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marylin monroe
Showing posts with label magnesium. Show all posts
Showing posts with label magnesium. Show all posts

Pomegranate for Statin Users, Magnesium for Cancer-Free Colons, Cialis for Diabetic & Healthy Women and Protein Supplementation for 0.81kg More Muscle & 13.5kg More Strength Gains Than Placebo (Data From Meta-Analysis)

As the data in the graphs at the bottom shows, only vigorous physical activity (right), yet not moderate (middle), let alone light physical activity (left) will help kids to stave off the bad visceral body fat, which increases their waist line from year to year. The photo in the background was by the way taken in 1989 on Orchard Beach, in the Bronx. If I remember correctly that's 6 years before the release of Nintendo's first "Game Boy". And yeah, I got one and it really doubled if not tripled my sedentary time!
7 minutes! That's the SuppVersity figure of the week and a number that should actually ring a bell with everyone of you who is following my advice and pays a daily visit to the SuppVersity Facebook Wall. "Seven minutes" that's what scientists from the University of Alberta and their Canadian colleagues believe would be the amount of "vigorous physical activities" our kids should get (Hay. 2012). I am not sure, if those scientists are still youths, but assuming they are not, I wonder if they cannot remember the amount of "vigorous activity" (which was back in the day simply called "play") they themselves or at least their parents or grand parents got, in the days when you still had to physically kick a ball, if you wanted to play soccer with your friends.

I mean, it's already bad enough that today's kids spend 70% of their time with sedentary activity, only 23% with light activity (like walking from the sofa to freezer ;-), 7% with modest and only 0.6% with vigorous physical activity, wouldn't it be wise then, to rather shoot for the stars and work towards a much higher amount of vigorous activity? After all, even Hay's own study shows that only vigorous activity was associated with a reduced waist circumference and lower markers of metabolic disease (see illustration on the right).

Even if the kids don't make it to the moon, but over to the neighbor's basketball hoop or a public playground that would be a major improvement over the 'exhausting' walks from the Playstation to the fridge and back, wouldn't it?
  • Pomegranate the better statin? Adding pomegranate phytosterol (β-sitosterol) and polyphenolic antioxidant (punicalagin) to a statin and reduce adipose tissue ROS production by a whopping 73%!  In their most recent paper Mira Rosenblat, Nina Volkova, Michael Aviram report that the administration of Simvastatin (15 μg/ml) to macrophages in the petri dish did only only "modestly decreased macrophage reactive oxygen species (ROS)" (Rosenblat. 2012), the presence of punicalagin (15 or 30 μM) almost 'extinguished the fire' cutting back inflammation dose-dependently by another 61% or 79%.

    As a regular here at the SuppVersity yo will still be aware that Pomegranate does also contain a potent plant version of CLA, called CLnA, no? Well then go back and read the full article!
    Intriguingly, β-sitosterol alone showed had minor pro-oxidant activity, when it was administered to the J774A.1 macrophages cell line the researchers from The Lipid Research Laboratory in Haifa (Israel) were analyzing,
    "the combination of simvastatin, β-sitosterol and punicalagin, clearly demonstrated a remarkable 73% reduction in ROS production."
    So what's the use of the statin, then? After all the scientists also found (but rather not mention in their abstract) that the combination of β-sitosterol and punicalagin actually suppressed macrophage cholesterol synthesis as effectively as low dose Simvastin or high dose Pravastatin (Click here to read about pomegranate in the SuppVersity news)
  • Organo-Magnesium stops colon cancer in its tracks by inhibiting inflammation, and the findings a group of researchers from the Gifu University Graduate School report in a soon-to-be published paper are not surprising. After all many epidemiological studies studies like Folsom & Hong (2006), for example, have already shown that there is a -23% reduced risk of developing colon cancer for 55-65 year-old Swedish women in the highest vs. lowers quantile of magnesium intake. Earlier this year Wark et al. conducted a randomized trial and meta-analysis of the hitherto published studies and found:
    "Our findings support the hypothesis that higher intakes of dietary magnesium are associated with lower risk of colorectal tumors. The consumption of magnesium-rich foods may be a new avenue to explore further in the search for cancer-prevention strategies." (Wark. 2012)
    Tabs or capsules? A 2010 study has the answer to the question which form of supplemental minerals is the best for you. Roswitha Siener and her colleagues from the University of Bonn in Germany found that magnesium oxide from effervescent tablets is better absorbed than from capsules and you can be pretty sure that similar results will be found for other forms of magnesium. My advice would yet be: Save the money and just go for plain magnesium citrate powder.
    The meta analysis yielded 13% lower risk of colorectal adenomas and 12% lower risk of colorectal cancer for every additional 100mg of magnesium per day. This does yet not mean that by eating pounds of magnesium you could render yourself 'cancer proof', but it is good evidence to make sure to get at least the into the 380-500mg range. And if you want to supplement, you really won't need the organ-magnesium Kuno et al. produced by mixing magnesium oxide (0.22 g), citric acid (0.55 g), malic acid (0.55 g), and glycine (0.22 g) - unless you can't tolerate it, cheap magnesium citrate will do just as well.
  • Taldalafil for insulin resistant and healthy post-menopausal women?! (Murdolo. 2012) A group of European scientists have found that the administration of 10mg of Taldalfil (the notorious PDE-5 inhibitor in Cialis) to both diabetic and healthy controls led to
    • an increase in permeability surface area product for glucose , and
    • skeletal muscle interstitial lactate levels r
    The forearm glucose uptake, as well as the arterial lactate levels showed differential responses, while there was a trend for increased glucose uptake in the healthy controls, the latter was absent in the diabetic group. The profound decrease in arterial lactate levels in the diabetic patients, on the other hand, was not present in the healthy controls, whose lactate levels had already been in the normal range (see figure 1).

