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

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

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

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

So what did the researchers do?

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

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

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

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

• 

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

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

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

Organic is not better than regular tea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Organic tea is a worse offender than regular

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

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

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

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

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

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

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

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

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

References:

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

Removal of Amalgam Fillings Associated With Reductions in Memory Loss, Fatigue, Anxiety, Confusion & Other Health Problems, Observational Study from Canda Shows

Amalgam removed = health restored?

While there is little doubt that mercury vapor poses a known health risk, there is neither a clearly established safe level of exposure, nor evidence that similar ill health effects can occur with chronic low grade exposure to mercury vapor from dental amalgam fillings.

As you may know amalgam is not 100% but "only" 50% mercury, but is that enough to represent a significant health risk? The objective of a recent study from the University of Calgary was "to determine if mercury exposure from amalgam fillings is associated with risk of adverse health effects" (Zwicker. 2014).

Mercury is among the reasons fish should not be your exclusive protein source

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Cod protein for recovery

Krill = Super Protein?

Farmed vs. Wild-Caught Fish

Fast vs. slow protein

5x More Than FDA Allows

To this ends, Zwicker et al. conducted a large longitudinal non-blinded study involving participants from a preventative health program in Calgary, Canada. The goal was to assess whether (a) there was an association between having amalgam fillings, the amount of mercury in the urine and reported health issues and (b) whether the 14 previously self-reported health symptoms would improve in a sample of persons who had their fillings removed compared to a sample of persons who had not had their fillings removed.

Figure 1: Summary data for study sample with urine mercury measures (Zwicker. 2014)

A brief glimpse at the baseline data reveals that the presence of 18.4 and 23.7 amalgam fillings on the tooth surfaces of the subjects in the treatment (amalgam fillings will be removed) and the amalgam control group (amalgam fillings will not be removed) have higher amounts of mercury in their urine.

What do previous studies say? Oskarsson et al. (1996) fount that mercury from amalgam fillings was the main source of mercury in milk. In fact, the amount of mercury babies were exposed to from breast milk ranged up to 0.3 μg/kg/d, of which approximately one-half was inorganic mercury and which corresponds to approximately one-half the tolerable daily intake for adults recommended by the World Health Organization (Oskarsson. 1996). Other studies present opposing results, though, and claim that fish, not amalgam fillings was the major source of mercury in breast milk (Drexler. 1998). Still, evidence from other studies, such as Nylander (1987), which report mercury vapor from amalgam fillings to be the major source of mercury in the organs of human subjects, support the notion that at least the "first generation" amalgam fillings are a major source of human mercury exposure. The correlation with subjective health symptoms, on the other hand, is less obvious. Studies like Ahlqwist et al. (1988) and a twin study by Björkman et al (1996) clearly refute the existence of a significant correlation.

What is interesting, but not actually what the scientists wanted to investigate is the fact that the mercury levels in women are generally higher (may be a result of a comparatively lower body size and mass and similar mercury exposure).

What do you think happened one year after the fillings were removed?

Well, let's see. As the data in Figure 2 indicates, the mercury levels in both amalgam groups declined in comparison to the baseline measure (follow up data for the amalgam free group is not available)

Figure 2: Changes in mean urinary mercury level after one year after the amalgam fillings
were removed / not removed (Zwicker. 2014)

The effects are, I guess you will agree with me on that one, not exactly impressive. Against that background the obvious question is: "Are the self-reported measured improvements in headache, memory loss, depression, fatigue, anxiety & co a result of a placebo effect?" I mean, the subjects obviously knew that their amalgam fillings were removed (remember: it's a non-blinded study!) and you bet that they've read some of the horror stories about mercury on the Internet.

Table 1: One year odds of symptom improvement and worsening in the group of subjects who had the amalgam fillings removed, controlled for age and sex | Odds ratio coefficients are the odds of change in treatment group relative to the positive amalgam group. {P values}; * indicates coefficient is different from 1 at size 0.05; ^ represents statistical significance at size 0.10 (Zwicker. 2014).

So, can we tell whether the "improvements" you see in Table 1 are actually brought about by the removal of the amalgam fillings or simply by the subjects psyche? I would say we can't and that's why I have my doubts about the validity of the researchers conclusion that "that mercury exposure from amalgam fillings adversely impact health and therefore are a health risk" (Zwicker. 2014) - not necessarily because I believe they are harmless, but rather because the data the scientists evaluated does not prove this claim.

