Pengetahuan Umum Praktis: omega 3

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Saturday, October 26, 2013

SuppVersity Science Round-Up Seconds: Supplement-Drug Interactions, Exercise and Psychology, Running vs. O-Lifting & Right Ventricular Hypertrophy, News on the N3-to-N6 Ratio, the CYP Enzymes, Endocannabinoids & Telomeres

The SuppVersity Science Round-Up every Thursday live on Carl Lanore's Super Human Radio -- tune in live at 1PM (EST= 6PM GMT)!

I hope that most of you have already had a chance to listen to yesterday's installment of the SuppVersity Science Round Up on Super Human Radio. In case you didn't, or have been waiting for me to post the link to the podcast (just a reminder: you can always download the latest show, from the navigation bar on the right, where it says: "Physical Culture for your Ears"), I'd suggest you go and download the podcast either now, or after going through today's SuppVersity Science Round Up Seconds.

The "Seconds" are as the name implies no "leftovers", but actually yet another selection from the selection of god knows how many interesting newsbits I usually pile up for the short 1h show, Carl and I are doing every Thursday. I would therefore encourage everyone to do both, listen to the podcast and read the "Seconds" one day later. After all, the things Carl and I discuss on the air won't reappear here, they are "SHR exclusives", so to say ;-)

Apropos, in yesterday's show, the topics we did cover were

premature ejaculation, and how only two hormones seem to make a difference,
peptides as prostate cancer vaccine, and how Harvard scientists build them from scratch,
supps vs. medications, and how fatal commonly overlooked interactions can be, and
copper, and why it may well matter than raw milk has 2-3x more than pasteurized milk

and before we go on with the actual "seconds", I must acquit myself of a promise -- the promise to provide you with more information on #3 on the above list.

Supplemental data: Supplement vs. drug interactions

Figure 1: Important supplement drug interactions based on Tsai (2013)

Those of you who have already listened to the podcast will probably be waiting eagerly for the supplemental material with more information about the potential pitfalls with supplement-drug interactions, Carl and I have been talking about on yesterday's show. With some digging, typing, searching, excerpting and formatting on my part, I have actually come up with a quite comprehensive and for people who are not familiar with all the funky drug names, probably even more understandable version (see figure 1) of the tabular overview H.H. Tsai and colleagues from the China Medical University Hospital and the College of Pharmacy at the University of Illinois at Chicago have included in their latest review of the literature (Tsai. 2013).

What I left out are the two pages (!) part on St. John's wort. With 147 drug (!) interaction ranging from "A" as in "amiodarone" to "W" as in "warfarin" and covering almost every drug type from anti-depressants, protease inhibotors, calcium channel blockers, PDE-5 inhibitors (viagra & co), SERMs, proton pump inhibitors, etc.. In view of the fact that these are only the known interactions, it would be easier to list those drugs with which St John's does not conflict, anyway. So, unless you have a study at hand which conclusively shows that St. John's is no problem, I would rather err on the side of caution, than end up in the ER.

Top 5 of the most frequent interactions observed with medication that act on (ranked by frequency, figure in brackets indicates percentage of all drugs in the study; based on Lin. 2013):

nervous system (19.6%)
cardiovascular system (17.7%)
antiinfectives for systemic use (14.7%)
alimentary tract and and immunomodulating agents (12.2%)
musko-skeletal system (6.4%)

As far as the supplement list in figure 1 goes, the most frequent potential side effect due to supplement-drug interactions affected drugs / supplements that play a role in blood coagulation. Danshen, evening primrose, gingko, glucosamine, white willow bark, garlic, vitamin E, fish oil to name only the most common ones, they all can increase the risk of bleeding not only, but specifically in patients who are taking warfarin (aspirin, ibuprofen, heparin and others were on the list, as well).

"What’s wrong with telling a patient, 'If you don’t hear from us with your lab results a few days, give us a call'? The answer is plenty, if that patient is receiving warfarin therapy. Because warfarin has a narrow therapeutic range and complex pharmacology, insufficient monitoring or errors in dosing can lead to severe and possibly life-threatening bleeding and clotting in patients receiving it." (Bush. 2002)

In view of the "top 5" above, this certainly sounds counter-intuitive, but we are dealing with a practical research bias here. As I mentioned on the air, there is simply an overabundance of research on potential interaction with warfarin, because finding the right dosage and adapting it appropriately is already hard even when there are no confounding variables, so that a sudden supplement-drug interaction and subsequent increase in the risk of bleeding can potentially be fatal (see the quote in the red box to the right)!

Regardless of what medication you may be on, rules that apply for a healthy individual that does not take any medication chronically (not even 'harmless' NSAIDs), don't apply to you! So please for one, follow the recommendation you find on each and every supplement to "talk to your medical practitioner" before you add another 'harmless' supplement on top of the 'harmless' over-the-counter or prescription drugs you are taking.

The Seconds: Interesting news that have been missing from yesterday's show

After this pretty lengthy addendum, let's get to three other items I had actually planned to have on the show, two of them are exercise, while the third one is a health and supplementation... and, when I come to think about it, obviously also diet related news-item:

Exercise makes you happy and puts an end to the greed for money! That's not exactly the result of a recently conducted study from the Charité in Berlin (Bothe. 2013), but it is more or less what follows from the differential response Bothe et al. observed in their untrained and highly trained subjects to monetary stimuli after they had completed a standardized running exercise (30 min at 60-70 % VO2max, T) or placebo (P).
Who would have thought that: Exercise reduces the anticipatory response to monitary incentive delay (MIT) test (Bothe. 2013)
"Acute exercise was found to influence gain anticipation. In the P compared to the T group a more pronounced anticipation-related BOLD response was found in mesolimbic and mesocortical dopamine-innervated regions like the VS, hippocampus (Hipp) and subgenual anterior cingulate cortex (sgACC). [...] Additionally, several brain structures potentially associated with motor preparation (primary and supplementary motor areas) as well as structures belonging to the ventral (lingual gyrus) and dorsal (cuneus, precuneus) visual pathway showed stronger BOLD responses to gain anticipation in the P group compared with the T group." (Bothe. 2013)
Moreover, according to the paper which is going to be published in one of the upcoming issues of Medicine and Science in Sports and Exercise, all 43 healthy men between the age of 20 - 32 years who participated in the study showed similar increases in mood (effect size F=11.70).

With both, the beneficial outcome of the positive and negative affect schedule and the decrease in anticipatory signalling (= the greedy "I am about to win!") in the psychological testing session (the so-called monetary incentive delay) in an fMRI brain scanner, being identical it becomes evident that you don't have to be an athlete to monetize (all puns intended ;-) on the beneficial psychological effects of exercise.

Figure 1: Changes in total lean mass, aerobic fitness, strength (mind the scaling with x10!), right ventricular mass and end-diastolic volume in subjects in the endurance (runners) and strength training arm (O-lifting) of the 24-week study (based on Spence. 2013)

Changes to the heart (right ventricular) due to exercise are mild, and if anything more pronounced in response to endurance than resistance training! " Left ventricular (LV) adaptation to exercise training has been the focus of 'athlete's heart' research to-date, information regarding right ventricular (RV) adaptation is sparse, due to its complex structure and imaging technique limitations." (Spence. 2013) So scarce, in fact, that this recent study that has been conducted by researchers form the The University of Western Australia, the University of Leeds, a and the Liverpool John Moore's University is the first to take a closer look at the impact endurance or resistance training have on the morphology of the RV.

