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Maximizing Excess Post-Exercise Oxygen Consumption aka EPOC | Run, Don't Cycle, Split Your Training Session in Two Intervals Instead of Doing One Long Session a Day!

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Bring the heart rate up with exercises that involve the whole body and do workout short, intense and frequent to maximize the excess post-exercise oxygen consumption, but don't fall for the falls believe that this alone would be enough to get you shredded.
It's pretty straight logical and with the publication of the accepted manuscript of a recent study from the Institute of Physical Education and Sports at the Laboratory of Physical Activity and Health Promotion of the University of Rio de Janeiro State it's scientifically proven, splitting your cardio training in two sessions kicks cardio's (=medium to high intensity steady state exercise's) ass, when it comes to maximizing the Excess Post-Exercise Oxygen Consumption (EPOC).

As Cunha et al. point out in the intoduction of their latest paper, "previous research investigating the effects of intermittent vs. continuous exercise upon EPOC superficially matched the exercise bouts for external work (same intensity and duration), the exercise volume was not matched by the actual EE [energy expenditure]" (Cunha. 2015).
Focus on muscle builders and use your diet to get shredded:

Tri- or Multi-Set Training for Body Recomp.?

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Battle the Rope to Get Ripped & Strong

Study Indicates Cut the Volume Make the Gains!
In other words, you if you want a fair comparison you have to make sure that the intra-workout energy expenditure is identical and cannot compare 10 minutes of steady state exercise to 2x5 minutes of steady state exercise, because it's not a given that the workload will be absolutely identical: Only if you standardize the workout volume by measuring the energy expenditure and make sure that the the exercise intensity and cardiorespiratory fitness levels of your subjects are taking into account you will be able to objectively compare the effects of continuous and intermittent exercise on the magnitude of EPOC.

In their latest study Cunha et al. tried to do just that, when they had ten healthy men, aged 23 to 34 yr, performed six bouts of exercise
  • firstly, two maximal cardiopulmonary exercise tests for running and cycling to determine exercise modality-specific peak oxygen uptake (VO2peak); and
  • secondly, four isocaloric exercise bouts (two continuous bouts expending 400 kcal and two intermittent bouts split into 2 x 200 kcal) performed at 75% of the running and cycling oxygen uptake reserve.
This means, the subjects expended the same 400kcal, but in one trial they did it in a single session, while in the other, they burned 200kcal in session 1 and 200kcal in session 2, exactly 1h later.
Beware! This is not a HIIT vs. LISS study! At first I thought that this would be another HIIT vs. LISS comparison, but this is not the case. It's a comparison of two forms of steady state exercise, where one is classic, i.e. training for roughly 30 minutes, while the other was designed to consume the exact same amount of energy, albeit in two sessions seperated by 1h of rest.
The exercise bouts were separated by 72 h and performed in a randomized, counter-balanced order. The VO2 was monitored for 60-min postexercise and for 60-min during a control non-exercise day.
Figure 1: It's quite obvious - the more muscle you train, the higher your EPOC is going to be. Plus: If you do interval training, your total EPOC will exceed the amount of fat burned after isocaloric continuous exercise (Cunha. 2015).
As it was to be expected, the VO2 was significantly greater in all exercise conditions compared to the control session (P < 0.001). More importantly, however, the combined magnitude of the EPOC from the two intermittent bouts was significantly greater than that of the continuous cycling (mean difference = 3.5 L, P=0.001) and running (mean difference = 6.4 L, P <0.001).

In the end, both, the exercise type (cycling = less muscle vs. running = more muscle) and modality (continuous vs. intermittent) both had a significant effect on net EPOC, where running elicited a higher net EPOC than cycling (mean difference = 2.2 L, P <0.001).
If you are training for max. EPOC, only, you are a fool | more.
In the end, the study does therefore provide convincing evidence that what most of you will probably already have assumed is in fact the case: "Intermittent exercise increased the EPOC compared to a continuous exercise bout of equivalent energy expenditure. Furthermore, the magnitude of EPOC was influenced by exercise modality, with the greatest EPOC occurring with isocaloric exercise involving larger muscle mass (i.e., treadmill running vs. cycling)" - or, as the title of today's SuppVersity article suggests: 'If a maximal EPOC is your goal, select an exercise that involves a maximal amount of muscles and split your X minutes of working out in two intervals.'

Whether that's something you must do, however, depends on how convinced you are that EPOC matters. In previous SuppVersity articles I have already dissected the myth that burning a few extra-calories from fat after the workouts will make the difference between being flubby and being jacked. In case you can't remember the result, i.e. that it probably doesn't make much of a difference, I suggest you take another look at the respective article | Comment on Facebook!
References:
  • Cunha, Felipe A., et al. "Effect of continuous and intermittent bouts of isocaloric cycling and running exercise on excess postexercise oxygen consumption." Journal of Science and Medicine in Sport (2015).

Acute L-Carnitine Tartrate Supplementation Boosts VO2-Max, Fat Oxidation & Endurance in Elite Wrestlers

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The VO2-max boosting effects of l-carnitine tartrate can be beneficial for almost every athlete.
After being the hype supplement in the 1990s, carnitine eventually sank into obscurity; and while the revelation that l-carnitine tartrate may increase the androgen receptor density is the main reason it can still be found in various T-boosters and pre-workout supplements, people appear to have forgotten that the original idea of carnitine supplementation was to increase the effectivity of the carnitine shuttle and thus to increase the oxidation of fatty acids.

As a recent study from the Shahid Chamran University in Iran shows, this could be a mistake. After all, Mostafa Dehghani and his colleagues were able to show that "supplementation of L-carnitine improved effectively the performance by increasing in [sic!] lipid metabolism" (Dehgani. 2015).
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But how did the researchers come to this conclusion and are the results relevant for you and me? Well, the first good news is that we are talking about a randomized controlled clinical human study, in which the subjects were not training noobs, but elite wrestlers.

The twenty healthy elite male wrestlers with a mean age of 22.05 ± 2.6 years, mean weight of 77.10 ± 11.65 kg, mean height of 1.79 ± 0.06 m, and mean body mass index of 23.79 ± 2.45 kg/m2 who participated in this single-blind clinical trial were randomly divided into two groups including test and placebo.
  • The test group received 3 g of L-carnitine tartrate in 200 ml water and 6 drops of lemon juice.
  • The placebo group consumed only 200 ml water and 6 drops of lemon juice.
Both, the active and placebo treatments were administered 90 minutes before performing the so-called Conconi Test for anaerobic and aerobic threshold, a test of lactate threshold using only heart rate (learn more). Blood samples were collected from brachial veins 90 minutes before the activity, immediately after the activity, and 30 minutes after rest and their serum lipids were measured. The results were analyzed using SPSS-16.
Figure 1: The carnitine supplement led to significant increases in VO2 max (fatty acid oxidation) and the maximal distance the subjects were able to cover in the Concoi test (Dehgani. 2015).
Speaking of results: As the previously quoted conclusion already gave away, 3g of l-carnitine tartrate lead to significant improvements in distance run performance. An effect that was probably at least partly mediated by a significant elevations of the the lipid metabolism and VO2 max.
Immediately after the workout there were transient changes in blood lipids that are surprising, but probably not (health-)relevant (Dehgani. 2015).
Overall, the study at hand does therefore appear to confirm the usefulness of l-carnitine tartrate supplementation in athletes. In that, it's very important that the subjects were highly trained wrestlers and not regular couch potatoes, because the former exhibit training-related improvements in the efficacy of the carnitine shuttle, anyway.

What remains to be seen, though, is whether the effects will still be visible after weeks of supplementation. You, as a SuppVersity reader, should know that acute supplement studies can be deceiving. Therefore, it would be great if we had a 6-week study that compared the performance increases in response to standardized training regimens with and without carnitine supplementation | Comment on Facebook!
References:
  • Dehghani, Mostafa, et al. "Effects of L-Carnitine L-Tartrate Acute Consumption on Lipid Metabolism, Maximum oxygen consumption (VO2 max), and distance run Following Aerobic Exhaustive Exercise on Treadmill in Elite Athletes wrestling." The AYER 2 (2015): 189-105.

Regular Ca-HMB Boosts Strength and Performance in Elite Athletes - Increased Performance Gains on High Volume Routines Confirm: HMB Excels On Insane Workouts

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In my comparison of leucine and HMB I have hinted at the unique anti-catabolic affects of HMB, already. Now, the accumulating evidence appears to suggest that the prevention of muscle damage is in fact the main pathway by which HMB exerts its ergogenic effects.
Free acid (or free form) HMB is one of the supplements I get the most questions about. It is yet by no means one of the best-researched supplements and another good example of how good write-ups sell supplements. Somehow it all reminds me of the not so good "old days", when HMB was still believed to be "as potent as a weak anabolic" until everyone had trialled it and realized that there were no steroid-like gains...

Well, enough of the ranting. Let's get to the actual reason I am talking about HMB. Scientists from the Federal University of Parana report in their latest paper that the good old calcium-bound form of HMB works. That wouldn't be important in view of the fact that there are at least two dozens of studies if it were not for the fact that the ~4 studies and the corresponding advertisement machinery for free acid HMB had been enough to make every bro believe that Ca-HMB didn't work, while free form HMB,... well, you know "is as potent as a weak anabolic steroid" ;-)
Learn more about HMB at the SuppVersity:

HMB For Fat Loss?

Hica & HMB in Yogurt

More on HMB Free Acid

Breakthrough HMB Science

HMB for Muscle Quality

HMB Hampers Fat Loss?
In said study, the researchers investigated the effects of 12-Weeks of Supplementation with β-Hydroxy-β-Methylbutyrate-Ca  (HMB-Ca) on athletic performance. In their prospective, randomized, doubleblind, placebo-controlled study Ferreira et al analysed the effects of HMB-Ca (37.5 mg/kg per day of the "regular" recently derided version of HMB also known as "Ca-HMB" or "Calcium-bound HMB") on body composition, athletic performance, and inflammatory mediators in 20 elite canoeists (age, 18.7 ± 1.49 yrs; body weight, 78.9 ± 3.3 kg).
Figure 1: Pre-post changes in strength parameters in the HMB and placebo group (Fereirra. 2015).
The athletes were supplemented and followed for a period of 12 wks during strength training. The results indicated that a dose of HMB-Ca could potentiate an increase in lean body mass (the exact values are not mentioned in the FT, which is strange, but the strength values developed significantly faster (see Figure 1) and the scientists claim there were increases in lean mass in the abstract; eventually both groups lost weight, though, so if there were lean mass increases there must have been a similar loss of body fat as in the Wilson study) commensurate with strength gains associated with endurance training in competitive athletes who lifted thrice per day for 6 hrs/week (1 to 3 sets of 2 to 8 repetitions at intensities ranging from 80 to 95% of 1 RM) on Monday, Wednesday, and Friday and performed an additional 10 hrs/wk of sprint-specific training and technical assistance with the boat.
Figure 2: In view of the training load, it is not surprising that all related parameter increased significantly in the placebo group; against that background it's yet all-the-more surprising that they decreased with Ca-HMB (Fereirra. 2015).
As Fereirra et al. point out, "[t]he mechanism by which this occurs is still unknown, but the results indicate that supplementation might decrease the damage to skeletal muscle when stressed before training with a significant difference in serum creatinine (P<0.05)" (Ferreira. 2015) - quite an interesting explanation that should remind you of one of the previously hinted at ~4 free acid HMB studies... which  one? Well, the one by Wilson et al. which used an overreaching regimen to produce extremely outstanding results (read up on the study). A study with a similarly insane (=high) training volume and trained subjects as the study at hand in which the elite athletes performed two daily sessions for a total of 11 training sessions per week.
It's a pitty there's no DEXA data that would allow us to quantify the changes in body composition, because other changes are not less astonishing than they were in the Wilson study.
With HMB you got to hit it hard! Considering the fact that the study at hand provides further evidence that HMB works (at least partly) by reducing the training induced actual muscle damage and thus speeding up the supercompensation response, I would like to remind you what I said about the previously mentioned Wilson study, already: HMB appears to excel, when you're training at the verge of doing so much that your progress is threatened by the way you train.

Plus: With the study at hand, we have (as I also suspected) the evidence that it doesn't have to be "free acid" or "free form" HMB to see results. The 2-3g of regular HMB that were spread equally on three doses (morning, afternoon, and evening) worked as well | Comment on Facebook!
References:
  • Ferreira, Heros Ribeiro, et al. "Effects of 12-Weeks of Supplementation with β-Hydroxy-β-Methylbutrate-Ca (HMB-Ca) on Athletic Performance." Journal of Exercise Physiology 18.2 (2015).
  • Wilson, Gabriel J., et al. "The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study." European Journal of Applied Physiology (2014)

Sweetener Update: Chronic Aspartame & Acesulfam-K Use Doesn't Mess W/ Your Microbiome | No Link Between Bad Lifestyle & Sweetener Use | No Good Advice from Dietitians

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There's no scientific evidence that any of the various forms of "natural" sugar replacements like brown sugar & co would be better than artificial sweeteners.
Since artificial sweeteners their (non-existent) impact on insulin and, more recently, their effects of the gut microbiome are recurring topics in the Facebook messages I receive, I thought it may be nice to briefly summarize potentially relevant results of some of the more recent papers which put a questionmark behind some of the commonly heard "anti-sweetener" arguments, ... including the recently voiced objection that they would mess up your microbiome.

To this ends, I have conducted a brief database search, the results of which I will summarize briefly in only one to two paragraphs:
You can learn more about sweeteners at the SuppVersity

Unsatiating Truth About Artif. Sweeteners?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Sweeter Than Your Tongue Allows!

Stevia, the Healthy Sweetener?

Sweeteners In- crease Sweet- ness Threshold
  • Recent intake of aspartame or Acesulfame-K is not associated with overall gut microbiome profile in adults (Frankenfeld. 2015).

    Unlike high-dose exposure to artificial sweeteners in rodents (Suez. 2015a,b), the chronic exposure to normal dietary amounts does not appear to induce significant changes in the gut microbiome. That's at least what the results of a recent study from the Global and Community Health George Mason University clearly indicate.

    In said study, Frankenfeld et al.  evaluated the gut microbiome in relation to recent aspartame and Acesulfame-K artificial sweetener consumption in thirty-one adults who completed a four-day food record and provided a fecal sample on the fifth day. The DNA analysis of the bacterial composition of the fecal samples showed that the bacterial composition of the participants (23%) who consumed aspartame and the participants (23%) who consumed Acesulfame-K did not differ significantly from the one of those subjects who did not use artificial sweeteners. As Frankenfeld et al. rightly point out, though, "[f]urther studies with more individuals are warranted to evaluate lower abundance microbial" (Frankenfeld. 2015).
  • No, sweeteners won't have you overeat. On the contrary: Epidemiological data suggests, people who consume more artificially sweetened foods and beverages have lower total energy, carbohydrate, and sugar intakes (Hunt. 2015).

    As the authors point out, "[t]he effectiveness of Low Calorie Sweeteners (LCS) for weight management is an area of debate", evidence on their use, however is lacking. To produce such evidence, Hunt et al. analysed the prevalence of LCS and macronutrient intake among US adults (19+y;n=9634, N=213,173,877) based on data from nonconsecutive 24 hr dietary recalls from NHANES 2007-2010. They categorized individuals into LCS usage groups as zero LCS use (56%; NO), LCS use 1-2x/2 day (23%; LO), or LCS use >3x/2 day (21%; HI) based on use of LCS in foods, beverages, and condiments. The classification shows that those in the highest LCS group, when compared to those who did not use LCS, were more likely to be: female, non-Hispanic white, age 51-70y, college educated, of higher income or BMI >30 kg/m² (all p<0.001).
    Figure 1: Data from NHANES 2007-2010 clearly indicates that people who use artificial sweeteners regularly can reduce their energy, sugar and carbohydrate intake significantly (Hunt. 2015).
    While this was more or less to be expected, the data in Figure 1, which reveals that "those who reported the higher LCS use evidenced mean total daily intake that was lower in total energy, carbohydrate, and sugar intake than those who did not use LCS" (Hunt. 2015), may be a bit surprising; and that despite the fact that these data are consistent with available published randomized controlled trials on the impact of use of LCS in weight management all of which show that they help to reduce the subjects energy intake and thus propel weight loss.

