Caffeine By Afrida: On Short Notice: PWO EAA Supps for Young & Old, Indoor Pools & Low Testosterone, Life-Savingly Low T3/rT3 Ratios, Copper-Zinc-Manganese, Lifting for Prostate Health +More

Image 1: It's neither just as much, nor just as serious, but I would still venture the guess that it will take you more than 30s to digest today's installment of "On Short Notice" - despite the fact that the new format has no lengthy "short news", anymore ;-)

For this installment of "On Short Notice" I have decided to go a somewhat different route than before: Originally, the first post you would have read after this short introduction would have dealt with the potential negative health effects of homogenized milk. What was intended as a "on short notice" item, did however become lengthier and lengthier, until it finally turned into an "almost full-length post" (a slightly extended version of this article is going to be published on Monday). This "incident" made me revisit the last installments of this series only to realize that the majority of the supposedly "short" On Short News items had become "almost full-length posts" and were thus either somewhat overblown or still to short for what the study / topic had to offer...

To cut a long story short, I decided to stick to the very short items, formerly known as "On Very Short Notice" from now on. If you have any reasonable objections against this practice, feel free to use the comment area of this post to complain. Do not forget, however, that you can still request a longer article on any particularly interesting topic or simply discuss the blurbs with me and others here or on the SuppVersity Facebook wall... Ready? Let's roll!

Figure 1: Ratio of muscle intracellular leucine to blood leucine concentration in response to
resistance exercise and ingestion of 20 g of essential amino acids in young and older men.
Older physical culturists can't "eat to grow" benefit from EAA ingestion - at least not to the same extend younger lifters do. And while this alone would hardly qualify as "news", the, or I should say one of the underlying reasons Jared M. Dickinson and his colleagues discuss in a paper that's scheduled to be published in the next issue of the Journal of Clinical Nutrition certainly is (Dickinson. 2012).
One hour after the 7 young (30 ±2yr) and 6 old (70 ±2yr) male "recreationally active" study participants had performed a standardized leg training program consisting of 8 sets of 10 reps on a Cybex leg extension machine at an intensity of 70%RM (3 min rest between sets) Dickinson et al. supplied them with a 500ml of a fluid that contained 20g of leucine enriched essential amino acids (EAA) (exact composition: histidine 8%, isoleucine 8%, leucine 35%, lysine 12%, methionine 3%, phenylalanine 14%, threonine 10%, and valine 10%). In the hours following the leg training the scientists measured the amino acid flux and took muscle biopsies from the vastus lateralis to quantify the amino acid transporter (the "shuttle" that carries the amino acids from the blood stream into the muscle) expression in the trained leg muscles of their subjects.
Contrary to what happened in the younger subjects, the expression of the transporter proteins was not further augmented (over exercise alone) in response to the ingestion of the EAA supplement in the older study participants. Consequently, the restoration of the intra- to extracellular amino acid ratio which was complete after 5h in the young subjects took more time and was not completed, when the third biopsy was taken at T=5h in the older subjects (see figure 1). A result, which (re-)emphasizes the paramount importance of physical activity in older people not just to become stronger, but also to ward off sarcopenia (=muscle loss) and subsequent frailty!

Figure 2: Unadjusted (top, middle) and adjusted (bottom) testosterone levels in adolescent boys depending on their exposure to chlorinated indoor-pool water before the age of 7y (bottom) and 10y (top, middle) respectively.

Michael Phelps & Co at high risk of low testosterone - That's at least what we'd have to conclude from a 2011 paper that was published in the International Journal of Andrology by Nickmilder et al. who found that there is a clearcut association with early life exposure to chlorinated indoor-pool water and low testosterone levels in adolescence (and probably later in life, although that was not part of the study; cf. Nickmilder. 2011)

As the data in figure 2 shows, the association with lower testosterone levels is most pronounced (p < 0.01) when the data was adjusting for inhibin B, FSH, age, time of blood sampling and breastfeeding (figure 2, bottom). With p < 0.05 (=5% chance that this is just coincidence) even the unadjusted values for pool water exposures of >250h before the age of 7 years were however statistically significant and as the scientists point out probably a result of the prolonged exposure of the "highly permeable scrotum" (Nickmilder. 2011) to chlorinated water.