For their randomized trial, the researchers recruited twenty-three young untrained men.. The men were assigned to either

endurance training (E; n = 10) - consisting of a progressively overloaded program of walking/jogging/running, divided into three training phases over the 24-week period, or
resistance training (R; n = 13) - with a focus on periodised R program was Olympic weightlifting with incorporated assistance exercises (e.g. deadlift, squat, bench press, overhead press) to develop overall strength and technique

for a total timespan of 6 months, in the course of which body composition, aerobic fitness, muscular strength, RV morphology (MRI) and function (speckle tracking echocardiography) were continously monitored.

The results Spence et al. are going to publish in one of the future issues of Medicine and Science in Sports and Exercise refute even two pieces of common "knowledge". Firstly, a still totally benign, right ventricular hypertrophy was exclusively observed in the endurance training group, yet not in the heavy lifters who were doing their squats, deadlifts and military presses (by 2.7g following E and by 1.4 g following R training). Secondly, both strength and size gains were no prerogative of the lifting weight group. Contrary to the increase in total lean mass (+1.3 kg vs. +2.1 kg), the strength increase of +53.8 kg vs. +35.3 kg was yet much significantly more pronounced in the weight lifters.

On the other hand only the endurance training group saw significant statistically improvements in their aerobic fitness level. This correspondence of endurance exercise, mild ventricular hypertrophy and increased fitness levels is unquestionably telling in terms of "how bad" a physiologically enlarged heart where the ratio of left-to-right ventricular mass remains intact (which was the case in the study at hand), don't you think so?

Omega-3s, omega-6s, telomere length, CYP enzymes, endogenous cannabinoid and the liver you need all of them to see the complete picture While the epidemiologists are still debating who will and who won't benefit from omega-3 supplementation, those who still care about how our bodies works and why their colleagues over at the epidemiology department are still debating, have made quite some progress as far as the underlying health benefits of rectifying the omega-3 to omega-6 balance are concerned.

Why are endocannabinoids problematic? One of the answers is: "They will make you fat!" Basically we have known that forever, but a recent study which tracked the conversion of dietary linolic acid (n-6) to it's endocannabinoid metabolits, 2-AG and anandamide has recently confirmed not just that, but also that the provision of no more than 1% of the total energy of the diet in form of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) can already make a huge difference (Alvhem. 2013). With the addition of the long-chain omega-3s, the rodents in the study had a 8:1 ratio of linolic acid (LA) to long-chain omega-3 fatty acids in their diets. Still much higher than what you will hear is necessary, but sufficient to reverse the overabundance of arachidonic acid, in the phospholipids of liver and erythroctes, and the +200% increase in endocannabinoid levels that had been brought about, when the researchers had increased the linolic acid content of the diet from 1% to 8% of the total energy intake. In view of the fact that the same goes for the increased food intake, feed efficiency, and adiposity the mice had developed on the 60% fat (total) diet with a high linolic acid content, this study - despite being done on rodents - clearly shows that it does not necessarily have to be a 1:1 ratio to grasp major health benefits.

If you get down from 30:1 to 8:1 you've come a tremendous way, already; and guess what: The easiest way to achieve that is to just cut out all seed and vegetable oils as well as processed foods that contain them.
In a recent review on the differential effects of fatty acids on human metabolism in the Italian journal Medical and surgical pediatrics G. Caramia emphasizes the role of omega-6 derived endocannabinoids:
"[E]ndocannabinoids like anandamide (N-arachidonoylethanolamine) and 2-arachidonoylglycerol [that arise from the enzymatic conversion of linolic acid by enzymes from the cytochrome P450 family at the liver are] capable of mimicking the pharmacological actions of the active principle of Cannabis sativa preparations such as hashish and marijuana (-)-Delta9-tetrahydrocannabinol. They act as true 'endogenous cannabinoids' by binding and functionally activating one or both [of the] cannabinoid receptor present on nervous and peripheral cell membranes." (Caramia. 2013; my emphases)
Unfortunately, the same enzymes which are responsible for the generation of those endocannabinoids, are also responsible for the conversion of n-3 PUFAs into more potent metabolites of EPA and DHA, which will actually do most of the the vascular- and cardioprotective magic that is commonly ascribed to "fish oil".

And how does all that relate to telomeres?

These competitive effects in turn segue directly into the observations of a double-blind 4-month trial that involved 106 healthy sedentary overweight middle-aged and older adults. The participants supplemented their diets with capsules containing either (1) 2.5 g/day n-3 PUFAs, (2) 1.25 g/day n-3 PUFAs, or (3) a placebo that mirrored the proportions of fatty acids in the typical American diet.

Now, it's not news that this led to decreases in inflammatory markers. I am not going to bore you with those, don't worry!

What is news, and in my eyes very important, is that neither the provision nor the dosage of additional long-chain omega-3s had an effect on telomere length, the only variable that mattered was were the changes in the n-6:n-3 PUFA plasma ratios, which "helped clarify the intervention’s impact: telomere length increased with decreasing n-6:n-3 ratios (p= 0.02)" (Kiecolt-Glaser. 2013).

That's it as far as today's seconds go... you want more? Man, I could certainly give you more, but you know that gluttony was once considered a sin, right? Tomorrow is another day, and if you can't wait, just head over to the SuppVersity Facebook wall, which is always bursting from the seems with the latest tidbits from the realms of health, exercise and nutrition sciences.

References:

Alvheim AR, Malde MK, Osei-Hyiaman D, Hong Lin Y, Pawlosky RJ, Madsen L, Kristiansen K, Frøyland L, Hibbeln JR. Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity. Obesity (Silver Spring). 2013 Oct;20(10):1984-94.
Bothe N, Zschucke E, Dimeo F, Heinz A, Wüstenberg T, Ströhle A. Acute Exercise Influences Reward Processing in Highly Trained and Untrained Men. Med Sci Sports Exerc. 2013 Oct 10.
Bush J. Preventing errors in your practice. Reducing risks for patients receiving warfarin. Fam Pract Manag. 2002 Jul-Aug;9(7):35-38.
Caramia G. [Essential fatty acids and lipid mediators. Endocannabinoids]. Pediatr Med Chir. 2013 Mar-Apr;34(2):65-72.
Kiecolt-Glaser JK, Epel ES, Belury MA, Andridge R, Lin J, Glaser R, Malarkey WB, Hwang BS, Blackburn E. Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial. Brain Behav Immun. 2013 Sep 23. pii: S0889-1591(12)00431-X.
Spence AL, Carter HH, Murray CP, Oxborough D, Naylor LH, George KP, Green DJ. MRI-derived Right Ventricular Adaptations to Endurance versus Resistance Training. Med Sci Sports Exerc. 2013 Oct 15.
Tsai HH, Lin HW, Simon Pickard A, Tsai HY, Mahady GB. Evaluation of documented drug interactions and contraindications associated with herbs and dietary supplements: a systematic literature review. Int J Clin Pract. 2013 Nov;66(11):1056-1078.

Friday, October 4, 2013

High Dose Omega-3 for Fat Loss? With 90% Lower Body Fat EPA Takes The Lead, DHA Second, ALA Distant Third... in Rats on Cornstarch or High Fat + High Sugar Diets

For Neo in the Matrix (courtesy of Warner Bros.) the choice was comparably easy. He had only two pills! You, however got to chose between ALA, EPA, DHA and, believe it or not, taking no pill at all!

I guess, those of you who are curious about the whereabouts of "your's truly" Adelfo Cerame Jr. will be disappointed to hear that he is currently so overwhelmed with clients and other duties that we have decided to turn the weekly contest prep series into a bi-weekly one.