    Against that background it's not exactly surprising that Drewnowski et al. (2015a) found that US adults who consume low calorie sweeteners and thus care about their sugar intake and health, have higher Healthy Eating Index (HEI 2005) scores and are more physically active. Similarly, "LCS use [is]more common among populations with a lower burden of obesity and related chronic disease, specifically, non-Hispanic whites and those with more education/higher incomes" (my emphasis in Drewnowski. 2015b).
Artificial Sweetened Foods Promote, Not Hinder Fat(!) Loss | more
Yes, yes and yes! Sweeteners will help you lose weight! Latest meta-analysis leaves no doubt: "Findings from observational studies showed no association between LCS intake and body weight or fat mass and a small positive association with BMI; however, data from RCTs, which provide the highest quality of evidence for examining the potentially causal effects of LCS intake, indicate that substituting LCS options for their regular-calorie versions results in a modest weight loss and may be a useful dietary tool to improve compliance with weight loss or weight maintenance plans" (Miller. 2014)
  • Dietitians' perceptions about sweeteners are uncertain, ambivalent and divergent, sometimes explicitly being linked to fears about adverse health effects (Harricharan. 2014).

    I must say that I am hardly surprised that artificial sweeteners are another thing dietitians should, but don't really know about. Data from France, Germany, Hungary, Portugal and the United Kingdom shows that whether "sweeteners are good" or "bad" depends on the dietitian you pick. While some argue (not totally unwarrantedly) that "they feel it is important for consumers to reduce their attachment to sweet tastes", the highly diverging "expert advise" makes it quite obvious why consumers are confused and that Harricharan et al. are right, when they demand "clear and authoritative guidance" (Harricharan. 2014) and evidence, not bro-science based recommendations from health-professionals.
Learn more about artificial sweeteners and more specifically about their non-existent effects on insulin in my previous article "Science Round-Up Seconds: The Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | more
Overall, there is no doubt that the deliberate and strategical use of artificial sweeteners, when you're dieting is useful. What remains to be seen is whether the results of the Frankenfeld study can be confirmed for other artificial sweeteners. If that's the case, the long-term consequences of artificial sweetener use on the gut microbiome and thus potential on health in general are probably irrelevant.

Assuming that there are unwanted consequences, the latter may explain the partly paradoxical results in epidemiological studies and would warrant investigations into the use of pre- and probiotics, i.e. substances that promote the growth of or replace those bacteria the count of which is reduced by artificial sweeteners | Comment on Facebook!
References:
  • Drewnowski, Adam, and Colin D. Rehm. "Consumption of Low-Calorie Sweeteners among US Adults Is Associated with Higher Healthy Eating Index (HEI 2005) Scores and More Physical Activity." Nutrients 6.10 (2014a): 4389-4403.
  • Drewnowski, A., and C. D. Rehm. "Socio-demographic correlates and trends in low-calorie sweetener use among adults in the United States from 1999 to 2008." European journal of clinical nutrition (2015b).
  • Frankenfeld, Cara, et al. "Artificial Sweetener Consumption and Microbiome Profiles in 31 Adults Living in the United States." The FASEB Journal 29.1 Supplement (2015): 262-5. 
  • Harricharan, Michelle, et al. "Dietitian perceptions of low-calorie sweeteners." The European Journal of Public Health (2014): cku171.
  • Hunt, Kelly, et al. "Low calorie sweetener and macronutrient intake in the US adult population: NHANES 2007-2010." The FASEB Journal 29.1 Supplement (2015): 254-6.
  • Miller, Paige E., and Vanessa Perez. "Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies." The American journal of clinical nutrition 100.3 (2014): 765-777.
  • Suez, Jotham, et al. "Non-caloric artificial sweeteners and the microbiome: findings and challenges." Gut microbes ahead-of-print (2015a): 1-7.
  • Suez, Jotham, et al. "Artificial Sweeteners Induce Glucose Intolerance by Altering the Gut Microbiota." Obstetrical & Gynecological Survey 70.1 (2015b): 31-32.

Placebo-Powered Turbo-Sprints - Study Confirms Possible Explanation for High Sales Ranks of Bullsh*t Supplements

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If it's not cancer, but something as simple as exercise performance believing that a pill will fix it will often suffice to fix it ;-)
Have you ever wondered why people spend bazillions of dollars on scientifically disproven supplements and claim that they work? Well, if you have read my previous article on "brocebos", you may already know the answer: It's the placebo effect.

Now, Danilo V. Tolusso, C. and colleagues from the Green State University did not investigate the subtle ways in which ads, sponsored athletes and the price of a supplement enhance its "efficacy", but their study which was designed give us "a more realistic understanding of the placebo effect in a sport or exercise session" is still enlightening with respect to the powers of belief.
The benfits of high(er) protein intake are not just placebo, bro ;-)

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Ten healthy, asymptomatic men (age = 22.2 ± 2.4, height = 1.8 ± .01 m, body mass = 81.2 ± 7.4 kg, body fat (%) = 8.1 ± 2.4) volunteered to participate in this no blind (if it was "blind" you could hardly have a good placebo effect ;-) study.
"To be included in this study,subjects must have reported performing sprint training or competition in an intermittent-type sport (e.g., basketball, football, tennis, soccer) at least two days per week. Prior to testing, subjects were instructed to refrain from drinking alcohol 24 hours and caffeine four hours before beginning physical activity. Subjects were also instructed to abstain from intense physical activities 48 hours before testing. Prior to each testing session, subjects were queried regarding adherence to the guidelines set for dietary intake and physical activity.

[...] The subjects must not have had a negative bias as to the effectiveness of ergogenic aids, as this may decrease the expectancy of the ergogenic aid to work and result in no placebo response. This was used as a criteria of exclusion to ensure that no subject had a preconceived bias against ergogenic aids (Tolusso. 2015)."
At the beginning of the study, all subjects were provided a brochure upon arrival to the laboratory. In the brochure the scientists claimed that the purpose of the study is to determine the impact of an "FDA approved substance has on performance during multiple sessions of repeated sprint work" (Tolusso.). The brochure contained an overview of previous research regarding the substance that they will be given- obviously one that was very beneficial.
How does "PLACEBO" work? This is how Tolusso et al. explain it: "In brief, the expectancy theory states that any resultant change in performance is largely mediated to the degree that an individual who was administered a treatment (i.e., placebo) believes it to be beneficial. Interestingly, improvements in performance are most commonly associated with the analgesic effect (i.e., pain mediating) that a placebo is known to induce, as research has confirmed that the anterior cingulate cortex, an area of the brain with a high concentration of opioid receptors, is similarly activated during placebo and opioid analgesia trials. This suggests that a placebo may elicit the same neural response associated with decreases in pain sensitivity owing to the binding of opioid receptors. This may yield increases in performance as studies have found that pain sensation can negatively impact performance" (Tolusso. 2015).
After the obligatory familiarization trial (obviously the whole study was designed as any good clinical study would be... well, with the exception of the blinding, obviously),  the subjects consumed 600 mL of the placebo beverage which contained nothing but distilled water and a commercially available, noncaloric, ‘water enhancer’ (sucralose + acesulfame-K) used to flavor the water. What is interesting is how this was done:
"The first dose of 600 mL was prepared in front of the subjects. Researchers extracted 1 mL of the ‘water enhancer’ from a beaker and extracted it into an Erlenmeyer flask containing approximately 600 mL of distilled water chilled to 10 ̊ C. The other doses of 150 mL were prepared beforehand, with the same concentration as the first dose. Subjects were informed the beverage they were consuming upon arrival and the additional doses of 150mL that they would be consuming during the sprinting trials were the same beverage and that they should expect the same ergogenic benefits listed in the expectancy brochure" (Tolussu. 2015). 
Immediately after ingestion of this 'powerful ergogenic' *rofl*, the subjects performed a standardized warm-up and three RAST protocols which consisted of 6x35m sprints + 10s active recovery in-between.
Figure 1: Overview of the study design (modified based on illustration from Tolusso. 2015).
After each RAST protocol, the subjects were allowed one minute passive recovery and had to rate their perceived exertion and pain on an RPE and VAS scale and were told to ingest more of their 'powerful' placebo super-supplement. To really mirror the typical supplement producer claim they were told to drink another serving after the workout, because beverage would promote overnight recovery (sounds familiar ;-).
Figure 2: Pretty neat performance gains (from Tolusso. 2015) for flavored water, right?
And guess what, it worked. As the data in Figure 2 tell you the subjects performed at significantly higher intensities (peak and mean power) "on" the powerful placebo supplement (the effect size is larger than with many "true" ergogenics in double-blind studies!); and that in the absence of any other significant difference in metabolic or perceptual strain (p > 0.05) - a fact that confirms the analgesic hypothesis (see lightblue box on the mechanism behind placebo effects in exercise science).
Brocebo? Add 10kg to Your Bench in Days with Sugar-Based "Anabolic Steroids". Old Study Shows, Many "Natural Anabolics" Could Work Solely via Placebo Effects | learn more.
Bottom line: I am not saying that your supplements don't work, but the fact that you or your bros feel much better "on" it is not exactly convincing evidence that a supplement works.

That being said, you may argue that it doesn't matter that it actually shouldn't work as long as it does work - who cares if the mechanism is psychological or physiological? I guess the people who produce and sell it don't and I am also quite sure that most of them are aware of that - I mean, why else would they pay MMA fighter and other pro-athletes to tell you that they use their supplements ;-) - what do you think, ha? | Comment on Facebook!
References:
  • Tolusso et al. "The Placebo Effect: Influence on Repeated Intermittent Sprint Performance on Consecutive Days." Journal of Strength and Conditioning Research (2015): Ahead of print.

D-Aspartic Acid (DAA): Does it Work, Not Work or Even Do the Opposite of What's Promised? Conflicting Evidence!

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If you do not like what you see, boys, you may already have taken too much testosterone reducing d-aspartic acid ;-)
You will probably have read the most-read SuppVersity article of all time "When Hype Meets Reality: D-Aspartic Acid (DAA) Turns Out to Be Another Supplemental Nonstarter in First Human Trial With Any Relevance for Healthy Young Men" (read more) and thus know that d-aspartic acid is not exactly half as potent as some of the shiny supplement adds would suggests.

Now, I've been waiting for new evidence on what exactly DAA does ever since the corresponding study has been published; and, guess what, the waiting was rewarded last week with not just one, but two new studies on the effects of DAA in relevant subject groups.
Workouts with powerful muscle builders, not amino acids build muscle!

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  • Study ä1: D-Aspartic acid sucks, big time (Melville. 2015, peer-reviewed) - As Melville et al. point out, there's abundant research on the hormonal effects of d-aspartic acid in rat models, but only limited research in humans.
    "Previous research has demonstrated increased total testosterone levels in sedentary men and no significant changes in hormonal levels in resistance trained men. It was hypothesised that a higher dosage may be required for experienced lifters, thus this study investigated the effects of two different dosages of d-aspartic acid on basal hormonal levels in resistance trained men and explored responsiveness to d-aspartic acid based on initial testosterone levels" (Melville. 2015).
    To find out whether their hypothesis was correct, the researchers randomly assigned 24 males, with a minimum of two years’ experience in resistance training (age, 24.5 ± 3.2 y; training experience, 3.4 ± 1.4 y; height, 178.5 ± 6.5 cm; weight, 84.7 ± 7.2 kg; bench press 1-RM, 105.3 ± 15.2 kg) to one out of three groups who received (a) 6 g/d plain flour (D0), (b) 3 g/d of d-aspartic acid (D3), or (c) and 6 g/d of d-aspartic acid (D6).

    Before the supplementation period, all participants performed a two-week training / supplementation washout period (to exclude effects of their previous training regimen and or supplement use) during which they trained on four days per week. The same standardized resistance training routine was continued through the experimental period (14 days), with participants consuming the supplement (or placebo) in the morning.
    Figure 1: Changes in total and free testosterone in response to two weeks of std. training in conjunction with 3g or 6g d-aspartic acid per day or placebo supplement (Melville. 2015).
    Serum was analysed for levels of testosterone, estradiol, sex hormone binding globulin, albumin and free testosterone was determined by calculation. The results show that DAA had no main effect for group in: estradiol; sex-hormone-binding-globulin (change in Figure 1 is not significant); and albumin.

    However, total testosterone was significantly reducedin the high dose D-aspartic acid group D6 (P = 0.03 | see Figure 1). Compared to the placebo group the D6 group exhibited significantly reduced free testosterone levels, as well. Since both effects were unrelated to the baseline testosterone levels (i.e. not just those with exceptionally high levels of T experienced a decline on DAA), this study clearly suggests that d-aspartic acid is not just useless as a testosterone booster, it's even worse than that: It reduces testosterone instead of boosting it!
  • Study #2: D-aspartic acid rules, small time (LaMacchia. 2015, not peer-reviewed) - This study comes right from the University at Buffalo and information about the results is available only in form of an abstract to a talk the authors presented at an undergrad research meeting. What is still interesting about it, is the fact that LaMacchia et al. determined (for the first time) the effect of D-aspartic acid supplementation on athletic performance in young male athletes.
    "After screening for ACSM low risk, 9 healthy male athletes (average age = 22y, body weight = 82.7 kg and body fat = 10.4%) were randomized to two groups for supplementation using a double blinded parallel arm experimental design. They ingested either 3 grams of d-aspartic acid (Aspartate, n=5) or a Placebo (n=4) for 14 days supplied in capsule form. Subjects recorded and replicated previous 3 day diets prior to testing. 
    Physical assessments were performed prior to and after supplementation included a peak VO2 test by cycle ergometer, 1 maximal repetition bench press and 1 maximal repetition squat (average values ±SD before supplementation were 41.7 ±6.4 ml/kg/min, 117.9 ±11.1 kg and 151.7 ±19.0 kg, respectively)" (LaMacchia. 2015).
    Now, in view of the results of the previously cited study by Melville, the results of LaMacchia's analysis of the performance data is surprising, to say the least:
    "The Aspartate group improved performance in 1 maximal repetition bench press by 4.5 ±1.6kg (average ±SEM, p=0.03) and 1 maximal repetition squat by 8.2 ±3.8kg (average ±SEM, p=0.04). No change in performance measures were observed in the Placebo group. Body composition did not change for either group" (LaMacchia. 2015).
    The fact that the body composition didn't change appears to suggest that the beneficial effects on bench press and squat performance were not of hormonal origin. Rather than that, one may speculate that they were triggered by DAA's effect on the central nervous system (Fuchs. 2005). What is questionable, though, is whether these effects (assuming they actually exist) can outweigh the long(er)-term negative effects on testosterone Melville et al. observed in their study.
Training "on" D-Aspartic Acid is not productive | more.
Bottom line: While it would appear as if it was undecided whether DAA is or isn't useful based on the studies at hand, alone, the previously discussed study by Willoughby (2013) (reread "When Hype Meets Reality: D-Aspartic Acid Turns Out to Be Another Supplemental Nonstarter in First Human Trial With Any Relevance for Healthy Young Men", here) tips the scale in favor of "clearly not useful" and "at high dosages maybe even counter-productive".

The neat presentation, LaMacchia et al. gave at the Suny Undergraduate Research Conference simply doesn't have enough weight to "outweigh" the already convincing peer-reviewed research that shows that athletes do not benefit from supplementing with d-aspartic acid | Comment on Facebook!
References:
  • Fuchs, Sabine A., et al. "D-amino acids in the central nervous system in health and disease." Molecular genetics and metabolism 85.3 (2005): 168-180.
  • LaMacchia, Zach, Peter Horvath, and Brian Williams. "Effect of Aspartate Supplementation on Athletic Performance in Young Men." (2015).
  • Melville, Geoffrey W., Jason C. Siegler, and Paul WM Marshall. "Three and six grams supplementation of d-aspartic acid in resistance trained men." Journal of the International Society of Sports Nutrition 12.1 (2015): 1-6.
  • Willoughby DS, Leutholtz B.  d-Aspartic acid supplementation combined with 28 days of heavy resistance training has no effect on body composition, muscle strength, and serum hormones associated with the hypothalamo-pituitary-gonadal axis in resistance-trained men.  Nutrition Research, Available online 15 August 2013. 

Low vs. High Load Resistance Training - Yes, You Can Gain Muscle W/ "Low" Loads - Non-Significantly More Even!

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It turns out, the biceps may even benefit from higher rep, lower weight training.
You probably remember my Facebook post about Brad Schoenfeld's then unpublished study which proves that you can gain muscle using low(er) weights, as well. Now, that the study has eventually been published, it would appear to be about time to take a closer look at the procedure and results in order to determine how relevant, the finding Schoenfeld, Peterson, Ogborn, Contreras and Sommez present in their not yet printed, but peer-reviewed and accepted paper in the Journal of Strength and Conditioning Research.

The purpose of the study, and that should be obvious considering what I already gave away, was to compare the effect of low- versus high-load resistance training (RT) on muscular adaptations in well-trained subjects.
According to the results of this study you better periodize to benefit from high & low loads!