Intriguingly, Bob Weinhold mentions in his otherwise rather critical comment on the study that Shanna Swan, a professor of preventive medicine at the Mt. Sinai School of Medicine, did not just criticize the "paucity of evidence from other studies", but also her hint at "effects from bath water exposures" as potential confounding factors (Weinhold. 2012). Against that background I suggest you go and take a very close look at the label of whatever cosmetic products you pour into your (male) children's bathwater.

Image 2: The dreaded low T3/rT3 ratio appears to be life-saving for critical ill patients. And when you come to think about it, it could well be a "natural mini coma" by which your body diverts all available resources to the one thing that's certainly more important than having a six pack: SURVIVAL!
Low T3/rT3 ratio protects critical ill from death! While 1000s of visitors of various bulletin boards and discussion groups on the Internet are whining about a too low ratio of the "active" to the "inactive" form of triiodothyronine, the observation Marijke Gielen and her colleagues made, when they studied the chance of critically ill patients to be released early and alive from hospital, would suggest that rT3 is way more than a nasty millstone around the neck of (over-)dieters. After all, Gielen et al. found that the patients with the best blood glucose control and lowest T3/rT3 ratios had a +19% increased chance of being released early and alive (Gielen. 2012). An increase in the T3/rT3 ratio, on the other hand, was independently of glucose management, associated with a -14% lower chance of being released early and alive!

I guess that this should be reason enough to rethink the generally touted "uselessness of rT3", wouldn't you agree? After all, it could well be that it is the rT3 induced metabolic slowdown that allowed for optimal recovery - much similar to the artificial coma physicians will induce in burn victims or other critically patients to have them recover faster / at all. This would yet also imply that having a very low T3/rT3 ratio is - as I've previously mentioned, by the way - a good indicator of other, non-thyroid related pathologies you should better try to spot and take care of before they will eventually show up and turn you into a subject for a follow up study for Gielen et al. (related: "T4+T3 Combination Therapy Instead of T4 Mono-Therapy")

Figure 3 (Zhu. 2012): Vitamin D3 is converted to the active metabolite 1,25(OH)2D3 by sequential 25-hydroxylation and 1a-hydroxylation.
Slow conversion of D3 to 25-OHD in the obese suggests: Low vitamin D is a result of obesity - not vice-versa! Within the past decade(s) many scientists have observed correlations between higher adiposity and lower vitamin D levels (e.g. Arunabh. 2003). Only within the last 5 years or so, however, those results have been interpreted as "scientific evidence" that low vitamin D levels play a causative role in the current obesity epidemic. First evidence for the opposite, i.e. a causative relationship between obesity and the occurrence of chronically low systemic vitamin D levels in obese individuals (90%+ of the obese women in the study had 25OHD level <50 nmol l⁻¹; Wamberg. 2012), does yet come from a study that has been published in the International Journal of Obesity a couple of weeks ago.
According to the Wamberge et al. present in their paper, the occurence of low 25(OH)D levels in the sera of obese individuals is a direct consequence of the sluggish bioactivation of vitamin D3 in the subcutaneous adipose tissue of obese patients. The latter is due to the -71% and -49% reduced expression of the two of the enzymes from the cytochrome P450 enzyme cascade (25-hydroxylase and 1α-hydroxylase, to be precise, see figure 3), which are responsible for the conversion of dietary or skin-derived (after sun exposure) vitamin D3 to 25(OH)D, which is the form of "vitamin D" your doctor will usually measure, and the "active" form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25(OH)(2)D(3) aka calcitriol.
Image 3: That's what active prostate cancer prevention can look like - no vaccine necessary!
Heavy lifting protects against prostate cancer! This is the result of yet another of a whole host of studies which finally acknowledge the value of weight training with respect to all sorts of health benefits that have previously been ascribed to aerobic training only (Teixeira. 2012). Published ahead of print in the online version of the Scandinavian Journal of Medicine & Science in Sports the paper by Teixeira et al. is the first one to report that strength training can reduce the risk of prostate cancer by (re-)establishing a healthy balance between natural cell death and growth.
In the course of a 91-day period a group of rodents were exposed to a daily "weight lifting regimen" (=jumping, 4x10 jumps with 50–70% of their body weight strapped to the thorax and 60–s rests between sets). This torture lead to an increase in corticosterone (=cortisol), DHT and testosterone levels, and brought about a healthier ratio of cell growth to apoptosis in the prostates of the animals than it was present in the age-matched sedentary control.
Figure 4: Building muscle requires more than just pumping existing fibers full of protein (click on the image to read up on the details)
Scientists confirm Intermittent Thoughts on Building Muscle: Myostatin allows cells to "blow up", but does not facilitate structural changes. What's funny though, is that Lee et al. obviously feel that this is a great thing; and while it may actually be in the context of sarcopenia (pathological muscle dystrophy), where agents that block myostatin could proof very valuable tools, it just confirms that these agents are of little use, if not counterproductive for athletes and physical culturists who would always have to be on the look-out not to outgrow the necessary (re-)construction process, of which I have argued in the Intermittent Thoughts on IGF-1 an Its Splice Variants, already that it is necessary to keep the ever-growing muscles functional.
So, in case you have a few vials of a real myostatin inhibitor lying around (not the hilarious egg-derived supplement that was sold a couple of years ago by snake oil vendors), you better talk to your medical practitioner about some growth hormone, as well, if you don't want to end up huge, but so weak that you can't make it up the five stairs in front of your gym ;-)

