of other researchers published ad paper on a novel all natural sweetener from the bark of a South African spiny-leafed, hardwood shrub that goes by the name of  Sclerochiton ilicifolius A.Meeuse (Fry. 2012).
  According to the Fry et al., the compound has a potency above 3000 at 5% sucrose equivalent, which would make it (theoretically) even sweeter than stevia. Since the latter hit the market, we do yet all know how unrealiable these theoretical values are so that we will probably have to wait until the first monatin-based sweeteners become available - and you as a SuppVersity would be the first to know what's in there ;-)
  If we assume that there are no hitherto undisclosed health issues with monatin and it does in fact taste sweet and not disgusting, metallic or whatever, it is also likely that we are going to see new "proprietary" blends of stevia + monatin, similar to their artificial counterparts you still see in Coke Zero & Co - the quasi "natural" way to get as close as possible to the "true sugar taste", people are still craving, these days... if they don't hurry, I do yet doubt that there will be a market for products like that very long, as we are more or less trained to crave the "real sugar" taste, but this would be the topic for another blogpost ;-)

• 

  Figure 1: Effect of different doses of pre-supplementation with magnesium aspartate on markers of LPS induced mitochondrial decay, antioxidant activity and oxidative damage (data calculated based on Ahmed. 2012)

  250mg/day magnesium counter the metabolic derangements from lipopolysaccharide (LPS) intoxication When Lamiaa A. Ahmed added 20mg/kg or 40mg/kg (~125mg or 250mg in human equivalents) of magnesium aspartate to the chow mice that were pretreated with LPS injections, the researcher from the Faculty of Pharmacy at the University of Cairo found that this regimen restored body temperature (low dose) and heart rate (high dose) of the profoundly inflamed to normal, restored the lowered glutathione levels (both doses) and reduced (low dose) and normalized (high dose) the elevated creatine kinase (marker of cell damage) and thiobarbituric acid reactive substances (TBARS; marker of oxidative damage) levels that had been elevated by the lipopolysaccharide treatment (Ahmed. 2012).
  The ATP:ADP ratio, the activity of the sodium potassium pumps and the creatine phosphate levels (CrPh protects the cell wall from damage as you remember from a previous installment, right?) were not completely restored to, but the pathological changes were minimized dose-dependently. In conjunction with the normalization of the lactate to pyruvate ratio, a sign of either exertional exercise or - if it occurs at rest, as it does here - mitochondrial failure, these observations indicate that Mg therapy could be a reliable protective agent in LPS-induced cardio- and general myotoxicity. In that it should be noted that higher, but not exorbitantly high (250mg is roughly 2/3 of what you should aim to get from our diet everyday, anyway) doses were more effective in reducing cell membrane damage as well as in improving the intracellular acidosis, energy production, oxidative stress and Na+,K+-ATPase activity and corresponded with a better perseverance of the mitochondrial ultrastructure.
  And while Ahmed sees the main application of Mg aspartate therapy in "critically ill" patients, I would say that the large group of patients (and non-patients) with other pathologies such as a leaky gut would benefit as well, since the defective gut barrier opens the door for the "excrements" of your gut bacteria, to induce all sorts of pathologies including mitochondrial damage and decay, but also depression, obesity, diabetes, etc. (Maes. 2008; Musso. 2010)... and before I forget to mention it is not unlikely that cheap magnesium citrate (if tolerated) would do the job just as well - maybe in a slightly higher dosage of say 300mg per day (best taken in divided doses with food).

• 

  Image 3: Coffee is full of wonders ;-)

  Antithrombotic effects of caffeine blunt platelet activity in response to interval training The use of 3mg/kg (equiv. to ~1 large cup of strong coffee or 2 smaller cups of regular coffee) of caffeine as an ergogenic aid during aerobic interval training cannot just improve your performance, it will also prevent the pro-thrombotic platelet function activation that occurs during exercise. That's the somewhat surprising finding of the one of the latest studies from the Health Innovations Research Institute at the School of Medical Sciences on the campus of the RMIT University in Melbourne, Australia (Whittaker. 2012).
  Whether this effect is of any importance to you certainly depends on your personal health. Personally, I would say that it is negligible for the vast majority of people who engage in strenuous athletic activities, if you belong to a risk group where platelet function is either high (risk of developing thromboses) or low (risk of bleeding) you may want to keep these results in mind.
  And if you don't care about platelet function, you may be considering to have another cup of coffee, when I tell you that ~3 cups per day appear to offer some protection against skin cancer, parkinson's and non-alcoholic-fatty-liver disease (click on the links to read the full stories on the SuppVersity Facebook Wall).

