Santa is Coming to Town and You Better Beware of His Gifts: Fat Gain, Muscle Loss and Increased Mortality Rates.

Image 1: The "modern" image of the Coke-drinking Santa. Do you really believe he is one of the good guys?

Finally, December 24th is there! The day we have all been waiting for, to get together with friends and relatives and wait for the portly, joyous, white-bearded man in the red coat to deliver "his" gifts. Interestingly enough, the word "gift" in German designates "poison" and while those of you who have been following the SuppVersity news earlier this week may now be speculating that this could in one way or another be related to the millions of iPhones Santa is going to be dropping down the chimneys in the night to come (cf. Mobile Contraception), it seems unlikely that the electromagnetic radiation from the gadgetry could explain the statistically significant +4.65% increase in cardiac and a + 4.99% increase in non-cardiac deaths during the holiday season. After all, the data based on which David P. Phillips, Jason R. Jarvinen, Ian S. Abramson, and Rosalie R. Phillips conclude that "the Christmas/New Year’s holidays are a risk factor for cardiac and noncardiac mortality" is from the pre-iPhone era (Phillips. 2004).

Is Santa not the good guy, the Coca Cola ads made us believe?

So, if its not the radiation, what else could it be? Could it be Santa Claus himself? Is he haunting us, just as his robotic counterfeit in the distant future of the year 2999, where an evil Santa robot is after the blood of the protagonists of Matt Groening's and David X. Cohens TV series Futurama? Or is it a result of the consumption of too many of the Coca Cola bottles Santa is supposed to have in his bag?

Image 2: One really has to marvel at how the soft drink producers dissolve the enormous amount of sugar on the right in the small amount of dark brew on the left.

Did you know that the Coca Cola company alone sells 1.6billion (!) servings of Coke per day? With 27g of sugar per serving, this equals 43,000 metric tons of pure sugar. The average American, who consumes an average of 150 to 170 pounds of sugar each year, would have to live into his/her 558th year of age to eat or drink her way through this sugar mountain. And while I have no doubt that there actually are people out there who would do that withing 100 years, I am not quite sure which of the ailments of our sweet convenience society would strike him / her first and put a spoke in the sweet-o-holic's plans: diabetes, cancer, heart failure or stroke? What would you say?

Phillipps et al. who report in a follow-up study based on the same dataset from the holiday periods between July 1, 1973, and June 30, 2001 that there was an "excess of 42,325 deaths from natural causes above and beyond the normal winter increase" (Phillips. 2010), exclude the possibility that the increased mortality rate was simply a result of the bad weather conditions and related respiratory diseases:

Respiratory diseases. Respiratory diseases increase during winter, and patients weakened by respiratory diseases can die from cardiac diseases. The respiratory hypothesis is undermined by 2 considerations: (1) People dying from cardiac diseases with respiratory disease listed as a secondary cause of death produce a smaller holiday peak than do people dying from cardiac diseases alone: 3.51% versus 3.77%. (2) Interaction between cardiac and respiratory diseases cannot easily explain the twin mortality spikes on Christmas and New Year’s.

So, in view of the latest headlines related to "holiday weight gain" here at the SuppVersity and elsewhere on the web, the next best plausible explanation (which would in fact come back to the "Coca Cola < > Santa Connection" ;-) would be gluttony, right?

Holiday weight gain: Distinguishing fact from fiction

Before we jump to any premature conclusions, here, let's initially have a closer look at how much body weight Santa actually has in his bag for you.I mean, the perceived weight gain is enormous, right? Well, science is however not about perceptions and feelings and it should thusly not really surprise you that, according to a US study which was published in the prestigious New England Journal of Medicine (Yanowski. 2000), the "average" American (in this study represented by 195 US adults with a mean age of 39 +/-12 years) gains no more than 0.37kg, or, expressed in terms of the mean weight of the study participants, 0.5% during the holiday period from from mid-November to early or mid-January.

Figure 1: Percentage of normal weight, overweight and obese subjects with "major weight gain", as defined in absolute or relative terms (data adapted from Yanowski. 2000)

And while the average weight gain hardly is something to speak of, there are two other particularly intriguing findings of this study I do want to draw your attention to. The first one relates to the the data in figure 1. As you can see, the number of overweight subjects among those study participants with major weight gain (as defined as >3% of the initial weight) is particularly high. While only 7.9% of the normal-weight (American normal weight ;-) subjects gained more than 3% of their initial body weight 11.1% of the already overweight subjects did. Interestingly, the number of obese subjects was slightly smaller (7.5%). The latter is yet a physical necessity as there simply is a phyiscal limit to the amount of weight you can gain in a given period of time and 3% for a person with BMI>30 is obviously way more than 3% for someone who is only "overweight" (25 < BMI < 30).

The real problem is: The weight does not magically disappear

The real culprit is however that the weight people gain during last weeks of the year "is not reversed during
the spring and summer months", so that he researchers' concern that

[t]he 0.48-kg weight gain of the subjects in this study between September or October and February or March might not appear to be  clinically important and could easily go unnoticed by both the subjects and health care providers [and that] the cumulative effects of yearly weight gain during the fall and winter are likely to contribute to the substantial increase in body weight that frequently occurs during adulthood.

A 2006 by Hull may not only provide a hypothetical explanation for the non-reversibility of the (minor) weight gain (Hull. 2006), it also provides some insights into the true fallacy of "holiday weight gain": The minor increase in total body weight goes at the expense of concomittant increases in body fat and reductions in lean tissue mass.

Figure 2: Relative changes in anthroprometric measures over the holiday season; left axis - overweight / normal weight, right axis + figures - all (data adapted from Hull. 2006)

In the 82 college students from the Hull study, this fat promoting, muscle reducing "recompositioning" effect of the holiday season (Thanksgiving to New Year) was even so pronounced that the study participants actually lost -0.1kg of their total body weight. This was unfortunately a direct result of a +0.8 increase in fat mass and a -0.4kg decrease in lean mass. And what's more, the effect on fat mass was again more pronounced in those subjects, who were already obese.

Beyond candy, coke & co: Five additional reasons why Christmas is potentially deadly

In spite of the fact that these highly unfavorable changes in body composition are certainly not beneficial for anyone's overall health, it stands out of question that their effects would be cumulative and can thusly hardly explain the empirically validated increased mortality risk during the holiday season. In a 2004 comment on the aforementioned paper by Phillips et. al., Robert A. Kloner thusly proposes five additional hypotheses which could explain the potentially fatal side effects of the holiday season (Kloner. 2004):

Image 3: If you do not want to be treated by "beginners" and unexperienced hospital personnel you'd better not get sick over the holidays; and in case you do, please make sure to "postpone your death" in order not to ruin everyone's holidays ;-)

1. Inappropriate delay in seeking medical attention - best way out: don't wait until all the presents have been wrapped out, when aunt Mary chokes over her food
2. Reduced levels of healthcare staffing or fewer staff members who are familiar with individual patients during holiday on-call schedules - best way out: better avoid getting sick in the first place if you do not want to be treated by the SCRUBS staff
3. Increased emotional stress - just ignore your nephew when he starts crying because he did not get the Nintendo Wii he wrote on his wish list
4. Decreased our of daylight - make sure to get as much of the little light there is during prolonged walks with the whole family (may also help cool down any raised tempers ;-)
5. "Postponement of death" - tell your 127 year old uncle that he has been waiting so long now that it would be very inappropriate to die now and ruin everyones' Christmas celebrations

Well, I guess, now that you know about all the terrible things that could happen and the best ways to avoid them, it is about time to wish you, your family, friends and loved ones a happy (death-free) holiday season! And in case you need a break from the festivities, there is no Christmas break, here it at the SuppVersity ;-)

Beyond Warding Off Holiday Weight Gain: 250-1000mg of Freeze-Dried Ginger Reduce Visceral Fat Even When Rodents Are Fed an Obesogenic "High Fat" Diet.

