4g of Conjugated Linoleic Acid Promote CYP17A1 + Leydig Cell Testosterone Production and Increase Cardio-Mediated Muscle, Strength and Endurance Gains

"That's all the exercise in induced T-response, bro. Now shut up, I got to squat!"

Yes, this is another of those rodent studies of which we simply don't know if the results will eventually translate to humans. In contrast to previous studies on CLA, which dealt with weight loss and produced marvelous results (see "CLA Destroys Body Fat & Increases Endurance!" | read more) which could not be reproduced in human trials.

This very recent paper from Italy deals with CLA's effects on exercise, testosterone, and potential gains in muscle mass and leaves the parameter body fat out of the equation (Barone. 2013).

"Hold on, that's not news, is it?"

When Roy Nelson shot me the link to the pertinent paper by Rosario Barone et al. (2013), the above, i.e. "Hold on, that's not news, is it?" was actually my first thought. After all, I had written about the purported muscle building effects of CLA in the past (see "Review Claims: CLA & Fish Oil Improve "Anabolic" Effects of Exercise - What Does the SuppVersity Sniff Test Say?" | read more). After briefly checking my previous article, I did realize, though: This is news!

The previous article did not discuss the same results. It did however come from the same team of Italian researches and made the claim that CLA & fish oil would be natural anabolics (read it!) - a claim I reviewed and wrote:

"[...] as far as ergogenic and/or anabolic effects are concerned, CLA is unquestionably the more promising fatty acid off the "two" (actually we are talking about four fatty acids, here: DHA + EPA = fish oil and cis-9,trans-11 and trans-10,cis-12 CLA)." (SuppVersity. 2013)

I have to admit, though, that I was thinking of CLA's ability to block the storage of body fat on a bulk, primarily - not so much about its not yet fully, but at least half-way established effects on exercise performance. The testosterone boosting effects, on the other hand, were something I discarded, so that it's about time to look at them more closely.

In vitro + in vivo - that's the way Barone et al. did it

In a first attempt to access the effects of CLA on the testicular androgen production, the scientists from the University and Hospital of Palermo conducted a couple of tests in the petri dish. Usually boring stuff, if it were not for geeks like me (and some of you) who always ask the nasty question: "Why".

Figure 1: The same research group published a paper that showed increased testosterone in young men on a resistance training regimen. It is therefore not totally unlikely that the results do translate to human beings; the figure shows the total testosterone before vs. after a workout in ng/dl (Macaluso. 2012)

In this case, we are lucky, because Barone et al. did not focus solely on the amount of steroids the the leydig tumour cells (don't worry that should work with regular cells, as well) were spilling out. They also tested for enzymatic changes and observed that as 17α-hydroxylase/17,20-lyase (CYP17A1), which converts progesterone into androstenedione and has  been demonstrated to have direct downstream effects on the testosterone production (Svechnikov. 2009; Weisser. 2011).

As every SuppVersity reader knows, the cytochrome P450 enzyme cascade is on of the most powerful and overlooked actors in the steroid orchestrate. While CYP17A1, which does effectively increase the production of testosterone pre-cursors and will thus exert an indirect beneficial effect on the testosterone production, other members of the cytochrome family facilitate the conversion and clearance of testosterone.

Against that background it was sound to expect to observe similar effects in the in-vivo part of the study. The interplay with other enzymes, however, could easily have thwarted the results. Outside of the petri dish the sheer number of variables that could change the outcome of the study makes it more or less impossible to predict the "exact" study outcome and - I want to emphasize this - the latter could well look slightly or completely different from what you see in Figure 2, when you went ahead and tried to support your training efforts with 4g of the patented Tonalin® FFA 80:

Figure 2: Free testosterone and CYP17A1 expression in the supplemented (CLA-) /  unsupplemented (PLA-) mice after 6 weeks of no (SED) or 15-60min (ramp up) of exercise 5x per week (Barone. 2013).

I hope you did notice the important hint I hid in the last sentence above Figure 2, where it says: "Support your training efforts..." If you didn't take a look at Figure 2 ... I guess, it's obvious to see that this short insert is of paramount importance: No training, no CLA bonus!

"The protein expression of CYP17A1 was significantly higher in both the trained groups (PLA-TR and CLA-TR) compared to the sedentary groups (PLA-SED and CLA-SED) (P <0.01). Moreover, CLA supplementation induced a further increase in CYP17A1 protein in the CLA-TR group compared to the PLA-TR group (P < 0.01)" (Barone. 2013)

In other words, training alone is a CYP17A1 powered testosterone booster and CLA is an adjuvant, which has no effect in the absence of 6 weeks with five "cardio" sessions/week at an ever-increasing pace and duration (15-60min and 3.2-4.8m/min from week 1-6).