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Schoenfeld et al. recruited eighteen young men who were - important fact! - "experienced in RT". More specifically, ...
"[s]ubjects were between the ages of 18-35, did not have any existing musculoskeletal disorders, were free from consumption of anabolic steroids or any other illegal agents known to increase muscle size for the previous year, and were experienced lifters (i.e., defined as consistently lifting weights at least 3 times per week for a minimum of 1 year, and regularly performing the bench press and squat). The range of lifting experience for all subjects was between 1.5 and 9 years of consistent training" (Schoenfeld. 2015).
The subjects were matched according to baseline strength, and then randomly assigned to 1 of 2
experimental groups:
  • a low-load + high rep resistance training routine (LL) where 25-35 repetitions were performed per set per exercise (n = 9), or
  • a high-load RT + normal rep routine (HL) where 8-12 repetitions were performed per set per exercise (n = 9). 
During each session, subjects in both groups performed 3 sets of 7 different exercises representing all major muscles. Training was carried out 3 times per week on non-consecutive days, for 8 total weeks (not other high intensity exercise was allowed during the study period;; dietary intake was monitored and didn't show sign. inter-group differences). The exercises performed were: flat barbell press, barbell military press, wide grip lat pulldown, seated cable row, barbell back squat, machine leg press, and machine leg extension. As Schoenfeld et al. point out, the "exercises were chosen based on their common inclusion in bodybuilding- and strength-type RT programs" (Schoenfeld. 2015).
The results of the study at hand put a question mark behind some, but not all of the recommendations in Kramer's paper. The ones on exercise order and workout structure (see above) are still valuable (Kramer. 2004)
So how can low load training build muscle? While it has long been shown that low(er) reps and higher weight are superior when it comes to building maximal strength and despite the fact that strength is an important prerequisite to induce the overload that's required to trigger adaptational changes in the form of skeletal muscle growth in response to resistance training, it is by no means clear that the latter, i.e. the induction of continuous progressive overload to trigger muscle growth wouldn't be possible with low reps - irrespective of the fact that Kraemer & Ratamess claim in their often cited paper about the "Fundamentals of resistance training: progression and exercise prescription" (Kraemer. 2004) that the high load was necessary, because it was required to recruit all motor units and thus fully activate the muscle and its growth potential.

Since even light load exercises can recruit a maximum amount of motor units if they are performed to failure, this argument is yet only relevant if we are talking about light load  + no-failure training. It is thus not surprising that previous studies comparing the muscular adaptations in low- versus high-load training programs yielded conflicting results. Results that were mostly generated in untrained subjects and are thus, much in contrast to the study at hand, pretty irrelevant for most of you.
"To facilitate recovery", the researchers provided the subjects with a supplement on training days containing 24g protein and 1g carbohydrate (Iso100 Hydrolyzed Whey Protein Isolate, Dymatize Nutrition, Farmers Branch, TX) which was consumed within one hour post-exercise, as this time frame has been purported to help potentiate increases in muscle protein synthesis after the workouts (cf. Aragon. 2013).

Figure 1: Overview of all relevant study results. Only the changes in squat strength and strength endurance as measure by 50% bench presses were statistical significant, there was a trend for greater increases in 1RM BP (Schoenfeld. 2015) 
As the data in Figure 1  tells you, both resistance training protocols yielded significant increases in biceps and triceps size. For biceps, the high rep training had a measurable, but non-significant edge producing 8.6% vs. 5.3% increases in biceps size (remember how people train their biceps, that's often ballistic, i.e. they are throwing high weights around, so maybe the benefits are simply a result of improved form).

For the triceps, the quadriceps (9.5% vs. 9.3%) and the biceps' antagonist, the triceps (5.2% vs. 6.0%) the differences were marginal and likewise non-significant. Now, it would be revealing, but boring if the results of high rep + low load and low rep + high load training were identical, right? Well, luckily, Schoenfeld et al. did find differences, as well. More specifically, they observed that the
"[i]mprovements in back squat strength were significantly greater for HL compared to LL (19.6 vs. 8.8%, respectively) and there was a trend for greater increases in 1RM bench press (6.5 vs. 2.0%, respectively)" (Schoenfeld. 2015).
In addition, and not much to your surprise, I guess, the upper body muscle endurance (assessed by the bench press at 50% 1RM to failure) improved to a greater extent in the low load (LL) compared to high load (HL) group (16.6% vs. -1.2%, respectively).
If there was a novelty effect that skews the results, this would only mean that you must periodize appropriately..
Overall, there's little to add to the authors' conclusion that their "findings indicate that both HL and LL [low load, high rep] training to failure can elicit significant increases in muscle hypertrophy among well-trained young men; however, HL training is superior for maximizing strength adaptations" (Schoenfeld. 2015); and while the latter is hardly news, the study is of particular significance in view of the ongoing debate about "go heavy or go home" as it proves a significant gain in muscle size can be achieved with both "going heavy" or "going light", as long as you don't go home, but train to failure.

What remains to be seen, though, is whether the high rep, low load training had the bonus of a novelty effect. After all, it can be expected that none of the subjects trained in a 25-35 rep range before they participated in the study. If that's the case and there is a novelty effect that bolstered the size gains, this wouldn't mean, though, that high rep training was useless. What it would mean, however, is that you'd have another reason to periodize your training properly - don't you think so? | Tell me about your experience and give me your thoughts. Comment on Facebook!
References:
  • Aragon, Alan Albert, and Brad Jon Schoenfeld. "Nutrient timing revisited: is there a post-exercise anabolic window." J Int Soc Sports Nutr 10.1 (2013): 5.
  • Kraemer, William J., and Nicholas A. Ratamess. "Fundamentals of resistance training: progression and exercise prescription." Medicine and science in sports and exercise 36.4 (2004): 674-688.
  • Schoenfeld, et al. "Effects of Low- Versus High-Load Resistance Training on Muscle Strength and Hypertrophy in Well-Trained Men." Journal of Strength and Conditioning Research Publish Ahead of Print. DOI: 10.1519/JSC.0000000000000958

Will "Muscle Building Supplements" Give You Testicular Germ Cell Cancer? Creatine & Protein Stand in the Pillory

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The study at hand makes protein and creatine look worse than prohormones - can that be right?
Maybe you've already seen a link to this study on Facebook, maybe not: "Muscle-building supplement use and increased risk of testicular germ cell cancer in men from Connecticut and Massachusetts" - that's the title of a study which claims to provide convincing evidence that "MBS use is a potentially modifiable risk factor that may be associated with TGCC" (Li. 2015), a study of which I don't have to tell you that it is of observational nature, a study based on interviews with 356 cases and 513 controls and thus a study that may and certainly is skewed by false recalls and deliberate lies - I mean, who would admit to have used illegal steroids if at Yale? Some may, but others certainly won't.
With dairy proteins being beststeller, the study is also an assault on whey& casein

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That being said, reason #1 to take the results of the study with the necessary skepticism is a combination of false recall and flat-out lies / not disclosing one's complete "supplement" regimen. Moreover, the fact that the subjects were asked about a finite set of 30 different types of MBS powders or pills which certainly didn't include powerful designer steroids made it even easier for the study subjects to conceal some o the "supplements" (haha) they actually took. Against that background it's a bold claim to say that
"Considering the magnitude of the association and the observed dose-response trends, muscle-building supplements use may be an important and modifiable exposure that could have important scientific and clinical importance for preventing testicular germ cell cancer development if this association is confirmed by future studies" (Li. 2015).
That's even more true in view of the fact that lies and recall errors are one thing that hampers the reliability of the results, while a statistically significant difference in the rate of (again) reported injuries to the groin which has long been shown to increase the risk of testicular cancer (Coldman. 1982; Oliver. 1994) is another one and reason #2 to take the results of this study with appropriate skepticism.
No, creatine does not give you cancer due to elevated DHT. As you know from a previous SuppVersity article, the increase in DHT that was observed in only one study may be statistically significant, but physiologically irrelevant (learn more).
The fact that the 95% confidence levels (95% CI: 1.11–2.46 total cancer risk, 95% CI: 1.34–3.63 cancer before 25, 95% CI: 1.39–4.74 long-term use) adds another question mark to the claim that using creatine once or regularly is going to give you germ cell cancer.
Figure 2: While both undescended testes and injuries to testes and groin can increase the risk of testicular cancer, only the latter shows a statistical significant inter-group difference between cases and controls (Li. 2015).
In conjunction with reason #3 which is the fact that there is absolutely no mechanism that would explain pro-carcinogenic effects of non-steroidal supplements in general and creatine and protein supplementation in particular (creatine has even been shown to inhibit breast cancer and general tumor growth | Miller. 1993; Juhn. 1998 and anti-tumor effects mostly in the colon, though, of whey protein have been reported among others by  Eason, 2004; Xiao, 2005 & 2006; Parodi, 2007; Attaallah, 2012; etc.), you may even call it "bad science" or "sensationalism" that that none of the several "reviews" of this study on the Internet mention the most important of all findings, which is the non-significance of the results of the TGCC subtype analysis and reason #4:
"Analyses by TGCC subtype suggested similar associations between use of MBS and the risk of seminoma and nonseminoma  (all the P-values for hierarchical coefficients tests were >0.05)."
Against that background I would be curious how the scientists were able to do an exploratory stratified analysis which found that "both creatine and proteins increased the risk of TGCC significantly (OR =2.55, 95% CI: 1.05–6.15)" (Li. 2015).
Table 1: Association Between MBS Use and the Risk of TGCC, Connecticut and Massachusetts, 2006–2010 (Li. 2015).
That sounds very odd considering the facts that (a) no associations were found for a complete analysis, that (b) there's no mention what exactly the data was stratified for and that (c) no previous epidemiological study provides the slightest hint that there may be a potentially causal association between supplement use and testicular cancer.

Speaking of causality, you are aware that the "odds ratios" from the case-control study like the one at hand provide extremely weak evidence? Evidence that cannot provide any information about cause and effect? If that's not your first visit to the SuppVersity you probably knew that already. If it's not, I believe it may be worth remembering that correlation and causation are two different pairs of shoes; or, like my friend Carl Lanore likes to explain it: Just because there are firefighters all over the place, whenever a house burns down (association), they're not the cause of the fire (causation).
Learn more about the old-wife's tale about creatine, DHT and hair loss.
Overall, it's probably rather the Yale and Harvard labels than the quality of the data that made this study pop up all over the Internet. With less than 1000 subjects, a possible reporting bias, error of recall, an interview that used a pre-compiled list of agents instead of just asking which product the subjects used and reconciling the data afterwards and the hushed up non-significance of the results of the full agent-specific analysis should be four good reasons not to freak out about possible increase of testicular cancer risk from 0.2% in the general population (Schottenfeld. 1980) to 0.6% which would be the corresponding 155% risk increase Li et al. report for creatine or protein supplements.

If anything, there may be a generally increased risk of prostate cancer due to high(er) protein intakes and correspondingly increased IGF-1 levels as it was observed among others by the scientists who conducted the European Prospective Investigation into Cancer (cf. Key. 2014). If you re-read my previous posts on dairy and cancer risk (article I, article II, article III, article IV), though, you will notice that even this association is a weak one that was observed in some, but by no means all studies on dairy intake and cancer risk. Corresponding evidence for creatine is - in spite of the existence of tons of long-term safety studies for what probably is the best researched ergogenic on the market, simply non-existent | Comment on Facebook!
References:
  • Attaallah, Wafi, et al. "Whey protein versus whey protein hydrolyzate for the protection of azoxymethane and dextran sodium sulfate induced colonic tumors in rats." Pathology & Oncology Research 18.4 (2012): 817-822.
  • Coldman, A. J., J. M. Elwood, and R. P. Gallagher. "Sports activities and risk of testicular cancer." British journal of cancer 46.5 (1982): 749.
  • Eason, Renea R., et al. "Dietary exposure to whey proteins alters rat mammary gland proliferation, apoptosis, and gene expression during postnatal development." The Journal of nutrition 134.12 (2004): 3370-3377.
  • Li, N., et al. "Muscle-building supplement use and increased risk of testicular germ cell cancer in men from Connecticut and Massachusetts." British journal of cancer 112.7 (2015): 1247-1250.
  • Juhn, Mark S., and Mark Tarnopolsky. "Potential side effects of oral creatine supplementation: a critical review." Clinical Journal of Sport Medicine 8.4 (1998): 298-304.
  • Key, Timothy J. "Nutrition, Hormones and Prostate Cancer Risk: Results from the European Prospective Investigation into Cancer and Nutrition." Prostate Cancer Prevention. Springer Berlin Heidelberg, 2014. 39-46.
  • Miller, Elizabeth E., Audrey E. Evans, and Mildred Cohn. "Inhibition of rate of tumor growth by creatine and cyclocreatine." Proceedings of the National Academy of Sciences 90.8 (1993): 3304-3308.
  • Oliver, M. C. "Social, behaviouraland medical factors in the aetiology of testicular cancer: results from the UK study." Br. J. Cancer 70 (1994): 513-520.
  • Parodi, Peter W. "A role for milk proteins in cancer prevention." Australian journal of dairy technology 53.1 (1998): 37-47.
  • Schottenfeld, Davit, et al. "The epidemiology of testicular cancer in young adults." American Journal of Epidemiology 112.2 (1980): 232-246.
  • Xiao, Rijin, Thomas M. Badger, and Frank A. Simmen. "Dietary exposure to soy or whey proteins alters colonic global gene expression profiles during rat colon tumorigenesis." Molecular Cancer 4.1 (2005): 1.
  • Xiao, Rijin, et al. "Dietary whey protein lowers serum C-peptide concentration and duodenal SREBP-1c mRNA abundance, and reduces occurrence of duodenal tumors and colon aberrant crypt foci in azoxymethane-treated male rats." The Journal of nutritional biochemistry 17.9 (2006): 626-634.

Metabolic Effects of Total Fasting Suggest: You Better Eat "Nothing" Than "Some" If You Want to Make Weight - The Metabolic Adaptation to Dieting is Yet Not All That Counts

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It is hard and it will cost you muscle, but dieting as in simply eating nothing for a few days won't kill your metabolism and it will shed a lot of weight (assuming you're as obese as the subjects in a new study).
Common sense dictates: The more you reduce your energy intake, the more your resting and total energy expenditure will decline. That's a normal adaptational process, right? Right, at least in the short run, however, the equation isn't that easy.

Scientists from the from the Newcastle University just published the results of an interesting experiment, in which they aimed to investigate whether three groups of obese men, exposed to different levels of negative energy balance (fasting, very low calorie diet (VLCD, 2.5MJ/day) and low-calorie diet (LCD, 5.2MJ/day)) in experimental controlled conditions, were characterised by distinct changes in resting and total EE after losing a similar amount of body weight (5% and 10%WL).

As the scientists point out, "[t]he study also provided the opportunity to test if the rate of WL and weight lost as FFM [fat free mass] were associated with the level of adaptive thermogenesis" (Siervo. 2015). The significance of the results for athletes and wanna-be athletes should thus be obvious.
Do you have to worry about fasting when your're dieting!?

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To collect the necessary data, the scientists recruited 18 obese men who were randomly assigned to one out of three groups. Group 1 did a total fast for 6 days (=no food!). Group 2 was meant to achieve a 5% weight loss in 3 weeks on a very low calorie diet containing only 2.5MJ/day (that's only 597.51kcal/day). Group 3 had an "easier" (?) job, as they were meant to lose 10% of their body weight in six weeks during which they consumed a low calorie diet containing 5.2MJ/day (that's 1 242.83 kcal/day).
Figure 1: Macronutrient intake in grams in the 3 diet groups (Siervo. 2015)
"[D]uring the 6-day baseline period subjects consumed a fixed maintenance diet (13% protein, 30% fat and 57% carbohydrate). After the 7-day baseline period, each group followed the specific diet to lose 5% and 10% of their baseline body weight. However, the duration of the fasting was of 6 days as ethical constraint allowed to fast subjects to lose 5% of their baseline body weight. The duration of the WL phases to achieve a 10%WL was of 3 and 6 weeks for the VLCD and LCD groups, respectively. Throughout the study, participants were residential in the Human Nutrition Unit at the Rowett Institute of Nutrition and Health (RINH), Aberdeen, UK.