Since this was more or less a last-minute decision, I just picked the next best study from my "interesting finds" folder and ... it turns out to be one of your, yet certainly not my favorite topics: Omega-3 fatty acids! That I am still skeptic about the usefulness, let alone necessity of respective supplements, does yet not change mean that I am deliberately ignoring interesting research on the unquestionable beneficial effects they have on lazy couch-potatoes and respective rodent models.

ALA, EPA, DHA - different acronyms, different effects?

Speaking of rodents, the soon-to-be published study by Hemant Poudyal, Sunil K. Panchal, Leigh C. Ward and Lindsay Brown from the Universities of Queensland and Southern Queensland in Australia unquestionably belongs into this latter category of "interesting rodent research on the benefits omega-3 fatty acids" (Pudyal. 2013). In order to differentiate the effects of alpha linoleic acid (ALA), the short(er)-chain brother to the long-chain omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) people often falsely refer to as "fish oil" (while fish oil contains them, the average fish oil cap has ~40% EPA/DHA or 400mg in a 1g gel cap), the scientists assigned 96 male Wistar rats (9–10 weeks old) randomly to one out of 8 different diets containing

Carbohydrate, fat and protein content (rel. to total energy)

corn starch,
corn starch +1.1g/d ALA-rich chia oil,
corn starch +0.7g/d EPA,
corn starch +0.8g/d DHA, or
high-carbohydrate, high-fat,
high carbohydrate, high-fat +0.7g/d ALA-rich chia oil
high-carbohydrate, high-fat +0.7g/d EPA oil and
high-carbohydrate, high-fat+0.6g/d DHA oil

The n-3 PUFA supplemented diets were prepared by adding 3% of the oil replacing an equivalent amount of water in the diet. n-3 PUFA supplemented diets were administered for 8 weeks starting 8 weeks after the initiation of the corn starch or high-carbohydrate, high-fat diet. The drinking water in all high-carbohydrate, high-fat fed groups was augmented with 25% fructose for the duration of the study.

Profound anti-obesity effects of EPA and DHA

Over the course of the 8-week supplementation period the researchers took daily measurements of body weight, food and water intakes. They performed two oral glucose (OGTT) and insulin tolerance tests (ITT) before and after the 16 weeks trial and measured the body composition by Dual-energy X-ray absorptiometric (DXA).

Figure 1: Body composition, lipid profile, glucose management (left to right) in rodents after 8 weeks on chia seed oil (ALA), EPA and DHA supplemented diets (date expressed relative to cornstarch non-supplemented control; calculated based on Poudyal. 2013)

If you take a look at my plot of the data, you may be surprised about the significance of the results. While it has to be said that even the "normal" control diet was not exactly what I would deem healthy (even for a rodent), it is nevertheless astonishing how pronounced the anti-obesity effects actually were.

Downstream benefits on organ health, ...

Figure 2: Contrary to what we have seen in previous studies (see TTA+fish oil), the high doses of the different omega-3s (HED ~20-30g!) had no effect negative effects on either the transaminase (ALT, AST), lactate dehydrogenase (LDH), alkaline phosphatease (ALP) or bilirubin values or the histology (histologies of hepatcytes not shown) of the liver of the rodents (data based on Poudyal. 2013)

Compared to the effects of the high doses of long-chain omega-3s the ALA treatment had a comparatively low impact on the adiposity. This could partly be a result of the fact that the omega-3 fatty acid metabolism in skeletal muscle and adipose tissue appears to be specific. While EPA and DHA
accumulated readily in these organs, when they were directly supplemented, the provision of ALA did not increase the contents of long-chain omega-3 fatty acids in either body fat or skeletal muscle tissue.

On the other hand, all omega-3 fatty acids showed beneficial effects on heart and liver the function of which had already been compromised by the 8 weeks on the extreme high carbohydrate or high sugar + high fat diet (reduced cardiac fibrosis, hepatic steatosis and inflammation in both the heart and the liver). In that, both, both, the improvements in body composition, as well as organ health, were more pronounced in the low-fat diet compared to the high-carbohydrate, high-fat diet.

... but negative effects on glucose management

Against that background it is actually surprising that none of the omega-3 fatty acids actually did what they are often hailed for: Neither ALA, nor EPA or DHA did improve the profoundly reduced glucose tolerance of the carb-o-holic rodents. On the contrary,...

"[...] EPA and DHA supplementation increased basal blood glucose concentrations, decreased intestinal glucose absorption and maintained the blood glucose concentrations for two hours after glucose loading with normal insulin sensitivity." (Poudyal. 2013)

Interestingly, this effect was probably brought about by yet another unexpected effect the high dose (human equivalent ~20-30g) omega-3 treatment had on the sympathetic nervous system:

"These effects were accompanied by increases in sympathetic activation seen as increased heart rate and cardiac output, increased force of left ventricular contraction and increased vascular responses to noradrenaline and sodium nitroprusside as observed with the hypothalamus–pituitary– adrenal axis response to stress and low blood glucose concentrations " (Poudyal. 2013; my emphasis)

As Poudyal et al. point out, this could also explain the profound weight loss effect in the cornstarch groups, and the "relatively smaller but significant changes in [high fat + high sugar] rats that still have an abundance of fructose and fat to meet the energy requirements."

From rodents to humans, from humans to... fishmen?

The latest on the usefulness of omega-3 supplementation for active individuals and athletes: One of the most recent reviews of the issue states: "[O]nly a few studies have evaluated the impact of omega-3 PUFA supplementation on exercise performance. It has been suggested that the ingestion of DHA of approximately 1-2 g per day, at a ratio of EPA to DHA of 2:1, may be beneficial in counteracting exercise-induced inflammation and for the overall health of an athlete. However, the human data is inconclusive as to whether omega-3 PUFA supplementation, at this dosage, is effective in attenuating the inflammatory and immunomodulatory response to exercise, and improve exercise performance." (Micleborough. 2013; my emphasis)

These (at least for me novel) effects of very high doses of EPA and DHA on the sympathetic nervous system as well as the modulatory effects of the baseline diet are certainly things to keep in mind. This is particularly true in view of the latest epidemiological data which suggests that the consumption of comparatively minuscule amounts of fish oil has a population (and thus probably diet-)dependent effect on diabetes risk (Wallin. 2013), with

17% increased risk of type-2 diabetes per 0.30 g per day increment in long-chain n-3 fatty acids in US residents, and
-2% reduced risk of type-2 diabetes per 0.30 g per day increment in long-chain n-3 fatty acids in Europeans

The same goes for the U-shaped dose-response curve, Crochemore observed in one of the most recent controlled trials in the course of which a low dose (1.5 g/d) fish oil supplement improved the body composition and fatty acid metabolism of 41 women (60.64 ± 7.82 years) with high blood pressure and diabetes mellitus, while only 1g more, i.e. 2.5g/day, did not simply yield less pronounced decreases in body mass and waist circumference, the "high" dose fish oil supplement also reduced the already highly compromised insulin sensitivity of subjects even further (Crochemore. 2013).

EPA & DHA can come to the rescue, but a healthy diet would render supplements obsolete

If I did not know that fish oil was an invention of the 1990s, I would speculate that the "fishman" in the 1954 horror blockbuster The Creature from the Black Lagoon (Universal Pictures) was a "fish oil fat loss supplementation experiment gone wrong" ;-) Or joke aside - you don't seriously consider popping 70 fish oil caps a day to get the human equivalent of the ~1g of EPA or DHA the rodents in the study consumed, do you?