If avoiding mercury from fish is a good thing, avoiding mercury exposure from amalgam fillings is a good thing, too. Irrespective of the fact that the study at hand provides only insufficient evidence of its ill health effects.

Bottom line: I personally had my one filling removed back in the day, but rather the necessary result of the fact that it was in a baby tooth ;-)

That being said, I still subscribe to the researchers assertion that "a safer alternative materials for dental fillings should be encouraged to avoid the increased risk of health deterioration associated with unnecessary exposure to mercury" (Zwicker. 2014), yet not because of the data in the study at hand, though, but rather based on the notion that you would want to limit any unnecessary exposure to heavy metals, no matter how small the amount that's leeching from the amalgam fillings may be, though.

On a side note: A study investigating the commonly heard claim that the removal of amalgam would only increase the load of mercury (at least temporarily) indicates that - if it's done properly - "[t]he uptake of amalgam mercury in the GI tract in conjunction with removal of amalgam fillings seems to be low" (Björkman. 1997). So if you are considering this procedure, it's unlikely that it will make whatever symptoms you believe to have as a consequence of having amalgam fillings more severe | Comment on Facebook!

References:

• Ahlqwist, Margareta, et al. "Number of amalgam tooth fillings in relation to subjectively experienced symptoms in a study of Swedish women." Community dentistry and oral epidemiology 16.4 (1988): 227-231. 
• Björkman, Lars, Nancy L. Pedersen, and Paul Lichtenstein. "Physical and mental health related to dental amalgam fillings in Swedish twins." Community dentistry and oral epidemiology 24.4 (1996): 260-267.
• Drexler, Hans, and Karl-Heinz Schaller. "The mercury concentration in breast milk resulting from amalgam fillings and dietary habits." Environmental research 77.2 (1998): 124-129. 
• Oskarsson, Agneta, et al. "Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women." Archives of Environmental Health: An International Journal 51.3 (1996): 234-241.
• Nylander, Magnus, Lars Friberg, and Birger Lind. "Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings." Swedish dental journal 11.5 (1986): 179-187.
• Zwicker, Jennifer D., Daniel J. Dutton, and John Charles Emery. "Longitudinal analysis of the association between removal of dental amalgam, urine mercury and 14 self-reported health symptoms." Environmental Health 13.1 (2014): 95.

Farmed vs. Wild-Caught: Pollutants and A Low Omega-3/6 Ratio - Is Wild Caught Fish Always the Better Choice? Plus: Krill, Fish Oil, or Whole Fish - What's Best for Your Health?

Wild caught or farmed? If you google it, it appears to be as if eating farmed  fish could be worse than eating no fish at all, but is this actually true?

Farmed fish is the ugly duckling in the "superfood" family. It is - at least that's what you'll read on the Internet - low in omega-3s, full of "bad" omega-6 fatty acids and laden with all sorts of pesticides. But wild caught fish is expensive and if we all ate it day in and day out not exactly eco-friendly, right?

In today's SuppVersity special parts of which you may have recently seen pop up for a few hours in interview form over at www.fighterdiet.com, before Pauline Nordin and I decided that due to its length and complexity it was rather an article than an interview and should thus be published as such, I am going to tackle the issue of "farmed vs. wild-caught" and "fish vs. fish oil" from all possible angles.

Do not underestimate fish as a protein source - fish is more than just omega-3!

Salmon Better Than Whey?

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Krill = Super Protein?

High EAA protein for fat loss

Fast vs. slow protein

5x More Than FDA Allows

I would like to start my elaborations with the results of a recent paper by Nichols et al. (2014). A paper, in which the scientists investigate whether the existing differences of the fatty acid profiles from farm-raised vs. wild-caught cold-water fish would depend on what the fish were fed.

The general consensus on the Internet appears to be that wild-caught salmon is in all ways superior to its "industrially produced" counterpart from the large fish farms. In that, the opponents of farmed fish consumption usually highlight the (I quote) "exorbitant" amount of allegedly unhealthy omega-6 fatty acids in farmed fish.

Now it is certainly undebatable that the ratio of omega-6 to omega-3 fatty acids in wild-caught vs. farmed salmon differs significantly. The previously mentioned study by researchers from the Commonwealth Scientific Industrial Research Organization does yet also show that this effect is not a result of "farming", per se. Rather than that, the increase in omega-6 and decrease in omega-3 fatty acids in today's industrially produced cold-water fish is a result of the ongoing reduction of the fish(oil) content in the fish food.