Image 1: If ginger works only half as good in humans as it does in rodents, you can drink your way to a leaner and healthier you with Alisa Profumo's delicious low-carb "Healthy REAL Ginger Ale".

Zingiber officinale, or, in plain English, Ginger, is unquestionably one of the most remarkable plant rhizomes that is known to mankind. It has been used in various cultures for treating common colds or fever, to aid digestion, treat stomach upset, diarrhoea or nausea, to alleviate rheumatic disorders, gastrointestinal complications and dizziness, and, as of late, it has received quite some attention as a possible adjuvant to treatment modalities of cancer (Peirara. 2011). In a pretty recent study, the administration of 500 mg/kg zinigiber officinale to streptozotocin-induced diabetic rats (cf. related study in CLnA, the Omega-3 Variety of CLA), was able to partly restore the deteriorated glucose metabolism (Abdulrazaq. 2011), and a 2010 study was able to show that 6-Dehydrogingerdione, an active constituent of dietary ginger stopped the growth of breast cancer cells in the petri dish. "That is all very well", you may now be thinking, "but what does that all have to do with warding off the holiday weight gain?" Well, the answer lies in the results of a very recent study, which have just been published in the International Journal of Pharmacology (Malik. 2011).

Ginger reverses diet-induced visceral obesity and restores blood lipids to normal

Z.A. Malik and P.L. Sharma, two researchers from the Department of Pharmacology at the ISF College of Pharmacy in Moga, India, investigated whether the administration of 0.25-1g/kg body weight of dietary ginger (freeze dried powder that was made from fresh ginger juice; human equivalent would be 40-160mg/kg) would have any beneficial effect on the high-fat diet induced deteriorations in body composition, energy, lipid and glucose metabolism of male Wistar rats. For eight weeks, the scientists fed the rodents a diet that consisted of 33% normal rat chow, 33% Nestlé milk powder, 7% sucrose, and 27% tap water.

Figure 1: This is probably the lowest fat "high fat diet", I've seen in some time (data adapted from Malik. 2011) - ridiculous, but hey, if the diet had really been "high fat", who knows if the rodents would have gotten obese, anyway ;-)

If you take a look a the macronutrient breakdown of the "high fat" and the "normal diet" in figure 1, it is quite obvious that the former is - if anything - higher in fat than the latter, but by no means what any sane individual would consider a "high fat diet" (I really have to check myself not to start ranting against the "high fat diet induced whatever" in rodent models, again ;-) But be that as it may, ... the data in figure 2 shows that the milk powder and the sucrose were obviously enough to really fatten the rats up, profoundly:

Figure 2: Relative increases in body weight (BW), white adipose tissue weight (WAT), visceral fat weight and brown fat in rats on the "high fat diet" (data adapted from Malik. 2011).

With a whopping +417% increase in the total white adipose tissue weight, the poor rodents became profoundly obese. Their visceral fat depots (mesenteric, epididymal  and retroperitoneal) more than doubled (on average +150%), whereas the weight of their metabolically active brown adipose tissue increased by "only" 107%.

Figure 3: Relative changes in body weight (BW), white adipose tissue weight (WAT), visceral fat weight and brown fat in rats on the "high fat diet" who were supplemented with 250, 500 or 1000mg/kg ginger (data adapted from Malik. 2011).

The addition of 250mg/kg, 500mg/kg and 1g/kg body weight of the freeze-dried ginger juice (now obviously in powdered form) to the chow dose-dependently ameliorated the weight gain and reduced the weight of both the visceral, as well as the brown fat to level that were below those of the rats on the "normal" diet (cf. figure 3). Intriguingly, the "low" dose of 250mg/kg body weight turns out to be the most effective one, when it comes to the reduction of the epididymal, retroperitoneal and mesenteric visceral fat pads.

Figure 4: Relative changes in triglycerides (TG), total cholesterol (TC), HDL and total cholesterol to HDL radio in rats on the "high fat diet" and rats who were fed the HFD with 250, 500 or 1000mg/kg ginger (data adapted from Malik. 2011).

The addition of ginger to the diet also kept the blood lipids in check (cf. figure 4) and normalized the glucose response to an oral blood glucose tolerance test in the "high-fat" fed rodents. Other than the scientists had speculated, it had no effect on energy intake and did not increase the fecal fat content. The two markers of hepatic health, AST and ALT, which were measured in the study, remained almost unchanged - in the 250mg group there was even a -17% and -13% reductions in the respective transaminases (I am thusly amazed why the study has the words "anomalies after chronic administration" in its title).

How does it work and how effective is it?

Let's finally have a brief look at a) the potential mechanism by which ginger exhibits its fat-burning magic and b) how effective ginger would be, as compared to other, better known, "tools" to ward off weight gain or induce weight loss. To check whether the mechanism of action involves increased beta-oxidation, Malik and Sharmaa mixed an additional 30mg/kg of the beta-blocker propranolol into the high fat, ginger-supplemented diets of the animals - and as you can see in figure 5, the addition of the beta-blocker led to a profound reduction in the ameliorative / fat burning effects of the freeze-dried ginger powder.

Figure 5: Relative increases (vs. control on normal diet) in body weight (BW), white adipose tissue weight (WAT), visceral fat weight and brown fat in rats on the "high fat diet" supplemented with ginger, ginger + propanolol, or sibutramine (data adapted from Malik. 2011).

And as far as its effectiveness is concerned, ginger stands the comparison to the (in-)famous weight-loss drug Sibutramine, of which you will probably have heard that Chinese manufacturers of otherwise ineffective herbal weight-loss remedies like to mix it into their products (obviously without mentioning this banned ingredient on the label).

So, if we assume that these amazing results translate to humans, the addition of a few ginger rhizomes to your holiday diet could be a very effective tweak to ward off unwanted weight gain. And if your plans for 2012 include getting rid of the nasty love-handles you have acquired in the course of the past 12 months, you better get accustomed to the spicy, yet fruity flavor of the rhizomes of this perennial reed-like plant. You could, for example start out by following Alisa Profumo's delicious low-carb "Healthy REAL Ginger Ale in Minutes"-recipe on the Super Human Radio webpage (cf. image 1). And just in case you are too lazy to juice and / or freeze-dry some fresh ginger rhizomes yourself, you may want to consider buying a bag of Carl Lanore's  standardized ginger extract, which is also available on the Super Human Radio website.

Adelfo Cerame - Road to Wheelchair Nationals '12: Getting Ripped For Christmas! Plus, Taking a Week Off Takes Some Courage, But Believe Me - It Will Pay Off!

Image 1: Adelfo at the Buckeye Classics, last year.

Actually, I wanted to start this installment of Adelfo's weekly contest-prep blog along the lines of "another Thursday, another ...", ... well, I guess that won't work out, because exactly those lines were the first words in the email with the weekly write-up Adelfo just sent me. So, I guess, I will just take the chance to sneak in a last-minute tip for a gift. Assuming that you have a friend or family member who really wants to make a change to the way he looks, feels and performs in the coming year, I think Adelfo is still taking new clients... but before he gets mad at me again, because I am pimping his services way too much for his liking, I better shut up now and let Adelfo tell you how he has been preparing for Christmas and his 12-weeks out mark on Christmas Day ;-)

Another Thursday, another blog…  

Damn! Aren’t you guys and, of course, girls ;-) getting tired of reading these Thursday write-ups? Well I hope not because there’s going to be about 13 to 14 more Thursday segments from yours truly ;-)

As you all know from the last installment of this series I am using this week as sort of a benchmark or test run for the show. With Christmas Day I will be hitting my 12-week mark and hopefully make myself an awesome present in terms of just about as lean and mean as possible before, ... well, before I will cram myself with every- and anything my little heart desires. What? You think that sounds stupid? Why would one diet down, just to ruin everything within one day? Well, I guess you have not read the previous installments of this series then. As I've already mentioned repeatedly, if you stay lean year round, keep your body accustomed to burning off extra calories by carefully planned cheat- and refeed-days and don't skimp on your workouts, the occasional holiday binge is not going to have any long-term detrimental effect on your physique. Enjoy your holidays - you have done your homework. It's the lazy rest of the world that's got to feel guilty, not you!