    Figure 1: Effects of 10mg of Taldalafil on arterial and intramuscular lactate concentration (Murdolo. 2012). The increase in intramuscular glucose oxidation (evidenced by the lactate that is generated during this process) could even be of interest to healthy women (and men?).
    Based on these findings, Guiseppe Murdolo and his colleagues argue that the results would suggest that acute Tadalafil administration can increase the capillary recruitment and nonoxidative glucose metabolism, without having consistent effects on forearm blood flow and regional lipolytic rate. However...
    "[...] notwithstanding the lack of measurable changes on forearm glucose uptake, the microvascular response to tadalafil emerged as an independent predictor of muscle glucose disposal in both T2D patients and insulin-sensitive controls."
    Well, and if those effects don't reach statistical significance, maybe 'others' will. After all a 2003 study by Caruso et al. suggests that Taldalafil can also increase "the frequency of sexual fantasies and of sexual intercourse, and enjoyment" (Caruso. 2003) in a group of  53 pre-menopausal women (age 22–28) years affected by arousal disorders. Maybe we should simply put Taldalfil into the drinking... ah, I am just kidding ;-)
  • Finally! Scientists determine 'exactly'*rofl* how much more muscle you can gain with supplemental protein (Cermak. 2012). I hope I do not have to point you towards the irony in the headline of this On Short Notice item. If this ain't your first visit to the SuppVersity you should by now be aware that calculations like add 1g of protein per day and gain x-amounts of lean muscle mass per month, year or whatever timespan are nonsensical and will provide, if anything, a very general orientation.

    That said, it is still interesting to see the actual results Naomi M Cermak et al.'s quantitative meta-analysis of 22 studies, of which 77% were conducted with untrained individuals (64% with young trainees) produced. Most studies, which had a duration of 6-24 weeks (median: 12 weeks), used 3-5 x whole body workouts / splits coupled with milk (mostly whey) protein supplementation in amounts that ranged from 10g to 106g - keep that in mind when you think about how 'exact' the following figures can actually be:
    • Size-wise and even more so strength-wise Arnold could still benefit from a protein shake after a workout. When it comes to the increases in type I and type II fiber CSA, his age could however put a spoke in his wheel.
      Fat free and fat mass - Compared with the placebo, protein supplementation significantly augmented the gain in FFM during prolonged resistance-type exercise training (weighted mean difference: 0.69 kg). A subgroup analysis for age showed that protein supplementation was beneficial for both the young and the old trainees, but that the total effect size in terms of fat free mass gains were ~1.7x higher in the young subject (+0.81 kg) than in the older ones (+0.48 kg;) subjects.

      What I find particularly surprising is that the subgroup analysis also revealed that training status had no significant and what's more, if anything a beneficial effect on the effect sizes in the young untrained (+0.75 kg) and trained subjects (+0.98 kg), respectively.

      As far as fat loss is concerned the scientists did not record any statistical significant differences compared to placebo and that despite the fact that the placebo in most of the 22 studies was a sugary carbohydrate drink.
    • Muscle fiber cross sectional area - As the gains in lean mass already suggest, the cross sectional area (CSA) of the muscle fibers increased: By ~ 212µm² in the type I fibers and 291µm² in type II fibers. Unfortunately, both the increases in type I and type II fibers were statistically significant only in the young trainees.
    • 1-RM Strength - The performance for the one-rep maximum (1RM) on the leg press improved across the board (+13.5kg more than in placebo) and that did work almost equally well for younger (+14.4kg) and older trainees (+13.1kg).
    I will leave it up do you what you want to do with this data and whether you think that studies like this are actually useful for the individual practitioner who does not - contrary to way too many dietitians - have to be convinced of the benefits of protein supplementation on top of the low 0.8g per body weight the dietary guidelines recommend.
That's it another saturdaily installment of On Short Notice and in case you feel that you could use some more educative news, tomorrow is another day ;-)

References:

  • Caruso S, Intelisano G, Lupo L, Agnello C. Premenopausal women affected by sexual arousal disorder treated with sildenafil: a double-blind, cross-over, placebo-controlled study. BJOG. 2001 Jun;108(6):623-8.
  • Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr. 2012 Nov 7.
  • Folsom AR, Hong CP. Magnesium intake and reduced risk of colon cancer in a prospective study of women. Am J Epidemiol. 2006 Feb 1;163(3):232-5.
  • Hay J, Maximova K, Durksen A, Carson V, Rinaldi RL, Torrance B, Ball GD, Majumdar SR, Plotnikoff RC, Veugelers P, Boulé NG, Wozny P, McCargar L, Downs S, Lewanczuk R, McGavock J. Physical Activity Intensity and Cardiometabolic Risk in Youth. Arch Pediatr Adolesc Med. 2012 Sep 10:1-8. doi: 10.1001/archpediatrics.2012.1028.
  • Kuno T, Hatano Y, Tomita H, Hara A, Hirose Y, Hirata A, Mori H, Terasaki M, Masuda S, Tanaka T. Organo-Magnesium Suppresses Inflammation-Associated Colon Carcinogenesis in Male Crj: CD-1 Mice. Carcinogenesis. 2012 Nov 3.
  • Murdolo G, Sjöstrand M, Strindberg L, Lönnroth P, Jansson PA. The Selective Phosphodiesterase-5 Inhibitor Tadalafil Induces Microvascular and Metabolic Effects in Type 2 Diabetic Postmenopausal Females. J Clin Endocrinol Metab. 2012 Nov 1.
  • Rosenblat M, Volkova N, Aviram M. Pomegranate phytosterol (β-sitosterol) and polyphenolic antioxidant (punicalagin) addition to statin, significantly protected against macrophage foam cells formation. Atherosclerosis. Available online 31 October 2012.
  • Siener R, Jahnen A, Hesse A. Bioavailability of magnesium from different pharmaceutical formulations. Urol Res. 2011 Apr;39(2):123-7.
  • Wark PA, Lau R, Norat T, Kampman E. Magnesium intake and colorectal tumor risk: a case-control study and meta-analysis. Am J Clin Nutr. 2012 Sep;96(3):622-31. doi: 10.3945/ajcn.111.030924. Epub 2012 Aug 1.