All food and drinks consumed by each participant during the study were supplied by the dietetics staff in the Unit. The participants were requested not to undertake any other strenuous physical activity during the study and they were asked to record their individual exercise sessions" (Siervo. 2015).
The actual energy intake (EI) of the subjects was measured daily. While the participants in the starvation group had access to water only, the diets of the other groups contained 32% of the energy as protein, 35% as carbohydrate and 33% as fat. More specifically,
  • the LCD weighed 1260g, with an energy content of 5.2kJ/g coming from protein 50.3g (17%), carbohydrate 155.7g (50%), and fat 45.4g (33%), while
  • the VLCD weighed 642g, with an energy concent of 2.55kJ/g coming from protein 49.4g (32%), carbohydrate 52.8g (35%), and fat 23.1g (33%) and was thus - in science terms - a high "protein diet", because it contained >30% of the energy from protein.
The resting energy expenditure (REE) was measured at baseline and at the end of each WL phase (5% and 10%WL) by indirect calorimetry over 30–40 min using a ventilated hood system (Deltatrac II, MBM-200, Datex Instrumentarium Corporation, Finland).
Figure 2: Changes in body composition in the three diet groups according to weight loss (Siervo. 2015).
If we take a look at the changes in body composition in Figure 1, we'll see that the Weight loss in the fasting group was 6.0 kg over 6 days. The VLCD group, who dieted far longer, lost 5.2 and 9.2kg over 11 and 21 days and the LCD group lost 7.2 and 12.6 kg over 21 and 42 days, respectively. Thus, the "[m]ean rates of WL during the 5% WL period were different between the fasting (-1.01 kg/d), VLCD (-0.52 kg/d) and LCD (-0.35 kg/d) groups" (Siervo. 2015).
Women watch out! It is not just possible, but in view of the association between the magnitude of daily energy deficit and the frequency of menstrual disturbances (Williams. 2015), women may see significantly more more side effects on harsh (fasting) diets.
What is far more important, though, is the fact that the allegedly "sanest" way of dieting, i.e. the LCD (=moderate deficit), produced the most significant fat mass loss. Accordingly, the "slow" diet had the upperhand in terms of fat free mass (FFM) losses, as well:
"The fraction of FFM to total WL after 5%WL was 46, 30 and 18% for the fasting, VLCD and LCD groups respectively. At 10% WL, the VLCD losses were 20% FFM and 80% FM compared with 9% FFM and 91% FM in the LCD group (Siervo. 2015).
Against that background it's quite surprising that (a) the VLCD and LCD showed a similar degree of metabolic adaptation for total EE (VLCD=-6.2%; LCD=-6.8%) and that (b) the metabolic adaptation for resting EE was greater in the LCD (-0.4MJ/day, -5.3%) compared to the VLCD (-0.1MJ/day, -1.4%) group.

Likewise noteworthy: The resting EE did not decrease after short-term fasting and no evidence of adaptive thermogenesis (+0.4MJ/day) was found after 5%WL. The rate of WL was inversely associated with changes in resting EE (n=30, r=0.-42, p=0.01).
Figure 3: Metabolic Adaptation - Percent of total and resting energy expenditure not accounted by changes in body composition (FFM and FM) after 5% and 10% weight loss (WL) in obese assigned to three different WL interventions (Siervo. 2015).
So what to make of these study results? If you scrutinize the results in Figures 2 & 3 and, most importantly, the ratio of fat free mass to fat mass loss, it's quite astonishing that the study confirms the common wisdom that slow weight loss will allow for a greater fat-specificity than fast weight loss. After all, the subjects losing 5% of their total body weight lost 88% of it in form of lean muscle (I wonder how much glycogen and thus water loss this was) in the total fast group, 42% in the very low calorie diet group (VLCD) and only 20% in the "moderate" = low calorie diet group. In this context, it's also noteworthy that "biggest losers", i.e. those who lost weight most successfully (cf. Tremblay. 2013) and achieved a 10% weight loss in the VLCD group had a sign. better fat free / fat mass ratio (23% vs. 42%) than those who managed to lose only 5% in three weeks.

Eventually, it may thus seem that the study at hand would confirm what we already know: Slow and steady is best, ... and that's true, but the fact that "slow and steady" produces the greatest reduction in resting metabolic rate makes me question whether the weight rebound after longer, but less severe dieting phases is actually smaller or not. Previous studies suggested there's no difference, but these studies used different protocols and stand in contrast to a plethora of studies like Sénéchal et al. (2012 | learn more). Whether it would be the same for the study at hand is thus questionable | Comment on Facebook
References:
  • Siervo, Mario, et al. "Imposed rate and extent of weight loss in obese men and adaptive changes in resting and total energy expenditure." Metabolism (2015): Accepted Article.
  • Sénéchal, Martin, et al. "Effects of rapid or slow weight loss on body composition and metabolic risk factors in obese postmenopausal women. A pilot study." Appetite 58.3 (2012): 831-834.
  • Tremblay, A., et al. "Adaptive thermogenesis can make a difference in the ability of obese individuals to lose body weight." International journal of obesity 37.6 (2013): 759-764.
  • Williams, Nancy I., et al. "Magnitude of daily energy deficit predicts frequency but not severity of menstrual disturbances associated with exercise and caloric restriction." American Journal of Physiology-Endocrinology and Metabolism 308.1 (2015): E29-E39.

News Quickie: Regular Eating Patterns May Boost Weight Loss | Protein Increases Satiety, Influence on Food Intake is Limited, Though | Sugar Reduction ≠ Weight Loss | More

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So you're eating "healthy"? Sure?
Time to clean my "may be worth an article" folder by putting out another installment of the SuppVersity short news. Today with a colorful potpourri of studies and experiments that were presented at the Summer Meeting of the Nutrition Society and are now subsequently published in the corresponding Proceedings of the Nutrition Society. 

Studies that are mostly, but not exclusively related to weight loss (or its prevention). Studies on protein, meal timing, appetite, eating for bone health and sugar reduction.
Learn more about the effects of your diet on your health at the SuppVersity

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5 Tips to Improve & Maintain Insulin Sensitivity

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  • Potassium and magnesium (not calcium alone) are necessary to keep your bones strong - In a random sample of 4000 individuals from the approximately 25,000 participants in the EPIC-Norfolk cohort scientists from the University of East Anglia were observed that combined dietary magnesium and potassium intake are positively associated with a quantitative measure of bone density (Hayhoe. 2015).
    Table 1: The higher the BUA (ultrasound attenuation), the stronger the bone. The higher the potassium and magnesium intake, the higher the BUA - it's as easy as that (Hayhoe. 2015).
    As the scientists point out, these results complement the limited literature studying other populations (Tucker. 1999; New. 2000; Rondanelli. 2013); and while the various beneficial effects of magnesium are widely appreciated (and on the web often totally overblown), the ones of potassium are still largely ignored (learn more about the low potassium epidemia).
  • Reduction of simple sugars alone is not enough to lose weight - In view of the fact that simple sugars are blamed to be driving the obesity epidemic, the appearance of tons of "sugar free" products of the market did not yet reverse the ever-increasing mean weights of the average Westerner, it appeared to be a smart move to examine the impact of an 8-week sugar reformulated product exchange on energy intake, energy expenditure (EE) and most importantly energy balance (EB), in a double-blind, randomised, controlled, crossover design Markey. 2015).

    Things look different in overweight individuals who consume artificially sweetened products | learn more
    For the study that was conducted by researchers from the University of Reading, forty five healthy, non-dieting, non-obese volunteers (14 male, 31 female; age: 32·0 (SD 9·8) years; BMI: 23·5 (SD 3·0) kg/m²) were randomly assigned to consume either regular sugar or sugar-reformulated food and drink products including confectionary, pasta sauces, baked beans, muesli, condiments and sugar-sweetened beverages for a 56 d period, with a 28 d washout period. The minimum target difference in dietary NMES intake between the regular and reformulated product exchange was 38 g/d (152 kcal). Weighed food diaries (4 d) and accelerometer data (7 d) were used to assess EI, EE and EB at baseline and following each dietary exchange period.

    In contrast to what the "bad sugar myth" would suggest, there was no significant effect of the intervention on body weight, EI, EE or EB; and that despite the fact that (1) the scientists had predicted a weight loss of at least 2.5kg body weight and irrespective of (2) the fact subjects actually reduced both their sugar and total carbohydrate intakes. Since much of the reduction in energy intake was compensated for "partly through increased voluntary fat intake", a blinded"sugar reduced diet" will not have significant effects on energy balance and thus body weight in either men or women.
  • Scientists confirm and quantify the satiety bonus of high protein breakfasts - "The fundamental contributing factor to the current obesity epidemic is energy imbalance," (Tolan. 2015) and I wish there were not a couple of dozen gurus who are debating that, but that's a different topic, so let's not lose sight of the context in which Tolan & Drummond wrote this statement.

    The researchers from the Queen Margaret University investigated if normal protein (NP; 15% energy), moderate protein (MP; 25% energy) and high protein (HP; 35% energy) quantities at breakfast proportionately increase subjective satiety and decrease within day energy intake. In the corresponding single blind three way crossover study, 12 healthy subjects (4 male, 8 female) (BMI = 23·9 ± 0·65 kg/m²) aged 21–31 years consumed three isocaloric breakfasts containing approximately 15%, 25% and 35% energy from protein, one week apart. Appetite parameters were measured via Visual Analogue Scale ratings before and after each breakfast and hourly thereafter.
    Figure 1: Macronutrient composition (g, left) and 8h fullness, hunger and desire to eat ratings  (Tolan .2015)
    The results in Figure 1 (right) clearly indicate a reduction in hunger and desire to eat and an increase in fullness that was however not linear. It is thus not surprising that there was only a trend in for a reduced mean energy intake between breakfast conditions. Only if this trend woul persist in the long run "this may prove to be a beneficial strategy within the multidisciplinary prevention or treatment of obesity" (Tolan. 2015).
  • Regular eating patterns may boost your weight loss efforts! And in this case regular does not mean "more frequently" it does simply mean that you stick to a plan like having breakfast at 6:00, lunch at 12:00 and dinner at 18:00.

    A recent study on "Breakfast Skipping" which found: "Whether Skipping Breakfast Increases Insulin, Hunger and Blood Lipids Depends on One's Breakfast Habits" seems to corroborate the results of the study at hand. After all, the findings suggest that breakfast skipping could increase your obesity risk only if you are not used to skipping it, i.e. if you lack a regular meal pattern.
    In a recent study from the University of Nottingham (Alhussain. 2015), 11 healthy weight women (18–40 years) were studied in a randomised crossover trial with two phases of 2 weeks each. In Phase 1, participants consumed either a regular meal pattern (6meals/day) or an irregular meal pattern (varying from 3 to 9meals/day). In Phase 2, participants followed the alternative meal pattern to that followed in Phase 1, after a 2-weeks washout period.

    In the two phases, identical foods were provided to a participant in amounts designed to keep body weight constant. Participants came to the laboratory after an overnight fast at the start and end of each phase. Resting metabolic rate (RMR) was measured by indirect calorimetry, in the overnight fasted state and during the 3 h period after consumption of a milkshake, test drink.

    In view of the short study period you cannot expect to see changes in body weight, but there was a significant difference in total postprandial energy expenditure (measured for 3 h) by visit (P = 0·04). More specifically, the postprandial energy expenditure after the regular meal pattern was significantly higher than at baseline (25·8 ± 6·8 and 17·5 ± 8·9 kcal respectively; P = 0·002) or than after the irregular meal pattern (14·8 ± 11·7 kcal; P = 0·04). Practically speaking this could, as the scientists point out, "contribute to weight loss and obesity management, but further studies are needed in obese participants" (Alhussain. 2015) - ah, since all subjects were women, it would be interesting to see if that's the same for men, because men are usually less susceptible to the effects of "fasting", so maybe they are also less susceptible to the effects of not getting their meal "in time".
Overfeeding 101: Get an Overview of the Consequences of Short- & Long-Term Overfeeding | read more
Bottom line: Weight loss requires a caloric deficit and that's not automatically induced by either reducing sugar intake or eating more protein - even if the latter may make you feel more satiated. This is by the way now scientifically proven, because Till et al. (2015) have recently been able to demonstrate that"appetite is not a reliable predictor of energy intake" (Till. 2015). In their review appetite and actual food intake were linked in only 19% of the 442 papers they assessed. This does also mean that in 81% the measured appetite scores had no significance in terms of the actual food intake.

In a similar vein, it is not yet clear if the increase in postprandial energy expenditure Alhussain et al. (2015) report in their paper is of real-world significance. In view of the fact that "irregularity" is one important characteristic of obesogenic eating habits, it would yet be foolish to negate it without longterm studies that disprove this hypothesis | Comment on Facebook!
References:
  • Alhussain, M, M. A. Taylor and I. A. Macdonald. "Influence of the constancy of daily meal pattern on postprandial energy expenditure in healthy weight women". Proceedings of the Nutrition Society, 74, E141 (2015): doi:10.1017/S0029665115001561. 
  • Hayhoe, et al. "Combined dietary magnesium and potassium intake is associated with greater bone density in women in the EPIC-Norfolk cohort". Proceedings of the Nutrition Society, 74, E120 (2015): doi:10.1017/S0029665115001354. 
  • Markey, O. and J. A. Lovegrove. "Dietary energy compensation in response to reduced sugar diet in non-obese men and women". Proceedings of the Nutrition Society, 74, E121 (2015): doi:10.1017/S0029665115001366. 
  • New, Susan A., et al. "Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health?." The American journal of clinical nutrition 71.1 (2000): 142-151.
  • Rondanelli, Mariangela, et al. "Update on nutrients involved in maintaining healthy bone." Endocrinología y Nutrición 60.4 (2013): 197-210.
  • Till, S, C. J. Harden, V. A. Grant and B. M. Corfe. "Appetite is not a reliable predictor of energy intake: interim reporting of a systematic literature review". Proceedings of the Nutrition Society, 74, E150 (2015): doi:10.1017/S0029665115001652. 
  • Tolan E. and S. Drummond. "An investigation into the satiating effects of differing quantities of protein consumed at breakfast." Proceedings of the Nutrition Society, 74, E130 (2015): doi:10.1017/S0029665115001457. 
  • Tucker, Katherine L., et al. "Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women." The American journal of clinical nutrition 69.4 (1999): 727-736.

Whey, Egg & Mixed Proteins - Effects on Muscle, Fat Cells and the Hypothalamus Suggest 70% Whey + 30% Egg May be Best for People Striving for Leanness & Muscularity

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Dairy or eggs? Why not just dairy and eggs - Protein mix exerts most promising effects on signalling proteins related to increased muscle mass and fat loss, analysis of the results of a study shows.
You will probably remember that the acute rate of muscle protein synthesis is not a valid proxy of the gains you can expect from a certain way of training or a specific type of supplement (Mitchell. 2015). Against that background you may very well ask yourselves why I am elaborating on the results of the latest study from the School of Kinesiology, Molecular and Applied Sciences Laboratory and the Auburn University which examined the acute effects of different dietary protein sources on skeletal muscle.

Well, despite the fact that this is a rodent study and irrespective of the questionable link between acute markers of protein synthesis and long-term gains, this is imho the first study to compare the effects whey and egg proteins have on skeletal muscle, adipose tissue and hypothalamic satiety-related markers at the same time.
You can learn more about protein intake at the SuppVersity

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To do so, Mobley et al. gave their lab rats (a) whey protein concentrate (WPC, n = 15), (b) hydrolyzed whey-to-hydrolyzed egg albumin at a ratio of 70:30 (70 W/30E, n = 15), the same mix at a ratio of (c) 50/50 and (d) 30/70 or (e) 1 ml of water with no protein as a fasting control.
Figure 1: Expression of protein synthesis and selected signalling proteins in skeletal muscle (PGC-1a, AMPK) and brain (POMC) in response to the different protein supplements (Mobley, 2015).
The detailed analysis of the protein signalling response revealed that that compared to CTL: (1) phosphorylated (p) markers of mTOR signaling [p-mTOR (Ser2481) and p-rps6 (Ser235/236)] were elevated 2–4-fold in all protein groups 90 min post-treatment (p < 0.05). Moreover,

  • WPC and 70 W/30E increased muscle protein synthesis (MPS) 104% and 74% 180 min post-treatment, respectively (p < 0.05), and 
  • 70 W/30E increased p-AMPKα (Thr172) 90 and 180-min post-treatment as well as PGC-1α mRNA 90 min post-treatment. 

A closer analysis of the protein responses in the subcutaneous (SQ) and omental fat (OMAT) depots of the rodents showed that

  • 70 W/30 W increased SQ fat phosphorylated hormone-sensitive lipase [p-HSL (Ser563)] 3.1-fold versus CTL and a 1.9–4.4-fold change versus all other test proteins 180 min post-treatment (p < 0.05); and 
  • WPC, 70 W/30E and 50 W/50E increased OMAT p-HSL 3.8–6.5-fold 180 min post-treatment versus CTL (p < 0.05). 