Image 2: No reason to feel guilty! I guarantee, "My 5 Simple Tricks For Guilt Free Thanksgiving Celebrations" will work for every holiday ;-)

How to minimize damage or even progress over the Christmas days? If you have not read them already, I strongly suggest you go back to"My 5 Simple Tricks For Guilt Free Thanksgiving Celebrations", where I describe in some detail how intermittent fasting and keeping your diet in check in the days before and after the holidays will help you to not only compromise your progress, but how you can even make use of a holiday binge as a strategic way of refueling your body and soul ;-) That being said, a related resource you may enjoy are the first issues (esp. Part 2 and Part 3) of the Intermittent Thoughts series, in which Dr.Andro digs into the physiology of intermittent fasting, which - as you all know - has helped me tremendously during this first half of my prep.

With only two more days to go, I am very pleased with how things are working out for me. It looks like I will be hitting my mark… As for the water retention issue, I have been seeing improvements in my physique this week, as in vascularity and separation within my shoulders, forearms, triceps and upper abs. I’ve been pounding at least 2 gallons of water a day to try and flush out as much water as I can. We will see what the end-result on Sunday will look like. I know that I will not be hitting my full potential in conditioning - if I did, the chances that I will be both as muscular, as well as as ripped as possible, on the day of the show, in 14 weeks would decrease, anyways.

Nevertheless, I do feel that I look now about as ripped as when I did the Buckeye Classic last April (cf. image 1). With another 13-14 weeks to improve, I am pretty damn sure that time (and obviously consistency as far as diet and training goes) will take care of the water retention and stubborn body fat I am still carrying. But enough about my 12-week mark! I’ve been bumpin’ my gums about it for the past two weeks, and I’m pretty sure you’re tired of it too. Note: I’ll have pictures up next Thursday on how my physique turns out this Sunday - promise ;-)

Rest, Rest, Rest... and? Well, I guess REST!

Rest, or what some people simply think of as "doing nothing", is in fact one of the most valuable training tools you have. More often than not, it is however taken for granted even by professional athletes and even I commit guilty of taking it for granted in the past, because I had that “gung-ho”,  “rest is for the weak”, or “I’ll sleep when I’m dead” type of mentality. Don’t get me wrong. There's nothing wrong with having a “gung-ho” mentality, but you should be aware of when your body is already "dead" and you begin to take steps back- not forward with every heavy lifting session... train hard, but train smart! Rest, when it’s time to rest, and learn how to listen to what your body wants.

Image 3: A brief update on my initial experience with Slinshot, Recycle and D-Pol by Purus Labs

Quick PurusLabs supplement update (Recycle, D-Pol and SlinShot): For my liking it is still too early to draw any conclusions, but as I promised to keep you up-to-date as far as my newest supplements are concerned, I thought I'd mention that I’ve been getting some pretty decent pumps in the gym, lately. While much of this could obviously be just in my head, I want to remind everyone that this is my deload week, so I’m basically just doing sissy workouts and lifting real light - still, the pump is really noticeable. And when I am practicing my poses, I feel like there was a major improvement in what people like to call the "mind and muscle connection", which is the ability to contract and flex individual muscles intentionally. As with every N=1 experiment, it is however difficult to judge how much of that can be ascribed to Recycle and D-Pol and what may be due to other parameters. With regard to the tarragon based insulin-sensitizer SlinShot, of which I told you that I'd save it for my refeeds, I will probably be able to tell you next week, whether or not it is working. I mean, the plan is to EAT BIG on Christmas, so we’ll see how much "damage" I can do, and whether or not SlinShot can help in repartitioning some of the "damage" into muscle glycogen ;-)

For me the incorporation of carefully planned rest days before it was too late, was the key to what I think is the most profound growth-spurt I have undergone in the past couple of month. Before, I did not only train 6 days a week, I also totally overlooked - or I should say - ignored the value of rest or deload weeks. Not hitting the gym for more than one day? Taking it easy, when you are not hurt? Impossible... no wonder I always felt burned out and sometimes even utterly unmotivated.

Taking more than a day off and the irrational fears of muscle loss, fat gain & co

At first I feared taking too many rest days, especially during contest prep, would hamper my progress. That being said, rationally, I was not even sure what the exact reasons for this gut feelings were. Maybe the fear of...

• losing muscle, when the latter was not constantly challenged during my diet
• not being able to get the most out of my body, or
• not having enough training days to help burn body fat, since I rarely did cardio. 

And, yes, I was one of those guys who used to lift weights constantly thinking about how that would help him burn off body fat, how many calories he would have "left at the gym" and what foods he was now "allowed" to eat after burning X amounts of calories in the course of his last workout. Thus, rather than focusing on increasing my strength and trying to build some lean muscle or at least maintain it, all my efforts in the gym were aimed at simply burning calories - a futile concept, as I have eventually come to realize.

The thought of not having done enough, alway hampered my progress

I know this may sound somewhat ridiculous, especially for the lazy guys out there, but it actually took me a whole lot of courage to finally incorporate more rest days into my training regimen, to take a week off or tick to a pre-planned deload week every 6-8 weeks. The results, however, were well worth it. Adequate rest alone, helped me to ...

• continously increase my strength on all major lifts
• make greater and more consistent muscle gains
• be able to hit the gym motivated and refreshed
• lift really heavy and not just heavy as my exhausted body would allow
• keep injury free

The latter, i.e. the ability to avoid major (and minor) injuries, may in fact be one of the most fundamental benefits you will get if you allow your body to fully recuperate. After all, what could be worse than not being able to hit the gym at all (look at Branch Warren with his torn quads!) For someone like me, who always seems to attract nagging aches, pains and tweaks during long hauls in his training, it was like a revelation, when I noticed that by just taking the necessary week off , I could totally avoid those tedious injuries.

Recipe of the week: In the good spirit of the Christmas Holidays & the birthday of Jesus Christ… I have put together a classic holiday recipe for you: Eggnog, but with an anabolic twist. Cheers!

Image 4: Eggnog - a classic recipe with an anabolic twist!

Anabolic Eggnog - ingredients:

• 4 whole organic eggs (blend in blender till frothy) 
• 1 c. non-fat milk 
• 40g of vanilla whey protein 
• 2 tsp. organic vanilla extract 
• 1 tsp. stevia 
• powdered or ground cinnamon (sprinkle to liking) 
• nutmeg (sprinkle to liking)
• Sailor Jerry’s spiced rum is optional ;-)
  
  Macros: 71g protein / 12g carbs / 20g fat

After blending the eggs till frothy, add all the other ingredients and blend till frothy, and you can add a couple more sprinkles of cinnamon on top to make your drink look fancy. ;-)

And just to make sure, you are getting the message: The type of Rest, we are talking about, here is not the time it takes to take a nip from your water bottle in-between sets (even if it has BCAAs in it ;-) It also does not mean hitting on the beautiful girl on the stairmaster instead of finishing you HIIT session. Rest, is the time you are spending out of the gym. A day, you spent with friends or family, where you treat your run down body with good nutrition and extra sleep. A day, where you get yourself a massage, take the dog for an extended walk and take your girlfriend out to a fancy restaurant that also carries bodybuilding friendly foods. And of course a day, where you have lot's of time to go and check out mine and Dr.Andro's posts, here at the SuppVersity, to learn new things about exercise and nutrition and to join the discussion... so, what are you waiting for, then? Go for it and rest... Merry Christmas, everyone!