Image 4: While some experts say otherwise it appears illogical that the increase in breast tissue density, that's characteristic of women with a non-android body fat distribution would increase breast cancer risk. The majority of studies still ascribes a much higher increase in cancer risk to abdominal obesity (=android fat).

Silicon boobs? Not necessary if you stay in shape! While the overall size still is a matter of genetics, the density of the female breast shows such a strong negative association with the android : gynoid ratio in young women (one standard deviation up corresponds to a -20% reduction in dense breast tissue; Dorgan. 2012) that it would seem as if simply staying in shape and thus avoiding the accumulation of body fit in the "unfemale" android areas could would (other factors like breastfeeding etc. aside) save one or another woman from a still very much underestimated and by no means just monetarily costly operation (cf. Bolton. 2012). And let's be honest: What are those silicon balls worth anyway, when the blubber starts shortly beneath? What certainly is bad news for the adolescent obesity generation , though is that childhood obesity is an even stronger predictor of low amounts of dense breast tissue. Even after adjustment for adult obesity each BMI z-score, i.e. one standard deviation upwards, was associated with a -27% decrease in tender breast tissue.

Against that background it appear dubious, whether or not the often touted association between dense breast tissue and breast cancer risk is by any means a causative one... after all Abu-Abid et al. report in their review on the literature that abdominal obesity, i.e. an android body fat pattern is one of the best predictors of increased risk for all cancers (Abu-Abid. 2002).