Lastly, the 70 W/30E and 30 W/70E increased hypothalamic POMC mRNA 90 min post-treatment versus CTL, an effect that suggests that an increased satiety response may have occurred in the former groups. An effect that was not counter by a compensatory increase in orexigenic (=appetite increasing) AGRP mRNA in the 70 W/30E group 90 min post-treatment versus and compensated by increases in orexigenic NPY mRNA in the 30 W/70E group 90 min post-treatment.
Why egg? Widespread interest has also surrounded the positive health benefits of dietary egg protein due to its high es sential amino acid (EAA) content and high digestibility (Buford. 2007). Similar to whey protein, egg protein feeding in rats has been found to significantly increase postprandial MPS (Norton. 2012). Likewise, one report suggests that bioactives isolated from egg protein down-regulate serum myostatin (MSTN | Colker. 2009 | this effect was not observed in the study at hand(!)); an effect which may enhance skeletal muscle hypertrophy with chronic supplementation. However, unlike the aforementioned whey protein re search, there is a paucity of data regarding the physio logical effects of dietary egg protein on other tissues (i.e., adipose tissue and the hypothalamus).
Practically speaking, the data would suggest that (1) the pure whey protein supplement had the most pronounced pro-anabolic effects on the muscle, while (2) the egg protein supplements had hardly any effect (this is different to studies, where egg supplements were given after workouts). (3) as far as the oxidative prowess of the muscles is concerned, the mix of whey + egg protein (70:30) was yet the only protein supplement to elicit significant changes in the "fat burning" protein AMPK and the mitochondrial builder PGC-1a.

Similarly, (4) with respect to the effects on the adipose tissue, the protein mix containing whey and egg protein at a ratio of 70:30 showed superior effects on the libid mobilizer HSL in both subcutaneous and omental fat depots, while (5) the 50:50 mix affected the release of fat from the adipocytes only in the belly (omental) fat. If we also take into account that (6) only the 70:30 mix increased the level of satiety related proteins in the brain without corresponding increases in satiety triggering hormones, the results of the study at hand would suggest that the pure whey protein may have the pro-anabolic edge, the addition of egg protein, however, appears to make the mix more suitable for body recomposition goals, because it will simultaneously increase the level of key proteins that could trigger an increase in fat oxidation and a decrease in energy intake. What reamains to be seen, though, is whether these effects translate into corresponding changes in body composition in longer-term human studies with an exercise component, though | Comment on Facebook!
References:
  • Buford, Thomas W., et al. "Journal of the International Society of Sports Nutrition." Journal of the International Society of Sports Nutrition 4.6 (2007): 6.
  • Colker, C. "Effect on serum myostatin levels of high-grade handled fertile egg yolk powder" (Conference abstract). J Am Coll Nutr. 28.3 (2009).
  • Mitchell, Cameron J., et al. "Last Word on Viewpoint: What is the relationship between the acute muscle protein synthetic response and changes in muscle mass?." Journal of Applied Physiology 118.4 (2015): 503-503.
  • Mobley, Christopher Brooks, et al. "Effects of protein type and composition on postprandial markers of skeletal muscle anabolism, adipose tissue lipolysis, and hypothalamic gene expression." Journal of the International Society of Sports Nutrition 12.1 (2015): 14.
  • Norton, Layne E., et al. "Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats." Cellulose (Fiber) 53.53.7 (2012): 53-7.

Toxic Fish Oils!? POPs Commonly Found in Comm. Fish Oil Supps Accumulate & Lower Your Anti-Oxidant Defenses

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You are probably popping POPs (per-sistent organic pollutants) with your fish oil supplements; and even if your blood lipids would suggest the pills are helping, you may slowly, but progressively be running down your anti-oxidant defenses.
From my previous articles about fish oil you will remember that the often-cited heavy metals may actually be the lesser of two evils of commercially produced fish oil. A recent study from the San Diego State University does now appear to confirm that lead and mercury could in fact be of less concern than the omnipresent persistent organic pollutants (POPs)

In fact, scientific studies show that the consumption of fatty fish and fish oil supplements is an important point of entry of POPs into the human food chain, exposing populations to toxic compounds such as polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCs). In that, Contamination with POPs in fish is not limited to certain regions or species. It is, rather, global and ubiquitous.
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PCBs were originally used as lubricants and cooling liquids for transformers, but their production was ceased in 1980 (Ortiz. 2011). Despite termination of their manufacture, PCBs still persist in the environment today and pose a threat as a toxic component in fish or contaminated fish oils. Clinical manifestations of PCB toxicity include endocrine, neurobehavioral, and developmental disruption (Marti. 2010).
Table 1: Comparison of POPs levels in samples of present study to those published in literature (Marti. 2010)
Organochlorines, another class of chlorine-containing organic pollutants such as dichloro-diphenyltrichloroethane (DDT), may also lead to endocrine disruption and pose a substantial carcinogenic threat (16). Previous studies have documented substantially increased breast cancer risk associated with PCB and OC concentrations in serum and breast adipose tissue (Aronson. 2000, Cohn. 2007).
"Given these concerns, there exist debates weighing the potential risks from POP intake against the benefits of n–3 FA consumption (19–23). A few studies examined the risks and benefits of consuming fish and fish oil containing POPs with the use of animal models (24, 25). However, no such study has investigated the effects of fish oil contamination with POPs on CVD risk factors. Therefore, we sought to investigate the effects of POP exposure through fish oil consumption on certain biological functions, including serum lipid modulation, oxidative stress, and inflammation. We hypothesized that the fish oil contaminated with POPs would negate the benefits by increasing oxidative stress and inflammation and decreasing antioxidant concentrations" (Hong. 2015).
To test this hypothesis twenty eight-day-old male Sprague-Dawley rats (n = 30) consumed diets of unmodified fish oil (FO) consisting of 15% fat by weight, persistent organic pollutant–contaminated fish oil (POP FO) (PCBs at 2.40 mg/g; OCs at 3.80 mg/g FO), or corn oil (control; CO) for 9 wk.
How can you protect yourselves? The easiest, but not exactly cheapest option is to buy molecularly distilled fish oils from which the producers have (hopefully) removed most of the pops. Since there's a reduction dependent loss of nutrients like vitamin D, E, K, cholesterol and unsaponifiable compounds (Oterhals. 2010), not all "distilled" fish oils will be 100% POP free, but the amount should be low enough to minimize the risks. Addendum: Just because people asked me: Products with the PuriMax (TM) Logo as they are sold by one of Europe's largest bulk suppliers are molecularly distilled.
Lipid profiles and C-reactive protein concentrations were assessed. Hepatic gene expression related to lipid metabolism was determined by real time quantitative polymerase chain reaction analysis.
Figure 1: In spite of the significant increase in POPs in the adipose tissue of the animals (left), there were still significant improvements in blood lipids (right | Hong. 2015).
After 9 wk of feeding, accumulation of PCBs and OCs in the fat tissue of the POP FO group compared with the other 2 groups was confirmed (P < 0.01 | see Figure 1 (left)).

In spite of the ongoing intoxication, though, the provision of fish oils showed the usual effects on HDL, trigs, LDL and CRP, with the former being increased and the latter being decreased.
Unfortunately, the POP FO group also exhibited a highly increased lipid peroxidation (5.1 6 0.7 vs. 2.9 6 0.9 and 2.6 6 0.6 mM) and a significantly reduced less antioxidant capacity (0.08 6 0.06 vs. 0.5 6 0.1 and 0.4 6 0.1 mM) compared to those rodents who consumed the corn oil and the purified fish oil diets  (P < 0.05).
Figure 2: Relative difference of TBARs (marker of lipid peroxidation) and total antioxidant capacity in the two fish oil groups compared to that of the rats receiving corn oil (Hung. 2015).
So what? In view of the fact that the levels of PCB, DDT and chloradane had been specifically chosen to mirror the concentrations of these compounds in commercially available fish and fish oil, the results of the study at hand are disconcerting.

Before further research quantifies whether the observed toxicity is mediated by other markers (e.g., IL-6, TNF-a, serum amyloid A, or fibrinogen) and investigates potential long-term effect, it is yet difficult to judge the real-world significance of these results which stand in contrast to the proven (and eventually still existing) cardio-protective effects of fatty fish and fish oil (Harris. 2008). And still, the authors of the study at hand are perfectly right, when they point out that "the current results prompt caution in their consumption" (Hang. 2015).

"For instance, research into the effects of different doses of contaminants and feeding durations is essential for the evaluation of long-term exposure and assessment of a critical window of exposure. In particular, the high accumulation of PCBs and OCs in the fatty tissue of the contaminated fish oil group raises concerns surrounding a generational effect through maternal transfer" (Hong. 2015)  | Comment on Facebook!
References:
  • Aronson, Kristan J., et al. "Breast adipose tissue concentrations of polychlorinated biphenyls and other organochlorines and breast cancer risk." Cancer epidemiology biomarkers & prevention 9.1 (2000): 55-63.
  • Cohn, Barbara A., et al. "DDT and breast cancer in young women: new data on the significance of age at exposure." Environmental Health Perspectives (2007): 1406-1414.
  • Harris, William S., et al. "Omega-3 fatty acids and coronary heart disease risk: clinical and mechanistic perspectives." Atherosclerosis 197.1 (2008): 12-24.
  • Marti, M., et al. "Persistent organic pollutants (PCDD/Fs, dioxin-like PCBs, marker PCBs, and PBDEs) in health supplements on the Spanish market." Chemosphere 78.10 (2010): 1256-1262.
  • Ortiz, X., et al. "Elimination of persistent organic pollutants from fish oil with solid adsorbents." Chemosphere 82.9 (2011): 1301-1307.
  • Oterhals, Åge, and Marc HG Berntssen. "Effects of refining and removal of persistent organic pollutants by short-path distillation on nutritional quality and oxidative stability of fish oil." Journal of agricultural and food chemistry 58.23 (2010): 12250-12259.

Shift Work, an Overlooked Motor of the Diabesity Epidemic? Revisiting the Impact of Continuous and Sporadic Shift and Night Work on Belly Size, Trigs and Glucose Control

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Stress at work only adds to the ill effects of shift work and night shifts will have on the health, body composition and life quality of  people who work when they're supposed to sleep.
You will probably remember the problems arising from shift work from the Circadian Rhythm Series. In said articles I did yet only scratch the surface of an underestimated problem that may ironically make (among others) those sick who are responsible for the well-being of us all: Nurses, doctors, flight controllers, etc.

The effects, this appears to be certain by now, can be triggered by both, irregular sleeping and eating patterns, and they relate to changes in melatonin, cortisol, ghrelin, and leptin. Changes with consequences that reach from the nasty but usually unproblematic ability to shed those last lbs of body fat covering your abs to cancer and death.
Even if you don't work shifts, melatonin may be a supplement to consider!

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You're asking yourself why this is a SuppVersity topic? Well with an estimated 20% of the economically active population in North America and Europe being engaged in some type of shifts involving night work (Harrington. 2001), it is very likely that a similar percentage of the visitors of this website are affected, too. And still, one thing that may distinguish the average SuppVersity reader on night shifts from the rest of the pack (hopefully) is that he or she does not share the same unhealthy lifestyle habits, such as smoking, poor diet, and sedentarism Costa et al. (2003) observed in their analysis of the lifestyle habits of in their 2003 study.

Overall, it is a complex mix of direct and indirect interrelationship of social problems and aspects related to misalignment of biological rhythms experienced by shift workers predisposes them to a number of deleterious health effects.
  • Figure 1: Especially older men & women and former smokers on shift work have a sign. increased abdominal obesity risk (Van Amelsvoort. 1999)
    Studies show that overweight and obesity are more prevalent in shift and night workers than day workers (Van Amelsvoort. 1999).
  • Shift and night work have been associated with increased risk of developing other metabolic disorders.
  • Shift and night workers are more likely to suffer from as insulin resistance, diabetes, dyslipidemias, and metabolic syndrome (Ulhôa. 2015).
  • And many shift and night workers suffer from an alteration in food intake (Esquirol. 2009; Crispim. 2012).
As Ulhôa et al. point out in a recently published review of the literature, a disruption of the circadian rhythm we've evolved as a means of adapting to environmental changes is an important motor of the endocrine abnormalities which are at the heart of many if not all of the previously listed health problems:
"The expression of biological rhythms takes place via interactions between central and peripheral endogenous molecular mechanisms, which enable the organism to adapt to changes in the external environment [24]. Circadian rhythms are aligned with periodic environmental events such as the light-dark cycle. In addition, circadian rhythms are interlinked; that is, there is a coupling of endogenous rhythms. These synchronized internal mechanisms ensure that all the physiological and behavioral rhythms occur in a coordinated fashion during the 24-hour cycle. This implies that the health of individuals whose timing between biological rhythms and environmental cycles is not kept in balance can be affected. Desynchronization is defined as a change in the relationship of phases between two or more rhythms, a situation that can have a number of deleterious effects on health" (Ulhôa. 2015).
As you will know, the main synchronizing agent of the central biological clocks in the control of circadian rhythms is the alternation between the light and dark cycle. Luminosity information is conveyed to the Central Nervous System (CNS) via the retinohypothalamic tract (Cipolla‐Neto. 2014), where melanopsin plays the role of key photoreceptor in this process.

Consequences of the absence or reduction in melatonin production. The consequences are of two types: those related to the metabolism leading to insulin resistance, glucose intolerance and dyslipidemia and those related to circadian synchronization of metabolic processes leading to chronodisruption (Cipolla‐Neto. 2014).
Driven by the light-dark cycle, the CNS orchestrates the circadian rhythms of many behaviors, tissues, hormones, and genes, as well as other physiological processes. In recent decades, studies have shown that molecular mechanisms occur in cells of peripheral tissues autonomously and that their circadian rhythms persist in vitro.

The synchronizers of peripheral clocks (located in organs, tissues, and cells) are neurohumoral factors such as glucocorticoids and melatonin, as well as social rhythms such as feeding and work times.

Biological rhythms modulate practically all physiological processes of mammals where circadian control over the endocrine system has been shown to be of vital importance. However, alterations in alignment of environmental cycles with rhythms of the organism may induce alterations in the complex mechanism of hormonal and metabolic timing.
This article may make shift work sound worse than it actually is, mostly because the data cited is based on "average Joes & Janes" who do not work out, make sure they get enough quality sleep, don't use blindfolds and ear-plugs to make the most of their daytime sleep, don't give a shit about what they eat and (ab)use cigarettes and snacks to keep awake during their shifts. Since I assume you are way above average, your personal risk is probably going to be much lower than that of the average shift worker.
Among permanent night workers, less than 3% exhibited complete circadian adjustment (Folkard. 2008), revealing that the majority of these workers experience misalignment of biological rhythms and its deleterious effects. While most of the abnormalities of the circadian rhythm are related to the circadian hormone melatonin, their real-world effects on our health are mediated by various hormones:

  • Cortisol - modulator #1 - It is well-accepted that there is a causal link between shift work and a messed up cortisol rhythm which should be characterized by a steep incline in cortisol in the AM and a progressive decline of the stress hormone from AM to PM (learn more).

    In a laboratory-based study showed that subjects whose usual 12-hour sleep pattern was inverted from night to day experienced misalignment and inversion of their circadian rhythm.
    "Circadian misalignment, when subjects ate and slept ≈12 h out of phase from their habitual times, systematically decreased leptin (−17%, P < 0.001), increased glucose (+6%, P < 0.001) despite increased insulin (+22%, P = 0.006), completely reversed the daily cortisol rhythm (P < 0.001), increased mean arterial pressure (+3%, P = 0.001), and reduced sleep efficiency (−20%, P < 0.002). Notably, circadian misalignment caused 3 of 8 subjects (with sufficient available data) to exhibit postprandial glucose responses in the range typical of a prediabetic state" (Scheer. 2009).
    The authors implicated this effect as the cause for the glucose increase and cardiometabolic consequences that occur acutely in jetlag and chronically in shift work (Scheer. 2009). These circadian rhythms changes, including alterations in cortisol expression, have been associated with the development of cardiovascular diseases and cancer (Machi. 2012). A pertinent question raised by the academic community concerns the type of shift that would be less harmful to workers’ health.
    Figure 2: Continuous vs. rotating types of shift work affect the cortisol rhythm differently (Wong. 2012).
    While all four, regular and irregular night and rotating shifts change cortisol level as compared to a daytime work schedule, night shifts are generally more strongly associate with stressors at the work place with regular shift work having a more pronounced effect on the cortisol rhythm (e.g. full suppression of AM rise in cortisol | Ulhôa. 2011). In spite of that, the study by Wang et al. (2012 | cf. Figure 2) suggests that rotating shift works have a more pronounced ill effect on endothelial function than continuous shift work.