• 

  Image 4: Remember last week's post on the mercury in fish and how it's not simply excreted with the selenium, let alone the cysteine it's bound to? It looks like the toenails of young Americans would confirm those lab results.

  Something fishy about toenail mercury levels I guess all of you will remember my "shocking" post about the mercury toxicity from fish (cf. "Mercury in Fish NOT Harmless, Regardless of Cysteine, Selenium, EPA or DHA!"), this one could actually go as sort of a follow up post, as it deals with the real-world consequences of mercury exposure and the subsequent deposition of the heavy metal in the toe nails of the 4,344 American male and female participants (age 20–32y) in the CARDIA Trace Element Study researchers from the Gillings School of Global Public Health and School of Medicine at the University of North Carolina have recently examined (Xun. 2012).
  I know, it may sound gross, but toenails have, among the various biological specimens you could theoretically analyze, the advantage of providing a relatively reliable long-term measure of Hg exposure (from a few months to a year), are easily collected, transported,stored, and cleaned and are relatively sheltered from environmental contaminants and less likely to be contaminated by shampoo, hair treatments, and medication (Morris. 1983, He 2011).

  

  Image 5: Who would have thought that your toenails provide a way better measure of the toxic load you have accumulated than your hair, for example? Just looking at them is yet not enough for a thorough analysis

  Since the Hg levels in toenails also have relatively high correlation with both mercury intake (r = 0.54; Ohno. 2007) and the mercury deposition in critical organs (spec. in the brain - r = 0.65 ; Bjorkman. 2007), it should be obvious that the association between toe nail mercury levels and fish intake in all, but those participants who lived in Oakland and had the lowest (0.45 servings per day) fish intake per day could have a significant impact on the health of the subjects that consume more than one serving of fish per day and have a 76% higher beta coefficient of the natural logarithm of toenail Hg level than those who consume fish / seafood less than once per day (this mean that the mercury in the toenails of daily fish eaters increases 75% more rapidly towards that level than in those who eat 0.35 to 1.03 servings). Interestingly this was particularly true for the Caucasian men in the study, where the beta coefficient was another 45% higher (beta = 0.64 vs. beta = 0.44).
  Despite the fact that these results seem to confirm that eating one dose of untested canned tuna (which would probably go as way more than one serving in the eyes of the scientists) is not necessarily the best idea. It does however not mean that you cannot have you once or even twice a weak salmon steak or sushi - just keep your diet more versatile and don't make fish (or any other single foodstuff your only "allowed" source of protein or fat.

• 

  Figure 2: Weight of castrated rats on TRT, TRT (50% dose) + Eurycoma longifolia  (EL) or Eurycoma longifolia, alone, at the end of the 6-week supplementation phase, ratio of bone building osteocalcin to CRX a marker of bone resorption and actual bone strength, as measure by maximal tolerable load and Young's Modulus; all data expressed relative to sham operated (=intact) rats (data calculated based on Saadiah Abdul Razak. 2012)