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

Image 1: "Please Dr. Andro tell me I can keep taking my essential multivitamin! I am just too busy to eat healthy..."
I must admit that I feel kind of awkward as I am about to defend one of those supplements, I consider to be the most dispensable within the dietary regimen of a physical culturist: the so-called multi-vitamin! In essence these small, and lately more often than not large pills do not even fall into the category supplement. With dose-equivalents way beyond what you would actually need, "multivitamins" are not even "replacements", they are madness or, I should say, the mad outgrowth of the prevalent "more is more" mentality that is beginning to harm us on every level of our society... but I am digressing, here. Let's take a look at the actual study which brought about such an upheaval in the supplement-addicted health community on the Internet.

Dietary Supplements and Mortality Rate in Older Women

Image 2: Is this you? No? Maybe she is "The Average American", then? No? Well, but the study says "vitamins are bad for YOU" and she could be one of the subjects (img. medscape.org)
The title alone, actually made me click the study away, back in the day when I first hit upon it, on one of my regular searches for new stories on the medical databases of the World-Wide-Web; and unless you are an old women (I would hope there were some older women reading the SuppVersity, but I guess there are none), you should have disregarded the study, as well. After all, we all know how the game changes after menopause and guess what, of those women, 98.6% were post-menopausal (in case you ever see studies done on ovariectomized rodents, remember that those are "menopausal", too ;-). Ah, and in case you are a post menopausal women with Africa-American or Hispanic background, there is likewise little reason for you to read on, because 99.2% of the women in the study were white (if you question whether or not ethnicity really matters, when it comes to the health effects of vitamins, I suggest you take a look at some reviews like Carmel. 1999).

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

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

So, let's see. What we have here is an offshoot of the Iowa Women's Health Study (IWHS), which is one of those highly over-estimate surveys, the media loves, because they boast of ten-thousands of "participants". In the case of the IWHS, "41836 women aged 55 to 69 years"... well, at least that were the women the scientists send their little questionnaires to back in 1986. Interestingly, this is also where the first bias (i.e. a deviation from "objectivity") came into play:
Respondents were slightly younger, had lower body mass index (calculated as weight in kilograms divided by height in meters squared), and were more likely to live in rural areas compared with nonrespondents.
So instead of the average American "older woman", the scientists suddenly had the "slightly younger" not just as obese, better off American older women, as their study object. Moreover, the number of participants dropped to 38772 women or, in other words, the scientists "lost" 7.3% of their study population even before the study actually began. Now, of those, the Mursu et al. selected 29230, who were the "elite" which responded to both the initial 1986 and the 2nd 1997 follow-up questionnaire.

Failure 1: Not representative of "The Average American"

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

The latter, i.e. the questionnaire, assessed the use of 13 supplements:
  • multi-vitamins; 
  • vitamins A, beta-carotene, B6, folic acid, B complex, C, D, and E; 
  • iron, calcium, copper, magnesium, selenium, and zinc
Now, the scientists show off their wealth of knowledge and state that "[d]ifferent forms of vitamin D, cholecalcif-erol (D3) or ergocalciferol (D2), were not distinguished". While this is obviously important, it would have been even more important to distinguish between different forms of vitamin B6 (pyridoxin vs. P5P), B complex (you can have a complete one, one with equal doses, one particularly high in one B vitamin, etc.), vitamin E (I suppose you read the first installment?), iron (heme, non-heme, chelated, etc.), copper / magnesium, selenium, and zinc (oxide, chelated, etc.), because we know that these different forms of vitamins and minerals are not only differentially absorbed, but also exhibit differential effects on our health and well-being.

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

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

Failure 3: Careless ignorance towards dosages

Raw foods are dangerous and so is raw data

Hence, the scientists got a set of data that was full of holes from a group of women who are by no means representative of "The Average American" (let alone every human being) - what did they do next? Well, obviously "raw data" is as dangerous as raw meat (or even raw milk), that is why the next step for every good scientists is data processing. In that Mursu et al. were particularly skilful as far as not revealing what they actually did was concerned:
In the minimally adjusted model, we adjusted the association for age and energy intake; in multivariable adjusted model, version 1, we additionally adjusted for educational level, place of residence, diabetes mellitus, high blood pressure, body mass index, waist to hip ratio, hormone replacement therapy, physical activity, and smoking status. For multivariable adjusted model, version 2, we added intake of alcohol, saturated fatty acids, whole grain products, fruits, and vegetables.
Even, or I should say, especially for a physicist, who is a 75% mathematician, the idea that by some sort of mathematical magic you could reliable subtract out all those influence, so that you get the "real picture" of what is going on, with an average human being is so hilarious that I avoid any further comment. Everything that goes beyond the "minimal adjustment" is so full of speculative hypothesis and mainstream paradigms (like "Whole grains are good for you! The more, the better!") that I will simply ignore this data... unfortunately these results of "3+3 = 666" mathematical manipulation were what the scientists (in their press releases) highlighted as their main results and what was accordingly taken up by the laymen (initially I wanted to write idiots, but that would be unfair, because laymen they are) in the editorial offices of the mass media.