Regardless of the "optimal dosage", we should not lose sight of the influence and importance of the basal diet, when we evaluate the effects of DHA and EPA on body composition, lipid metabolism and not the least glucose management. It is, for example, very unlikely that we would see anywhere similarly pronounced effects in humans who are following a whole-foods based, "paleo-esque" diet without tons of cornstarch in it (control group), or plain sugar (and 17% additional fructose) that are on top of that hilariously protein-deficient (5%-6% is - if anything - enough not to die).

If you chose grass-fed over regular butter / dairy (makes sense only for high fat dairy), eat fish once or twice a week and replace the grain-based oils in your diet with coconut and olive oil, anything that goes beyond the occasional one or two fish oil caps will probably do more harm than good. And let's be honest, you don't really believe that you would get rid of the blubber that may still be covering your abs by copying the supplementation protocol of the study at hand and taking 70 fish oil caps every day to get your 20-30g of EPA and DHA, do you?

References:

Crochemore IC, Souza AF, de Souza AC, Rosado EL. ω-3 polyunsaturated fatty acid supplementation does not influence body composition, insulin resistance, and lipemia in women with type 2 diabetes and obesity. Nutr Clin Pract. 2013 Aug;27(4):553-60.
Mickleborough TD. Omega-3 Polyunsaturated Fatty Acids in Physical Performance Optimization. Int J Sport Nutr Exerc Metab. 2013 Sep 4.
Poudyal H, Panchal SK, Ward LC, Brown L. Effects of ALA, EPA and DHA in high-carbohydrate, high-fat diet-induced metabolic syndrome in rats. J Nutr Biochem. 2013 Sep 28. pii: S0955-2863(12)00207-0. .
Wallin A, Di Giuseppe D, Orsini N, Patel PS, Forouhi NG, Wolk A. Fish consumption, dietary long-chain n-3 fatty acids, and risk of type 2 diabetes: systematic review and meta-analysis of prospective studies. Diabetes Care. 2013 Apr;35(4):918-29.

Sunday, August 18, 2013

On Short Notice: Teas & Prostate, Metformin & Amenorrhea, Stevia & High, Omega-3 & Low Cortisol, Aminos & Weight Control, Nordic Hamstring Exercise & 20% More Power!

Image 1: This would be a case where metformin probably won't help you to get your menses back - unless this is just one of your "yous" and you are taking high doses of anti-psychotics, of course.

In view of the fact that I have piled up way more "On Short Notice" items than I can possibly squeeze into one installment, today's news on the right tea (green or black) for prostate cancer, the purported anti-obesity effects of leucine and alanine, which turn out to be inferior to those of whole protein, the anti-amenorrhea and weight loss effects of metformin in women on anti-schizophrenic drug and how this relates to PCOS, the surprising N=1 cortisol-raising, high blood pressure and water retaining effects of stevia, the stress and weight loss reducing effects of omega-3s and high DHA levels in the brain, and an effective yet rarely used hamstring exercise, the "Nordic hamstring exercise", will be complemented by another installment of "On Short Notice" either tomorrow (in case I don't find the time to write the next installment of the Circadian Rhythm Series) or earlier next week... but enough of these organizational matters, let's see what we have in stock, here:

Differential effects of green and black tea on prostate cancer risk While we are, yet again, only dealing with epidemiological shenanigan in a population living in a, if not the juggernaut of the far east, the >50% increase in hazard risk in the 27,293 men from the Singapore Chinese Health Study Julia A. Montague and her colleagues report for men who drink 1 cup of black tea per day is somewhat alarming (Montague. 2013). The fact that the hazard risk decreases to +17% with more than 2 cups of black tea does yet suggest that this is nothing but a statistic outlier. That said, black tea is (at least based on the results of this study) overall probably as benign as green tea, which is totally devoid of statistical beneficial or detrimental effects on prostate cancer risk in this cohort of normal-weight men in their middle to late 50s.
This result does by the way not conflict with previous research, which did - if anything - only suggest a "borderline significant" beneficial effect of green tea and absolutely no effect of black tea on prostate cancer risk (Zheng. 2013). Apropos prostate cancer, just in case you missed it I highly suggest you take a look at my brief write-up on the recently published "red meat will give you prostate cancer study" before you decide on whether or not you got to stop eating meat for the sake of your prostate.
Figure 1: If ~50g of leucine and alanine /kg chow are good, then 500g of whey are magic; makes you wonder, why you would want to add just one amino acid, instead of more protein, no?
"Dietary L-leucine and L-alanine supplementation have similar acute effects in the prevention of high-fat diet-induced obesity", that's the somewhat ill-chose title of a recently published paper by Anne Freudenberg, Klaus J. Petzke, Susanne Klaus from the German Institute of Human Nutrition in Potsdam-Rehbruecke which does not show that the ingestion of l-leucine or alanine, but rather an isocaloric high protein diet version of the high-fat diets the researchers fed their 10-week-old male C57BL/6 mice, prevented them from getting obese (Freudenberg. 2013).
While the high fat + complete protein mice hardly gained any body fat, the high fat + leucine and high fat + alanine (both diets were "adequate" in protein and contained 100g whey + 60g leucine and 100g whey + 45g alanine, respectively) got only significantly less fat compared to their peirs on the 100g whey only diet control HFD diet. Now, the high protein mice (500g of whey per kg chow; =5x over baseline) simply consumed less energy, but so did the mice on the leucine and alanine enhanced diets, so that the title of the study is not just misleading, it also disguises the most important result of the study, which is high protein diets keep mice lean.
"Cure-it-all-drug" metformin helps with anti-psychotic induced amenorrhea and weight gain, as well. If metformin was not (a) no longer protected by patent rights and (b) would not basically work via similar mechanisms as exercise I would really begin to smell fraud over the ever-extending list of pathologies this 1920s medication is good for (this is when it was originally discovered, it took however until 1958 before researchers realized the potentials and a pharma company introduced it to the UK market). New to the list are the negative side-effects women experience in response to anti-psychotic treatments. In a recently documented experiment, 48 women (ages 18-40 years) with amenorrhea and weight gain in response to clozapine, olanzapine, risperidone, or sulpiride (all anti-psychotic drugs administered to treat schizophrenia) received a dose of 1,000mg of the wonder-molecule per day (Wu. 2013). After 2 months 25% of the women had resumed menstruation, after another 2 weeks it were 80% and after 3 months all women were eumenorrheic, again (of the placebo group only 2 resumed menstruating). Instead of gaining another 2kg of body weight, they had lost 2kg and the previously thwarted prolactin, LH, and testosterone levels, as well as the LH/FSH ratio had normalized.
Probably, some of you may now ask themselves: Will this work for me as well - though I am not taking anti-psychotics? I would love I could answer this question, but aside from polycystic ovarian syndrome (PCOS), where we have a couple of trials in which metformin was used with success (cf. Velazquez. 1998; Bela. 2009; Palomba. 2009), the scientific evidence is scarce and in view of the fact that we know even less about the underlying mechanisms by which risperidone & co cause amenorrhea and weight gain than about the almost magical omnipotence of metformin I honestly can't tell. One thing that comes mind, where metformin is yet very unlikely to of any use is diet or exercise induced amenorrhea (overtraining and undereating), because this form of amenorrhea presents with a totally different hormonal profile, with low levels of basically all reproductive hormones.

Stevia as cortisol promoter? Case study: Bloating, high blood pressure and malaise in a young previously healthy woman. Before I go on, let me briefly remind you that the events that are described in a recent case report from the University of Iowa Hospitals and Clinics may should be regarded with the degree of caution that is indicated whenever we are talking about case reports, specifically because stevia does actually have a pretty decent safety profile (aside from the occasional allergic reactions you will see with almost every foreign molecule you put into your body, obviously).

