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This delicious Artichoke, Kale, and Ricotta Pie would make an elegant dish for any time of day.



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Baked Mini-Frittatas with Mushrooms, Cottage Cheese, and Feta are great for Meatless Monday.

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It just doesn't get much easier than these Grilled Zucchini and Sausage Kabobs!


(For Phase One Fridays I feature Phase One Recipes from the past that have been my personal favorites, and this recipe for World's Easiest Grilled Zucchini and Sausage Kabobs is something I've made over and over with beef, chicken, or turkey sausage.)


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This Slow Cooker Southwestern Beef Stew with Tomatoes, Olives, and Chiles can be perfect for anyone who's eating Paleo; just skip the sour cream!



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Jake and I loved everything about these Fish Taco Cabbage Bowls!



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Low-Carb and Gluten-Free Swedish Meatballs, and they're baked instead of fried.



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These Stuffed Peppers with Turkey Italian Sausage, Ground Beef, and Mozzarella are great for Phase One

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Kalyn's favorite Phase One Recipes for October 2013 were Greek Salad Spaghetti Squash Bowl,  Slow Cooker Chickpea Stew, Chicken Paprikash, and Turkey and Black Bean Mexican Cabbage Bowl.

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This festive Cranberry Apple Crisp is made with low-calorie natural sweeteners and it's gluten-free!

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Roasted Brussels Sprouts with Pecans and Gorgonzola, wow! Or make them without the Gorgonzola if you prefer!


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So I reached the part of my diet where I need to maximize the amount of fat Im eating, so I thought Id share what Ive been eating.

Im no masterchef but I realize Im not the only one, so this is for people looking for something simple.

• 3 egg omlette 
• 68g salami 
• 60g cheddar cheese 
• 25g butter
• 12g Boursin cheese
• 2 tbl spoons Heavy Cream 

What happens to your muscle, when you train on a low protein diet?

With the publication of Alan Aragons and Brad Schoenfelds excellent paper "Nutrient timing revisited: is there a post-exercise anabolic window?" (Aragon. 2013), the over-estimated importance of the so-called window of opportunity after a workout has been knocked back into reasonable shape. Neither of the two would yet probably tell you to copy the experimental design of a recently published study that was conducted by a team of researchers from the Maastricht University in The Netherlands, the McMaster University in Canada and the University of Nottingham in the UK.

Protein "starvation" and growth potential

Much contrary to the average "window of opportunity study", Snijders et al. did not look at the benefits of post-workout protein supplementation, but at the detriments of not consuming any protein before and after a workout.
To this ends, the scientists put their 21 ± 2 year old male subjects on iso-caloric (=same amount of total kcal) diets with highly different protein content. While

• Table 1: Subject data (Snijders. 2013)

  the normal protein group (NPD) feasted on 1.2g protein/kg ↳ 88/474/60g PRO/CHO/FAT

the poor guys in

• the low protein group (LPD) received only 0.1g of protein/kg ↳ 11/502/56g PRO/CHO/FAT

over the course of the 4 day tightly controlled study period. After following this diet for one day the subjects had to perform a single bout of resistance exercise which consisted of two different exercises, each of which was performed for six:

• horizontal leg press machine - 6 sets x 10 reps @ 75% of the 1RM
• leg extesions - 6 sets x 10 reps @ 75% of the 1RM

The equipment they used were standard Technogym machines and thus as representative of what the average trainee may find in his gym as the antroprometric, body composition and fitness data of the study participants (see Table 1) was representative of the average novice trainees stats.

Figure 1: Total number of myostatin(+) satellite cells per type II fiber - left; rel. change (% of baseline) in type I+II fiber SC number and size 72h after the workout - right; (Snijders. 2013)

It is thus not unrealistic to assume that the data the scientists got from muscle biopsies of the vastus lateralis that were collected before and 12, 24, 48, and 72 h after the workout are representative of what would happen to any young, normally trained individual, on a quasi no-protein fast:

• A note on satellite cells: As Snijders et al. point out. Mere protein synthesis appears to be enough for short term growth, in the longer run, however, "SCs are required to provide additional myonuclei to allow muscle fiber hypertrophy". Thats old news. The thing the study at hand adds, though, is the fact that the exercise induced recruitement of satellite cells "does not affect the increase in muscle fiber SC". The study at hand is thus the first to show that "the SC response to exercise is essentially dissociated from dietary protein intake and is likely evolutionary conserve" (Snijders. 2013).
  No acute differences in the net reduction in myostatin(+) satellite cells (SCs) - The fast wont have any effects on the number of myostatin(+) satellite cells (SC), in general. In other words, the training will acutely losen the "protein synthesis brake" irrespective of whether you consume or dont consume enough protein.
• Persistent decreases in myostatin(+) satellite cells only in the LPD group - The restoration of the number of myostatin(+) SCs in the fast twitch type II muscle fibers of the vastus will however be blunted - or, put differently, the myostatin expression will remain suppressed for at least 72h.
• Overall increases in total satellite cell content and size around the muscle fibers - The crowding of satellite cells around type I and type II fibers (Figure 1, right) is a crucial step in postworkout recovery, because the SCs "are thought to be the sole source for providing new myonuclei, thereby supporting skeletal muscle reconditioning" (Snijders. 2013).