  Low dose testosterone + long jack better than TRT alone? The results Saadiah Abdul Razak et al. present in the latest issue of Evidence Based Complementary Medicine don't actually look like they were interesting for muscle heads, I mean "androgen dependent osteoporosis", where are the word hypertrophy, skeletal muscle, or at least ripped & jacked? And I have to admit that of these only "skeletal muscle" makes its appearance somewhere in the introductory remarks of the discussion and only in the context of the "auxiliary functions" of testosterone as a growth hormone and IGF-1 booster and muscle builder. I do still believe that the data in the figure 2 on the right is going to get your attention - after all, the combination treatment of testosterone + Eurycoma longifolia did not "just" restore the balance of the "bone builder" osteocalcin to the "bone eater" ORX (actually it's just a marker of bone resorption) to normal (=sham levels), it did also effectively build the strongest bones, with the highest maximal load in Newton and the greatest elastic stability, as measured by the Young's Modulus.
  What's interesting, as well, is that all treatments were equally effective in restoring normal body weight - who knows maybe 15mg/kg/day (HED: 2.4mg/kg; ~170-250mg/day) of Eurycoma longifolia (EL) extract would even make a valuable stand alone (no pun intended ;-) testosterone booster for mild cases of real hypogonadism (not the one where your diet is shitty, your training sucks and it's your "low T" that you believe is to to blame that you make no gains), or an adjunct to HRT that would allow you to use only half the regular dose (this was done in the study at hand) and see similar results!? That it's good for sperm quality and testosterone, when it's administered in ~13x higher dosages in rodents (Chan. 2009) and for sperm health in men (at about the dosage used here; cf. Tambi. 2010) has already been established.
  And still, the "major gap" of which Bhat et al. postulated that it existed "in [sic!] providing scientific base for commercial utilization and clearance of the Tongkat Ali products with regard to consumer's safety" is still in existence. Moreover, the same could be said about our knowledge with respect to the individual effects of the potentially biologically active component(s) in the plant and respective extracts. Before those issues are not solved, the "extract" you may buy could be anything from uberpotent to simply toxic... although I suspect that it is still most likely that it will simply be ineffective.

What? That went too fast? Don't worry, it's just two days to the Thursdaily Science News Roundup on SHR, four days to the next official installment of "On Short Notice" and just one click away from a handful of additional up-to-the-minute news on the SuppVersity Facebook Wall such as

• the correlation of low growth hormone levels with NAFLD (= non-alcoholic fatty liver disease), 
• a study on how digestion potentates the antimicrobial activity of coconut oil,
• a potential successor to metformin that triples muscular glucose uptake in the absence of insulin 

and all the other interesting tidbits I have already and am still going to post there even before the next SuppVersity news is going to be published right here, tomorrow! Ah,... and by the way it's not prohibited to share articles you like on Facebook and other social media outlets ;-)

References:

• Ahmed, L.A., Protective effects of magnesium supplementation on metabolic energy derangements in
  lipopolysaccharide-induced cardiotoxicity in mice. Eur J Pharmacol. 2012.
• Bhat R, Karim AA. Tongkat Ali (Eurycoma longifolia Jack): a review on its ethnobotany and pharmacological importance. Fitoterapia. 2010 Oct;81(7):669-79. Epub 2010 Apr 29. 
• Bjorkman L, Lundekvam BF, Laegreid T, Bertelsen BI, Morild I, Lilleng P, Lind B, Palm B, Vahter M. Mercury in human brain, blood, muscle and toenails in relation to exposure: an
  autopsy study. Environ Health. 2007; 6:30 
• Chan KL, Low BS, Teh CH, Das PK. The effect of Eurycoma longifolia on sperm quality of male rats. Nat Prod Commun. 2009 Oct;4(10):1331-6. 
• Fry JC, Yurttas N, Biermann KL, Lindley MG, Goulson MJ. The Sweetness Concentration-Response of R,R-Monatin, a Naturally Occurring High-Potency Sweetener. J Food Sci. 2012 Aug 27.  
• He K. Trace elements in nails as biomarkers in clinical research. Eur J Clin Invest. 2011;  41(1):98–102.
• Maes M, Kubera M, Leunis JC. The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuro Endocrinol Lett. 2008 Feb;29(1):117-24.
• Morris JS, Stampfer MJ, Willett WC Dietary selenium in humans: toenails as an indicator. Biol Trace Elem Res. 1983; 5:529–537.
• Ohno T, Sakamoto M, Kurosawa T, Dakeishi M, Iwata T, Murata K. Total mercury levels in hair, toenail, and urine among women free from occupational exposure and their relations to renal tubular function. Environ Res. 2007;103(2):191–1.
• Saadiah Abdul Razak H, Shuid AN, Naina Mohamed I. Combined Effects of Eurycoma
  longifolia and Testosterone on Androgen-Deficient Osteoporosis in a Male Rat Model. Evid Based Complement Alternat Med. 2012;2012:872406. Epub 2012 Aug 9.
• Whittaker JP, Linden MD, Coffey VG. Effect of Aerobic Interval Training and Caffeine on Blood Platelet Function. Med Sci Sports Exerc. 2012 Aug 29.
• Xun P, Liu K, Morris JS, Jordan JM, He K. Distributions and determinants of mercury concentrations in toenails among American young adults: the CARDIA Trace Element Study. Environ Sci Pollut Res Int. 2012 Aug 25.