Figure 1: Fatty acid profile of farmed and wild-caught baramundi in 1998, 2002 and 2010 (left) and the corresponding omega-3 to omega-6 ratios (right) – it's worth noticing that "back in the day" of high fish oil diets, the farmed barramundi had a more favorable omega-3 to omega-6 ratio than their wild-caught relatives (Nichols. 2014)

In 2001, for example, when farmed barramundi (Lates calcifer | another cold-water fish that is raised in large aqua-farms these days) were still fed a high percentage of dietary fish oil, the farmed fish actually had a more favorable omega-3 to omega-6 ratio than its wild-caught counterpart (see Figure 1).

Over the past 13 years, the fish farmers have yet replaced large amounts of the increasingly expensive fish oil in the feed by cheap poultry oils. The consequences are obvious: While this practice may reduce the levels of dioxins and dioxin‐like PCBs (Berntssen. 2005), the substitution of fish oil with vegetable oil in the feed lead to decreases in the total amount of PUFAs, most specifically omega-3s, though. Thus, the originally highly favorable omega-3/omega-6 ratios of 5:1 for farmed salmon and 3:1 for farmed barramundi has declined to a meager 1:1 (Nichols. 2014).

High omega-6 in today's farmed cold-water fish - a problem? For the average physical culturist who is following a diet that is comparatively low in potentially pro-inflammatory omega-6 fatty acids (they are only bad for you, when they are consumed in excess), tehe deterioration of the omega-3 to omega-6 fatty acid ratio in modern farmed vs. wild caught fish is relatively unproblematic. Unlike it is the case for the average Westerner, who is in dare need of high omega-3 and low omega-6 foods to balance his or her excessive omega-6 intake from vegetable oils and industrially processed foods, farmed salmon is thus still a good source of protein and fats for those of us who are following a whole foods diet with a balanced fatty acid profile.

So, if the relatively high omega-3 content is not a problem, because the effects of "high omega-6" farmed fish on your omega-3 to omega-6 ratio is still neutral (that's the case if the ratio is approx. 1) there is no reason to avoid farmed fish, right?

From "high omega-6" to high levels of organic and inorganic pollutants

Unfortunately the high omega-6 content is not the only problem farmed fish is supposed to have.  Next to the previously discussed issue, the occurrence of various pollutants in farmed fish is another of the topics that will be mentioned in almost every online- or gym-debate on the consumption of farmed fish. Rumors have it that farmed salmon was loaded with toxic chemicals. And guess what!? To a certain extend that is absolutely true.

Figure 2: Fish is by far not the only POP source in our diets. Each 0.5 serving of the above foods is associated with the given increase in µg of urinary phthalate and phenol biomarkers in the urine of 6-8 year old girls and may thus increase their breast cancer risk later in life (Mervish. 2001)

When we are taking a closer look at the latest scientific evidence on the real world effects of thes persistent organic pollutants (POPs), it turns out that a high fish consumption has no measurable impact on the concentration of this potentially cancerous endocrine disruptors (they mess with your hormones) in our blood and adipose tissue. In fact, the latest study by Hausken et al. clearly indicates that the POPs in the blood of their fish fed subjects and the corresponding control group have different food products as their main sources (Hausken. 2014).

It is thus no wonder that the researchers from the University of Bergen did not find any change in serum or adipose tissue POP levels, when they had their subjects, 42 outpatients with different metabolic disorders, increase their intake of farmed salmon or salmon oil and compared their subjects' serum and fat pollutant levels to a non-fish eating control group.

The results were unambiguous: The consumption of farmed fish did not affect the steady-state of organic pollutants in either the blood or fat tissue of the subjects.

High levels of persistent organic pollutant (POPs) - a problem? The ever-increasing amount of POPs in our diet and other consumer goods (deodorants, perfumes and cosmetics are another source of POP) is a problem and a potential threat to our health, but farmed fish is not the item on your plate or cupboard that will tip the scale.

Due to the ever-increasing pollution of the oceans, rivers and lakes, POPs and other pollutants are no "farmed fish" phenomenon, anyway. If you look at the results of a recent study from the Hong Kong Baptist University, for example, you will have to concede that "eating wild caught only" is not going to protect you from being exposed to chemicals like BPA (Wei. 2011).