Unfortunately we do not have the corresponding protein synthesis data, but I would bet that the ostensibly "negative" increase myostatin the subjects in the normal protein group experienced after 48h (+86%) and 72h (+88%) is actually a good indicator that the muscular protein pool was replenished (or even supercompensated) at this time point.

From the Intermittent Thoughts on Building Muscle you will probably remember that the increase in myostatin and the corresponding reduction in protein synthesis would be a perfectly normal - in fact, a very healthy response. A response that prevents the development of huge, but dysfunctional skeletal muscle (learn more). Consequently, we would have to interpret the myostatin reduction in the low protein group as a reaction to the loss, or at least constantly low skeletal muscle protein, a status the consequences of which are similar to those that occur, when you empty your glycogen stores: The muscle cells will do their best to replenish the said nutrient. In this case, this means that lower myostatin and generate an anabolic potential that cannot be fulfilled, though, as long as there is no protein to be "pumped" into the muscle.
References:

• Aragon, A. A., & Schoenfeld, B. J. (2013). Nutrient timing revisited: is there a post-exercise anabolic window?. Journal of the International Society of Sports Nutrition, 10(1), 5.
• Snijders, T., Verdijk, L. B., McKay, B. R., Smeets, J. S., van Kranenburg, J., Groen, B. B., ... & van Loon, L. J. (2014). Acute Dietary Protein Intake Restriction Is Associated with Changes in Myostatin Expression after a Single Bout of Resistance Exercise in Healthy Young Men. The Journal of nutrition, jn-113.

This is what Photoshop and creativity can tell us about aging men.

It has been a while since weve taken a closer look at the effects of testosterone deficiency and its replacement aka TRT. Basically thats why I decided not to waste the interesting findings from a recently published study in the The Journal of Clinical Endocrinology and Metabolism (Yeap. 2013) in the Facebook News. In combination with the findings Xu et al. report in a paper on the difference in testosterone concentrations in young healthy US versus Chinese men the Yeap study does after all make a decent addition to the 269 of hitherto ~1500 archived SuppVersity articles that deal in one way or another with the famous androgen.

Virile men live longer! Ca. 30% longer, to be precise.

If you take a look at the link between serum testosterone, free testosterone and DHT and the all-cause mortality risk of the 16,451 community-dwelling older men from Perth in Western Australia it should be obvious that the third quartile of all these serum values, is where you want your androgen levels to be, if you intend to live to see your 90th birthday.

Figure 1: Relative reduction in all-cause mortality with total and free testosterone levels, as well as dihydrotestosterone levels in quartile 2,3 & 4 vs. quartile 1 (Yeap. 2013)

To quantify: You want to have your total testosterone levels in the 12.56 – 15.75 nmol/L (362ng/dl - 454ng/dL), your free testosterone levels in the 182.66 – 216.34 pmol/L (5.3-6.2 ng/dL) and your dihydrotestosterone (DHT) levels in the 1.34 – 1.83 nmol/L (DHT; 39-53ng/dL) range if you dont want to miss a couple of years of your life.

And while your androgen levels shouldnt be significantly lower, you also dont want them in the fourth quartile, where the all-cause mortality risk begins to rise again. Unless you dont want to lose the ~30% all-cause mortality of being in the zone, you shouldnt let the rumors about a causal (not corollary) link between testosterone replacement therapy (TRT) and the incidence of prostate cancer upset you. Why, well because ...

"[...] to date, no study or review has definitively shown that androgen replacement therapy is an independent risk factor for development of prostate cancer." (Fisher. 2012) 

The thing you should ask yourself is thus whether you really want to give up on this 30% reduction in all-cause mortality, or the decrease in fatal cardiovascular events, Ramasay et al. list next to the reduction in body fat mass, and insulin resistance among the proven benefits of TRT in their 2012 review of the literature.

Its your decision and therefore you should make sure that its you and not your doctor who takes this decision. If you decide to help your low testosterone levels along, its your doctors job to help and assist you by ordering and interpreting regular hormone and, as Fisher et al. suggest, PSA tests.

Informed decisions, require information, lab values, and reference ranges!

Speaking about "interpreting" hormone panels. One of the problems youll be facing is that nobody can actually tell you what your normal testosterone level should look like. Of course, every med-school graduate will believe that he knew exactly whats good for you, but when its all said eand done, scientists (and doctors) tend to be a bit too egalitarian, when it comes to "normal ranges". So egalitarian, in fact that they simply assume that a lightweight Chinese pencil pusher must have the same testosterone levels as a 6.6 ft tall, 300lbs heavy Caucasian strongman.