Are manboobs a sign of intelligence? Could be if we put any faith into the relation between the size of your hippocampus and your intellectual capacity, the findings Janine Bayer and her mostly female colleagues (this could be important, who knows maybe this is a feminist conspiracy!?) report in their latest paper on the effects a certain genetic polymorphicism (rs700518) in the aromatase enzyme CYP19A1 will have on both systemic as well as hippocampal estrogen levels and had the volume of the posterior hippocampal gray matter (Bayer. 2012). Unfortunately most manboobs today are a simple result of overaromatization due to obesity and whether this is a hallmark feature of superior intelligence appears at least questionable to me (suggested read: "Chest Fat, Bitch Tits, Chesticles and How to Get Rid Off Them")
Image 5: 1x 1g of taurine = 1.5% faster 3k-times in trained middle distance runners - another benefit of the underrated sulfur amino acid, taurine
Taurine works for 3k-runs as well that's the simple message of a recently published study by Balshaw et al. In the randomized, double-blinded crossover experiment the ingestion of 1,000mg of taurine immediately prior to a 3km run increased the time-trial performance of the eight trained middle-distance runners by statistically significant 1.5%, on average (Balshaw. 2012); this does allegedly not sound like much, but if you take into consideration that this was a single serving effect it is actually quite impressive compared to the the ~1% performance increment in the narrow range of 90-120s activities that has recently reported to come out of weeks of beta alanine supplementation.
So, if the testosterone boosting, anti-diabetic effects of taurine (see "Up to 180% Increase in Testosterone & More From Taurine") did not already convince you to invest the ~$20 for a 500g batch of this sulfur amino acid, maybe these results and a couple of hours in front of the TV watching track & fields events at the Olympic Games '12 can ;-)
Figure 5: Glucose metebalism markers of oxidation and nitric oxide (top) calculated artheorscleortic risk (bottom, left) and body weight gain (bottom right) in the different groups
Differential and common effects of zinc, copper and manganese supplementation on body weight gain, glucose metabolism and cardiovascular health have recently been reported by scientists from the Usmanu Danfodiyo University in Nigeria. In their paper that has been published in the Journal of Oxidative Medicine and Cellular Longevity Muhammad et al. report that the provision of high copper (4mg/kg), high manganese (10mg/kg) and high zinc (20mg/kg) diets or the addition of all three supplemental minerals to the diets of salt-loaded hypertensive male Wistar rats all offered at least some protection against the oxidative stress, dyslipidemia, and insulin resistance that's associated with hypertension.
As the data in figure 5 goes to show, the provision of additional copper does yet appear to exert the most benefits. In view of the short duration of the study, it would yet be more than premature to recommend copper only supplementation regimens in the absence of proven and most importantly specific deficiencies. Rather than that those of you who are suffering from the triumvirate of elevated blood pressure, insulin resistance and dislipidemia would probably be better off if they increased their overall intake of these trace minerals.
Image 6: Sounds stupid, but if you are concerned about your dopamine receptor count, you better make sure to eat the bun and order an extra large coke (the original with tons of sugar, of course ;-)
High fat / low carb = reduced striatal dopamine receptor availability this is the quintessence of a short communication that has been published in the International Journal of Obesity three days ago. According to E van de van de Giessen and his co-workers, rats on a high fat high fat diet (this is no typo but the way of the researchers to acknowledge that the "original high fat diet" as it is interpreted by most scientists is almost equally high in carbohydrates (calorie-wise) as it is in fat; not so for the "High Fat High Sugar High Fat" (HFHS hf) diet in the van de Giessen study. Compared to the regular high fat diet, the HFHS-hf diet ameliorated the increase in energy intake, but reduced the availability of D2 & D3 receptors in the nucleus accumbens.
Overall, the ratio of fat to carbohydrate in the diet and not as it has previously been speculated the degree of adiposity or the total energy intake were the most and only significant correlate of the central dopamine receptor downregulation the researchers observed in their test animals (Giessen. 2012). In view of the fact that Fetissov et al. speculated in 2002, already, that "[l]ow D2 receptor expression may be causal for an exaggerated dopamine release observed in obese rats during food ingestion" (Fettisov. 2002) this is bad news - as it would indicate that the low carb induced reduction of dopamine receptor density could precipitate to reward driven episodes of overeating... an emphasis is on the conditional, here, as the majority of low-carb dieters will probably confirm my gut feeling that during the low carb diet, the exact opposite appears to be the case (at least as long as we are talking about even more fatty foods ;-).
Image 8: According to Hwang et al. it does not matter how you cook your broccoli, if you want to keep the glucosinolates intact. The main point is that you do it fast!
Cooking your veggies without water reduces cholesterol oxidation and improves potassium status that's what a group of Japanese researchers who declare they do not have any affiliation with the producer of multi-ply cookware, Vita Craft Japan Ltd, found in a 2-week intervention study in the course of which both the "just eat your veggies" and the "eat your veggies, but cook them without water in multi-ply cookware(TM)" (the product reference is #5123) increased their beta carotene and vitamin C levels and decreased their LDL and total cholesterol levels, but only the "without water cookers" had significantly reduced oxidized LDL and profoundly improved (=lower) Sodium : Potassium ratios in their urin (Mori. 2012).
Now, while this sounds as if it would make sense to buy this cooking "gear" things look somewhat different, when you take a look at the absolute differences and outcomes. While the oxidized LDL levels did in fact improve more in the muli-ply group this brought them just back into the exact same range where they were hovering in the other groups, as well. Similarly, the Na:K ratio was better, but it did improve in the "regular cooking" group as well and would thus probably end up in the same range, after another 2-6 weeks of vegetable eating - regardless of whether you cook them with water or not. Things would probably not be much different for the glucosinolate content of broccoli of which Hwang et al. report in the same issue of the International Journal of Food Sciences and Nutrition report that, they decreased significantly and time-dependently during boiling, steaming and microwaving (Hwang. 2012)
Black tea, lemon and honey: Can you stack it? Yes, you can! Camellia sinensis, Citrus limon and Apis mellifera all have a record of being potent antioxidants, but according to a paper in the August issue of the International Journal of Food Sciences and Nutrition lemon-flavoured black tea becomes an even more potent health drink, when you "spike" it with honey (Pereira. 2012).
Moreover, Pereira et al. found that the darker species of the different honeys from Lavandula stoechas, Erica sp. pl. and other indigenous floral species from north-east Portugal they tested were more potent than the light amber varieties.