Failure 4: Over-"analysis" of the data

Let's get to the raw truth

This would not be the SuppVersity, if I did not have something to offer that goes beyond the angry rants and criticism (see above) you probably have read elsewhere, anyways. So, I went through the pains of compiling and comparing the "real", i.e. the N=X data and not the calculated hazard ratios for you.
Figure 1: Raw data and minimally adjusted (age and caloric intake) data on the effect of taking vitamin A, beta carotene, vitamin C, vitamin D, vitamin E, and finally the multivitamins on overall mortality (data calculated based on Mursu. 2011)
Now, I want you to take a close look at the data for vitamin A, beta carotene, vitamin C, vitamin D, vitamin E, and finally the multivitamins. I don't know what you see, but I see only vitamin A and beta carotene scratching at the increased mortality margin of 1.0 (cf. dotted red line in figure 1). And, just for a better understand, two examples:
  • the 1.04 as for vitamin A (minimally adjusted) in 2004-08 indicates a +4% higher risk and 0.80,
  • the 0.80 for vitamin E (raw data) in 2004-08 indicates a -20% decrease in mortality risk
So, what would you say, how "dangerous" is taking vitamin pills if you do not process the data to death? Interestingly, things get really nasty, from here. And moreover, they get nasty, where you probably would not have expected it unless you are a very diligent student of the SuppVersity and are thus aware that messing with the methylation cycle via B6 or folic acid supplementation for no reason is not a good idea.
Figure 2: Raw data and minimally adjusted (age and caloric intake) data on the effect of taking vitamin B6, folic acid, B-complex, calcium, and magnesium on overall mortality (data calculated based on Mursu. 2011)
Given the fact that an increasing amount of "old" people are taking magnesium supplementation, I would say that in this case the age-adjustment is probably necessary - if you also consider that back in the 1980s this bias was smaller, since people were not told that taking mg supplements would be necessary for older folks, the respective adjustment will be "too small" and thus I would simply ignore the fact that the 1996 value still signifies a +2% greater risk of dying when you take a magnesium supplement (add to that that the study participants could have taken magnesium in the 10x recommended dosage and the scientists would not know that /see comment on dosage, above). What really surprises me, though is the enormous benefit that is (even in the raw data) associated with calcium supplements - 22% reduced risk according to raw data and 21% reduced risk with age/energy adjustment - impressive!
Figure 2: Raw data and minimally adjusted (age and caloric intake) data on the effect of taking iron, copper, zinc, and selenium on overall mortality (data calculated based on Mursu. 2011)
Last but not least - the worst offenders, the dreaded "heavy metals" ;-) Ok, I guess iron really is a bad guy (at least for post-menopausal women), but even copper, which has gotten such a bad rep, lately turns out to come pretty handy in the female part of the aging American population, ... interestingly only in the early to late 2000s - how come? I'll leave it up to you to make up your mind on this and other questions, but I assume that now, that you know the raw truth, you will not blindly follow Bjelakovic's campaign to "wake up [regulatory authorities] to their responsibility to allow only safe products on the market" (Bjelakovic. 2011), but rather scrutinize his "invited comment" to the Mursu study, which was published in the same issue of the Archives of Internal Medicine and has caused such an upheaval among the increasingly health conscious American and International public.

Spot Reduce Abdominal Fat With Green Tea, Green Clay & Magnesium Sulfate Soaked "Plaster Body Wrap"... Really!?

No. Some green slime + cellophane is not going to make this possible within 5 weeks ;-)
I have been making fun of doing sit-ups to shed body fat in the midsection only recently on the SuppVersity Facebook Wall and what do I see today? A study that claims that a "plaster body wrap" could help you burn abdominal fat... what the f...at!?

First things first: In the "conflicts of interest" declaration at the end of the paper that is still in the "accepted manuscript" form, the authors declare no interest. If that's correct - and I simply assume it is - they probably have not yet patented their green tea + green clay + magnesium sulphate infused "plasters". This does not only mean that it is unlikely that the scientists "improved" the results of the treatment group; it does also mean that this could be your chance to make a fortune as a fat burning patch or fat burning oil, -creme or -whatever producer :-)

Why don't you test it yourself!?