True or False? Glycine & Proline Supplements Ramp Up Collagen Synthesis & Improve Joint Health. Plus: The Tripeptide Advantage of Collagen Hydrolysates

The "Paleo" cult has repopularized eating and preparing your own (Chicken) bone broth, but will this also help with bone and cartilage health?

Although you're probably thinking of collagen as the stuff that's important for joint health, its implications in human health are more far-reaching than most of us believe.

In fact, collagens are the most abundant group of organic macro-molecules in human and animal body. Because of their tensile strength, they perform numerous structural functions within the body - specifically in connective tissues which include among other tissue also organs as your heart, your intestines, your lungs and the parenchymal organs like the liver and the kidneys and even the fibrous matrix of skin and blood vessels.

As I already said, collagens are yet by far best known as structural components of the protein matrix of the skeleton and its related structures, like bones, teeth, tendons, cartilage and ligament, which bring us back to the original question that bothered me after assuring Chris who emailed me asking about the necessity of taking glycine and proline supplements in the absence of any other protein (my answer was "that's bullocks"): Do glycine and problem supplements even help with collagen synthesis and joint health? Or is the supplement vendor next door the only person who benefits?

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We do have evidence (from rodent studies) that the ingestion of low molecular weight (=small peptides) collagen hydrolysates with intact glycyl-prolyl-hydroxyproline tripeptides that actually make it through the gut into the bloodstream and will increasee the organic substance content and decreased the water content of the left femur (Watanabe-Kamiyama. 2009). Previous studies had already shown hat the content of an orally administered gelatin hydrolysate will be incorporated into the cartilage tissue of rats (Oesser. 1999). Similar observations have been made by Iwai et al. for human volunteers and porcine gelatine hydrolysate, as well.

"After the oral ingestion, the peptide form of Hyp significantly increased and reached a maximum level (20-60 nmol/mL of plasma) after 1-2 h and then decreased to half of the maximum level at 4 h after the ingestion. Major constituents of food-derived collagen peptides in human serum and plasma were identified as Pro-Hyp. In addition, small but significant amounts of Ala-Hyp, Ala-Hyp-Gly, ProHyp-Gly, Leu-Hyp, Ile-Hyp, and Phe-Hyp were contained." (Iawai. 2005)

If we assume a similar physiological effect as it was observed by Watanabe-Kamiyama in rodents, the ingestion of (large) quantities of gelatine could thus very well, after it's hydrolysation in the gut, have similar effects on human cartilage tissue as the collagen hydrolysate that was used in the Watanabe-Kamiyama study.

Table 1: Summary of Structure and Recovery of Food-Derived Collagen Peptide in Human Serum or Plasma after Oral Ingestion of Gelatin Hydrolysates (Iawai. 2005).

With respect to the occurence of glycyl-polyl-hydroxproline tripeptides, of which the Watanabe-Kamiyama study suggests that they may be responsible for the beneficial effects on cartilage synthesis it should yet be said that it occurred in human plasma only after the ingestion of chicken, but not in porcine collagen in the Iawai study (see Table 1). If that's no coincidence, HARIBO, which is usually made with porcine gelatine is no "collagen builder", a real chicken soup, cooked with bone, on the other hand, could be.

Given that your stomach is working properly a nice paleo bone broth (preferably from chicken bone) could thus produce similar results as a collagen hydrolysate of which a recent review in Current Medical Research and Opinion says that its ingestion stimulates a statistically significant increase in synthesis of extracellular matrix macromolecules by chondrocytes.

There is more to collagen hydrolysates than joint health: In 2009 Saito et al. were able to show that fish collagen hydrolysates affect lipid absorption and metabolism in rats and may be useful in suppressing the transient increase of plasma triglycerides (Saito. 2009). Moreover, Spanish researchers showed that the daily dietary intake of hydrolyzed collagen seems to have a potential role in enhancing bone remodeling at key stages of growth and development in 60 children (9.42±1.31 years) who had been randomly assigned to either placebo or collagen (+ calcium) supplementation. In spite of these benefits, the ingestion of corresponding supplements is not necessary for people with healthy collagen metabolism who exercise regularly and eat clean.