Figure 2: If you block the 11bHSD2 enzyme that will convert cortisol into inactive cortisone, you are in trouble and a bloated tummy is certainly your least problem, not because "cortisol is bad", as common sense would dictate, but because not being able to manage it is bad (img. Michael. 2008)

When a 32 year old Caucasian woman presented with generalized edema (feet, hands and face) that had persisted for over six months at her Dr office and was found to to suffer from pre-hypertension (138/88 mmHg) and hypokalemia (3.4 mM/l) that was brought about by a decline in serum aldosterone and plasma renin activity and corroborated by a concomitant increase in the plasma cortisol/cortisone ratio, most Dr.'s would probably have thought of licorice intoxication. As it turned out, it were neither the glycyrrizinic acid, not the glycyrrhetinic acid from licorice which brought about these problem, but rather the stevia the lady had been using for over 9 months, now. Obviously, the sweetener (from an undisclosed brand) had blocked the 11 beta-hydroxysteroid dehydrogenase Type 2 (11-beta-HSD 2, see figure 2) enzyme that's responsible for the conversion (="deactivation") of cortisol to cortisone - with all the negative side effects of the subsequent 12x elevation of the ratio of active to inactive corticosteroids (Esmail. 2013).

Now, I am certainly not suggesting that this is going to happen to everyone, but it could well be that the frequent reports of headaches people are developing after a couple of days "on stevia", could also be related to the effects the sweetener has on people with a certain genetic disposition. So, if you get a headache or start holding water like crazy, when you use stevia / stevia sweetened products, first try using a different brand (there have been issues with toxins in some products), make sure you have a pure stevia sweetener and not one with other sweeteners added (thx. to Amit for the reminder about erythritol that's in many products), switch to another preparation, e.g. from pure stevisoids to a a more "natural" extract and if all that does not help, just turn your back on it - you can live without it, I guarantee ;-)

Omega-3's modulate adrenal activity What many people know from going overboard on fish oil has now been established in a recently published rodent study by Marie Hennebelle and her French (resident) colleagues (Hennebelle. 2013). The researchers fed a group of rodents a totally ALA free energetically restricted diet to produce male rats with brain phospholipid DHA levels that were 50% lower than those of the normal control. The 6 month-old rodents were then subjected to chronic restraint stress (6 h/d) for 21 days. As expected the rodents on the alpha linolic acid deficient diets had a much harder time coping with the torture they were exposed to and showed higher corticosterone levels, more pronounced behavioral abnomalies and slightly more pronounced weight loss in the 3-4 week of the 1-month experimental period. What's intriguing though is the the remarkable stress resistance (one could also say adrenal hypofunction ;-) in the rodents in a third experimental group, who had received an omega-3 enriched diet that boosted their brain DHA levels to 10% above normal: Compared to both the normal, as well as the omega-3 deprived rodents they had ~30% lower cortisol levels during week two and three of the experiment and lost only 50% of the weight their normal and ALA deprived peers did.
That this is not necessarily a good thing for everyone is probably nothing I have to tell you. After all, the number of people who are hardly functioning due to over-supplementation with fish oil and (as this study would suggest) below normal stress responses is ever increasing. As with so many nutrients and supplements, it thus comes down to specificity and hitting the right ratios for you as an individual, again. And what's most important: Before you even start thinking about "fixing your adrenals" you should first take a look at the various stressors in your life. After all, the aforementioned fatigue is not simply a result of two much fish oil, but of its combination with a lifestyle which simply requires a robust and healthy cortisol response. You would not smoke weed to calm yourself down minutes before running away from a saber-toothed tiger, either, would you?
Video 1: These young ladies show you how it's done - well almost, you better go a little slower (click image to watch.
Scientists confirm efficacy of nordic hamstring exercise - up to +20% increase in peak torque! What? You don't know the nordic hamstring exercise - I bet you do, but probably not by this name. Check out video 1 to the right and you will know what the 18 male players from a club in the English professional soccer leagues (mean±SD; age, 22.9±3.6 years; stature, 1.81±0.08 m; body mass 78.0±9.7 kg) did for 1x 2x5, 2x 2x6, 3x 3x6 and 3x 3x8 (sessions per week x sets x reps) during week 1-4 of the study period to improve their peak torque by up to 21% in all assessment conditions (90-61°, 60-31° and 30-0° of knee extension; cf. Iga. 2013).
What is yet important is that you stick to an adequate temp and don't mess around and hurt yourself. In the study at hand, the velocity of the movement was standardized to 30°/s. If we assume that you go over the full ROM it must therefore take you 3s until your nose hits the ground (if you are afraid to hurt your nose, you may be interested in the SuppVersity EMG Series and the Best Leg + Hamstring Exercises ;-)

I hope you enjoy this more digestible format, having 20 of these items in one installment is - at least in my view - somewhat beside the point. Not that this would not be possible, but if I go by the average attention span of my real-life students, multiply it by 2x to accommodate for your superior cognitive abilities and personal interest in the topic, it appears prudent to call it a day for today. And if can't stand the 24h for the next SuppVersity news to be released, I suggest you simply like the SuppVersity Facebook Wall, where you will find another seven allegedly shorter news-items... about the wheat-allergens in soap (+ scary pic of what can happen, when you use those), for example or the news photo-based cholesterol test (a photo of your hands is all it takes), which is probably going to give the sales of statins another boost.

References:

Billa E, Kapolla N, Nicopoulou SC, Koukkou E, Venaki E, Milingos S, Antsaklis A, Adamopoulos DA. Metformin administration was associated with a modification of LH, prolactin, and insulin secretion dynamics in women with polycystic ovarian syndrome. Gynecol Endocrinol 2009; 25:427–434
Esmail S, Kabadi UM. Edema, Enigma: 11 B-Hydroxysteroid dehydrogenase Type 2 Inhibition by Sweetener “Stevia”. Open Journal of Endocrine and Metabolic Diseases, 2013, 2, 49-52.
Freudenberg A, Petzke KJ, Klaus S. Dietary L-leucine and L-alanine supplementation have similar acute effects in the prevention of high-fat diet-induced obesity. Amino Acids. 2013 Jul 31.
Hennebelle M, Balasse L, Latour A, Champeil-Potokar G, Denis S, Lavialle M, Gisquet-Verrier P, Denis I, Vancassel S. Influence of omega-3 Fatty Acid status on the way rats adapt to chronic restraint stress. PLoS One. 2013;7(7):e42142.
Montague JA, Butler LM, Wu AH, Genkinger JM, Koh WP, Wong AS, Wang R, Yuan JM, Yu MC. Green and black tea intake in relation to prostate cancer risk among Singapore Chinese. Cancer Causes Control. 2013 Aug 3.
Palomba S, Falbo A, Zullo F, Orio F Jr. Evidence-based and potential benefits of metformin in the polycystic ovary syndrome: a comprehensive review. Endocr Rev 2009; 30:1–50
Wu RR, Jin H, Gao K, Twamley EW, Ou JJ, Shao P, Wang J, Guo XF, Davis JM, Chan PK, Zhao JP. Metformin for treatment of antipsychotic-induced amenorrhea and weight gain in women with first-episode schizophrenia: a double-blind, randomized, placebo-controlled study. Am J Psychiatry. 2013 Aug 1;169(8):813-21.
Velazquez EM, Mendoza S, Hamer T, Sosa F, Glueck CJ. Metformin therapy in polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure while facilitating normal menses and pregnancy. Metabolism 1994; 43:647–654
Zheng J, Yang B, Huang T, Yu Y, Yang J, Li D. Green tea and black tea consumption and prostate cancer risk: an exploratory meta-analysis of observational studies. Nutr Cancer. 2011;63(5):663-72.