Image 9: The powdery Matcha tea is not only already high in catechines, it will also release>130x more of it's EGCG content into the brewing water than most regular green teas! And as if that wasn't enough, it has a 64% higher caffeine concentration (6.4 vs. 3.9mg/g), as well.

Matcha tea has an uber-potent 137x increased EGCG content! This is one of the "oldie but goldie" studies I hit upon when I did "colleteral research" in response to a Highbrow Paleo member complaining that the over-potent Matcha tea literally blew him away. Actually not very surprising in view of the fact that it contains 137x more EGCG than regular green tea (brand China Green Tips; cf. Weiss. 2003). And while the selection of a specifically catechin rich fraction will figure here, as well, much of the effect is probably simply a result of the increased surface area and thus the greater efflux of the bioactive ingredients into the brew the tea is steeped in.

In view of the previously reported negative effects very high doses of green tea catechins can have on your testicular health all matcha lovers out there should better limit their daily consumption to one or two cups of the exclusive brew (see "20% Reduction in Testosterone with 5 Cups of Green Tea").

Oral anti-oxidants restore glutathione in diabetic skin At least in rodents this works pretty damn well. According to Sokmen et al. all it takes to restore the natural antioxidant defense system in the skin of streptozotocin-induced diabetic rats (model of type II diabetes) are 250 mg/kg vitamin C, 250 mg/kg vitamin E and 0.2 mg/kg selenium (Sokmen. 2012). The human equivalent of these orally supplied antioxidants would be 40mg/kg vitamin C, 45 IU/kg vitamin E and 30µg/kg selenium - all much too high to benefit anyone who is not diabetic, by the way.

Image 10: Usually I am really enthusiastic about new technologies, but looking at how careful physicists handle nanomaterials, and how food designers and the cosmetic industry unleash them on the costumers, like the US and UDSSR unleashed the a-bomb radiation on their own soldiers, ignorant of the (un?)known dangers.

Nano-sizing fish oil doubles absorption - This is the result of a recently conducted rodent trial by Tanmoy kumar Dey the results of which are soon going to be published in Food Research International (kumar Dey. 2012). The more than +50% increased absorption the scientists found for their nano emulsified fish oil in the small intestine of the lab rats is - at least in my humble opinion - somewhat frightening. Firstly, I am really not sure we really need the hilarious amounts of fish oil, where the use of respective products would make sense (it should be said, though, that this new formula has been developed for parenteral nutrition, specifically). We have, secondly, not the slightest idea if those nano-sized fish oil molecules behave anywhere similar to their fluffy large brethren - who tells us that they don't have the exact opposite effect on our health?

And third and lastly, if nano-sized fish oil is absorbed 100% more efficiently, all other nanomaterials - especially those that are nor increasingly popular in the cosmetic industry - will have a similarly increased "bioavailability" and could thus not only reach places in our body they were never intended to reach, but do just that in very significant amounts!

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