Figure 1: Physician rated (top) and subject-rated (bottom) improvement in joint pain walking (left) and standing (right) in the Clark study (Clark. 2008).

The authors, researchers from the University of Illinois College of Medicine at Chicago and the University of Kiel in Germany add:

"These findings suggest mechanisms that might help patients affected by joint disorders such as OA. Four open-label and three double-blind studies were identified and reviewed; although many of these studies did not provide key information – such as the statistical significance of the findings – they showed collagen hydrolysate to be safe and to provide improvement in some measures of pain and function in some men and women with OA or other arthritic conditions." (Bello. 2006)

Subsequent studies such as Benito-Ruiz et al. (2009) or Clark et al. who evaluated data from 97 athletes from a varsity team or a club sport in Pennsylvania support Bello's conclusion (see Figure 1).

Similar beneficial effects were also observed by  et al. in a more recent study with "normal" subjects with articular pain in response to 1,200mg/day of collagen hydrolysate (Bruyère. 2012). When we're looking into the effects of single amino acids, however, things look different. If they're ingested separately, glycine and proline are not going to form a tripeptide in the course of the digestive process. And while they may still serve as a raw material for the endogenous synthesis of such peptides the chance that they actively promote the synthesis of new collagen is slim.

Biologically active tripeptides, not just glycine & proline is what you want!

Bottom line: Collagen hydrolysates with intact tripeptides seem to have a beneficial effect on collagen synthesis. Classic broth and gelatine, both best made from chicken bones (absorption data on beef is not available), could have beneficial effects on collagen synthesis. In view of the chance that and rate at which the physiologically relevant  glycyl-prolyl-hydroxyproline tripeptides (see image to the right) are produced during the natural digestion process it does yet appear certain that you would have to garble down tons of it on a daily basis to actually trigger collagen synthesis and not just to do what individual amino acids could probably do as well: provide the necessary substrates without actually accelerating collagen synthesis.

Chris' original question whether you'd have to take glycine and proline supplement on their own and in the absence of any other proteins and amino acids would thus actually be obsolete (you shouldn't take them at all), but I guess it may be worth mentioning that doing that, i.e. taking them on their own will only increase the "risk" of both being used by the liver as a substrate for glyconeogenesis (proline for example has the 3rd highest potential for gluconeogenesis 75% of the most glycogenic amino acid, i.e alanine; cf. Ross. 1967) - especially if you top "taking them on their own" with "taking them during a fast".

References:

• Bello, Alfonso E., and Steffen Oesser. "Collagen hydrolysate for the treatment of osteoarthritis and other joint disorders: a review of the literature." Current Medical Research and Opinion® 22.11 (2006): 2221-2232.
• Benito-Ruiz, P., et al. "A randomized controlled trial on the efficacy and safety of a food ingredient, collagen hydrolysate, for improving joint comfort." International journal of food sciences and nutrition 60.S2 (2009): 99-113. 
• Bruyère, Olivier, et al. "Effect of collagen hydrolysate in articular pain: a 6-month randomized, double-blind, placebo controlled study." Complementary therapies in medicine 20.3 (2012): 124-130.
• Iwai, Koji, et al. "Identification of food-derived collagen peptides in human blood after oral ingestion of gelatin hydrolysates." Journal of agricultural and food chemistry 53.16 (2005): 6531-6536.
• Oesser, Steffen, et al. "Oral administration of 14C labeled gelatin hydrolysate leads to an accumulation of radioactivity in cartilage of mice (C57/BL)." The Journal of nutrition 129.10 (1999): 1891-1895. 
• Ross, B. D., R. Hems, and H. A. Krebs. "The rate of gluconeogenesis from various precursors in the perfused rat liver." Biochem. J 102 (1967): 942-951.
• Saito, Masataka, et al. "Effect of collagen hydrolysates from salmon and trout skins on the lipid profile in rats." Journal of agricultural and food chemistry 57.21 (2009): 10477-10482.
• Watanabe-Kamiyama, Mari, et al. "Absorption and effectiveness of orally administered low molecular weight collagen hydrolysate in rats." Journal of agricultural and food chemistry 58.2 (2009): 835-841.