    It is yet not just the continuity that matters. Ulhôa et al. point out in their previously cited 2015 review of the literature, most individuals who work very early mornings (morning shift) have partial sleep deprivation, obesity, and low morning cortisol concentration compared to those who work the afternoon shift. They also highlight that "[c]ircadian rhythm misalignment, including alteration in cortisol expression, is further aggravated in the presence of job strain" (Ulhôa. 2015). In that, work stress and sleep loss synergize and maximize the alterations in cortisol rhythm, "[t]herefore, it can be asserted that endocrine alterations are influenced by shift work, sleep, or circadian system changes or by a combination of these factors" (Ulhôa. 2015).
  • Diet and triglyceride metabolism - modulator #2 - Besides the well-known risks, such as poor diet and sedentarism, shift and night work have been similarly associated with weight gain, one of the central features and driving motors of obesity. In their previously cited review Ulhôa et al. report that "[e]pidemiologic evidence shows that shift and night work are associated with elevated risk of metabolic disorders, perhaps as a result of poor physiological adaptation to sleep loss, leading to chronic sleepiness and feeding at unfavorable circadian times, which in turn contribute to chronic circadian misalignment" (Ulhôa. 2015). In that, not all the negative affects are triggered by circadian misalignment.
    Figure 3: Nigh time (squares) eating / snacking is associated with increased triacylglycerol levels (left) and worsened glucose clearance and insulin sensitivity (right | Al-Naimi. 2004)
    People who work on shifts or do night work have fewer opportunities to practice physical activity, they exhibit a reduced meal frequency and consume more snacks (according to Kroencke et al. the increased snack intake adds an average of 200-300kcal, mostly from "junk", to the shift workers diets | probably a result of messed up leptin and ghrelin levels specifically in those who switch back and forth between night and day shifts; cf. Fogteloo. 2003; Scheer. 2009; Marqueze. 2013). In addition, scientists have found that both, the quality and quantity of foods consumed, suffers and increases respectively.

    Next to these behavioural influence, the nocturnal decline in digestive efficacy (Al-Naimi. 2004), the already increased trigylceride levels (our biological rhythm dictates higher levels at night than during the day; this is because we'd need them during sleep to fuel our energetic demands | Al-Naimi. 2004; Holmbäck. 2003). Since high triglycerides inhibit the uptake of glucose and in view of the fact that night-time eating triggers a greater response of triacylglycerol compared to day-time eating, it is no wonder that night time workers exhibit a blunted insulin sensitivity. Due to the elevated insulin and triglyceride levels body fat storage kicks in and it is only a question of weeks or months before the effects will become visible on the scale and in the mirror. 
  • Insulin resistance and full-blown diabetes - modulator #3 - While I did already touch on the triglyceride driven reduction in insulin sensitivity with modulator #2, the "trigs" are not the only contributor to an increase in insulin resistance in shift workers.

    There is also a direct reduction in GLUT4 glucose transporter expression, which would normally be sustained by melatonin. The impact of reduced GLUT4 expression could also explain that laboratory-based experiments have shown that individuals who sleep outside normal times have reduced sensitivity to insulin, without a commensurate increase in insulin secretion (Leproult. 2014).  With often chronically elevated insulin levels, it's also no wonder that the risk of a high β-cell activity was increased almost threefold in shift workers who work at night and very early shift.
    Figure 4: Relative risk of developing type II diabetes in shift workers according to age (Ika. 2013).
    In conjunction with the severe circadian misalignment, the downstream effects of shift work are thus significant promoters of the development of diseases such as insulin resistance and diabetes, independently of factors such as job strain and physical activity. In fact, previous studies have suggested a twofold greater risk for developing type 2 diabetes mellitus (Figure 4 | Ika. 2013 | see Figure 4), as well as poor glycemic control among shift workers compared to nonshift workers. Interstingly, though, no clear association, however, was observed between seasonal shift work and diabetes mellitus. 
This is how your melatonin levels should look like (Altun. 2007). By supplementing you may partly restore the normal ups and downs even if you're working night shifts.
As you can see, the link between shift work, obesity and chronic disease is complex too complex to actually believe that the mere ingestion of a melatonin supplement 30min to 1h before you go to bed would counter all the negative effects of chronic and/or temporary shift work / night shifts. What you can expect from 3-5mg is yet an improvement in your ability to fall asleep (Sadeghniiat-Haghighi. 2008), improved daytime sleep and night alertness (in night workers | Jorgensen. 1998), and - assuming you don't take the unphysiological time-release preparations no hangovers (Sharkey. 2001)... ah, and yes, melatonin may also help with the increased cancer risk I discussed in previous articles about melatonin | Comment on Facebook!
References:
  • Al-Naimi, S., et al. "Postprandial metabolic profiles following meals and snacks eaten during simulated night and day shift work." Chronobiology international 21.6 (2004): 937-947.
  • Altun, A., and B. Ugur‐Altun. "Melatonin: therapeutic and clinical utilization." International journal of clinical practice 61.5 (2007): 835-845.
  • Cipolla‐Neto, J., et al. "Melatonin, energy metabolism, and obesity: a review." Journal of pineal research 56.4 (2014): 371-381.
  • Costa, Giovanni, Claudia Roberta de Castro Moreno, and Lúcia Rotenberg. "Saúde e trabalho em turnos e noturno." Trabalho em turnos e noturno na sociedade 24 horas. Atheneu, 2003. 79-98.
  • Crispim, Cibele Aparecida, et al. "Adipokine levels are altered by shiftwork: a preliminary study." Chronobiology international 29.5 (2012): 587-594.
  • Esquirol, Yolande, et al. "Shift work and metabolic syndrome: respective impacts of job strain, physical activity, and dietary rhythms." Chronobiology international 26.3 (2009): 544-559.
  • Fogteloo, A. J., et al. "Impact of meal timing and frequency on the twenty-four-hour leptin rhythm." Hormone research 62.2 (2003): 71-78.
  • Folkard, Simon. "Do permanent night workers show circadian adjustment? A review based on the endogenous melatonin rhythm." Chronobiology international 25.2-3 (2008): 215-224.
  • Harrington, J. Malcolm. "Health effects of shift work and extended hours of work." Occupational and Environmental medicine 58.1 (2001): 68-72.
  • Holmbäck, Ulf, et al. "Endocrine responses to nocturnal eating–possible implications for night work." European journal of nutrition 42.2 (2003): 75-83.
  • Ika, K., et al. "Shift work and diabetes Mellitus among male workers in Japan: does the intensity of shift work matter?" Acta Medica Okayama 67 (2013):9-23.
  • Jorgensen, K. Michael, and Michael D. Witting. "Does exogenous melatonin improve day sleep or night alertness in emergency physicians working night shifts?." Annals of emergency medicine 31.6 (1998): 699-704.
  • Leproult, R., Holmbäck, H., Van Cauter E. "Circadian misalignment augments markers of insulin resistance and inflammation, independently of sleep loss." Diabetes (2014).
  • Machi, Mari S., et al. "The relationship between shift work, sleep, and cognition in career emergency physicians." Academic Emergency Medicine 19.1 (2012): 85-91.
  • Marqueze, Elaine Cristina, Melissa Araújo Ulhôa, and Claudia Roberta de Castro Moreno. "Effects of irregular-shift work and physical activity on cardiovascular risk factors in truck drivers." Revista de Saúde Pública 47.3 (2013): 497-505.
  • Sadeghniiat-Haghighi, Khosro, et al. "Efficacy and hypnotic effects of melatonin in shift-work nurses: double-blind, placebo-controlled crossover trial." Journal of circadian rhythms 6.1 (2008): 10.
  • Scheer, Frank AJL, et al. "Adverse metabolic and cardiovascular consequences of circadian misalignment." Proceedings of the National Academy of Sciences 106.11 (2009): 4453-4458.
  • Sharkey, Katherine M., Louis F. Fogg, and Charmane I. Eastman. "Effects of melatonin administration on daytime sleep after simulated night shift work." Journal of sleep research 10.3 (2001): 181-192.
  • Ulhôa, Melissa Araújo, et al. "When does stress end? Evidence of a prolonged stress reaction in shiftworking truck drivers." Chronobiology international 28.9 (2011): 810-818.
  • Ulhôa, M. A., et al. "Shift Work and Endocrine Disorders." International Journal of Endocrinology 2015 (2015).
  • Van Amelsvoort, L. G., E. G. Schouten, and F. J. Kok. "Duration of shiftwork related to body mass index and waist to hip ratio." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 23.9 (1999): 973-978.
  • Wong, Imelda S., et al. "Job strain and shift work influences on biomarkers and subclinical heart disease indicators: a pilot study." Journal of occupational and environmental hygiene 9.8 (2012): 467-477.

BroScience Research: "What do Bros Say About AAS Use and the Prevention of Shut Down & Infertility?"

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Are today's "muscle men" not going to be able to procreate?
If you are frequenting any of the popular fitness and bodybuilding bulletin boards, you will know that "broscience" is a mixture of anecdotal evidence and hilarious claims that is spiked with cherry picked scientific references.

Against that background it may sound funny that researchers from the New Castle Fertility Center devoted a complete study to the analysis of drugs and protocols highlighted by the online community of users for prevention and/or mitigation of adverse effects of steroid use. If you think about it, however, it's only logical that doctors will be better able to help their patients if they understand what brought them in a situation in which they have to see a doctor at a fertility clinic.
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With the ever-increasing lifetime prevalence of AAS use in men being currently estimated to be between 3 0 and 4 2% (de Souza. 2011), it is after all not unlikely that many of the future patients of fertility clinics all over the world may suffer from the long-term consequences of AAS abuse - regardless of whether they belong to those 50% of AAS userswho tell their doctor about their stroid history or not (cf. Pope. 2004). This mistrust does not exist by chance, though. As Karavalos et al. (2015) point out in the paper at hand,
"[...] mainstream academic endocrinology rather lost credibility with the ‘performance-enhancement community’ in the 1980s and 1990s, by persisting overlong in (a) doubting whether further enhancement of athletic performance could be achieved through raising serum T levels above the physiological reference range and (b) questioning whether any therapeutic separation of androgenic and anabolic actions was achievable, due to the single androgen receptor (cf. Pope. 2004)" (Karavalos. 2014).
And let's be honest. Someone who actually believes that superphysiological doses of AAS were not performance enhancing might actually learn something something from the broscientific expertise of his clients... well, as long as he is willing to listen to what they have to say.
Figure 1: Illustration summarizing the keywords (left) the scientists used to select the top 20 websites, blogs and forums (right) they researched for information on the use of AAS and means to prevent side-effects (Karavalos. 2015).
As previously mentioned, Karavalos, Reynolds, Panagiotopoulou, McEleny, Scally an Quinton, the authors of the paper at hand were  willing to listen. They used Google, the most popular online search engine (Search Engine Watch, 2012), along with the search terms listed in Figure 1 to identify Internet sites related to methods and substances used to counteract the symptoms of hypogonadism secondary to exogenous steroid use and selected the top twenty links generated by their search (Figure 1) and navigated through them to obtain details of
  • the methods and substances advised to counteract the side effect of hypogonadism and
  • the quality of medical information and advice provided online
Unsurprisingly, the best, i.e. most relevant not "best" as in medially correct, results were yielded by utilizing the terminology the AAS users commonly use, such as ‘postcycle therapy’, ‘stacking’ or ‘steroid recovery’.
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"We found that online discussions and advertisements concerning agents that can be used to combat the side effect of hypogonadism are very common. There was a mixture of information available from online communities (forums), AAS user blogs and from websites attempting to sell products such as anabolic steroids and substances directly related to hypogonadal recovery. Roughly one-third of the Internet sites we reviewed also offered to sell these drugs without prescription. Information was also available from official public health websites, such as the Welsh government funded and image-enhancing drugs website (SIED Sinfo.co.uk). The later provided risk reduction advice by provid ing information on safe injection practices" (Karavolos. 2014)
As I already hinted at in the introduction the information on forums consisted of anecdotal reports and advice from unverifiable sources (some claiming to be medically qualified). These sources referenced mainstream scientific papers and abstracts on the issues discussed.
"However, there were clear flaws to this superficially ‘evidence-based approach’. The papers quoted were of only limited generalizability to AAS users, ASIH, or to the argument proposed by the ‘expert’. Equally most users were unable or unwilling to progress beyond subscription paywalls, leaving them to draw conclusions from the abstracts or the ‘expert opinion’ alone" (Karavolos. 2014).
The most commonly named drugs and supplements to bring back normal endocrine and liver function were clomid or nolva, toremifene, and raloxifene, various AIs (anastrozole, letrozole and exemestane) as well as stacks consisting of milk thistle blended with a multitude of ingredients, such as vitamins (notably vitamin D), minerals (most often zinc), amino acids, herbal extracts and compounds such as L-carnitine. While the effects on the HPTA were discussed in detail, potential long-term effects on spermatogenesis were largely ignored. In fact,
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"[...] discussions often lead to misunderstanding the pathophysiology of spermatogenesis and its impairment, leaving users to believe that return to normal serum testosterone levels translated to normal spermatogenesis.

In most discussions, men seemed to equate regaining endogenous steroid production to normal fertility, ignoring long-term effects on quality of sperm, such as poor morphology and motility, which might potentially be irreversible." (Karavolos. 2014).
The problem with this assumption is that normal spermatogenesis is associated with intratesticular T levels some 30-fold higher than serum T levels. Exogenous administration cannot deliver anything remotely approaching this requisite T concentration within the seminiferous tubules; indeed, it will tend to markedly reduce it by suppressing endogenous LH-mediated T secretion.
It is hard to predict how long the natural T production will be suppressed: Aside from the drugs that were used and the duration, age appears to be an important factor, with younger users recovering significantly faster than older ones (Moretti. 2007).
Of the treatments mentioned on the boards, only two have some degree of scientific backup, albeit not exactly in form of reliable long(er)-term studies on former steroid users:
  • Figure 2: A meta-analysis of the use of  oestrogen antagonists (clomiphene or tamoxifen) as medical empiric therapy for idiopathic male infertility shows significant increases (∆ in %) in pregnancy rates, sperm concentration and motility as well as the "sperm production trigger" FSH in response to treatment (Chua. 2013).
    HCG, which has been successfully used for the treatment of T deficiency and/or induction of spermatogenesis in gonadotrophin-deficient adults (typically with concomitant FSH therapy in the latter role) and in treating hypogonadotrophic pubertal delay (Liu. 2002), and
  • SERMs such as clomiphene, tamoxifen and raloxifene which have long been used off-label for the treatment of male gynaecomastia and infertility, for which studies show highly variable success rates ad most promising data for clomiphene or tamoxifen in the treatment of idiopathic male infertility (Chua. 2013). How many of the subjects in the studies were infertile due to AAS (ab-)use is unknown, but in view of the low number of AAS users who speak openly about their steroid history, the rate could be high.
For disclosed steroid induced infertility there are yet only case reports available that suggest that either of these agents is an effective method to restore fertility in former AAS users. Strong evidence for the use of aromatase inhibitors (AIs) is absent.
In theory, SARMs may build muscle without any of the ill side effects of androgens, but their effects on fertiltiy as well as their long-term safety has not yet been studied sufficiently. Keep that in mind when you read my recent overview of the literature here and if you are seriously considering their use.
Bottom line: The study at hand confirms that most of the information you will find about the use of AAS on the Internet generates the false impression that "AAS use is safe with manageable adverse effects." This is in part due to the non-awareness of potentially long-lasting anti-fertility effects that may persist, for months if not years even if the normal HPTA function is restored.

Karavolos et al.'s comparison of bro- and pro-science does yet also reveal that not all the advise you can find "on the boards" is total bogus. The use of SERMs and HCG, for example, appears to be a still unproven, but at least promising strategy to normalize both, the production of testosterone and sperm after an AAS cycle. Still, far more research is necessary before we would be able to quantify the risk of long-lasting negative effects of AAS use on the endocrine axis and, even more so, on sperm production and function | Comment on Facebook!
References:
  • Chua, M. E., et al. "Revisiting oestrogen antagonists (clomiphene or tamoxifen) as medical empiric therapy for idiopathic male infertility: a meta‐analysis." Andrology 1.5 (2013): 749-757.
  • de Souza, Guilherme Leme, and Jorge Hallak. "Anabolic steroids and male infertility: a comprehensive review." BJU international 108.11 (2011): 1860-1865.
  • Karavolos, Stamatios, et al. "Male central hypogonadism secondary to exogenous androgens: a review of the drugs and protocols highlighted by the online community of users for prevention and/or mitigation of adverse effects." Clinical endocrinology (2014).
  • Liu, Peter Y., et al. "Predicting pregnancy and spermatogenesis by survival analysis during gonadotrophin treatment of gonadotrophin-deficient infertile men." Human Reproduction 17.3 (2002): 625-633.
  • Moretti, E., et al. "Structural sperm and aneuploidies studies in a case of spermatogenesis recovery after the use of androgenic anabolic steroids." Journal of assisted reproduction and genetics 24.5 (2007): 195-198.
  • Pope, Harrison G., et al. "Anabolic steroid users’ attitudes towards physicians." Addiction 99.9 (2004): 1189-1194.

(Super-)slow vs. Traditional Weight Lifting Affects Satellite (=Muscle Progenitor) Cells, Fiber & Domain Sizes Differently

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In know one could argue that you may see different results for other body parts than legs which were the only muscle group trained in the study at hand.
While the overall majority of currently available studies appears to suggest that traditional resistance training regimen with cadences of 1-2s on the concentric and eccentric parts of the exercises are superior to their (super-)slow counterparts, the debate is far from being settled.