Figure 3: Polycyclic aromatic hydrocarbon (PAH) content of farmed and wild-caught salmon samples (Easton. 2002).

Moreover, the amount of organic pollutants in farmed fish could be easily reduced if the producers were willing to invest more money into quality fish food. The results of a 2002 study by Easton et al. clearly indicate for example that the increased polycyclic aromatic hydrocarbon (PAH) content of farmed vs. wild caught salmon could be easily reduced if these organic pollutants were not already present in hilariously high quantities in the feed the fish are fed. Buying uncontaminated fish food would thus give the farmers a degree of control fishers whose wild caught chinook salmon can contain up to 4.8x  more PAH than farmed salmon (see Figure 3) will never have.

Fish oil can be POP free, but not everything that glitters is gold

Fish oil is a highly processed substance. If the processing is done right, it is possible to remove large parts of the previously discussed POPs, as well as inorganic pollutants like mercury from the fishy sludge. The fact that it can be pollutant-free, however, does not necessarily mean that your fish oil caps will actually be free of any harmful substances.


The fact that fish oil producers may not do their job properly is yet not the only reason I am a strong proponent of consuming whole vs. "capped fish" and a whole foods vs. processed "supplement diet.  Why? Well, fish is by far not the only so-called "superfoods" for which we have seen time and again that the isolation of certain ingredients, of which we think that they are what makes these foods so "super", is not going to yield the results we are looking for.

In fact, recent studies which highlight the benefits of fish proteins for man and women who strive to build and maintain a muscular physique (learn more in a previous SuppVersity article) clearly suggest that the often-cited high selenium content of fish is not the only "good thing" you'd miss if you ditch your salmon, tuna and other fatty fish for cheap and convenient fish oil caps.

Warning! "Whole fish" does not include fried fish as you will find it on a "fish mac" or fish & chips and/or fish sandwiches. An increased consumption of these "fish" meals has been shown not to influence the cardiovascular mortality risk of 3910 adults aged 65+ years in a 2003 study by Mozaffarian et al. Moreover, the previously discussed amount of environmental pollutants in the fish is another determinant of its beneficial health effects.

In an editorial comment in the Journal of Internal Medicine Jacobs, Ruzzin & Lee highlight that "[t]he evidence that environmental pollutants can affect the health benefits of fish is supported by previous experimental studies" (Jacobs. 2014). In rodent studies, only decontaminated farmed salmon oil ameliorated the negative effects of high fat feeding. A POP-laden salmon oil from Atlantic salmon, on the other hand, accelerated the development of insulin resistance-related disorders in the lab animals (Ibrahim. 2011). The question, whether we should eat fish and take fish oil supplements is thus intricately related to the question whether we can obtain POP-free fish and fish oil products.

Table 1: The amount of organochlorides in various types of fish oil supplements bought on the Canadian market can be significant - similar results have been found on other markets | ^aΣ of 1,2,3,4 tetrachlorobenzene, 1,2,3,5 tetrachlorobenzene, and pentachlorobenzene; ^bΣ of α-HCH, β-HCH, and γ-HCH; ^cΣ of oxychlordane, trans-chlordane, trans-nonachlor, and cis-nonachlor; ^dΣ of p,p′-DDT and p,p′-DDE.(Rawn. 2009).

And even if you're not interested in being muscular, a recent study by Brazionis et al. clearly suggests that getting your 1g of long-chain omega-3 fatty acids from fish vs. fish oil supplements "may have additional cardiovascular benefits beyond the omega-3 effect". Effects which lead to a significant reduction in blood pressure the scientists observed only in those subjects who consumed fresh salmon (two 150 g servings per week of John West fresh Atlantic salmon), but not in their peers in the fish oil arm of the study (Brazionis. 2012).

Is fish oil the safer alternative? If you buy your fish oil from a manufacturer who can prove that each and every batch is tested for its POP and heavy metal content, it may be safer, but in view of the synergistic effects of protein, fat, certain peptides and a plethora of micronutrients you will be missing if you scrap your two weekly servings of fatty fish and turn to fish oil caps instead, this does not mean that it will be healthier.

When we are talking about toxic substances in fish and fish oils, we obviously cannot dismiss the heavily debated issue of heavy metal contaminations.

Heavy metals are clearly no farmed-fish exclusive!