CLnA, the "Omega-3 Variety" of CLA from Pomegranate & Co, Has Potent Anti-Obesity Effects and the Potential to Become More Than Just Another Anti-Diabetes Drug.

Image 1: Pomegranate - I loved to eat them even before I realized that their seeds are the #1 dietary source (83%) of punic acid.

While more and more people are beginning to grasp the notion that with (naturally occurring) fats - as with everything else in life - there is no simple "good" and "bad", no clearcut "black" and "white" and no definite "beneficial" and "detrimental". The number of different fatty acids and their respective effects on the human metabolism is so vast that it is pretty hard to keep track of all those varieties of saturated and unsaturated carboxylic acids. I would thusly not be surprised if you simply assumed that the "n" in the headline of this blogpost was a type that had slipped in because poor Dr.Andro is chronically stressed from Christmas shopping... well, while the latter is actually correct, the former is not: CLnA is actually the omega-3 variety of the famous conjugated linoic acid (CLA), which in and out of itself is not a single but a group of 28 different trans- and cis-isomers that occur in our diet mainly in the shape of high and full-fat meat and dairy products.

CLnA - Conjugated Linolenic Acid is not a typo ;-)

Within the last couple of years even the medical establishment has come to realize that the chronic omega-6 (n6: linolic acid) overload in our diet is killing us. The "heart-healthy" PUFAs have now become the more and less heart-healthy PUFAs with the totally healthy *rofl* omega-3s and the not just as healthy omega-6s - both, of course, still totally "essential" and WAY better than saturated fats,... (attention: the afore statements are full or irony! Saturated fats are of course NOT the bad guys. Sorry, David if that lead to confusion)... but I am getting derailed, here. So let's get to the point. What every reasonable person appears to agree on, these days, is that we have to lower the ratio of n6:n3 fatty acids in our diets. Now, I am asking you: Has it ever occured to you that CLA essentially is an omega-6 fatty acid? I mean its conjugated linoleic acid - "linoleic" as in omega 6 = linoleic acid! Probably not, right? The reason for that is yet (hopefully ;-) not that you are dump, but simply that the existence of an omega-3 "variety of CLA", namely conjugated linolenic acid, or short, CLnA, is something about which you will only hear, when you read blogs (such as the SuppVersity ;-), which do not stick to copying, pasting and commenting the stuff the authors have read on one of the major news-portals.

Table 1: CLnA isomer content in natural sources (data adapted from Hennesey. 2011)

From a molecular perspective,  CLnA isomers combine the conjugated double bond system of the classic conjugated linolic acid, you know, with the octadecatrienoic fatty acid (C18:3) structure of omega-3s, i.e. linolenic acid. Interestingly, this make-up confers these fatty acids with a high bio-active potential. Now, while this may sound like one of the frankenfood test-tube results of the gene-technology laboratories of Monsanto, we know at least 10 CLnA isomers which occur naturally in foodstuff or as byproduct of fermention processes (cf. table 1).

Adiposity, hyperlipidemia, cancer - CLnAs could help with all!

Image 2: Even if CLnAs would just prevent obesity, this illustration I borrowed from multiplemyelomalifeexpectancy.tk, shows that not being / getting obese alone would prevent a plethora of related maladies. Such as kidney failure, arthritis, gallbladder disease, infertility, asthma, fatty liver disease, sleep apnoea, depression, heart disease, hyperlipidemia, diabetes,... basically every major ailment the increasingly obese convenience society of the Western hemisphere is suffering from.

Due to their anti-adipogenic (meaning preventing the accumulation of body fat) effects CLnA fatty acids have been investigated as potential candidates for the treatment of the obesity epidemic for quite some time, now (Hennesey. 2011). In a 2002 article that was published in the Journal of Applied Biochemistry and Biotechnology, Nishimura et al. report that CLnA isomers exert apoptotic effects on mouse preadipocyte 3T3-L1 cell - or, in plain English, incubation with CLnA did not only hinder the "pubertal" fat cells from becoming mature adipocytes, it actually killed them. In vivo studies with rodents, such as Arao et al. (2004), where the administration of a diet that was enriched with 1% pomegrenate seed oil lead to a 27% reductin in omental white adipose tissue, were able to confirm the "rodent-real world signficance" of these test-tube results.

Other studies showed a normalization of hyperlipidemia in rodent models of the metabolic syndrome and a hand full of studies have explored the usage of CLnA isomers as cytotoxins in the treatment of cancer. In their concise review of the literature, Hennesey, et al. thusly rightly conclude that with their "potent inflammatory and immune modulating properties", their ability to "reduce the risk of obesity, improve cardiovascular health, and mediate strong anti-carcinogenic activity", the use of CLnA isomers or dietary enrichments could offer treatment strategies for pathologies, which "represent some of the greatest mortality risks to humans in the Western world and have been inextricably linked with diet" (Hennesey. 2011).

Adding diabetes to the list of potential targets for CLnA

For today, we are however going to focus on the most recent result from the research front: The effects of CLnAs on diabetes, or, to be precise, the increases in blood glucose, and decreases in anti-oxidant capacity that go hand in hand with the latter. In a recently published study (Saha. 2011), Siddhartha S. Saha and Mahua Ghosh from the Department of Chemical Technology at the University College of Science and Technology of the University of Calcutta (I don't have to tell you that this is in India, do I?) injected male albino lab rats with 60mg/kg streptozotocin (STZ) - this is a common and well-established method to induce a metabolic state that serves as a model of type II diabetes - and fed them diets that contained either no, or 0.5% of the total fat in the form of alpha-eleostearic acid (from bitter gourd, cf. table 1) or punic acid (which was in this case taken from snake gourd oil, but could as well have been extracted from the eponymous pomegrenate, cf. table 1).

Figure 1: Relative blood glucose levels vs. non-STZ injected control in streptozotocin injected rats over the course of the dietary intervention (data calculated based on Saha. 2011)

As you can see in figure 1, this 100% natural "food additive" had a more than pronounced effect on the +300% (vs. non STZ-injected control) elevated blood glucose levels of the "type-2 diabetic" rodents.

Figure 2: Relative level of lipid peroxidation (left) and total antioxidant capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)

And while the glucose levels were still 150% above those of the healthy control levels, the streptozotocin-induced lipid peroxidation in plasma, pancreas and erythrocytes of the lab animals was ameliorated by the snake gourd oil treatment (remember that is the stuff from pomegranate) and even reversed by the bitter gourd diet. Judged by the standardized FRAP assay, the "diabetic animals" that were fed a diet that contained 0.1% alpha-eleostearic acid (of the total diet, which had 20% fat) even exhibited a 10% greater total antioxidant capacity than the totally healthy control!

Figure 3: Relative expression of inflammatory cytokines, TNF-alpha and interleukin 6 in plasma capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)

Snake gourd oil, on the other hand, exhibited more profound effects on the elevated TNF-alpha, interleukin-6 and NF-kappaB levels of the STZ-treated rodents (cf. figure 2) and thus, at least this is my humble opinion, render punic acid the overall more promising agent with respect to the treatment of all sorts of inflammatory (or related diseases). After all, disturbances in the regulation of the nuclear factor kappa-light-chain-enhancer of activated B cells  (NF-kappaB) and the downstream over-expression of TNF-alpha and IL-6 are hallmark features of allmost all the aforementioned ailments of the increasingly obese western convenience society. This is also why I am quite certain that we are going to hear much more about the CLnAs in the month to come... and I guess, I don't have to tell you that right here, at the SuppVersity, is where you will read about respective studies first!

Mobile Contraception: 850Mhz GSM Mobile-Phone Radiation Reduces Sperm Vitality, Membrane Integrity and Motility.