Accordingly, the results of a recent study from the Ohio University are highly interesting. The findings Jennifer R. Herman-Montemayor, Robert S. Hikida and Robert S. Staron present in their latest paper could after all explain why "classic" resistance training resistance outperformed their (super-)slow cousins in the majority of studies.
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As the authors rightly point out, previous investigations have paid little attention to the role of satellite cells during exercise-induced adaptations in human muscle (Kadi. 2005). In untrained muscle, most satellite cells are in the non-proliferative, quiescent state in. As Herman-Montemayer point out, they can however be activated by various stimuli linked to exercise:
"Several studies have shown an increase in the satellite cell population following resistance training in young and old, male and female subjects. Although additional research is needed to fully understand the various factors which may influence satellite cell response, it is clear that exercise provides a sufficient stimulus for satellite cell activation, proliferation, and possibly incorporation" (Herman.Montemayer. 2015).
The process of incorporating satellite cells into the muscle is, as I've pointed out in previous articles, highly relevant not just for the repair, but also for the growth of skeletal muscle, because the subsequent increase in the number of myonuclei and thus reduced domain sizes will allow for a reduction of the exercise induced increases in myostatin which is a key factor that limits the influx of protein into the muscle and will thus allow for increased muscle growth.
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Why are satellite cells important? O’Connor et al. have suggested that muscle hypertrophy consists of several phases in which early up-regulation of transcription and translation in existing myonuclei is then followed by satellite cell activation, proliferation, and potential incorporation (29). A processes that is required to stall the myostatin induced blockade of muscle protein synthesis that occurs when the maximal domain sizes (number of myonuclei per muscle area) could be exceeded and the functionality of the muscle be compromised. In this context, I would also like to remind you of a recent SV News on vitamin A and myogenesis | more.
In their latest study, the scientists from the Universities of Rocky Vista and Ohio were thus interested in the training-specific effects of two standardized 5-week resistance training programs. To this ends, thirty-four, untrained females were divided into: slow speed (SS), traditional strength (TS), traditional muscular endurance (TE) groups as well as a non-training control (C) group. All groups performed the same three sets each of leg presses, squats, and knee extensions twice a week the first week and 3 days/week for the following 5 weeks. In that, ...
  • the SS group performed 6-10 repetitions maximum (6-10RM) for each set with 10 s concentric (con) and 4 s eccentric (ecc) contractions for each repetition, while 
  • the TS and TE group performed 6-10RM and 20-30RM, respectively, at “normal” speed (1-2 s/con and ecc contractions). 
In contrast to previously untrained men and women who had been randomized to the TE and SS who trained at the same intensity (40-60% 1RM), the subjects in the TS group trained at 80-85% 1RM.
To determine the individual effects of the workouts, the scientists performed pre- and post-training muscle biopsies that were then analyzed for fiber cross-sectional area (CSA), fiber type, SC content, myonuclear number, and MND.
Figure 1: Changes in muscle fiber size, domain size and myonuclear number (Herman.Montemayer. 2015).
As the results of the biopsies revealed, the satellite cell (SC) content of type I, IIA, IIAX, and IIX fibers significantly increased in the traditional strength training group (TS). Doing the same exercise at a significantly reduced pace, on the other hand, lead to increases in satellite cells only in the "intermediat" type IIAX and IIX fibers.

Compared to the strength endurance group, which did not see any increases in satellite cell activity, that's still a plus, though. Of greater practical relevance than the increase in satellite cell number is yet the myonuclear number which did not change in any group.
No increase in myonuclei number? So does it not matter after all? That would be the case if there had not been another, very important, but not unexpected result.

Please note that "superslow" and doing slower eccentrics, but performing regular eccentrics (fast up, slow down) are two completely different ways to train. In fact, studies indicate that the latter way of training may actually increase your gains | read more.
While the traditional strength training regimen lead to significant increase in type I, IIA, IIAX, and IIX mean myonuclear domain sizes, while the mean diameter of the domains and thus the effective "size" of the fibers increased only in type IIA fibers in the subjects in the super slow (SS) group. No increases in fiber size were observed in the TE or C groups.

Overall, it is thus warranted to conclude that "slow-speed resistance training increased SC content and MND [myonuclear domain size] more than training with a similar resistance at normal speed". It is yet just as warranted to say that "high-intensity, normal-speed training produced the greatest degree of fiber adaptation for each variable" (Herman-Montemayor. 2015) including the most relevant one, the cross sectional area | Comment on Facebook!
References:
  • Kadi, Fawzi, et al. "The behaviour of satellite cells in response to exercise: what have we learned from human studies?." Pflügers Archiv 451.2 (2005): 319-327.
  • O'Connor, Roddy S., et al. "Last Word on Point: Counterpoint: Satellite cell addition is/is not obligatory for skeletal muscle hypertrophy." Journal of Applied Physiology 103.3 (2007): 1107-1107.

HMB + Whey = Useless? Performance Markers Up, CK, IL-6 and DOMS Down - Recent Study Suggest Faster Recovery, Study Design Limits Significance of Results, Though

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To actually confirm the marketed "more complete recovery", I'd like to see more relevant study outcomes (who does CMJs?) to be tested, EAS ;-)
If you've read my comments on previous HMB studies you will know that I am skeptical if the promising results that have been observed in studies using 2-3 grams of calcium bound or free acid HMB would persist if the subjects did what most of you will do: Consume 20-30g of whey protein after every workout.

I guess Kraemer et al. (2015) may have had similar doubts, when they designed their latest study. A study in which they compare recovery from highly demanding resistance exercise with whey protein (WP group) alone or a supplement containing whey, HMB, and a slow-release carbohydrate (isomaltulose | RP group).
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Now, I have to admit that due to the lack of a "HMB + whey only" group it is difficult to tell how much of any potential benefits the subjects in the WHI group may have experienced can be ascribed to HMB. As we are going to see in the discussion of the results, a comparison to previously observed effects of HMB do yet suggest that the addition of HMB may have had an effect,... but hey, I am anticipating here. Let's first take a closer look at what exactly the researchers from the  Ohio State University did.
"Thirteen resistance-trained men (age: 22.6 +/- 3.9 years; height: 175.3 +/- 12.2 cm; weight: 86.2 +/- 9.8 kg [at least one year of RT experience]) completed a double-blinded, counterbalanced, within-group study. Subjects ingested EAS Recovery Protein (RP; EAS Sports Nutrition/Abbott Laboratories, Columbus, OH) or WP twice daily for 2 weeks prior to, during, and for 2 days following 3 consecutive days of intense resistance exercise" (Kraemer. 2015).
The workout sequence included heavy resistance exercise (day 1) and metabolic resistance exercise (days 2 and 3 | see Table 1 for details) and was specifically designed to provide "excessive demands" on the recovery process.
Table 1:  Three-Day Workout Sequence. Workouts were performed on consecutive days at the same time of day. Rest period represents time in minutes between each set (Kramer. 2015).
The subjects performed no physical activity during day 4 (C24 hours) and day 5 (C48 hours), where recovery testing was performed. Before, during, and following the 3 workouts, treatment outcomes were evaluated using blood-based muscle damage markers and hormones, perceptual measures of muscle soreness, and countermovement jump performance.
Figure 1: Creatine kinase levels (left | RP < WP ), pain scores (right, top | RP << WP) and countermovement jump performance (right, bottom | RP >> WP) at baseline, 24h and 48h after (Kraemer. 2015).
Now, while none of the markers the scientists evaluated is indicative of the real-world long-term effects the supplementation regimen may have on what really matters, i.e. strength and size gains, the improvements in creatine kinase (CK), a purported marker of muscle damage, IL-6 (not shown in Figure 1), a marker of the inflammatory response to exercise, DOMS, a potential reason you may not be able to get back to the grind and countermovement jump performance, a proxy (albeit not a good one) for potential performance declines, appear to suggest a statistically significant advantage for the whey + HMB + isomaltose mix.
In a previous comparison of leucine and HMB I have already hinted at the unique anti-catabolic affects of HMB. Effect that don't depend on the form of HMB you take, as a recent study suggests | more.
So how much of the effect is due to HMB? It is obviously impossible to answer this question conclusively, but a 2010 study by Cooke et al. indicates that the creatine kinase buffering effects of whey protein are significantly more pronounced than those of an isocaloric amount of carbohydrates. This does not mean that the isomaltose content of the RP supplement didn't contribute to the reduction in creatine kinase, but it does at least suggest that there is room for additional benefits from HMB, of which you will remember from one of my more recent articles on HMB that its benefits may partly be ascribed to its ability to buffer the muscle damaging effects of highly intense exercise.

Still, the study at hand allows for only one conclusion which is "that during times of intense conditioning, the recovery benefits of WP [whey protein] are enhanced with the addition of HMB and a slow-release carbohydrate [isomaltose]" (Kraemer. 2015).

This does also mean that Kraemer's study does not provide the missing evidence that consuming 1.5g of HMB (calcium bound) alone on top of 20g protein would be superior to 20g of whey alone on a protein sufficient (subjects consumed 0.8-1.2g/kg), let alone a high protein diet; and that's not just because it was (EAS-)sponsored research and thus as some people may apparently assume "biased", but rather because the study design doesn't allow for a conclusion like that, because (a) the main outcomes don't tell us anything about potential strength gains on relevant exercises like squats or bench presses and/or long(er)-term muscle gains, and because (b) the use of a supplement containing both carbohydrates and HMB on top of whey protein makes it impossible to disentangle the effects of the individual agents | Comment on Facebook!
References:
  • Kraemer, William J., et al. "The Addition of Beta-hydroxy-beta-methylbutyrate and Isomaltulose to Whey Protein Improves Recovery from Highly Demanding Resistance Exercise." Journal of the American College of Nutrition ahead-of-print (2015): 1-9.

L‑Alanylglutamine Blunts Allegedly Catabolic Signaling Proteins After Exercise - Does This Mean Sustamine™ is a Potent Anti-Catabolic Agent We All Should be Using?

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Can a few grams of Sustamine™, i.e. L‑Alanylglutamine, prevent protein breakdown after an intense workout? How significant are reduced AMPK and NF-kB protein levels? And lastly: Do we even care about 20 min? 
Glutamine dipeptides such as l-alanylglutamine (AlaGln) have been designed to improve upon the low solubility and stability of regular l-glutamine and are used in more and more sports drinks and health products. Maybe you have even used one of them without knowing? Just take a look at the labels. Does any of your "proprietary blends" contain Sustamine™? Yes? I am by no means surprised.

Due to its increased stability and correspondingly higher absorption rates for intact glutamine, AlaGln dipeptide facilitate greater increases in plasma glutamine concentration compared with glutamine or wheat protein, which has the highest glutamine content of all common protein formulas (Harris. 2012; Rogero. 2006).
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Cruzat et al. report in their 2010 study that AlaGln administration can attenuate muscle damage, but their results are based exclusively on the observation of lower inflammation biomarkers following prolonged endurance exercise (Cruzat et al. 2010). A more significant outcome parameter was measured recently by Wang et al. (2015). In their study, the scientists investigated
"the effects of acute Sustamine™ (SUS) supplementation, a dipeptide composed of alanine and glutamine, on the signaling pathways controlling MPS and MPB post resistance exercise. Comparisons were made relative to whey protein (WP) supplementation" (Wang. 2015).
In that it is a bit disappointing that the subjects" of the study were eighty-nine male Sprague–Dawley rats who had been familiarized with the standardized exercise protocol, before they had to do latter climbing 10 times with a weight equal to 75 % of their body mass attached at the base of the tail.
Figure 1: Levels of the alleged markers of protein breakdown, NF-kB, AMPK and FOXO3A, 20 min (A) and 40 min (B) after the workout (Wang. 2015).
Before the exercise trial, the rats had been fasted, afterwards, blood was collected before the rats received either (1) whey protein (WP = 0.4 g/kg), (2) a low dose of Sustamine™ [LSUS = 0.1 g/kg, l-alanylglutamine (AlaGln); Kyowa Hakko Bio. Ltd., New York, NY], a high dose of Sustamine™ (HSUS = 0.5 g/kg), or placebo (PLA = 0.52 g/kg glycine, isonitrogenous to the HSUS) by intubation.  The results of the extensive testing the scientists conducted on their hairy subjects indicate that (Wang. 2015):
  • Figure 2: Unfortunately, Wang et al. forget that NF-kB is only "bad" for your muscle if it's chronically elevated (Kramer. 2007)
    All supplements elevated the phosphorylation of FOXO3A above SED at 20 min post exercise, but only the SUS supplements significantly reduced the phosphorylation of AMPK and NF-kB p65. 
  • SUS supplements had no effect on mTOR signaling, but WP supplementation yielded a greater phosphorylation of mTOR p70S6k, and rpS6 compared with PLA at 20 min post exercise. 
  • By 40 min post exercise, phosphorylation of mTOR and rpS6 in PLA had risen to levels not different than WP. 
At first sight, it may thus in fact seem as if "SUS blocks the activation of intracellular signals for MPB [muscle protein breakdown], whereas WP accelerates mRNA translation" (Wang. 2015). Upon closer scrutiny of the results it does yet turn out that exercise-induced increases in AMPK are not only highly transient (please don't fall for the common bullsh*t concept that you could "lose muscle" over the 20 minutes where AMPK is higher in the WP and PLA group), but also not necessarily catabolic (I have discussed this at length in a previous article and won't repeat the whole sermon here | learn more). Rather than an inhibition of protein breakdown, the decrease in AMPK may rather trigger reduction in fat oxidation and glucose uptake both of which are elevated by AMPK - an effect you probably don't expect from a useful dietary supplement.
Figure 3: I am not sure, but personally I would say that the reduced mTOR response in the low dose Sustamine™ group may actually be the most significant result of the study at hand. After all, most supplements contain less than the 1.3g of this patented and thus expensive agent that would be the human equivalent of the 0.1g/kg used in the LSUS group.
So what about NF-kB is that irrelevant, as well? While the change in NF-kB is likewise transient, it is undebatable that NF-kB is involved in skeletal muscle atrophy (Li. 2008). To think of NF-kB as a merely proteolytic would yet be short-sighted, because it is also involved in the adaptational process to exercise. As the figure from Kramer et al. shows, only chronic elevations of NF-kB are truly catabolic. Transient elevations of NF-kB on the other hand are a motor of "improved fuel homestasis, increased antioxidant capacity, tissue regeneration" and thus all the "beneficial physiolog[ical]" (Kramer. 2007) effects of exercise training.

The fact that FOX-O, another protein that's involved in the breakdown of muscle protein (Sandri. 2004), isn't decreased by Sustamine™ either, I  personally do have my doubts that the alleged anti-catabolic effects Wang et al. believe to have observed are practically relevant. But hey, maybe Kyowa Hakko Bio Co who were paying for the study at hand want to sponsor a study with a more relevant study design to prove that one of their best-sellers is actually worth spending money on ;-) | Comment on Facebook!
References: 
  • Kramer, Henning F., and Laurie J. Goodyear. "Exercise, MAPK, and NF-κB signaling in skeletal muscle." Journal of Applied Physiology 103.1 (2007): 388-395.
  • Li, Hong, Shweta Malhotra, and Ashok Kumar. "Nuclear factor-kappa B signaling in skeletal muscle atrophy." Journal of molecular medicine 86.10 (2008): 1113-1126.
  • Sandri, Marco, et al. "Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy." Cell 117.3 (2004): 399-412.
  • Wang, Wanyi, et al. "l-Alanylglutamine inhibits signaling proteins that activate protein degradation, but does not affect proteins that activate protein synthesis after an acute resistance exercise." Amino acids (2015): 1-10.

Nutrition & Age-Related Muscle Loss - Overview of Some Recent Studies: It Does not Take More Than Well-Timed ~20g of Milk Protein to Turn Muscle Loss into Gain + More

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Ladies and gents, if you want to keep up with the youngsters and be able to play with your grand and grand-grand children you better put an emphasis on more than adequate protein intakes.
Initially I wanted to talk about only one of the studies that were presented at the latest meeting of the Nutrition Society, but in view of the facts that (1) we are all going to be old one day, (2) we all have parents and grand parents at risk of muscle loss and sarcopenia and (3) we all are interested in some good research, I thought it may be a good idea to summarize the most important findings of three additional relevant presentations.

Ah, before I get started: I would like to emphasize that the corresponding full papers have not been published, yet. I do thus apologize in advance that I won't be able to answer detail questions about the methods, side findings and allegedly interested, but hitherto unknown stuff like that.
Read more short news on various topics here at the SuppVersity

Exercise Research Uptake Nov '14 1/2

Exercise Research Uptake Nov '14 2/2

Weight Loss Supplements Exposed

Exercise Supplementation Quickie

Exercise Research Uptake Jan 12, 2015

Read the Latest Ex. Science Update
  • It does not take more than ~20g of milk protein to turn muscle loss into gains (!) - It does sound almost too easy to believe, but researches from the University of Limerick were able to show that adding 0.33g/kg body weight milk protein may be all it takes not just to conserve, but actually to build lean muscle mass in people aged 50-70 year old.