While the heavy metal issue is still a matter of open scientific debate, the epidemiological evidence in favor of the profound health effects of regular fish consumption appears to suggest that it is less of an issue for the general population than the hysteric news on the Internet may make you believe.

Figure 4: Mean (bottom axis) and max (top axis!) mercury content (mg/kg) in fish (FDA Monitoring Program. 1990-2010 from a 2012)

For fitness junkies and bodybuilders who are trying to satisfy their alleged protein "requirements" of 3-4g of protein per kg body weight by shoveling down one can of tuna after the other, however, the heavy metal content of the cheap fish cans may become a problem.

Or maybe I should say: I personally would not use canned tuna as my primary protein source, when aiming for a protein intake of 3-4g per kg of body weight.

And this goes regardless of the fact that I believe that the risks associated with consuming tuna containing 0.10-0.75ppm methyl mercury (Yess. 1993) may be overblown in some of the sensationalist articles on the Internet and other mainstream media.

Similarly, I am reluctant to rely on the purported protective effect of the high amounts of cysteine and selenium in seafood. A protection, by the way, of which scientists have recently shown that is cannot mitigate the loss of cardioprotective effects of high omega-3 intakes in individuals with high hair mercury levels (Virtanen. 2009 | learn more).

So mercury is less on an issue than people claim? Probably yes. I would subscribe to the FDA recommendation to limit your fish intake to 2-3x fish meals a week. More specifically, you should forget about the idea of tuna as a "healthy snack" you can eat as often as you want to and stay away from more than one fish meal if you are pregnant or trying to become pregnant. In this case buying either mercury controlled fish or fish oils may in fact be the better choice  – I mean: "Better save than sorry", right?

Speaking of fish oil, there is an increasing trend towards krill oil as the "hype" omega-3 supplement. A trend of which you, as SuppVersity readers know that it appears to be unwarranted, although krill oil has the advantage of providing a large amount of the omega-3 fatty acids in their phospholipid-bound form (learn more in a previous SuppVersity article).

Figure 5: Plasma, liver and white adipose tissue (WAT) levels of triglyceride (TL) and phospholipid varieties of DHA+EPA after 9 weeks on HFD diet with (w3TL or w3PL) or  w/out 30mg/kg chow DHA + EPA (Rossmeisl. 2012)

Compared to triglycerides, the phospholipid-bound version is easier to assimilate. Accordingly, it is not very surprising that Rossmeisl. et al. (2012) were able to show that phospholipid-bound long-chain omega-3 fatty acids increase the plasma and liver omega-3 content to a significantly greater degree than the same amount of triglyceride-bound omega-3 fatty acids. An effect that was – at least in rodent studies – associated with a significantly more pronounced reduction in fat cell size and insulin sensitivity (Rossmeisl. 2012).
A more recent study by Tillander et al. (2014) adds to the evidence that krill oil may have an edge over fish oil, as an anti-NAFLD agent, because it will epigenetically reduce the fatty acid synthesis in the liver (read more).
 
The very ability to reduce the synthesis of fatty acids in the liver makes krill oil particularly interesting for overweight and obese people.

The increased fatty acid oxidation in response to the ingestion of fish oil (vs. krill oil) the researchers observed in the same study, on the other hand, may be something that could be of interest for lean individuals who are trying to lose weight (learn more in previous SuppVersity article).

Fish or krill? It depends... The previously presented evidence does thus make one thing very clear: It is more than likely that it will depend on your goals and current health status which of these omega-3 sources you should prefer. Overall, there is yet still a paucity of independent research, which is why I would not be surprised if the previously made conclusions were refuted by future studies.

If not weight loss, but muscle gains and fat loss are your goal, though, neither fish nor krill oil will do - at least not in the absence of one of the previously mentioned synergists: Fish protein!

Fish protein, an overlooked anabolic?

What wanna-be bobybuilders need is protein. Fish protein, to be precise. In 2009, for example, Ramel et al. were among the first to observe that using fish, or more specifically cod protein as the major protein source in the diet of their overweight subjects would yield improved outcomes in terms of fat loss and lean mass retention (Ramel. 2009; see Figure 6).

Figure 6: Decreases in anthropometric measurements after the 8-week intervention with isocaloric energy reduced diets having in obese subjects consuming no, three or five servings of lean fish per week (Ramel. 2009).