Image 1: If you carry your phone in your pocket, you reduce your sperms chances to hit a home run ;-)

I don't know if you actually realized that there is a separate category "sex" in the navigation bar of the SuppVersity. Well, I guess if you have, you will probably have been disappointed when you hit the respective button, because sexually exciting news from the realms of exercise and nutrition science are scarce and even today's blogpost is probably not exactly what you would expect when you read the word "sex" on the Internet. If you come to think about it from the increasingly popular paleolithic point of view, sex is however nothing but a means of reproduction, our ancestors have been practicing... well you know the whole ancestral litany ;-)

2,000,000 infertile couples in the US and the figures keep rising

What I am really driving at, here, is that for way more of your fellow human beings than you may think sex becomes a meticulously planned undertaking in a pairs hitherto futile endeavor to parent a child. According to the most recent figures from the American Pregnancy Association, a total of 2,000,000 married couples are considered "infertile" and the figures keep rising year by year and while infertility can have many reasons, of which stress, bad nutritional habits, diabesity and metabolic syndrome are recurrent topics here at the SuppVersity, the "contraceptive potential" of electromagnetic radiation is largely ignored by the iPhone-addicted American (and European) public. Thusly, I personally found it not very surprising that the most recent scientific evidence for the anti-feritility effect of GSM mobile radation (850Mhz, yes the same your beloved iPhone uses) comes from a study that was conducted by a team of researchers from Saudi Arabia, Egypt and Libya, countries where having more than a single spoiled child is still the norm and not the exception - even among academics.

Image 2: Would you buy underwear from this guy if I told you that he is from the Swiss company Isa Bodywear and sells what he claims is radio-protective slips for 29CHF per piece? No? Even if I told you that the experimental approach from the study at hand was valid?

Update: A brief note on a clever objection regarding the real world significance of this kind of artificial experiment. Darko Zdravić, argued not without good reason on Facebook, that putting a mobile phone next to some sperm in a dish was not exactly a perfect model for the little buggers in your scrotum; and without question, Darko is right. I had in fact thought about that myself before and dug up an even more recent study that is going to be published in the physics journal Health Physics in January 2012, which deals with the validity of this approach and then simply forgot to mention that in the "original version" of this article. According to Mouradi and his co-workers, who constructed an artificial scrotum to test the "protective" effect the multiple tissue levels under which your sperm usually reside, the model is adequate, but you would have to subtract 0.8-1.2cm from the distance that is used when no absorbing tissue is placed in between the sperm and the EMR emitting device (Mouradi. 2012). That being said ~4cm is still about the mobile to sperm distance you would get when you put your phone right into the pocket and don't forget that your beloved iPhone radiates even more intensely than the Nokia phone used in the study ;-)

For their research, Mohamed A. Dkhil and his colleagues collected semen samples from 20 healthy donors, including only donor specimen, which had sperm parameters within the normal range defined by the WHO. The subsequent separation procedures, which somehow sound like they were events in the SpermOlympics, involved a so-called "swim-up test" (I guess I don't have to tell you what part of the lifecycle of a sperm requires some serious up-ward swimming ;-), by the means of which the "best" swimmers, which would obviously have the greatest chance to inseminate the ovocyte, were selected. 50% of these "performance athletes" were subsequently exposed to the electromagnetic radiation of a Nokia73 GSM phone (SAR 1.46W/kg which is about the same specific absorption rate the independent German computer magazine measured for the iPhone4S with 1.62W/kg in UMTS mode) at 5 cm distance, which is similar to carrying the phone right in the front pocket of your jeans.

Figure 1: Reductions in vitality, membrane integrity and mobility of previously healthy (elite ;-) sperm after 60-min exposure to cell-phone radiation (data adapted from Dkhil. 2011)

If you take a look at the data in figure 1 you will have to realize that 60 min of this "totally benign" type of EMR reduced the number of vital sperm (as measured by eosin test), increased the number of sperm with membrane defects (as measured by HOS test) and reduced their total motality by ~88%. If I do now tell you that all those effects had a statistical significance way below the cut off of p<0.05, I hope that you will probably agree with the scientists assessment that their results provide an experimental validation of previous epidemiologic data from Fejes et al. (2005) Erogul et al. (2006) and others, who have been warning the public for years that "the prolonged use of cell phones may have negative effects on the sperm motility characteristics." (Fejes. 2005).

And by the way, even if your sperm survive the chronic electromagnetic assault, chances are that the chronic stress of being within everybody's reach 24/7 will finish them off. So, regardless of whether you want or do not want to father a child in the near future, I suggest you reconsider whether or not it is really necessary, let alone desirable to be enslaved by an electronic gadget and the people at the other end of the wireless line.

The Fat Truth Behind the Dairy Weight Loss Miracle: MUFA and PUFA Impair, Saturated Fat and Plenty of Micronutrients Drive Full-Fat Dairy-Powered Fat Loss.

Image 1: Kids who drink more milk, tend to be leaner... and that despite (?) the fact that this stuff comes out of an animal and is full of bad cholesterol and fat - outrageous ;-)

Plenty of interesting news, lately, so this one - just like the recently released hypertrophy / hormone correlation study by Stuart Phillips, about which I have been talking in yesterday's installments of the Intermittent Thoughts got somewhat delayed. With the Christmas holidays and the approaching and all those New Year's weight loss resolutions (I would prefer the term "fat loss resolution", though ;-) already on your mind, I do yet think that it is about time to break the news on the "fat" reason for the purported beneficial effects an increased consumption of dairy products during periods of caloric restriction appears to have on weight and more specifically body fat loss (Linn. 2000; Peirara. 2002; Shahar. 2010).

Dairy, calcium or simply the right macronutrient composition?

The scientific results I am going to present are taken from a study that was published in the Journal of Nutrition and Metabolism a few weeks ago (Smilowitz. 2011). In a randomized, placebo-controlled study Jennifer T Smilowitz and her colleagues from the USDA-funded (keep that in mind, when interpreting the results, or rather the scientists interpretation of the latter ;-) Western Human Nutrition Research Center assigned their 62, against the background of the rampant obesity epidemic, only slightly overweight young subjects (mean age: 25y; BMI ~28) to a calorically restricted diet (-500kcal) that was specifically designed to "provide comparable levels of macronutrient and fiber, to approximate the average consumption in the US" (35% fat, 49% carbohydrate, 16% protein and 2-3g fiber), which contained either

• 0-1 servings of dairy, with 500mg dietary calcium (from the whole diet) + placebo,
• no dairy (still 500mg calcium from diet), 900mg of supplemental calcium carbonate, or
• 3 servings of dairy, with 1400mg of dietary calcium (from the whole diet) + placebo

Thusly, the study basically mimicked, what would happen if you told the average American to just keep their usual sedentary life-style (the subjects were instructed not to start to exercise or anything like that) and either just reduce his caloric intake by 500kcal, to do the former and to make sure to have three servings of dairy per day, or to just take an additional "healthy" calcium carbonate supplement.

Eat dairy + whatever you want and lose weight?

Now, interestingly, the subjects were not only free to chose whether they wanted to consume the dairy from low or normal fat cheese, milk and/or yoghurt, they were also relatively free as far as the rest of their dietary choices were concerned so that the detailed analysis of their food-logs allowed for conclusions to be drawn that went beyond the initial scope of the study... but let's take one thing after the other.

Figure 1: Dietary intake (macronutrients in kcal/day) of the subjects before and at the end of the 12-week study period and relative changes in carbohydrate, protein and fat intake (data calculated based on Smilowitz. 2011)

If you take closer look at the analysis of the dietary records the subjects had to keep, you will notice that the minor differences in the dietary prescriptions induced quite profound changes as far as the macronutrient composition of the respective diets was concerned. While the subjects in the non-dairy groups, regardless of whether they received a calcium supplement or placebo, cut back on all the three major macronutrients, the requirement to incorparate three servings of dairy into their meal-plan, alone appeared to suffice to keep the protein intake of the dairy group at a reasonably high level (~72g; which would be 0.96g/kg body weight). The protein intake of the two non-dairy groups, on the other hand dropped to 57g (0.75g/kg) and 54g (0.7g/kg) for the calcium and placebo supplemented groups, respectively.