Overweight or Just "Heavy Bones"? Recent Studies Provide Insights Into How Your Bones Affect Your Metabolism

Image 1: The yellow bone marrrow fat
turns out to be more than a filler.

In Germany there is a common saying that is predominantly used by the mothers of fat kids: "My son, overweight? No. He just has some really heavy bones." Well, I guess few of these proud mothers will be aware that recent research from the Boston Medical School (Fulzele. 2011) and the University of Toledo suggests that there may be more to the bone-bodyweight connection than even they may have thought.

In a comprehensive review of the latest findings on bone metabolism (Fulzele. 2011) Keertik Fulzele and Thomas L. Clemens state that the "contemporary model [which] assigns IGFs [insulin like growth factor] as central regulators of cell profileration, survival, and organism growth" and reduces the influence of insulin to the "level of regulation fuel utilization, storage, and energy expenditure" is too simplistic to to accommodate the overlapping roles of IGF and insulin in several physiologic processes, one of which is the recently discovered and previously unappreciated skeletal action of insulin. Via skeletal insulin receptors, the latter is intricately involved in

• osteablast [=bone cells] bone acquisition
• osteocalcin production

Of these, the production of the noncollagenous peptide ostecalcin could be of special interest with respect to the metabolic function of bone, as its undercarboxylated form (carboxylation of osteocalcin occurs in the presence of vitamin K and "activates" the peptide hormone, so that it can fulfill its bone-building function), which has a low affinity for bone matrix, appears to function as a hormone on the systemic level. On the other hand, insulin has lately been found to increase the accumulation of undercarboxylated osteocalcin, which "in turn acts in an endocrine fashion to regulate pancreatic insulin secretion and peripheral insulin responsiveness". It is this hitherto unknown mechanism by which your bones factor in the complex hormonal game that is your metabolism and by which skeletal energy-sensing pathways may manage fuel production, storage, and expenditure in a similar vein as their analogues in muscle and fat tissue.

Figure 1: Metabolic and endocrine functions of white (WAT) and brown (BAT) adipocytes in your bone marrow
(based on Czernik. 2011)

As the scientists point out, we are just beginning to understand the sophisticated role our bones play in the orchestration of our metabolism. Questions that still have to be answered relate to the ways, osteablasts "sense" glucose and other fuels, whether they simply burn amino acids and glucose as fuel and whether and to which extent medications that influence bone resorption could also be used for blood sugar management.

Answers to these questions will expand our understanding of the biology of the skeleton and should have implications in the diagnosis and management of patients with metabolic diseases, including osteoporosis and diabetes.

More information on the underlying mechanisms by which your bones directly influence your metabolic rate, and thus your weight, can be found in a Special Issue of the Journal 'Bone', entitled "Bone and Fat". In her paper (Czernik. 2011), Beata Lecka-Czernik elaborates on the possible influence the yellow bone fat, which - believe it or not - occupies a significant portion of your bone marrow cavity, could have on your metabolism, both locally, as well as systemically.

Did you know? The fat distribution in your skeleton is site, age, and gender specific (men have more bone fat than women). In adults the bone marrow cavity of long bone, for example, is entirely filled with fat, while the ileac crest marrow contains only ~40% fat. The overall amount of bone fat can double in the course of your life and the WAT- and BAT-like adipocytes appear to have similar metabolic and endocrine functions as their white (WAT) and brown (BAT) analogues on your hips, your belly and your neck.

In this context, the integrative models of Ferron et al and Fulzele et al. are of particular interest, as they could help elucidate the link between the anabolic effects of insulin signaling in osteoblasts and the regulation of insulin sensitivity in peripheral organs. And who knows, even if its not the "heavy bones" that contribute to the obesity pandemic,"fat bones" could well become a novel target in its prevention and treatment.

SuppVersity World Cup Special: What Football Can Do For Your Health & Performance Now & As You Age - It's Better for Heart & Bones (!) Than Lifting

Soccer! For Young & Old, Heart & Bones, Blood Sugar & Body Fat Now & Beyond World Cup 2012

Ok, I have to admit, in spite of the fact that the World Cup starts today, I wouldn't have produced this article, if the editor(s) of the Scandinavian Journal of Medicine & Science in Sports didn't have a similar idea and I wouldn't have "early view" access to a bunch of soon-to-be-published on the beneficial and not so beneficial effects of what I call "football" and most of you call "soccer".