Wednesday, August 14, 2013

You Are What You Eat? Not Really! Rodent Study Shows Mice Are What the Salmon Ate That's in Their Chow

Image 1: Farmed Atlantic salmon Raised an fried with soy *yummy*

Health conscious as you are, you will probably make sure to get grassfed beef, pay extra for the delicious Kerrygold butter and ask your farmer whether the chicken that lay the eggs you are just about to buy were pastured or received the standard feed and tons of antibiotics... right? Ok, but do you know what the fish that's lying there right in front of you had as his last supper? No? Well, after reading today's SuppVersity news, you will probably give your fish monger the third degree... but one thing after the other.

We are what that what we eat ate!

In a soon to be published study in the British Journal of Nutrition, Anita R. Alvheim and her colleagues from the National Institute of Nutrition and Seafood Research, the Department of Biomedicine at the University of Bergen in Norway, the National Institute on Alcohol Abuse and Alcoholism in Rockville, USA, and the Department of Biology at the University of Copenhagen in Denmark, report which astonishing (or should I say frightening?) downstream effects it can have when the fish farmer who supplies your local fish monger with salmon wants to save a couple of bucks and replaces the fish oil in the diet of his farm-raised Atlantic salmon with some cheap (and hip / at least among vegans ;-) soybean oil.

Table 1: Fatty acid composition of rodent chow (top) and change in fa content of salmon due to soy oil feeding (rel. fish oil fed salmon, bottom; Alvheim. 2013)

To elucidate the downstream effects of this practice, the researchers raised Atlantic salmon on either soy or fish oil based diets (250g of each added to the diet), slaughtered the animals, filleted them and used the fillets to prepare two calorically identical rodent chows. A practice, by the way which was not as easy as it may sound, after all the salmon that had received the soy-based diet was significantly fatter (33% fat in the fillet of the soy fed vs. 26% fat in the fish oil fed salmon), so that the scientists had to make up for the lack of fat. The 6-week old mice were then randomly assigned to one of the two experimental diets to which they had ad libitum access for 6 weeks.

As the data in figure 1 goes to show the rodents on the "soy-salmon" diet had a significantly elevated hepatic alpha linoleic acid and arachidonic acid (AA) content in the hepatic phospholipids. After 9 weeks on the diet, there was a trend towards increased body weight gains that reached statistical significance in week 15 - and that in the absence of statistically significant differences in energy intake.

Figure 1: Linoleic acid, Arachidonic acid and Arachidonoylglycerol (endocannaboid) content of liver phospholipids (left, data expressed relative to fish oil diet group), body weight development (right; Alvheim. 2013)

Moreover, compared to the rodents on the diet that contained the "normal" salmon the rodents on the soy fed salmon diet had significantly lowered EPA and DHA levels in the phospholipid fraction of their liver, erythrocytes and white adipose tissue. This lead to an overall decrease of the omega 3-index from 23 to 16 and increased the relative abundance of n-6 highly unsaturated fatty acids from 19 to 39 % percent. The histological analysis of the adipose tissue did also reveal that the rodents who received the diets with the soy fed salmon exhibited significantly more of the so-called crown-like structures which are remnants of macrophage (immune cells) invasion into the inflamed and partly necrotic (=dead) adipose tissue. The presence of this structures is associated with major increases in local and systemic inflammation and their has been implicated as one of the major driving forces of obesity induced metabolic disturbances in mice and humans (Bremer. 2011). Furthermore the adipocyte size in the groin area (=inguinal WAT) was increased.

Figure 2: I must admit I did not check if AP got the data in this chart right, but if they did, the increase in AA and AA-related endocannaboids is only part of the problem and you better stick to grass-fed beef if you can't afford wild salmon.

Implications: Overall, the weight gain may be negligible, the intricate differences in the phospholipid structure of various cells and even the presence of the crown-like structures relatively harmless and still, with the overall increase in soybean oil consumption in the US (from 2.2% of the total energy to 7.3% of the total energy intake) and the constant decline of natural (not supplemental!) DHA and EPA in the diet of the average US citizen, in the course of the 20th century (Blasbalg. 2011), the indirect or "second feed" assault from all sorts of animal products may well be the literal "last straw that brakes the camels back". After all, there is accumulating evidence for a direct relation between the diet-induced increase in arachidonic acid derived endocannaboids like 2-arachidonoylglycerol (cf. figure 1) in rodents and humans and the modulating effects of dietary fat intake on the latter.

With the study at hand, Alvheim et al. show pretty conclusively that the effect of certain foods, specifically oils, can be "handed down" in the food chain an effect that is hitherto largely ignored by scientists and nutritionists. In conjunction with reports that show that the DHA and EPA content of Atlantic salmon is already on the decline, while the linolic acid content has increased from 1.1 g/100 g in 2005 to 1.6 g/100 g in 2010 (NIFES. 2011), this raises the question of whether salmon, which is still considered to be the go-to protein and fat source for health-conscious customers, has not already been turned into another Frankenfood and puts another emphasis on the importance of knowing not just what you eat, but also what whatever you eat ate or grew on... but the latter is, I guess a topic for another blogpost ;-)

References:

Alvheim AR, Torstensen BE, Lin YH, Lillefosse HH, Lock EJ, Madsen L, Hibbeln JR, Malde MK. Dietary linoleic acid elevates endogenous 2-arachidonoylglycerol and anandamide in Atlantic salmon (Salmo salar L.) and mice, and induces weight gain and inflammation in mice. Br J Nutr. 2013 Aug 10:1-10.
Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011 May;93(5):950-62. Epub 2011 Mar 2.
Bremer AA, Devaraj S, Afify A, Jialal I. Adipose tissue dysregulation in patients with metabolic syndrome. J Clin Endocrinol Metab. 2011 Nov;96(11):E1782-8. Epub 2011 Aug 24.
Massiera F, Saint-Marc P, Seydoux J, Murata T, Kobayashi T, Narumiya S, Guesnet P, Amri EZ, Negrel R, Ailhaud G. Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern? J Lipid Res. 2003 Feb;44(2):271-9.
NIFES. National Institute of Nutrition and Seafood Research. Research on nutrition;
feed for fish and fish as food. < www.nifes.no/sjomatdata > retrieved Aug 14, 2013.

Sunday, August 4, 2013

On Short Notice: Ghrelin & GH Boosting Fats for Intermittent Fasting, 4-AD, 5-AA, Testosterone & Co in "Pod", Too Much Vitamin D for Your Prostate, Estrogens in Milk & More

Image 1 (fidged-group.co.uk): Being average may not be sexy, but one thing I did not mention in the summary of what you are going to learn today is that an average amount of body fat (not the new average American though ;-) could hold the key for a longer life - ah, I almost forgot: This is only valid if it comes with an appropriate amount of lean mass, which is still the best predictor of a long and healthy life!