Figure 2: Changes in body composition and measures of insulin sensitivity after 12-weeks on the high dairy, calcium supplemented or placebo supplemented diets (data calculated based on Smilowitz. 2011)

In view of the facts that the subjects had to stick to the calorically restricted diet for 12 weeks, it should not surprise you that all of them lost a statistically significant amount of body weight (cf. figure 1) and improved their insulin sensitivity (as indicated by reduced insulin levels and HOMA-IR values).What should yet strike your eye are the increased reductions in body fat and waist circumference and the greater increase in lean mass-% in the high dairy group. Now, you will probably assume that this was a result of the higher protein intake, and that may in fact have been the case, as one of my beloved model calculations by which scientists "adjust" their data for whatever they want (usually until the result is in accordance with their hypothesis ;-) revealed that

Dairy product consumption was found to be significantly associated with reduced WC [waist circumference] and %BF [percent body fat], however, these relationships were no longer significant after adjustment [my emphasis ;-] for protein and energy intake and physical activity.

Figure 3: Scatterplot of the partial correlations between reported 12-week mean dietary fat intake expressed as % of total energy and changes in lean body mass (LM) and body fat % (taken directly from Smilowitz. 2011)

Assuming that this "adjustment" yielded valid results it is all the more interesting what a subsequent analysis of the "adjusted" data revealed:

When expressed as a percent of total energy, dietary fat composition was correlated with changes in anthropometrics. Reported MUFA at 12 wk was inversely and positively associated with changes in % LM and % BF, respectively.

Or, in the words of the layman: The greater the relative monounsaturated fatty acid (MUFA) content of the subjects' diets, the more lean mass was lost and the more body fat was retained during the study period (cf. figure 3). Similarly, a higher intake of polyunsaturated fatty acids (PUFA) was associated with lower reductions in waist circumference, and while  the scientists claim that the n3:n6 ratio did not matter, it should make you wonder if it could actually be coincidental that the n6:n3 ratio in the dairy group was 6.6, while the ones in the calcium and placebo groups were 8.7 and 7.9, respectively.

And what about saturated fats? 

Moreover, the USDA scientists mention only "in the small print" that most fundamental (and statistically significant) distinguishing feature of the dairy group, who unquestionably had more favorable weight loss results despite an overall greater caloric intake, was (and I am quoting this from the paper) "a significantly higher intake of SFA [saturated fats] and lower intakes of MUFA and PUFA compared with the calcium supplement and placebo groups". Now, guess where this "bad" saturated fat came from? Well, probably from full-fat dairy! And guess why those "good" MUFAs and PUFAs were missing from the diets of the high dairy group. Well, probably because the subjects ate less "healthy vegetable oils"... ah, and did I already mention that the dairy group also ingested disproportionally (relative to their caloric intake) higher amounts of biotin, vitamin B12, vitamin D and - God forbid! - cholesterol?

Image 2: Even if you like animals, eating their eggs and full-fat dairy products won't hurt them.

So, while the scientists do their best to conceal that all those "bad things", like a high protein intake and nutrient dense real non-processed animal products with their original (saturated) fat, cholesterol and micronutrient content left untouched, are the true driving forces of successful weight loss (and, you bet, also maintenance), I am quite confident that you, as a diligent student of the SuppVersity, would not have needed the doctored... ah, pardon me, ... I obviously meant the well-adjusted results of this study to know that. After all, you are probably just enjoying a rib-eye steak with some delicious melted butter from grass-fed cows, right?

Intermittent Thoughts on Building Muscle: IGF-1 and its Splice Variants MGF, IGF-IEa & Co - Master Regulators or a Bunch of Cogs in the Wheel of Muscle Hypertrophy?

Image 1: With regard to IGF-1 and its splice-variants like MGF, there is probably 10x-100x more bro- than pro-scientific data out there - this does not help us, though, since you never know which of the bro-reports is bogus and which is not.

In view of the fact that we have not covered much ground with the last installment (we did build a pretty solid foundation, though ;-), I will try my very best to steer a middle course between presenting impressive amounts of facts and explaining the complex and in part not even completely elucidated physiological underpinnings of skeletal muscle hypertrophy, or, as the bros would say, getting big and buffed! A pros pros Bro, you will unquestionably have read on one of the myriads of bodybuilding-related bulletin boards how the injection of X amounts of IGF-1 right into the muscle made BigGuns, or whatever the poster's pseudonym may have been, grow "3 inches in 2 weeks"... ok, his profile picture looks impressive, but is that credible? Does IGF-1 really have such profound effects on muscle growth? And about what type of growth are we talking here? The myostatin-negative "ballooning up" of the muscle, which leaves you with overblown myogenic domains and dysfunctional muscles?

IGF-1: Insulin, growth hormone, or what?

To be able to answer these and related question we will first have to understand what exactly this "insulin-like growth factor 1" actually is. From a (bio-)chemical perspective it is nothing but a bond of 70 amino acids which are entangled into a specific peptide structure that is characteristic for somatomedin C, as IGF-1 is also called. Both the "growth" in IGF-1, as well as the "somato" in its old-fashioned appellation already suggest that what we are dealing with, here, is a "growth hormone related" polypeptide. And in fact, the synthesis of IFG-1, which, in the case of the systemically available fraction, takes place primarily in the liver, and is triggered by systemic growth hormone (somatotropin) levels.

Figure 1: Changes in systemic IGF-1 levels after 5-weeks on either a "normal" (=55:15:30 carbs:protein:fats) or a low carb "high protein" (=20:30:50) diet in 8 men with untreated type II diabetes (data adapted from Nuttal. 2006)

The "insulin" in its name, however, is pretty misleading... or I should say people mislead themselves, by not reading  the name correctly: It's not "insulin-growth factor", but "insulin-like growth factor" and the "like" refers to the structure of the molecule and does not imply that it is released in response to insulin spikes, as you may have read it on one of the aforementioned bulletin boards. If you do take a look at the growth hormone and IGF-1 levels of eight male subjects in a 2006 study on the metabolic of 5-weeks on what the scientists call a "high protein, low carbohydrate diet" (Nuttall. 2006), you will see that an increase in protein and fat from 15% to 30% and 30% to 50%, respectively elicited an 34% increase in serum IGF-1 levels over the treatment period, a finding that is corroborated by the recently published results of Matthew B. Cooke and his colleages from the Department of Health, Human Recreation and Performance at Baylor University.

Figure 2: Serum IGF-1 levels in response to whey vs. maltodextrin supplementation and subsequent lower body resistance training (data adapted from Cooke. 2011)

In their randomized double-blinded cross-over study, Cooke et al. had a group of 10 recreationally active men (2-3 non-resistance training exercise sessions per week) perform a lower body exercise program (leg presses and knee extensions, 4 sets, 8-10 reps at 80% of the individual 1RM) with either 10g of maltodextrose or 10g of whey 30 minutes before the exercise bout (Cooke. 2011). The results of the study (equal IGF-1 response regardless of whey or carbohydrate supplementation) imply that even in the short term, in healthy subjects and in conjunction with exercise the ingestion of carbohydrates is not superior to the provision of fast acting protein sources as a means to either increase or maintain systemic IGF-1 levels.

On a side note: The insulin-mediated induction of Akt, which subsequently triggers the phosphorylation of the mammalian target of rapamycin (mTOR) and thusly does its bit to elevate protein synthesis, has no direct relation to IGF-1, which - I cannot emphasize that enough - has a structure resemblance to insulin, nothing more, nothing less. And what's more, the insulin response in the aforementioned study by Cooke et al. was identical in the whey vs. maltodextrin arm of the study.