But enough of the prelude, let's take a look at what I have to report, here: Schmidt et al. present the amazing cardiovascular adaptations they observed in response to 4 and 12 months of football or strength training in 65- to 75-year-old untrained men.

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The study was conducted at the Copenhagen Centre for Team Sport and Health of the University of Copenhagen and involved, as you would have guessed, 26 untrained men (age: 68.2 ± 3.2 years). The guys were randomized to football training (FTG; n = 9), strength training (STG; n = 9), or control (CG; n = 8).

Football (soccer), older hearts will love it!

Maximum oxygen consumption (VO2max; L/min) and resting heart rate (RHR; bpm) in elderly healthy 65- to 75-yearold men at baseline, after 4 & 12 months of football training (FTG), strength training (STG), and control (CG) - Schmidt. 2014

Aside from the impressive improvements in VO2max (vs. no improvement in either the strength training or the control group; see Figure 1), the researchers observed the following beneficial structural changes of the heart:

• increases in left ventricular diastolic diameter +8%
• increases in end-diastolic volume +21%
• increases in ventricular mass index +18%

Unlike the improvements in ejection fraction (+8% in FTG vs. +5% in STG), these changes were "football"-exclusive.The systolic longitudinal two-dimensional strain increased by 8% (FTG) and 6% (STG), whereas the right ventricular systolic function improved (P < 0.05) by 22% in FTG, but not in STG and CG.

In conjunction with the football-exclusive increases in diastolic mitral inflow (E/A) ratio and peak early diastolic velocity (E') improved (25% and 12%, respectively), your 3x1h of training may thus be better spend on football than on resistance training if your main goal is to improve your VO2max and kick heart disease's ass.

If we look at the benefits the older guys in the Schmidt study derived from their soccer training it can hardly be surprising that Anderson et al. (2014a) report similarly "hearty" benefits in 31 untrained males with mild-to-moderate hypertension who were randomized 2:1 to a football training group (n = 20) and a control group receiving traditional recommendations on healthy lifestyle (n = 11).

While the football group exhibited significant (P < 0.05) changes in cardiac dimensions and function after just 3 months similar to those in the Schmidt study, as well as significant reduction in arterial blood pressure, the results in the "traditional take this *bs* advice" group were mediocre tat best. Consequently, the researchers conclude that even in the short term (3-6 months)...

"football training improves LV diastolic function in untrained men with mild-to-moderate arterial hypertension [and] improve longitudinal systolic function of both ventricles." (Anderson. 2014a)

 Now, SuppVersity readers are not generally hypertensive, and I am gathering that the few highly appreciated "best agers" in my readership are also in the minority. Against that background it's worth mentioning that the heart is not the only part of your body that will benefit from soccer practices - your bones will, too. Ok, I see you laughin' cause you're hittin' the weights, regularly, but what would you say if I told you that ...

"4 months of recreational football for elderly men had an osteogenic effect, which was further developed after 12 months, whereas resistance training had no effect."  (Helge. 2014)

I see, I've got your attention, now! Well, the authors, again researchers from the Copenhagen Centre for Team Sport and Health speculate that the anabolic response may be due to increased bone turnover, especially improved bone formation which was obviously promoted to a greater extent in those 9 of the initially 26 healthy sedentary men (age 68.2 ± 3.2 years) who had been randomized to the  football (F; n = 9) and not the resistance training (R; n = 9) group - and that despite the fact that both trained two to three times weekly for a total of 45–60 min training.

Playing soccer is good for your health, watching it... well, watching it can increase your risk of being hospitalized for acute myocardial infarction minimally (+1%; cf. Barone-Adesi. 2010), unless, of course, your team wins! During the 1998 World Cup, which was won by France, the myocardial infarction risk of French men was actually reduced by 35% (Berthier. 2003)

When it comes to improving the functional ability and physiological response to submaximal exercise, in older men, however, it's difficult to pinpoint a difference between three football and three resistance training sessions per week. Unsurprisingly, study #4 in today's review did yet report that only football trainign "additionally elevates maximal aerobic fitness and exhaustive exercise performance." (Anderson. 2014b).

What's left to discuss, oh yes! Anderson. 2014c and the effects on glucose management!