Figure 2: Total and bioavailable testosterone levels in US and Chinese young men (Xu. 2013)

Its thus quite refreshing that Xu et al. followed a different path and followed the heavily underused "Equal, but different!"-princple, when they decided to conuct what they claim is the first study to analyze and compare the total (TT), calculated free (FT), and bioavailable testosterone (Bio T) levels of healthy young men (18–29 years) from the Third National Health and Nutrition examination Survey (NHANES III) in the United States (US) to those of men living in a region of China with a similar living standard to the US, i.e., Hong Kong.

By this means, the researchers wanted to find out whether the potentially existing differences in androgen levels in Caucasian vs. Asian young men would warrant a revision / specification of the "normal" range for men from different ethnic backgrounds.

As you can see the results are not exactly easy to interpret (Figure 2) - is this a difference, or not?

If we take another look at the data in Figure 2 and compare the relative differences between the total testosterone levels of young US vs. Chinese men to those that made a significant difference, in the previously discussed study by Yeap et al. (see Figure 1), we will have to concede that the xisting differences can hardly be significant. They are after all a magnitude smaller than the quartiles in the Yeap study.
That being said, there are at least three additional reason that speak against establishing specific testosterone cut-off values for different ethnic groups based on the Xu study:

1. The Xu study is not representative of "all" Chinese young men: The Xu study compares US citizens in the US to Chinese citizens in China. Who tells us that the values they obtained for young Hong Kongers are valid for 2nd generation Chinese immigrants to the US, as well? Environmental conditions, dietary factors, etc. all that could just as well be the reason for the measured differences as ethnicity-specific genetic differences.
2. The Xu study, or rather the NHANES data is not representative of a specific ethnicity: By analogy to (1), the Xu study, which uses data from NHANES III to gauge the average testosterone levels of male US citizens, relies on data from Asian, African American, Native American, Hispanic and Caucasian US citizens. How on earth would you establish ethnicity specific normal values based on that?
3. Using the Yeap study as a reference to determine "optimal levels" is unwarranted: With old men as study participants, the significance of the optimal total testosterone levels from the Yeap study (12.56 –15.75 mmol/L ≡ 362- 454ng/dL) is about as questionable as the assumption that older men are actually supposed to have significantly lower testosterone levels.

And even if you wouldnt agree that these objections are valid, there would be a simple, yet effective solution to end this discussion once and for all: Measure (or calculate) the free testosterone levels!

If you do that, i.e. compare free instead of total testosterone levels, you will find that the purported ethnic differences disappear. And this is true not solely for the comparison of the data from Chinese and US men Xu et al. analyzed, but also for the existing differences between Mexican-American, non-Hispanic black and non-Hispanic white men in the NHANES study by Rohrmann et al. (2007). Specific reference ranges for Asian, Caucasian, African American, Hispanics, ... are thus probably unwarranted (not sure about Aliens, though ;-).
References: 

• Ramasamy, R., Fisher, E. S., & Schlegel, P. N. (2012). Testosterone replacement and prostate cancer. Indian journal of urology: IJU: journal of the Urological Society of India, 28(2), 123.
• Yeap, B. B., Alfonso, H., Chubb, S. P., Handelsman, D. J., Hankey, G. J., Almeida, O. P., ... & Flicker, L. (2013). In Older Men an Optimal Plasma Testosterone Is Associated With Reduced All-Cause Mortality and Higher Dihydrotestosterone With Reduced Ischemic Heart Disease Mortality, While Estradiol Levels Do Not Predict Mortality. 
• Perry III, H. M., Miller, D. K., Patrick, P., & Morley, J. E. (2000). Testosterone and leptin in older African-American men: relationship to age, strength, function, and season. Metabolism, 49(8), 1085-1091. 
• Rodriguez, A., Muller, D. C., Metter, E. J., Maggio, M., Harman, S. M., Blackman, M. R., & Andres, R. (2007). Aging, androgens, and the metabolic syndrome in a longitudinal study of aging. Journal of Clinical Endocrinology & Metabolism, 92(9), 3568-3572.
• Rohrmann, S., Nelson, W. G., Rifai, N., Brown, T. R., Dobs, A., Kanarek, N., ... & Platz, E. A. (2007). Serum estrogen, but not testosterone, levels differ between black and white men in a nationally representative sample of Americans. Journal of Clinical Endocrinology & Metabolism, 92(7), 2519-2525.
• Traish, A. M., Miner, M. M., Morgentaler, A., & Zitzmann, M. (2011). Testosterone deficiency. The American journal of medicine, 124(7), 578-587. 
• Vermeulen, A., Verdonck, L., & Kaufman, J. M. (1999). A critical evaluation of simple methods for the estimation of free testosterone in serum. Journal of Clinical Endocrinology & Metabolism, 84(10), 3666-3672.
• Xu, L., Au Yeung, S. L., Kavikondala, S., Leung, G. M., & Schooling, C. M. (2014). Testosterone concentrations in young healthy us versus Chinese men. American Journal of Human Biology, 26(1), 99-102.