Now, you all know that money doesn't grow on trees. So aside from a proper amount of entrepreneurship you will also need the will and patience to (1) massage your tummy with an alcoholic extract of green tea (alcohol at 96%) for five minutes (2) apply a solution of ~34g of green clay combined with ~19g of magnesium sulphate in ~17ml of distilled water to belly, (4) plaster your abs with plaster bandage that was previously impregnated with 3g of a green tea and another 7g of magnesium sulphate and finally (5) wrap yourself up in cellophane - go for it! If it works, it's your chance to make a fortune ;-)
In case you missed the recent SuppVersity Facebook post on "spot reduction": A Study from the 1980s says "5007 sit-ups won't shrink your belly by an inch" - I guess the 27-day sit-up challenge the scientists had their subjects perform will remind you of the "six-back" or "flat belly" specials in the Men's H. and Sh*pe magazines of this world; programs of which I can assure you that they will yield the exact same results as the one in the study: NONE → "Body weight, total body fat (underwater weighing), and fatfolds and girths remained unaltered." (Katch. 1984)
I guess the tone in the previous paragraphs has probably given away that I am still somewhat skeptical about the magical fat burning prowess of this "beer-belly remedy", but if you look at the results the 10 normal / pre-obese women in the active arm of this 5-week study you will have to concede: That's pretty impressive! Especially in view of the fact that ll they did to achieve that were two "fully wrapped" up endurance exercise sessions at 50% of their individual maximal heart rate reserve (=maximal heart - resting heart rate) per week.
Figure 1: Difference (active - control) in body fat / skinfold thickness (in cm) and calculated total body fat (caliper data) after 5 weeks with only two "fully wrapped" up 30min endurance sessions (Moreira. 2013)
Alright, I have to admit that the changes you see in figure 1 are pretty pathetic compared to the boastful promises the supplement industry uses to get rid of some Chinese herbal waste they label as "fat burner", "fat incarcinator", or "proven thermogenic". Nevertheless the mere idea that cellophane powered kitchen-sink approach to spot redution could actually work is impressive - don't you think so?
SuppVersity Suggested Read: "High Reps for "Spot Reduction" Works - Yet Not the Way Trainees Believe. Fat Loss Occurs in Untrained Body Parts" | read more
Make of the results whatever you want... and in case you feel inspired to try the "recipe", let me know how it worked. I promise I am not going to patent it before you can ;-)

Ok, enough of this nonsene. I guess, before you get totally psyched and wrapped up, it's worth mentioning that there is no specific information about the time-point when the ultrasound and skinfold measurements were taken. This may sound irrelevant, but if this was anywhere close to the last workout it is possible that the 10 subjects in the "patch" group simply lost more subcutaneous water than the 9 ladies in the control group and all those "significant results" were just measuring errors (in the broadest sense).

References:
  • Katch et al. Effects of Sit up Exercise Training on Adipose Cell Size and Adiposity. Research Quarterly for Exercise and Sport. 1984; 55(3).
  • Moreira JS, Carneiro Pinto de Melo AS, Noites A, Couto  MF,  Argel de Melo C, Freire
    de Almeida Adubeiro NC. Plaster Body Wrap: Effects in Abdominal Fat. Integrative Medicine Research. 2013 [accepted manuscript]

Which Micro- & Macronutrients Intakes Are Associated With High HDL Levels? Study Shows Magnesium & Folate Are, High Carbohydrate & Total Animal Fat Intakes Are Not!

The advantage of HDL is its stability that reduces the risk of plaque build-up in the intestinal wall, which is clogged by the remnants of oxidized LDL and causes heart disease & co.
First things first: We are not talking about "hard experimental evidence" as you could generate it in a randomized controlled trial in a metabolic ward. The data I am reporting today is from a cohort with 1,566 participants with extensive lipid phenotype data completed the Harvard Standardized Food Frequency Questionnaire to determine their daily micronutrient intake over the past year - an epidemiological study that used stepwise linear regression was used to separately evaluate the effects of dietary covariates on adjusted levels of HDL-C, HDL-2, HDL-3, and apoA1.

Interestingly, this is the first study with a quality data-set that determined the association between specific dietary micronutrients with HDL-C, HDL-2, HDL-3, and apoA1, and how these dietary associations differ across the various measures of HDL - not just one.
Learn more about HDL, cholesterol, heart health & co at the SuppVersity

Prohormones mess with your cholesterol.

Every other day fasting for your lipids
Dairy Protein Satiety Shoot-Out: Casein vs. Whey

Fish oil & oleic acid counter their ben. effects

Eggs increase cholesterol reverse transport

Does roasted coffee increase bad LDL?
To identify the HDL-promoters in the diet, the scientists use demographic and clinical variables in the base model. What they found was that numerous dietary intakes increased total HDL-C variance.
The results of their stepwise linear regression model in Table 1 indicate - probably for some people much surprisingly - that all alcohol intake levels were positively associated with HDL-C.
"In addition, magnesium, folate, and the saturated fat, myristic acid (14:0), were all positively and independently associated with HDL-C. Carbohydrate intake, iron, and % of fat derived from animal sources were each negatively additive for HDL-C." (Kim. 2014)
Similar effects from dietary intakes were observed for HDL-2, of which we know that it is decreased in women with rheumatoid arthritis (Arts. 2012) and individuals with other inflammatory diseases (including metabolic syndrom) and associated with a slightly higher reduction in acute myocardial infarction risk than "regular" HDL in several studies (Salonen. Salonen. 1991; Stampfer. 1991; Buring. 1992; Gaziano. 1993) for all alcohol intakes, magnesium, folate, and myristic acid (14:0), eicosapentaenoic acid (20:5, a ω-3 EPA), all of which were positively and independently associated with HDL-2 levels.
Table 1:  Best-fit model from stepwise linear regression predicting HDL-C levels using dietary intake data (Kim. 2014)
The opposite was the case for arachidonic acid (20:4, an ω-6 ARA), carbohydrate and iron intakes, which were both negatively associated with HDL-2 (see Table 1).

Don't forget to put things into perspective!

And just to make sure, I don't get angry emails from bulletproof coffee drinkers: Your coffee is fine, the content of the only "good" saturated fat, i.e. myristic acid, happens to be especially high coconut oil (41%; Sodamade. 2013) and relatively high in butter (12% independent of whether it's grass-fed or not; Couvreur. 2006) - surprised? Not really, I guess. As a SuppVersity reader you are by now aware that the bad reputation coconut oil and butter have for being mostly saturated fats is no longer supported by contemporary scientific evidence (Dias. 2014).