    In their study, Norton et al. (2015) observed a highly significant increase in lean tissue mass of 1% in 24 weeks when the subjects who consumed a protein sufficient diet with 1.2g protein/kg body weight (that's 50% higher than the FDA minimum of 0.8g/kg) added only 0.3g/kg milk protein to their diets. The protein came from two shakes that were - and this may be important - consumed with the lowest protein meals of the day.
    Figure 2: Change sin lean tissue mass (relative and absolute) in response to 24-weeks of supplementation with two servings of 0.15g/kg body weight milk protein (total 0.3g/kg) or placebo in 50-70 year olds (Norton. 2015).
    So, assuming your grandma eats a high protein breakfast, has no appetite at lunch and consumes only a few slices of bread at dinner, she'd take the protein shakes with lunch and dinner. Depending on cultural and personal habits, the distribution is yet probably rather breakfast + launch (US) or dinner (Europe).
Don't be a fool! Nutrition is an important factor that will help you keep your muscle functional, but without proper "exercise" in the form of adequate physical activity and some form of "strength training" (body weight squats and push ups if you have no equipment) you will not be able maintain optimal muscle function, no matter how much protein you consume.
  • Which reminds me: It would have been very interesting if the scientists had had one group of subjects consume all the milk protein with their larges meal of the day. If we believe in the "protein timind does not matter" mantra that has recently become popular (cf. Schoenfeld. 2013), it should not matter. Somehow I do believe, however that it would.
  • DHA as performance booster for your grandma - In another recent study Dyall et al. observed that short-term supplementation with an enriched DHA supplement was associated with significant increases in blood DHA content and there were significant positive relationships between increased DHA status and improved fast walking speed and vertical jump height.

    Meta-Analysis Says: Fish Oil Does Not Help You Lean Out! Plus: Why you Should Still Eat Fish | more
    What is particularly interesting is that only potentially relevant inter-group difference the scientists testes was the DHA level which was significantly increase in response to the ingestion of the supplement that contained 1 g DHA, 160 mg EPA, 240 mg gingko biloba, 60 mg phosphatidylserirte, 20 mg d-alpha tocopherol, 1 mg folic acid and 20 pg vitamin B12 per day for 6 months. No other significant differences were found. A fact that suggests that "the effects were mediated via changes in DHA, rather than the other components in the treatment" (Dyall. 2015).
Can drinking protein shakes outperform dietary protein when it comes to protecting aged muscle from diet induced catabolism? Find out in this previous SuppVersity article @ March 2015 | read more
On short notice: Next to these findings, scientists also found that the majority of Britons still gets the lion's share of their dietary protein from animal products, with the average contribution of animal protein to the diets of men and women being 10.1% and 10.8% of the total energy intake (vs. 4.7% from plant protein | Bain. 2015). Since bone loss usually goes hand in hand with muscle loss, it may also be worth mentioning that one's susceptibility to seasonal changes in 25OHD levels are associated with increased bone resorption, i.e. the "deconstruction" of bone material (). That's an interesting observation researchers from the University of Sheffield have made - one that provides another good argument to (a) test your 25OHD levels regularly and to supplement if necessary (specifically during fall and winter) | Comment on Facebook!
References:
  • Bain, LKM., et al. "Contributions to dietary protein intake in a British adult population". Proceedings of the Nutrition Society, 74, E179 (2015): doi:10.1017/S0029665115001974. 
  • Darling, AL. "Increased bone resorption is associated with greater seasonal fluctuation or ‘cycling’ of 25-hydroxyvitamin D". Proceedings of the Nutrition Society, 74, E177 (2015): doi:10.1017/S0029665115001950. 
  • Dyall,SC. et a. "Blood levels of the omega-3 fatty acid docosahexaenoic acid are associated with gait and lower limb power in older females". Proceedings of the Nutrition Society, 74, E168 (2015): doi:10.1017/S002966511500186X. 
  • Norton, C,  et al. "Effect of 6 month supplemental milk protein intake on lean tissue mass in healthy adults aged 50 to 70 years". Proceedings of the Nutrition Society, 74, E181 (2015): doi:10.1017/S0029665115001998. 
  • Schoenfeld, Brad Jon, Alan Albert Aragon, and James W. Krieger. "The effect of protein timing on muscle strength and hypertrophy: a meta-analysis." J Int Soc Sports Nutr 10.1 (2013): 53.

True or False? Your Back Pain Will Vanish Forever if You Train Your "Core"! Plus: What Actually is the F*** "Core"?

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Do people really suffer from back pain because they are not doing exercises like this everyday, or are we rather dealing with a more fundamental problem? One that is related to the general reluctance to move further than from the couch to the fridge and back? What do you think?
You will probably be aware that the #1 trigger of back pain in today's society is our sedentary lifestyle. Today, more than 50% of the US adults are affected by chronic back pain (Rozenberg. 2008). Against that background it appears logical to assume that it would help if you strengthen you deep trunk muscles, but is that actually true? And how does one do that (best)?

Currently, no standardized system has been established analyzing and comparing the results of core strength training and typical resistance training. Therefore, Wen-Dien Chang, Hung-Yu Lin, and Ping-Tung Lai conducted a systematic review of the results of previous studies to explore the effectiveness of various core strength training strategies for patients with chronic low back pain.
You can find more True or False articles at the SuppVersity

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In general, their results appear to confirm the hypothesis that appropriate "core training" will "assist in the alleviation of chronic low back pain" (Chang. 2015). The efficacy of different training modalities and training different muscle groups does yet have significantly different effects on chronic low back pain.

Before we delve any deeper into the specific exercise modalities I do however want to do something many people forget, when they are talking about strengthening the "core muscles". This "something" that is so often forgotten is to define the muscle groups that constitute the core,... or rather the muscles that are capable of stabilizing our (lower) backs in a way that renders them "pain proof". As Chang et al. point out, the core muscles, which are the primary muscle group for maintaining spinal stability, can be divided into two groups according to their functions and attributes (from Chang. 2015):
  • The first group of muscles is composed of the deep core muscles, which are also called local stabilizing muscles. These muscles primarily include the transversus abdominis, lumbar multifidus, internal oblique muscle and quadratus lumborum. The lumbar multifidus is directly connected to each lumbar vertebral segment, and the transversus abdominis and lumbar multifidus activate a co-contraction mechanism. The abdominal draw-in that occurs during contraction provides spine segmental stability and maintains the spine within the neutral zone. In additional, these muscles provide precise motor control and are thus primarily responsible for spinal stability.
  • The second group of muscles comprises the shallow core muscles, which are also known as global stabilizing muscles, including the rectus abdominis, internal and external oblique muscles, erector spinae, quadratus lumborum, and hip muscle groups. These muscles are not directly attached to the spine, but connect the pelvis to the thoracic ribs or leg joints, thereby enabling additional spinal control. These muscles produce high torque to counterbal ance external forces impacting the spine; thus, this group of muscles is secondarily responsible for maintaining spinal stability. 
The function of this muscle can be best described as a "natural brace" that maintains segmental stability, protects the spine, and reduces stress impacting the lumbar vertebrae and intervertebral discs. If the muscles are weak or their power is unbalanced, this can trigger chronic back pain. Depending on which of the two is the reason for your back pain (imbalance or weakness), the goal must thus be to strengthen all or specific core muscles.
Figure 1: Overview of the four exercise types used in the studies reviewed by Chang et al. (2015).
In their study, Chang et al. compared the results of four out of 142 reviewed studies which study the effect of four core strength training exercises (i.e., trunk balance, stabilization, segmental stabilization, and motor control) on deep core muscles strength, stability and back pain (see Figure 1). One reason the studies by Akbari et al. (2008), Andrusaitis (2011), França (2010) and Gatti (2011) were selected was their design.
Table 1: Intervention, assessment and results of reviewed articles (Chang. 2015) | VAS: visual analogue scale; OSWDQ: Oswestry disability questionnaire; RMQ: range minimum query; PBU: stabilizer pressure bio feedback unit; BPS: back performance scale | *p < 0.05, statistically significant difference between experimental group and control group.
To make sure that any potential benefits of the exercise protocols were in fact core-training specific, all of the control groups in the four reference studies performed typical resistance training to strengthen their trunk and lower limb muscles (e.g., curl-ups, straight-leg raises, and pushups) and this is exactly where things become dodgy, because in only one of the studies the pain reduction was significant, compared to the control group.
Impingement No More: Study Outlines 6 Week Protocol That Reduces, in 15% of the Cases Even Resolves Shoulder Pain | more
So, core training worked, but the efficacy that was evaluated by various questionnaires, as well as biofeedback and ultrasound was not exactly mind-boggling with pain reductions in all studies.

Since the benefits were not significantly more pronounced than the benefits of regular strength training it is questionable how smart it is to tell patients to do core exercises which provide only non-significant benefits over standard training routines with free weight or machines considering the fact that unlike core training the latter will also have potent metabolic effects.

If you want to do core exercises on top of a sound resistance training routine, fine! If you are like the lazy or busy Westerner who has the willpower and/or time to spend only 20 minutes on your workouts it would be plain out stupid to waste the time on core exercises, when a sensible resistance training workout (that's not doing bench presses, biceps curls and 200 sit-ups everyday for 10 years, bros | learn how to program a sensible routine) will reduce your diabetes and obesity risk and help you improve your body composition, no? | Comment on Facebook!
References:
  • Akbari, Asghar, Samane Khorashadizadeh, and Gholam Abdi. "The effect of motor control exercise versus general exercise on lumbar local stabilizing muscles thickness: randomized controlled trial of patients with chronic low back pain." Journal of Back and Musculoskeletal Rehabilitation 21.2 (2008): 105-112.
  • Andrusaitis, Silvia Ferreira, et al. "Trunk stabilization among women with chronic lower back pain: a randomized, controlled, and blinded pilot study." Clinics 66.9 (2011): 1645-1650.
  • Chang, Wen-Dien, Hung-Yu Lin, and Ping-Tung Lai. "Core strength training for patients with chronic low back pain." Journal of Physical Therapy Science 27.3 (2015): 619-622.
  • França, Fábio Renovato, et al. "Segmental stabilization and muscular strengthening in chronic low back pain: a comparative study." Clinics 65.10 (2010): 1013-1017.
  • Rozenberg, S. "[Chronic low back pain: definition and treatment]." La Revue du praticien 58.3 (2008): 265-272.

Battling Fat W/ Fat: Subcutaneous Fat Implant Improves Glucose Tolerance and Alleviates Inflammation | Plus: Beware of the Potential Ill Health Effects of Liposuction

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BMI is not a good predictor of metabolic health. One reason it isn't is the differential contribution of visceral and subcutaneous body fat on diabesity an CVD risk. The rodent study at hand demonstrates that quite drastically.
It is absolute bogus to deny the contribution of the ever-increasing amount of fat many of us are carrying around day by day to all sorts of potentially fatal diseases. In that, it is yet important to differentiate between the accumulation of intra-abdominal or visceral adipose tissue (VAT) which is associated with type 2 diabetes, dyslipidaemia and hypertension and high amounts of subcutaneous fat which are (comparatively "benign").

As Hocking et al. (2014) highlight in their latest paper, "[t]his relationship [between VAT, type 2 diabetes, dyslipidaemia and hypertension] was originally attributed to increased NEFA [non-esterified fatty acid] flux from VAT into the portal circulation" (Hocking. 2014).
HIIT is an excellent way to shed both subcutaneous and visceral body fat!

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone
A closer look at the low relative contribution of VAT to the total NEFA concentration in our blood does yet suggest that other factors, such as the proinflammatory cytokine production that is particularly pronounced in visceral (vs. subcutaneous) would be at least as important as the constant efflux of non-esterified fatty acids.

To probe the differential acute and chronic effects of subcutaneous (non-inflammatory) and visceral adipose tissue on glucose metabolism and whole body inflammation, researchers from the Garvan Institute of Medical Research in Australia conducted an interesting experiment in which they performed time course studies to investigate the short- and long-term effects of inguinal subcutaneous→visceral (SubQ→Vis) and  epididymal visceral→visceral (Vis→Vis) adipose tissue transplantation in HFD-fed mice.
Figure 1: The transplantation of subcutaneous fat into the intra-abdominal cavity of the mice did not just improve the glucose tolerance it did also (albeit non-significantly) blunt the HFD-induced weight gain (Hocking. 2014).
Yes, it may sound hilarious, but instead of removing intra-abdominal fat, the scientists transplanted subcutaneous or visceral fat into the abdominal cavity of their lab animals. Ca. 150-225mg of fat that's tantamount to 13% of their total body fat that was thus redistributed.
Yes, the study at hand does also underline the fallacies of liposuction: Unlike lifestly-induced weight loss that will target both visceral and subcutaneous body fat (for the obese the visceral fat will usually go first), liposuction will remove only subcutaneous fat. It is thus not surpFrising that liposuctions will have no effect on insulin action and risk factors for coronary heart disease (Klein. 2004). With significant increases of 16% (range 13 to 21 percent) in women and 13 (10-17%) of the visceral to subcutaneous fat ratio, as they were observed by Matarasso et al. (1998), and post-liposuction gains in total visceral fat, the removal of unaesthetic subcutaneous fat may eventually even worsen a patients' metabolic health (assuming the liposuction is not complemented by profound lifestyle changes | no energy surplus, no fat gain!).
Now, what is intriguing, though, is that "sick" were only those rodents who had been transplanted with metabolically active and highly inflammatory visceral fat. The rodents who harbored an additional 13% of formerly subcutaneous fat in their abdominal cavity actually experienced significant improvements in glucose tolerance and inflammation within the 6 week post-transplantation study period and that despite the fact that they received the same obesogenic high energy + high fat diet as the rodents who were sham operated or received visceral donor fat.

A closer examination of the underlying mechanisms revealed that the SAT transplantation prevented HFD-induced hepatic triacylglycerol accumulation and normalised the expression of hepatic gluconeogenic enzymes.
"Grafted fat displayed a significant increase in glucose uptake and unexpectedly, an induction of skeletal muscle-specific gene expression. Mice receiving subcutaneous fat also displayed a marked reduction in the plasma concentrations of several proinflammatory cytokines (TNF-α, IL- 17, IL-12p70, monocyte chemoattractant protein-1 [MCP-1] and macrophage inflammatory protein-1β [ΜIP-1β]), compared with sham-operated mice. Plasma IL-17 and MIP-1β concentrations were reduced from as early as 4 weeks after transplantation, and differences in plasma TNF-α and IL-17 concentrations predicted glucose tolerance and insulinaemia in the entire cohort of mice (n=40)" (Hocking. 2014).
That's in contrast, mice receiving visceral fat transplants who were glucose intolerant, with increased hepatic triacylglycerol content and elevated plasma IL-6 concentrations.
Being heavy is not the problem. The problem is being fat. Even if your BMI is in rance, men and women with body fat levels >25% / 35%, respectively have significantly increased risks of developing one or all of the central features of metabolic syndrome (Oliveros. 2014) 
Is this a viable treatment option for humans? Probably not, but the results of the study at hand highlight the often overlooked of invisible intra-abdominal fat. Specifically women appear to be at high risk of being "skinny at" or "normalweight obese", which means that they have a normal BMI but body fat levels far above the normal range of <30%. As the data from a 2014 study by scientists from the Mayo Clinic in Rochester indicates, their risk of suffering from one or even all of the features of the metabolic syndrome is significantly increased.

Specifically for this group of subjects, a subcutaneous → visceral fat transplant may actually alleviate he symptoms, but whether that's a sensible treatment option is more than questionable. Rather than that, diet and exercise the unbeloved standard recommendations are still the way to go. In conjunction they are the #1 visceral fat burner - with meds being necessary only for the severely obese to bring the into a situation where they are actually able to adhere to the necessary lifestyle interventions | Comment on Facebook!
References:
  • Hocking, Samantha L., et al. "Subcutaneous fat transplantation alleviates diet-induced glucose intolerance and inflammation in mice." Obesity Research & Clinical Practice 8 (2014): 99-100.
  • Klein, Samuel, et al. "Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease." New England Journal of Medicine 350.25 (2004): 2549-2557.
  • Matarasso, Alan, Richard W. Kim, and John G. Kral. "The impact of liposuction on body fat." Plastic and reconstructive surgery 102.5 (1998): 1686-1689.
  • Oliveros, Estefania, et al. "The concept of normal weight obesity." Progress in cardiovascular diseases 56.4 (2014): 426-433.
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