It is thus quite obvious that there must be something special to fish proteins more common dietary protein sources do not provide.

This hypothesis is also supported by previous evidence from rodent studies. One of these studies that was conducted by Frédéric Tremblay et al. (2003) at the Laval University Hospital Research Center suggests that the benefits may be related to the potent anti-inflammatory effects of fish proteins, which will thus increase the muscular insulin sensitivity and favor fat over muscle loss and muscle over fat gain.

A more recent study by Vikøren et al. (2013) seems to confirm this hypothesis.

The overweight adults who participated in the corresponding experiment experienced significant improvements in glucose metabolism, increases in lean and decreases in fat mass, when the scientists added 3 g of fish protein per day to their diets for the first 4 weeks and 6 g/d for the last 4 weeks of the 8 week intervention.

Figure 7: Macronutrient composition of the diets at baseline, after 4 weeks and 8 weeks and changes in body composition compared to baseline (Vikøren. 2013 - learn more in a previous SuppVersity article)

What is particularly noteworthy about this study is the fact that these effects occurred in spite of the fact that "[p]hysical activity and energy and macronutrients intake did not change during the course of the study" (Vikøren. 2013).

More recent evidence from a rodent study by Kawabata et al. (2014) strengthens the "anti-inflammatory" hypothesis. In their experiments, the researchers compared the effects of casein and fish protein in a tightly controlled dietary intervention and found similar increases in muscle mass and improvements in glucose metabolism in their hairy subjects as Vikøren et al. did one year before in overweight adults (learn more in a recent SuppVersity article).

Why don't we use our consumer money to force producers to make a change? I hope my previous elaborations have made it clear that living off fish as your only protein and fat source in the diet is probably not the best idea. On the other hand, similar issues with antibiotics (ab)use, persistent organic pollutants (POP) and even mercury exist for other foods, as well – with the exception of antibiotics which are only used to produce animal products all these pollutants can also be found in veggies and fruits (so no "vegan advantage").

We would thus be good advised to use our most powerful weapon, i.e. consumer money, to steer the food industry away from doing everything to cut the production costs and buy fish from those farms that don't use cheap poultry instead of fish oils, intoxicate the water with antibiotics and buy the cheapest, yet POP-laden food from questionable sources in China to feed their fish.

Time to draw some conclusions: Based on the existing evidence there is no reason to shy away from either fish consumption, in general, or the consumption of farmed fish, in particular. The overwhelming majority of epidemiological evidence indicates that consuming two servings of fatty fish a week will have nothing but beneficial effects on your overall health and that in spite of the fact that the fish was not controlled for organic or inorganic pollutants in any of these studies.

Whether it makes sense to consume large quantities of fish on a daily basis is yet as questionable as the routine use of fish oil supplements. Most of us will be able to cover our fundamental omega-3 needs with the previously mentioned two servings of fish per week. Consuming more than that in supplemental form is – in my humble opinion – not necessary for healthy individuals, unless they need to balance their exuberant intake of omega-6 fatty acid from large quantities of vegetable oils and processed foods in their diets –both products of which I highly recommend that people limit their intake to a minimum.

Moreover, imbalanced diets that are dominated by a single food source have repeatedly been shown to increase one's risk of running into severe health problems in the long run. So why don't we combine fish with dairy products, grass fed beef, pork and vegetable protein sources to create a varied, tasty, health and physique promoting high protein diet we can follow for the rest of your lives, instead of looking for the one "superfood", of which I would hope that most of the people who read this interview will know by now that it doesn't exist, anyway.

References:

• Brazionis, Laima, et al. "The effects of fish or fish oil on the omega‐3 index." Nutrition & Dietetics 69.1 (2012): 5-12.
• Berntssen, Marc HG, ANNE‐KATRINE LUNDEBYE, and Bente E. Torstensen. "Reducing the levels of dioxins and dioxin‐like PCBs in farmed Atlantic salmon by substitution of fish oil with vegetable oil in the feed." Aquaculture Nutrition 11.3 (2005): 219-231.
• Easton, M. D. L., D. Luszniak, and E. Von der Geest. "Preliminary examination of contaminant loadings in farmed salmon, wild salmon and commercial salmon feed." Chemosphere 46.7 (2002): 1053-1074.
• Hausken, Trygve, et al. "High Consumption of Farmed Salmon Does Not Disrupt the Steady State of Persistent Organic Pollutants (POP) in Human Plasma and Adipose Tissue." Journal of Toxicology and Environmental Health, Part A 77.20 (2014): 1229-1250.
• Ibrahim, Mohammad Madani, et al. "Chronic consumption of farmed salmon containing persistent organic pollutants causes insulin resistance and obesity in mice." PloS one 6.9 (2011): e25170.
• Mervish, Nancy, et al. "Dietary predictors of urinary environmental biomarkers in young girls, BCERP, 2004–7." Environmental Research 133 (2014): 12-19.
• Mozaffarian, Dariush, et al. "Cardiac benefits of fish consumption may depend on the type of fish meal consumed the cardiovascular health study." Circulation 107.10 (2003): 1372-1377.
• Nichols, Peter D., et al. "Readily available sources of long-chain omega-3 oils: is farmed Australian seafood a better source of the good oil than wild-caught seafood?." Nutrients 6.3 (2014): 1063-1079.
• Rawn, Dorothea FK, et al. "Persistent organic pollutants in fish oil supplements on the Canadian market: polychlorinated biphenyls and organochlorine insecticides." Journal of food science 74.1 (2009): T14-T19.
• Rossmeisl, Martin, et al. "Metabolic effects of n-3 PUFA as phospholipids are superior to triglycerides in mice fed a high-fat diet: possible role of endocannabinoids." PLoS One 7.6 (2012): e38834.
• Tillander, Veronika, et al. "Fish oil and krill oil supplementations differentially regulate lipid catabolic and synthetic pathways in mice." Gene expression 24 (2014): 28.
• Tremblay, Frédéric, et al. "Dietary cod protein restores insulin-induced activation of phosphatidylinositol 3-kinase/Akt and GLUT4 translocation to the T-tubules in skeletal muscle of high-fat-fed obese rats." Diabetes 52.1 (2003): 29-37.
• Vikøren, Linn A., et al. "A randomised study on the effects of fish protein supplement on glucose tolerance, lipids and body composition in overweight adults." British Journal of Nutrition 109.04 (2013): 648-657.
• Virtanen, Jyrki K., et al. "Serum long-chain n-3 polyunsaturated fatty acids and risk of hospital diagnosis of atrial fibrillation in men." Circulation 120.23 (2009): 2315-2321.
• Wei, Xi, et al. "Assessment of risk to humans of bisphenol A in marine and freshwater fish from Pearl River Delta, China." Chemosphere 85.1 (2011): 122-128.
• Yess, N. J. "US Food and Drug Administration survey of methyl mercury in canned tuna." Journal of AOAC International 76.1 (1993): 36.

Lose(!) 33% Body Fat in 10 Days!? The Heavy Metal Obesity Link: Study Shows "Preventive Role" for Inorganic Cobalt in Obesity-Related Diseases.

Image 1: Cobalt - certainly not what you would expect to see at a health food store or pharmacy; with Kawakami et al.'s study this may change in the future (img Alchemist-hp)

"We are living in a toxic world!" - you have probably heard or read this sentence more than once and while I cannot deny that the environmental load of, among others, heavy metals appears to be increasing, I can however tell you that, according to a recent study from scientists from the Tukushima Bunri University in Japan, exposure to some of those heavy metals produces quite unexpected results in a rodent model of the metabolic syndrome and in lean controls. Instead of making them gain weight even more rapidly, the "toxic" (maybe we will have to reconsider that, just as we did in the case of chromium) heavy metal cobalt did not only reduce the weight of the white adipose tissue of the rodents, it increased leptin, adiponectin, and HDL-cholesterol, as well, and thusly "may have a preventive role in obesity-related diseases" (Kawakami. 2011)

This is certainly the 1001st time I am writing this, but I cannot emphasize often enough that the "high fat diet" researchers use in their studies has (in most cases) nothing to do with the Atkins or even a low-carb diet. Its main characteristic is that it is hypercaloric and high in fat and carbs. Please keep that in mind whenever you read about another study on the detrimental health effects of "high fat diets".

For 24days Kawakami et al. fed a group of seven-weeks-old male mice either a standard diet with 357.6kcal/100g or a hypercaloric (cf. red box above) high fat diet (HFD), where the latter induced obesity and dislepidemia within 2 weeks. After this initial phase, i.e. when the HFD mice were already obese and metabolically deranged, the scientists injected the animals with Sodium Arsenite (NaAsO2: 1.0 mg/kg bw), Mercuric Chloride (HgCl2: 1.0 mg/kg bw), Manganese Chloride (MnCl2: 5.0 mg/kg bw), Cobalt Chloride (CoCl2: 0, 1.3, 5.0, 7.5 mg/kg bw) or saline (control).