And with respect to the total animal fat intake - for the average Westerner that's a good measure of how much processed meat he / she eats, so I would not overrate the small negative association (1/80 of the one of having a ton of carbohydrates in your diet!) the scientists found in the study at hand.
Eggs are unquestionably and exception from the "animal fat" is bad for HDL rule | learn more.
Bottom line: With the exception of folate, which has previously not been reliably associated with increases in HDL, let alone speficic HDL subfraction, the improvements with alcohol, magnesium and EPA are not exactly news. The same is true for the decreases in response to increased intakes of (all) animal fat, arachidonic acid, carbohydrates and iron.

In the end, the study confirms what we already know: The way you eat (and train; see Leon. 2001) can directly affect the level of the heart-healthy HDL fractions in your blood.

One thing you should keep in mind, though, is that it's the ln = logarithmus of these macronutrients and micronutrients that's associated with increased / decreased HDL and its subfractions. This means that small changes are not really important. Things that would count are eating low carb vs. extreme high carb or eating no folate containing foods vs. a significant amount of these.
References:
  • Arts, Elke, et al. "High-density lipoprotein cholesterol subfractions HDL2 and HDL3 are reduced in women with rheumatoid arthritis and may augment the cardiovascular risk of women with RA: a cross-sectional study." Arthritis Res Ther 14.3 (2012): R116.
  • Buring, J. E., et al. "Decreased HDL2 and HDL3 cholesterol, Apo AI and Apo A-II, and increased risk of myocardial infarction." Circulation 85.1 (1992): 22-29.
  • Couvreur, S., et al. "The linear relationship between the proportion of fresh grass in the cow diet, milk fatty acid composition, and butter properties." Journal of dairy science 89.6 (2006): 1956-1969.
  • Dias, C. B., et al. "Saturated fat consumption may not be the main cause of increased blood lipid levels." Medical hypotheses 82.2 (2014): 187-195.
  • Gaziano, J. Michael, et al. "Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction." New England Journal of Medicine 329.25 (1993): 1829-1834. 
  • Kim et al. "Effects of dietary components on high-density lipoprotein measures in a cohort of 1,566 participants." Nutrition & Metabolism 2014, 11:44.
  • Leon, ARTHUR S., and OTTO A. Sanchez. "Response of blood lipids to exercise training alone or combined with dietary intervention." Medicine and science in sports and exercise 33.6 Suppl (2001): S502-15.
  • Salonen, Jukka T., et al. "HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men." Circulation 84.1 (1991): 129-139. 
  • Sodamade, A¹, and O. S. Bolaji. "Fatty acids composition of three different vegetable oils (soybean oil, groundnut oil and coconut oil) by high-performance liquid chromatography." Chemistry and Materials Research 3.7 (2013): 26-29.
  • Stampfer, Meir J., et al. "A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction." New England Journal of Medicine 325.6 (1991): 373-381.

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
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.

On Short Notice: Red Onions For Glutathion & Jiagulan For Muscle Glycogen, Low Iron & Obesity, Sodium Caprate, Useless Probiotics & Leaky Gut, Perivascular Fat & Heat Shock Proteins for Your Heart & Magnesium vs. Migraine