Yeah, with 21 middle-aged men (49.8 ± 1.7 years ± SEM) with T2DM as subjects, this study will certainly appeal to all the Average Joes out who unfortunately don't get their daily dose of SuppVersity wisdom, yet (Anderson. 2014c).

The said middle-aged subjects were divided into a football training group (FG; n = 12) and an inactive control group (CG; n = 9) - the absence of a strength training "control" is a pity... but alas, after the 24-week intervention period, in the course of which the sick guys covered only During 4.7 ± 0.2 km at a mean heart reate of 83 ± 2% of HRmax per 1h soccer training, they experienced a 11% increase in VO2peak and lost 1.7 kg and 12.8% of their total fat and android fat, respectively.

Against that background it's not that surprising that Anderson et al. report concomitant improvements in plasma glucose and an increased expression of the glucose transporters (GLUT-4). Most importantly, however, the Danish researchers did also observe an overall time effect for glycosylated hemoglobin (HbA1) and thus significant and continuous improvements in glucose management in the soccer group.

Bottom line: "There you have it" ... that's actually something my good friend Carl Lanore from www.superhumanradio.com like to say. There you have the benefits of playing soccer. Improved heart health, fat loss and reductions in blood glucose in type II diabetes are probably nothing, you wouldn't have expected, anyways, right?

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Well, what about the benefits on bone health, then? I personally was surprised that the impact of soccer training was more pronounced than the one of strength training. In the end, I would yet expect equal results if the latter, i.e. the strength training had included free-weight squats and/or deadlifts. Those and not sissy curls and lat pulldowns are true bone builders, but honestly - when I see some of the 60+ agers at my gym do them I think to myself: You better leave that to true physical culturists, like my previously mentioned friend Carl Lanore (www.superhumanradio.com) and head over to the soccer training, folks ;-)

References:

• Andersen, L. J., Randers, M. B., Hansen, P. R., Hornstrup, T., Schmidt, J. F., Dvorak, J., Søgaard, P., Krustrup, P. and Bangsbo, J. (2014a), Structural and functional cardiac adaptations to 6 months of football training in untrained hypertensive men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12237 
• Andersen, T. R., Schmidt, J. F., Nielsen, J. J., Randers, M. B., Sundstrup, E., Jakobsen, M. D., Andersen, L. L., Suetta, C., Aagaard, P., Bangsbo, J. and Krustrup, P. (2014b), Effect of football or strength training on functional ability and physical performance in untrained old men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12245
• Andersen, T. R., Schmidt, J. F., Thomassen, M., Hornstrup, T., Frandsen, U., Randers, M. B., Hansen, P. R., Krustrup, P. and Bangsbo, J. (2014b), A preliminary study: Effects of football training on glucose control, body composition, and performance in men with type 2 diabetes. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12259
• Barene, Svein, et al. "Soccer and Zumba as health-promoting activities among female hospital employees: a 40-weeks cluster randomised intervention study." Journal of sports sciences ahead-of-print (2014): 1-11. 
• Barone-Adesi, Francesco, et al. "It is just a game: lack of association between watching football matches and the risk of acute cardiovascular events." International journal of epidemiology 39.4 (2010): 1006-1013.
• Berthier, Fabrice, and Frédéric Boulay. "Lower myocardial infarction mortality in French men the day France won the 1998 World Cup of football." Heart 89.5 (2003): 555-556.
• Helge, E. W., Andersen, T. R., Schmidt, J. F., Jørgensen, N. R., Hornstrup, T., Krustrup, P. and Bangsbo, J. (2014), Recreational football improves bone mineral density and bone turnover marker profile in elderly men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12239.
• Ramírez-Campillo, Rodrigo, et al. "Effects of In-Season Low-Volume High-Intensity Plyometric Training on Explosive Actions and Endurance of Young Soccer Players." The Journal of Strength & Conditioning Research 28.5 (2014): 1335-1342.
• Schmidt, J. F., Hansen, P. R., Andersen, T. R., Andersen, L. J., Hornstrup, T., Krustrup, P. and Bangsbo, J. (2014), Cardiovascular adaptations to 4 and 12 months of football or strength training in 65- to 75-year-old untrained men. Scandinavian Journal of Medicine & Science in Sports. doi: 10.1111/sms.12217