Figure 1: Modulatory effects of 10 days of heavy metal injection in mice on a high fat diet; values expressed as changes relative to animals on a normal diet (data calculated based on Kawakami. 2011)

Now, if you look at the data in figure 1, you will notice that the administration of Mercuric Chloride may have been most "effective" in ameliorating the HFD-induced increase in white adipose tissue (WAT) mass (HFD +70%; HgCl2 -14% vs. normal fed control), but those "fat burning" effects went hand in hand with profound elevations of the liver enzymes AST, ALT (in this case we can safely assume that these were not coming from the muscle tissue of the animals) and the blood urea nitrogen (BUN) levels, which indicate deteriorations of the kidney metabolism. Manganese and cobalt, on the other hand, had negligible or even beneficial effects (compared to HFD alone) on liver and kidney health and ameliorated the weight gain to +10% and +17%, respectively.

Figure 2: Adiponectin and leptin serum levels and mRNA expression in mice after 10 days on a high fat diet with simulatenous injection of mercury or cobalt; data expressed relative to normal fed control (calculated based on Kawakami. 2011)

What is particularly interesting about cobalt, though, is that it did not simply starve out the adipose tissue by poisoning it (like that was probably the case for mercury), but triggered exactly those metabolic adaptations scientists have been trying to provoke with drugs for years now: elevations in adiponectin and leptin (cf. figure 2), the two adipokines, researchers currently believe to be essential for successful weight loss / maintenance.

Figure 3: pAMPK/AMPK ratio after injection of different dosages of Cobalt chloride (calculated based on Kawakami. 2011)

In a follow up experiment, the scientists, also found that cobalt dose-dependently increases AMPK phosphorylation (for more on AMPK, I would like to refer you to the Intermittent Thoughts series) in white adipose tissue (WAT), muscle and liver of the animals (cf. figure 3). Of the three tested dosages, administration of 5mg/kg CoCl2 per day resulted in the most beneficial AMPK response, while with the maximal dose of 7.5mg/kg the negative / toxic effects appear to prevail (another of these bell-shaped dose-response curves, I guess).

Figure 4: Glucose tolerance test in mice on high fat diet with or without cobalt injections compared to mice on standard diet (control); values in mg/dl (data adapted from Kawakami. 2011)

Now, you are probably asking yourselves: "So what's the catch?". A brief look at figure 4 tells you that is ain't glucose intolerance, as the cobalt treated animals had the exact same response to the glucose tolerance test, as the mice on the normal diet - in other words: cobalt completely reversed the HFD induced glucose intolerance, and it did so not only without negative effects on blood lipids, but in the presence of a profound elevation of HDL levels and a reduction in LDL levels (cf. figure 5).

Figure 5: Relative (to normal fed control) changes in blood lipid in mice on a high fat diet with or without heavy metal injections (calculated based on Kawakami. 2011)

And as if that was not enough, the cobalt injections also eradicated the iincreases in free fatty acids and ameliorated the increase in triglycerides.

From the lab to the bedside?

Last but not least, and I hardly dare showing you this graph, because I would expect that some of you will already be googling a source of injectable cobalt (which would be plain out stupid, before any reliable safety data and confirmation of these results in controlled human trials are available), cobalt had almost identical effects when it was injected to the mice on the normal diet.

Figure 6: Relative changes in body composition and liver and kidney parameters due to heavy metal injection in non-obese mice on a standard diet (calculated based on Kawakami. 2011)

As figure 6 goes to show the mice lost 33% of their white adipose tissue and liver, as well as kidney function did not take a beating (HDL stayed the same, LDL decreased by -1%). Whether we will see a obesity or even just a weight-loss drug based on cobalt in the near future, does yet still seem questionable. In view of the fact that the number of "bad things" (cobalt is in fact an essential nutrient as it is the active center of vitamin B12 = cobal-amin) that have unexpectedly positive health effects is increasing day by day, we do yet obviously have to ask ourselves, whether there may be some major flaws in our current understanding of how our body works and how it deals and is effected by "toxins", oxidants and co.

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. 
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