Image 1: You may already have read it on the SuppVersity Facebook Wall; "Sacrificing sleep in order to study won't improve your college grades..." it could however easily whack your circadian rhythm and give you headaches. If those turn into a migraine, you may be happy to have read about beneficial effects of magnesium on the incidence of these crippling and painful attacks (see last item in this installment of "On Short Notice" ).
In order to avoid having another weekend of "On Short Notice" posts, I decided to post the first collection today, already. The topics are, as usually, only loosely related and I hope that each and everyone of you will find something he or she considers interesting. We'll start out by having a brief look at the amazing antioxidant effects of red onions, and then delve deeper into the connection between obesity and low ferritin levels and a brief reminder that sometimes good things can become bad, if they are not handled properly, next on the list are the tight gut junction opening effects of sodium caprate which may be a good thing if your goal is to increase the bioavailability of berberine, but a very bad thing, if other molecules take the opportunity and pass through the open doors, as we are then going to see Dr. Shirota's probiotics are probably not going to help you avoid this problem and they are certainly not helping patients with metabolic syndrome: The latter is probably also true for PPAR-gamma antagonists, which may help prevent visceral fat accumulation, but could at the same time precipitate to heart disease by decreasing the surprisingly heart-healthy perivascular fat.
Although more of an ergogenic, Gynostemma penthaphylum (aka Jiagulan) is probably a more promising strategy to get in better shape. If it allows you to train harder, it will also allow you to make better use of potential systemic health effects of exercised induced heat shock protein expression... and just in case all that was so much information that you are having a headache once you have arrived at the end of this blogpost, a 500mg dose of magnesium could help you reduce the incidence of migraine attacks by more than 60% whether additional 500mg of carnitine make this treatment even more effective does yet remain to be elucidated!
  • Do your liver and body antioxidant system a favor and add a couple of red onions to your diet! That's the straight forward take home message from a recently conducted study by a group of Korean scientists (Lee. 2012). The researchers had investigated  the effect of red onion on the total activity of antioxidant enzymes in 18-week-old Sprague-Dawley rats. To this ends the rodent had been kept on a diet enriched with red onion peel, flesh or both (all pulverized and mixed into the standard chow for a total content of 5g per 100g) for for weeks.
    Figure 1: The red onions outperformed easily outperformed their uncolored white brethren and cousin, white onions and garlic, in the in vitro dish and had profound antioxidant boosting effects in the in vivo study (Lee. 2012).
    The results, (a) a significant increase in plasma SOD activity in the red onion peel and red onion (peel + flesh) groups, (b) a significantly higher GPX (enzyme that recycles glutathione) activity in the in the red onion flesh group and (c) a general tendency towards higher catalase and ORAC activity in the livers and profoundly reduced liver malondialdehyde (=marker of lipid peroxidation) levels in the red onion groups provide an in vivo (allegedly only "in rodent vivo" ;-) confirmation of the in vitro data in figure 1 which is - as usual - to be treated with caution before respective experiments in complex, real organisms confirm that they are more than artifacts of the respective essay.
  • Low iron (ferritin) associated with obesity in adolescents, but simple eating more iron probably won't solve either the iron deficiency, nor the (central) obesity. That's at least what the results of a recent investigation in normal and fat Greek kids would suggest, after all the fat kids did already consume more iron in their diets than their lean age-mates (Moschonis. 2012).
    What makes this study worth mentioning is the (as usual hasty) conclusion that iron must be a bad guy, when just its mismanagement (probably as a result of adiposity induced liver problems, or, as a handful of older and recent studies would suggest vitamin A deficiency; e.g. Arruda. 2009; Citelli. 2012; Yohsikawa. 2012) is a problem - so don't get fooled, donating blood every other week won't lean healthy people out, it will just drain them out.
  • Figure 2: Sodium caprate won't "open" the tight gut junctions for berberine, only, but also for all sorts of other, mostly unwanted junk - self-induced temporary leaky gut so to say!
    Sodium caprate opens tight junctions of the gut and let's berberine in. The consequence is an amplification of the hypoglycemic effects of berberine (Lv. 2012), but at the same time it is likely to amplify the effects of whatever you else put into your mouth or the critters that live in your stomach are pooping out - I guess it should be obvious that I am referring to the LPS assault from your gut microbiome, here and that the potential increase in lipopolysaccharide could well outweigh (in a negative sense) the benefits you would see from an increased bioavailability (~1.5-2.3 fold; cf. Lv. 2010) of berberine.
    Against that background I am really not sure how sensible the use of sodium caprate or other "tight junction openers" of natural or pharamacological origin really is. But hey, that's just me - maybe you are less cautious...  if there are not yet any products like that on the market, it probably won't be long until the first "enhanced" berberine appear in the line-ups of the large "health supplement" vendors on the Internet.
  • Image 2: Patented lactobacillus strains are all the rave, and probably big business... that does yet not mean that they work - regardless of whether they carry the name of famous Drs or not ;-)
    Probiotic supplements don't cure everything - although many ads may give just this impression. In a recently published study, Swiss researchers were not able to show any beneficial effects of the patented L. casei Shirota strain on the increased gut permeability of 28 patients with metabolic syndrome (Leber. 2012). In the course of the three months study period, it rather exasperated the already elevated C-reactive protein levels, due to liposaccharide leakage through the leaky gut into the system and I bet the only reason that the conclusion states that the dosage may have been too low instead of "this is initial evidence that the use of L. casei Shirota is not useful if  not counter-indicated in to treat gut permeability in patients with MetS", was the financial support by Yakult Europe the patent holder of L. casei Shirota ;-)
  • PPAR-gamma ablation leads to loss of perivascular adipose tissue (PVAT). What may at first sound great could in fact be deadly. The recently published results of Chang et al. show quite clearly that non-tissue-specific blockade of the "fat builder" PPAR-gamma (cf. "Tangeritin, Natural Metformin from the Rind of Mandarin Oranges Hits the OFF-Switch on Diet Induced Obesity") is a dangerous undertaking. While keeping the differentiation and growth of body fat at bay, especially in the abdominal region, would be a good thing, the high rate of atherosclerosis among the mice from the laboratories of the University of Michigan confirms that "not all body fat is created evil" (Chang. 2012).
    Figure 3: Fitzgibbons et al. were already able to show that the UCP-1 expression, which is a marker of metabolic activity, in PVAT is equally high as in the meanwhile infamous brown adipose tissue. In short - PVAT just like BAT will not just store superfluous lipids, it will also burn them and prevent them from accumulating in the vasculature (Fitzgibbons. 2011)