Somehow these On Short Notice posts become increasingly longer... I had to "outsource" a couple of items, to reduce today's installment to a manageable length, but don't worry a couple of them will turn up in the next installment or make it into the regular news in the days to come. For now you will have to settle for valuable and at least in part surprising insights into the broad range of effects different types and loads of dietary fat can have on your appetite, metabolism and your, or rather your bacterial subtenants' methane production. You will also learn what TAC means and why you want more than 1,080 units of it in every 100g of whatever you are stuffing down your pie-hole. You will be surprised to hear that SuppVersity student FatFree instinctively chose the low estrogen variety of dairy, when he "downed 1l of raw goat's milk" from his local farmer earlier today (see respective comment) and you will attend another lesson of the "what's good for your obese neighbor, is not necessarily good for you" class. All that will be topped of with some testosterone laden, WADA prohibited "pod", too much vitamin D for your prostate to handle and a glass of bone-conserving wine for the habitual drinkers among the ladies ;-)

Fat Interactions - MUFA, PUFA, SUFA and How They Influence Your Metabolism

The idea that "not all fats" are created equal is meanwhile broadly accepted. What is still a matter of constant debate, though, is which of the three main classes, i.e. saturated, mono- and polyunsaturated fatty acids exert beneficial and which of them detrimental effects on our health. A recently published on the differential effects of butter (saturated fat), olive oil (mono-unsaturated; oleic acid + a relative high amount of omega-6), fish oil (polyunsaturated; high omega-3) and soybean oil (polyunsaturated; mainly omega-6 + some omega 3) on the expression of the purported "hunger hormone" ghrelin (note: acetylghrelin, which was measured in this study, is the "active" variety of ghrelin) may yet help to get a better grasp of what exactly we should be looking for (Saidpour. 2013), when it comes to the downstream metabolic effects of high amounts of certain fatty acids - and no, it is not for maximal ghrelin suppression.

Figure 1: Food intake (in g, left), body weight (relative to control group on regular diet, middle) and acetylghrelin levels in the fasting and fed state during the 8-week experimental period (data based on Saidpour. 2013)

As the data data in figure 1 shows, the 5-week old male Wistar rats who had been randomly assigned to either standard rodent chow or calorically identical (3.98kcal/g of food) high fat diets who were fed ad libitum every other day only to maximize the ghrelin response) for 8 weeks did not, as common sense would suggest, eat the least and gain the least on the saturated fat (butter) diet with its long lasting satiety effect (as evidenced by the lowest fasting ghrelin levels).

In fact, the exact opposite was the case: The acute satiety effect of the fish oil and olive oil diets (as evidenced by the plummeting acetylghrelin levels in the fed state) turned out to be the main determinant of the amount of food the rodents, who were effectively intermittently fasted (though with a pretty long fasting window of 24h), consumed. And while the low ghrelin levels in the fed state reduced the food intake, the fasting induced rise of acetylghrelin to 23% higher levels than in the butter fed animals has probably given them the metabolic advantage of elevated growth hormone levels. At least this is what we must expect based on the ability of ghrelin to directly bind to the GHS receptor and induce the release of the fat annihilating 191-amino acid, single-chain polypeptide from the lateral wings of the anterior pituitary gland (Kojima. 1999).

Bottom line: While this is certainly only another small piece to the oftentimes puzzling effects of fatty acids (check the "On Very Short Notice" items in this installment for more "puzzling" effects ;-), it does not only provide another mechanism by which the original "Mediterranean diet", which is rich in both fish and olive oil and by no means as fat free as its latest mainstream interpretation would suggest, could in fact provide a metabolic edge. And though the "intermittent fasting" feeding pattern may reduce the significance of the results for the "average" inhabitant of the Western hemisphere, who can hardly go 2h without a Snickers bar or at least a sugar-laden coffee, it does suggest that all the "lean gainers" and "intermittent fasters" out there could derive great benefits from a huge piece of salmon and couple of tablespoons of high MUFA olive, macadamia or artichoke oil in their "feeding windows".

A Diet High in Dietary Antioxidant Keeps you Lean & Healthy

Image 2: Clover is among the most potent antioxidant foods.

You know that I am very critical when it comes to the supply of exogenous antioxidants (cf. "Multivitamins, a question of Faith?!"; more on multivatmins), but would never even remotely consider limiting the supply of whole foods that are rich in antioxidants. I was thus not very surprised, when I read that the consumption of high amounts of dietary antioxidants was associated with statistically significant lower body weight and abdominal fat gain in a 3-year longitudinal (this is where scientists analyze data from the same persons on different time-points) study from the University of Medical Sciences in Teheran (Bahadoran. 2013).

Foods	TAC
Cloves (see image), Cinnamon, Oregano, Tumeric, Acai (all dried or grounded)	300,000 -100,000
Cacao, Parsley, Basil, Currry, Sage, Peppercorns, Mustard, Ginger, Marjoram	100,000 -25,000
Rice bran, Chili, Pecans, Paprika, Choke berries, Elderberries, Kidney Beans (dried), Oregano, Walnuts	25,000 -10,000
Hazelnuts, Cranberries, Artichoke hearts, Blueberries, Prunes, Pistachios, Blackcurrant, Artichokes, Plums, Blueberries (cult.) Lemon balm (fresh) Blackberries, Garlic, Coriander,	10,000 -5,000
Raspberries, Basil (fresh), Almonds, Apples, Dates, Strawberries, Figs, Peanuts, Raisins, Cherries, Asparagus, Spinach	5,000 -2,500
Cornflakes, Red Cabbage, Gooseberries, Cashews Avocado, Pears, Peaches, Oranges, Oats, Macadamia, Tangerines, Broccoli, Potatoes, Grapefruit, Red grapes	2,500 -1,500
Carrots, Olive oil, Green grapes, Mango, Lettuce, Radish Eggplant, Kiwi, Banana, Red pepper, Pineapple, Artichoke, Nectarines, Pine nuts, Cauliflower, celery	1,250 -500
Leeks, Lettuce, Baby carrots, Tomatoes, White wine, cantaloupe, Honeydew, Watermelon, Cucumber	500 -100

In particular, Zarah Bahadoran and her colleagues found that the consumption of foods with an average total antioxidant capacity equal to 1,080µmol TAC essay units per 100g - something your would get from oats + blueberries or a handful of pecans and an apple - was associated with a -38 % decrease in the risk of central obesity (note: The TAC essay is an experimental measure of the total antioxidant capacity of food and is independent of whether it's phenols, vitamins, thiols or whatever that contribute to the antioxidant effects of a food; the clear disadvantage of this method is that it does not really tell you what exactly the compounds will do outside of a petri dish, but, but this is the topic for another blogpost ;-)

And while some of the confounding factors have been eliminated from the above hazard risk calculations, it is still worth to take note of the fact that...

people with the highest antioxidant intake consumed food with the lowest energy density (so they cannot be eating nuts and chocolate only ;-)
women consumed significantly more antioxidants than men, with +10% more women in Q3 (959-1080µmolTE/100g) and +15% more women in the critical Q4 (>1,080µmol/kg) quartiles
the more leisure time the subjects had, or I should say allowed themselves, the higher was their antioxidant intake
high antioxidant consumers were also dairy lovers with 81% more dairy consumption in the highest quartile, exactly those people, thus, who consumed the >1,082 µmolTE/100mg diets
needless to say that people who are reckless enough to smoke also consumed the least antioxidants

Aside from these significant differences, the non-existence of other differences people often take for granted, such as the notion that education and job activity, or different macronutrient compositions would have an impact on the total amount of antioxidants you consume, is certainly worth mentioning.