Systemic vs. local IGF-1 expression: A crucial distinction

If you have been following the daily research updates here at the SuppVersity over the last months, you may now be wondering why I am even caring about those growth hormones (after all you should, after reading the first paragraph, realize that IGF-1 is something like the active incarnation of somatotropin), when Stuart Phillips lab has quite conclusively shown that even the exercise induced elevation of testosterone does not correlate with subsequent increases in muscle protein synthesis. Certainly a good question, but nevertheless not difficult to answer:

1. The previous installments of the Hypertrophy 101 (Part 1, Part 2) should have made it quite clear that protein synthesis alone is not sufficient to grow. Without intra-muscular restructuring / reorganization and the recruitement of new myonuclei from satellite cells, you would sooner or later grow beyond the maximally allowed myonuclear domain sizes (assuming that by whatever means you block the healthy upregulation of mystatin that will prevent that) and end up as an over-muscled but completely dysfunctional wrack.
2. In a very recently published study, the results of which I have actually been holding back, because I thought I would get to them much earlier in this series, the very same Stuart Phillips whose studies are "responsible" (in fact it is the way they are discussed by the lay-press and abused by the supp-companies that is actually "responsible") for the current over-emphasis on acute increases in the protein synthetic response to exercise and/or supplements, reports that there actually was a statistically significant correlation between exercise induced growth hormone release and increases in mean type I fiber (p<0.06) and type II (p<0.04) cross-sectional area (CSA) in 56 healthy previously non-resistance trained healthy young men in response to a 12-week, 5-day per week resistance training regimen (West & Phillips. 2011).
3. While we have hitherto been talking about systemic IGF-1, it has become evident in the course of the last decade that the hepatic IGF-1 output, which is the main determinant of circulating IGF-1 levels, has little to no impact on the IGF-1 induced increases in skeletal muscle mass and remodeling of muscle tissue that has been previously studies in Petri dishes. In fact, recent research suggests that, just like the liver produces IGF-1 for "the whole body", muscles produce their own IGF-1, or I should say, their own IGFs-1, whenever they are challenged to grow and/or repair (Velloso. 2010), and that the decline of muscle mass with age is at least in parts attributable to a defect / reduction in the expression of local IGF-1 splice variants (for an explanation of what this is, see red box below).

If we now count 2. and 3. together the result is not 5. but rather that it is the growth hormone mediated, exercised-induced local expression of IGF-1 splice variants, which drives the repair and restructuring process that allows for continuous (healthy) muscle growth.

Did you know that the intra-muscular (=autocrine, meaning directly in the tissue where it is supposed to work) "construction process" of the mature 70 amino acid polypeptide IGF-1 gives rise to three different splice variants of insulin-like growth factor (note: the structure of IGF-1 gene does theoretically allow for 6 variants)? And though we are just beginning to understand the physiological roles of IGF-IEa, IGF-IEb and IGF-IEc, also known as MGF (mechano-growth factor), their distinctly timed expression in response to physical overload appears to constitute one of the major driving forces of myocellular hypertophy.

In order to fully understand the role "the" insulin-like growth factor 1 plays in the physiology of muscle growth, it is thusly important to realize that the common perception of IGF-1 as a systemic hormone is, at best, incomplete - I would even venture to say that it is totally flawed.

MGF?! Yeah, I have heard of that one!

Figure 3: Stained myocyte migration (top) and infiltration (bottom) essays for IGF-1 and MGF; more stains = greater effect (taken from Mills. 2007).

Of the three primary splice variants that are expressed in skeletal muscle, IGF-IEc, or MGF (Mechano-Growth Factor) has probably received the greatest attention - so much attention that even the aforementioned bros, will probably have grasped the notion that this is somewhat of a local isoform of IGF-1 which is expressed in response to exercise induced muscle damage and could potentially be the magic bullet to grow beyond what we have hitherto believed to be possible... and, guess what, in essence this appears to be correct.

In one of the earlier studies on the cellular effect of MGF, Yang et al. were able to show that MGF stops the IGF-1 mediated cell differentiation process (in practice this means that it stops the satellite cells from differentiating = specializing and becoming muscle cells) and increases their proliferation. Or put more simply: While in vitro exposition to IGF would suffice to build muscle, as long as there are enough progenitor cells (satellite cells) available, MGF is necessary to replenishes the satellite cell pool of which you have learned in the previous installments that it is necessary to a) repair damaged muscle tissue and b) increase the number of myonuclei in order to grow beyond the physiological growth limit that arises due to the muscle-type-specific upper limit to the myonuclear domain size (cf. previous installments).

Figure 4: Cell proliferation data in response to MGF treatment after blocking the IGF-I receptor.

As the data in figure 4 goes to show the effects of the complete polypeptide IGF-1 and its splice variant MGF appear to be mediated, at least partly via distinct receptors. And while recent research suggest that MGF also exerts similar effects on tendon (Olesen. 2006), brain (Dluzniewska. 2005) and nervous tissue (Aperghis. 2004), our primary concern here, is its pivotal role in muscle repair, which involves the activation of satellite cells, their proliferation (Yang. 2002) and migration (Mills. 2007).

A series of studies by Hammad et al., which was originally intended to investigate the effects of age on the expression of the different IGF splice variants, goes to show that the "muscle (re-)building effects" of MGF are not restricted to the test tube. In their 2002 study (Hamed. 2002), the researchers were able to show profound increases in the MGF expression in the quadriceps muscles of 8 healthy young men (age 29.5 ± 1.5 years, body mass 81.1 ± 2.4 kg, height 179.3 ± 1.8 cm) 2.5h after a single muscle-damaging leg-extension exercise (10 sets of 6 repetitions at 80% 1-RM, 2 min rest between sets):

Figure 5: MGF (ng mRNA / 10^8 µg RNA) and IGF-IEa ng mRNA / 10^5 µg RNA) expresion in quadriceps muscle of young subjects before and 2.5h after 10 sets of 6 repetitions at 80% 1-RM on a leg-extension machine with 2min rest between sets (data adapted from Hamed. 2002)

If you take a closer look at the data in figure, you will probably notice that there was one subject with an extreme MGF response, the scientists explain by a particularly high type-IIx fiber content of the quadriceps of this individual. If you remember the mouse studies and the analysis of the muscle composition of bodybuilders from the previous installments, you will be aware that the shift from type IIb to type IIx muscle fibers is one of the main characteristics of "getting real big". The extreme MGF response (>10x higher than the mean MGF expression across the other subjects) in this subject thusly suggests the increased growth capacity of type IIx muscle fibers is in part due to their ability to release MGF in response to strenuous exercise and thusly multiply / replenish their satellite cell pool to prepare for future growth.

Figure 6: MGF (ng mRNA / 10^8 µg RNA) and IGF-IEa ng mRNA / 10^5 µg RNA) expresion in quadriceps muscle of young subjects after eccentric HIIT exercise on cycle ergometer (data adapted from Hamed. 2008)

Interestingly, a 2008 follow up study (this time involving nine healthy young men aged 20–27 years, cf. Hamed. 2008) with a completely different training protocol that consisted of

60min of opposing the rotation of the pedals down to 60 r.p.m. Subjects performed the following program of six working intervals: six working intervals: 0–6min at 50%, 6–12min at 75%, 12–20min at 100%, 20–25min at 130%, 25–40min at 100% and 40–60min at 75% of the load  eliciting concentric VO2max

illicited surprisingly similar results (cf. figure 6). And in both cases, it appears to be the MGF splice variant not the IGF-IEa variety that drives the short term (hours to days) response to strenuous exercise.

HIIT and resistance training a dynamic duo for MGF expression

Assuming that you are following each and every post here at the SuppVersity (you know you should be ;-), this should remind you of a previous blogpost of mine (cf. "HIT Your Satellite Cells to Increase Your Gains!"), in which I explained that one of the many advantages of high intensity training (not even interval) over classic "cardio" training is that it can increase satellite cell proliferation. Now, with this installment of the Intermittent Thoughts you finally understand, why this is the case.