    As it turned out, PVAT, rather than being proinflammatory and hazardous, actually has a protective function on the vasculature it is sourrounding. In fact, the results Chang et al. are presenting in the latest issue of Circulation suggest the assumption that PVAT is anti-inflammatory and functionally similar to the metabolically active brown adipose tissue that has gotten quite some attention by experts ad laymen as of lat. When it's suddenly missing, the lipids inside the vascular can no longer be cleared into the perivascular adipose tissue where they would be oxidized and disposed of. In addition, the ensuing pro-atherogenic coupled with the absence of PVAT-derived prostacyclin, a prostanoid that's metabolized from endogenous arachidonic acid through the cyclooxygenase (COX) pathway and acts as a potent vasodilator (cf. Ruan. 2010) could thus easily set you up to die before your time - regardless of how lean you may have become...
    And though it is very unlikely that this is going to happen from the use of one of the freely available herbs with anti-PPAR-gamma effects (e.g. tashinones from Salvia miltiorrhiza, or the previously cited tangeritin), it certainly is a good reminder of how fatal our constant black-and-white thinking can be, when it is injudiciously applied to such complex matters as our own body.
  • Image 4 (dracoherbs.com): Gynostemma penthaphylum is also known as Jiaogulan, is often mentioned in the same breath with ginseng in TCM
    Gynostemma penthaphylum boosts endurance by ROS scavenging and multiplying skeletal muscle glycogen stores. Not yet another potent anti-oxidant was what I first thought,when I hit upon the soon-to-be published study from Shaanxi Normal University in Xi'an, China, but after taking a closer look it turned out that the way this century old adaptogen that goes by the name jiaogulanin TCM and is an herbaceous vine of the family Cucurbitaceae (cucumber or gourd family) indigenous to the southern reaches of China, northern Vietnam, southern Korea, and Japan, could actually make quite an exciting supplement (Chi. 2012). After all its high ROS(radical oxygen specimen) scavenging abilities are only part of what allowed the rodents in the study by Chi, Tang, Zhang & Zhang that had been treaded with isolated polysaccharides from this plant to go significantly longer during a standardized exercise performance test.
    The more intruiging part of the performance boost, however came from the direct pro-gluconeogenic and glyocogen storage promoting effects of the alpha variety of the three Gynostemma penhaphylum polyssacharides the scientists had extracted. If similar effects would be seen in humans, GP would certainly make a valuable addition to the regimen of anyone who does not just perform 1-rep maxes day in and day out - and let's face it: In view of the fact that the glycogen can't be synthesized from nothing, it could also help to burn body fat, by it's repartitioning effects.
  • Figure 4: It would certainly be an unwarranted overgeneralization to ascribe all beneficial effects of exercise to the systemic expression of heat shock proteins. But still, there is increasing evidence that their controlled expression does at least contribute to the numerous beneficial effects exercise has on our brains, hearts and other organs; interestingly these effects are likewise mediated by the breakdown and the protection and "recycling" of organ tissue.
    Will training your biceps, heal your heart and protect your brain!? You probably know that the scientists at the McMaster University have put the myth of the pro-anabolic effects of systemically circulating hormones that are released response to isolated muscle training (eg. "train your legs to increase your testosterone and see your arms grow") at rest, years ago. Now, a study that's soon going to be published in theh Journal of Experimental Biology suggests that testosterone, growth hormone and co. may not be the only molecules we should be looking for, when we talk about possible non-localized effects of exercise (Jammes. 2012). Another class of proteins that has gotten quite some attention esp. in the context of the profound effects of occlusion training, the so-called heat-shock proteins, which are released in response not just to heat, but to exhaustive contractions / trauma / hypoxia / etc., could in fact play a likewise, probably more important role not so much in skeletal muscle growth, maybe, but in the overall systemic response to exhaustive skeletal muscle contractions. 
    After all, Jammes et al. observed a delayed, but significant elevation of non phosphorylated HSP25 and HSP70 in skeletal and respiratory muscles, kidney, and brain. Now, of HSP70, for example, it has long been known that it exerts cardio-protective effects (Martin. 1997). In addition to its anti-apoptotic effects, it does yet also contribute to the proteolysis (=protein breaking) that's a necessary part of the continuous clean-up processes that remove the "junk" and "clutter" (defect protein structures) from your body in order to keep everything functional (Lüders. 2000). Similarly, HSP25 (aka HSPB1) exerts both cytoprotective effects due to its ability to modulate reactive oxygen species and raise glutathione levels, as well as proteolytic effects and is working hand in hand with HSP70 by inhibiting protein aggregation and stabilizing partially denatured proteins, so that they can be refolded by the former. That the latter could be of particular importants in view of the neuroprotective effects of exercise is also supported by a couple of trials in which HSPB1, to be precise, its exogenous administration or endogenous overexpression, have been evaluated as treatment or preventive strategies in ALS (Lou Gehrig's Disease), Huntington's, Parkinson's, Stroke and acute nerve injury (for an overview see table 3 in Brownell. 2012).
  • Figure 5: The benefit of l-carnitine is questionable, despite the fact that the serum l-carnitine in the Mg group dropped to a similar extent as in the control group; over time the carnitine depletion could however become important (Tarighat Esfanjani. 2012)
    Headaches? Magnesium and l-carnitin help! At a dosage of 500mg/day magnesium oxide, alone did already have significant beneficial effects on the occurrence of migraine in  106 females and 27 males volunteers who were diagnosed with headache according to the International Headache Society criteria, were between the age of 18 and 55 years old and "had severe and continual headache lasting from 4 to 72 h, unilateral and pulsating headaches with moderate or severe intensity, migraine with or without aura, at least two attacks per month, headaches which were aggravated by routine physical activity and associated with nausea and/or photophobia, and phonophobia" (Tarighat Esfanjani. 2012).
    So, if that sounds like you (I don't hope it does) magnesium should be the least you should take, the additional 500 mg/day L-carnitine is questionable - just as whether ALCAR may have provided greater benefits. Apropos, you do realize that this is neither transdermal nor any fancy chelated magnesium or at least magnesium citrate that did the trick? Yeah, right: The same "worthless" (put name of random nutrition guru, here) mg-oxide you find in the cheapest fizzy tablet from the supermarket did the trick!
If you are now thirsty for more, I suggest you check out the SuppVersity Facebook Wall (which is by the way updated several times a day), like the career-boosting information that sacrificing sleep in order to study is a bad idea, that Caucasians, compared to Asians, lose weight relatively easily, but have a hard time getting rid of their bellies, or, if all that ain't for you, how the wise producers of "functional foods" are planning to add a little wood aka methylcellulose into your yogurts and smoothies to curb the cravings you probably would not have, if they had not removed all the fat from it, before ;-)

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