On Very Short Notice

Figure 2: "Pod" contains a hell lot of steroids. Unfortunately, most of them will be dumped by right into the urine specimen for the WADA agents (data based on Thevis. 2013)
"Pod" doping could get you banned, but probably won't increase your performance - While I cannot tell you what the swimmers at the Olympics have been taking to break world record after world record (some even in consecutive races on the same day), I can tell you that it were not the reddish-brown musk grains from the dried secretion from the preputial follicles of the male musk deer , which are located in the "pod", a small sac in close proximity to the preputial orifice (see figure XYZ, upper right), because none of these athletes would have passed the WADA doping controls had he or she taken a couple of grams of those steroid-containing staples of Traditional Chinese Medicine.
Now, despite the fact that we do see "classics" such as 4-AD, Androsterone, Epiandrosterone, DHEA and even minuscule amounts of the "Big T" (1-6µg/g with the highest level in the pod from the zoo animals from Leipzig, Germany - read more about testosterone's ability to build muscle in the "Intermittent Thoughts on Building Muscle") testosterone , the total amount of those compounds which could actually induce noticeable performance increases may be high enough to show up during doping controls as the five cases during the last FIFA Women World Cup show(cf. Thevis. 2013), it does not appear reasonable to assume that the rumored performance enhancing effects of musk (pod) extracts would stand the test in a placebo controlled supplementation trial.

Figure 3: When administered at a HED of ~750mg/day sodium salicates reduce the glucose (left axis) and insulin (right axis) levels in response to a standardized intraperitoneal glucose injection in obese mice, they do the opposite in lean mice (based on Nixon. 2013).

Salicates block cortisol expression in fat cells and increase insulin sensitivity in obese mice, but... as we have seen for alpha lipoic acid (see "ALA? You are Better of Without the Purported Nutrient Repartitioner") and tons of other "wonder-supplements", things that are good for your obese neighbor will rarely work out for lean folks like, yourself; and thus it should not come as a surprise that the blockade of adipose tissue 11-beta-HSD, the enzyme that converts cortisone, the inactive form of cortisol into it's active twin, exerts no, if not the exact opposite effect (see figure 3; adapted from Nixon. 2013).

So, if you are lean and want to stay lean, leave the aspirin, the 7-ketos and other overpriced 11-beta-HSD inhibitors or "cortisol blockers" to those who need them - inflamed, overweight (pre-)diabetics.

Purportedly anti-carcinogenic high vitamin D levels increase risk of prostate cancer - Swedish scientists found a statistically significant trend towards an increased risk of developing prostate cancer with rising vitamin D levels. In the 7th and 8th decile which corresponds to plasma vitamin D levels of 91-97 nmol/L the calculated risk of developing prostate cancer was 67% higher than in the lowest decile (Brändstedt. 2013). Other than previous studies which reported associations between high calcium intake and prostate cancer risk, Brändstedt et al. observed an association between high serum calcium levels and prostate cancer levels only among men aged 55-65 who had a BMI < 25. It is thus very unlikely that the underlying reason of the pro-carcinogenic effects was an increase in calcium absorption... hmm, I don't have to remind you of (a) the antagonism between vitamin D and vitamin A and (b) last weeks news on the anti-carcinogenic effects of the latter, do I?

Image 3: Although the scientists controlled the compliance by measuring the serum concentration of fatty acids instead of using unreliable food logs, there are still a lot of uncontrolled confounding variable, here. Hower, the same can be said of those studies on which the concept of the pro-inflammatory omega-6s is based. Anyway, I will still eat butter, not margarine and if olive oil is one of staple sources of dietary fat, you will be getting plenty of omega-6 from this purported GH booster (see previous new item)

High omega-6 diet reduces insulin, total/HDL-cholesterol ratio, LDL cholesterol, and triglycerides - Helena Bjermo and her colleagues from the Uppsala University in Sweden report that feeding 67 abdominally obese patients (15% were diabetic) either a butter-based high saturated fat diet or a diet that was particularly rich in linoleic acid (omega-6 mainly from sunflower oil; 15% of the total energy intake) for 10 weeks had very differnt effects on the hepatic fat content an other highly relevant markers of metabolic health. Despite the fact that both diets were isocaloric, the butter-based high saturated fat diet increased the hepatic fat content of the study participants (measured by MRS) by 10% while the subjects in the high PUFA group were able to reduce the fat content of their livers by -35%. Similarly, the basal insulin level, triglycerides, as well as total and LDL cholesterol increased in the butter eaters and decrease or remained the same in the 15% linoleic acid group.

The results are honestly not what I had expected, but in essence only further evidence there is still a lot to learn about the shades of grey that exist between the dichotomous black and white that is still so characteristic of the way we think about fats.

Goat's milk is the better choice for people concerned with limiting their intake of exogenous estrogens - According to analyses that were conducted at the Laboratory of Proteomics and Analytical Technologies in Frederick (Farlow. 2013), cow's milk contains significantly more estrogens (estrone and 17beta-estradiol) than goat's milk and that irrespective of whether it was organically produced or not. Bad news for the reproductive health of the North Americans and Europeans, where the consumption of cow's milk exceed that of goats milk by several magnitudes and good news for the fertility of the rest of the world, where goat's milk still is the "milk of choice".
Image 4: Looks like this was not the only potential side effect of methane producing bacteria in your gut.
High fat diets increase the ratio of methane producing to other bacteria and thus increase obesity risk - Most of you will probably remember the finding that mice without gut microbiome are more or less resistant to dietary induced obesity. A recent study does now suggest that (as it was to be expected) not all bacteria are created evil.. ah, pardon... equal ;-) In the lab mice of Ruchi Mathur and his colleagues, the tendency to develop obesity correlated with the amount of gastrointestinal (GI) methanogens, including Methanobrevibacter smithii, and was independent of the presence of other bacteria (Mathur. 2013).
With the pro-methanogenic (=allows those little bastards to grow) effects of high fat diets Mathur et al. may in fact have found another potential co-founder in the development of the metabolic syndrome. Interestingly enough Methanobrevibacter smithii is also the predominant methanogen in patients with constipation-dominant IBS and methane breath (Kim. 2013) - so if that is you, this could be one of the few cases where the use of a broadband antibiotic could save you from a lot of ailments, because you would thus not have to care about contradictory results from Million et al., as well as dozens of other studies, each of which identifies another type of bacteria as 'the root cause' of the obesity epidemic - in Million's case the name of the scapegoat is Lactobacillus reuteri, by the way (Million. 2013).
Mediocrity guarantees a long life - At least when it comes to body fatness being too lean and being too fat are equally detrimental to the life expectancy of male 65+ agers (Toss. 2013). If you are women, though, the results Fredrik Toss and his colleagues published in the latest issue of Age and Ageing suggest that being on the chubbier side of things can actually be life-saving, as long as you carry the fat in the gynoid and not the abdominal area. Most importantly, however, lean mass, or as my buddy Carl Lanore calls it, "metabolic currency" is yet still the most significant predictor of survival in older subjects - in other words: Don't even think of emulating the skinny fat celebrities with their starvation diets and endless cardio sessions if you intend to live your grand- and grand-grand-children, better check out yesterday's news on the "Iranian HIIT Solution for Improved Insulin and Leptin Sensitivity".
Image 5: If you are concerned about bone health, menopause is not the best time to stop drinking... unless you start weight lifting, of course ;-)
Don't stop drinking alcohol in menopause! At least if you don't want to increase bone-resorption, i.e. the leeching of calcium from your bones. This is the surprising result of a recently published study by Jill A. Marrone and colleagues, who had investigated the effects of total abstinence from alcohol in 40 healthy postmenopausal women (mean ± SE age, 56.3 ± 0.5 y) who consumed the alcohol equivalent of ~1 glass of wine per day (Marrone. 2013). Interestingly, the bone formation marker osteocalcin and the resorption marker C-terminal telopeptide (CTx) returned to their normal values, once the women resumed their former drinking habits.
In view of the fact that there was also a significant correlation between baseline bone-density, as measured dual-energy x-ray absorptiometry, and the extent of mild to moderate alcohol consumption, these results raise the question whether "bone health" would be another factor to add to the list of the "minimalist approach" to alcohol consumption.