Image 2: This is not the kind of muscle damage you should be aiming for in the gym.

Now, while protein synthesis and increases in domain size are partly mediated via nutrition, the intra-muscular expression of the IGF-IE splice variants appears (at least based on the current research) to depend solely on exercise, or I should say the wear and tear that goes hand in hand with heavy exercise. In that it seems to be less important, whether you are "pumping away" or "cycling like maniac", as long as its "hard" - to put that into perspective, in the 2008 study by Hamed et al. the subjects underwent ~3600 eccentric muscle contractions in only 1 h, their creatine kinase (CK) levels (marker of muscle damage) increased by +183% and all subjects reported profound muscle soreness.

This controlled amount of muscle damage ties in nicely with the topic of next week's installment which will center around the the intricate relation of the inflammatory response to exercise, the expression of the well-known and less known inflammatory cytokines, TNF-alpha, IL-6 and IL-15 (sorry, Trevor, I have already gone overtime, so your question will have to wait till next week ;-) and the muscle (re-)building effects of IGF-1 and its intra-muscular children.

A Fat D-Ficiency! Do You Really Need More Vitamin D or Simply More Fatty Foods? Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat.

 Image 1: Fatty fish and organ meats aside, whole eggs and full-fat dairy are your best food choices to raise vitamin D levels - I would even venture the guess that they (combined with fish and organ meats) would make supplementation obsolete, even in the Nothern hemisphere (if you "load up" on sun in the summer).

Those of you who have been following my daily blogposts, here at the SuppVersity for more than the last couple of days will be aware that I am one of the few outspoken vitamin D (-supplementation) skeptics. I am by no means doubting the scientific data which clearly indicates that low vitamin D levels (low in medical, not in "Internet blogosphere" terms) are associated with all sorts of diseases. I do not question the hypothesis that, from a biomolecular perspective, vitamin D has more of a hormone than of a "vitamin" (=essential nutrient). And I do not challenge the use of vitamin D(3) supplements by people with low or even borderline low vitamin D levels (although this blogpost may change the way you ingest them ;-). What I do yet call into question is the hilarious idea that every Joe and Jane in the Western hemisphere could benefit from taking "at least 2.000IU of vitamin D" per day.

Re-thinking dietary (=supplemental) vitamin D

Hitherto, the only Joes and Janes who have profoundly benefited from this one-(XL-)size-fits-it-all approach are the producers of respective supplements. Convincing scientific data from controlled studies which would show that the consumption of large amounts >1.000 IU of vitamin D capsule or pill form, exert any verifiable health benefit for someone with normal (or even low-normal) vitamin D levels is absent. The (remote?) possibility that there actually is no benefit, aside, there are yet a few other possible explanations why - epidemiological data aside - scientific evidence for the benefits of vitamin D3 supplementation in a non-vitamin-D-deficient cohort is still lacking:

Image 2: Who would buy all those toxic, but expensive drugs, if it turned out that by taking a non-patentable "vitamin" the diseases they were invented for could be prevented?

1. Lack of financial interest from the side of the pharma companies: Vitamin D is obviously non-patentable and if it could, as many people believe, prevent diabetes, stroke, heart disease and cancer, the use of respective supplements would obviously put the pharmaceutical industry out of business.
   
   Note: The pharmaceutical industry has already been trying to come up with patentable vitamin D analogues, of which they claim that they would lack the largely non-existent negative side-effects of the real vitamin - I guess, you can you tell which way the wind is blowing?!
   
   Financial revenue could thusly be a major factor, as it is obviously pretty costly to set up a tightly controlled, appropriately powered randomized, placebo-controlled study on healthy people. Even large scale epidemiological studies, on the other hand, can be done by a group of graduate students, by just plugging into respective databases and doing some more or less sophisticated statistical evaluations on existing data sets.


2. Insufficient dosing or study periods that are simply too short to yield results: I have, in the past seen studies, even I, as a avowing skeptic, would not cite to underline my argument that we do not have enough scientific evidence that supplemental vitamin D is not the savior people may make you believe. I mean, if you assign a group of say 20 people to 400IU of vitamin D for 4 weeks and see no changes in a handful of pretty random markers of health and disease, this is unquestionably not an argument against the potential usefulness of vitamin D supplementation.


3. Adding vitamin D3 supplements to a "healthy" low fat diet: Assuming that this point has immediately caught your eye, I want to encourage you to read the rest of this blogpost, as this, i.e. the necessity of adequate amounts of dietary fat, to absorb vitamin D3 is what the rest of this post will revolve around.

Fatty fish, eggs, organ meats, full fat organic (raw) dairy products - all those good foods which have been banned from YourPlate (at least if it contains what the US government's MyPlate suggests is healthy) are not only high in vitamin D, they are also high in fat. Against that background and in view of the fact that our ancestors did not buy their vitamin D at the local health food store, it is only reasonable to assume that our digestive tract was designed to absorb the little additional vitamin D we are supposed to get from foodstuff (you know that I am a firm believer in the power of sunlight - even beyond vitamin D) in the presence of fat. And guess what, a recent study, which was obviously not published in the Journal of the American Medical Association (cf. 1. in the previous list of possible explanations for the lack of conclusive scientific evidence on the usefulness of vitamin D supplementation), shows exactly that: without the concomitant presence of significant amounts of dietary fat, even 50.000IU of supplemental vitamin D3 have no effect on the serum levels of 25(OH)D, the active form of vitamin D (Raimundo. 2011, cf. figure 1).

Figure 1: 25(OH)D levels of 30 healthy men and women after ingestion of 50.000IU vitamin D3 supplement in conjunction with a normal or low fat breakfast (data calculated based on Raimundo. 2011)

And, as the detailed macronutrient breakdown in figure 1 (right) shows, the "high fat" breakfast the 30 young (~27y), healthy, non-obese, vitamin-d sufficient men (n=12) and women (n=18) ingested with a 50.000IU vitamin D3 capsule in the morning after an overnight fast, did not even consist of eggs and bacon. It was comprised of whole milk, white bread with bologna, and vegetable oil margarine and the whole milk aside, probably not much healthier than the skim milk, white bread with fruit jelly, and fruit salad breakfast the low-fat group had to eat. The additional 23.9g of fat did nevertheless make a huge difference, as far as the absorption and subsequent utilization of the vitamin D3 supplement is concerned.

No fat, no sun, no vitamin D - regardless of supplementation

Image 3: Get your D from the sun, if you can!

In view of the fact that the subjects were advised to "avoid sun exposure and changes in their usual eating pattern [which were probably low in dietary vitamin D] for the next two weeks", it is thusly hardly surprising that contrary to the "high fat" (I deliberately labeled it "normal fat" in figure 1 ;-) group, the subjects in the low fat breakfast group suffered a -11% decline in 25(OH)D serum levels over the 14-day follow up period, which other than the inter-group difference of 35% (!), did not reach statistical significance (mainly due to the small number of participants, where inter-subject variability renders even relatively profound differences "statistically non-significant").


And while the scientists concede that the small scale of the study, the lack of detailed recordings of the subjects' dietary vitamin D intake in the course of the 14-day follow up period and the reliance on 25(OH)D level as single surrogate for serum vitamin D levels (remember that we are actually talking about a whole host of "vitamins D") are limitations of their study, Raimondo et al. are nevertheless right to conclude that their "findings can have important implications to define the adequate dietary intake of vitamin D"... implications, which may well go beyond the mere recomendation to take your vitamin D with fat. After all, increased absorption would mean decreased need for supplementation and who knows whether you could not easily satisfy your dietary vitamin D requirements without any supplements, if you just set the "low-to-no fat, no dangerous organ meats" dietary recommendations at naught?