Figure 4: Body weight gain, and force/body weight gain  (in %; top) and distance traveled relative to SED-PLA group (Barone. 2013)

"Wow that's exciting, isn't it?" Actually no - not really. The increase in testosterone alone would hardly be worth the paper this article is probably never going to be printed on. What is at least borderline exciting, though, are the increase in muscle gains, strength and running distance the rodents covered in a standardized test (see Figure 3).

Yeah, I have to admit: The data does look exciting, but that can be said of the previously referenced study by Macaluso, as well. The said human trial (see Figure 1), however, tells us that it's probably unrealistic to expect similarly pronounced effects with even more CLA (6g in the Macaluso study from 2012) in men.

Personally, I would save the money, but if you want to try it: Go ahead... and tell us if it works ;-)

I, for my part, am missing anecdotal evidence (You can't tell me that there is no one who has tried that already - so where are the "CLA is king, bro!" posts on the various boards?), the confirmation of this or at least similar effects by other scientists and a 'Conflict of Interest' declaration at the end of a paper that puts such an emphasis on the "®" in  Tonalin® FFA 80.

References:

• Barone, R, Macaluso F, Catanese P, Marino Gammazza A, Rizzuto L, et al. Endurance Exercise and Conjugated Linoleic Acid (CLA) Supplementation Up-Regulate CYP17A1 and Stimulate Testosterone Biosynthesis.  PLoS ONE 8(11): e79686.
• Macaluso F, Morici G, Catanese P, Ardizzone NM, Marino Gammazza A, Bonsignore G, Lo Giudice G, Stampone T, Barone R, Farina F, Di Felice V. Effect of conjugated linoleic acid on testosterone levels in vitro and in vivo after an acute bout of resistance exercise. J Strength Cond Res. 2012 Jun;26(6):1667-74.
• Svechnikov K, Spatafora C, Svechnikova I, Tringali C, Söder O. Effects of resveratrol analogs on steroidogenesis and mitochondrial function in rat Leydig cells in vitro. J Appl Toxicol. 2009 Nov;29(8):673-80.
• Weisser J, Landreh L, Söder O, Svechnikov K. Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells. Mol Cell Endocrinol. 2011 Jul 20;341(1-2):18-24. doi: 10.1016/j.mce.2011.03.008.

Honey, Smoke & Testosterone: One Tablespoon of Honey Protects Your Leydig Cells From Oxidative Damage

Image 1: A beehive in one of the beehives Koompassia excelsa (‘Tualang’) trees which grow in the Rain Forest of Kedah, Malaysia.

"Have you already had your tablespoon of honey, Honey?" If that's what your girlfriend or wife asked you this morning, she is probably concerned about your testicular health... A group of Malaysian scientists has recently been able to show that 1.2g/kg/day (human equivalent: 0.2g/kg/day or about 1 tablespoon for an average adult man) of a off-the-shelf Malaysian Tulang honey protected the testis of rats, who had been exposed to cigarette some for 8 minutes three times per day, from damage and oxidative stress (Mohamed. 2011).

Before the experiment, the scientists had conducted FRAP and DPPHI assays to determine the in-vitro antioxidant activity of the sweet gummy superfood from "beehives built on a tall tree, Koompassia excelsa (locally named as ‘Tualang’ tree) that grows in the Rain Forest of Kedah".

Figure 1: Total phenolic content (Eq/kg), antioxidant activity (FRAP; µmol of Fe Eq/L), free radical scavenging activity (DPPH assay % inhibition of DPPH radicals) and sugar composition of the Tulang honey used in the study (data adapted from (Mohamed. 2011).

As the data in figure 2 shows, the anti-inflammatory, anti-oxidant effects of the honey (cf. figure 1), were so pronounced that the +234% increase in TBARS (thiobarbituric acid reactive substance) cigarette exposure induced in the unsupplemented group was completely abolished by the Tulang honey "supplement" (I deliberately put this into quotation-marks, because I would not consider the "human equivalent", i.e. putting a tablespoon of honey in the tea you have with breakfast as "supplement").

Figure 2: Effect of 13 weeks of honey supplementation (H: 1.2g/kg/day), exposure to cigarette smoke (CS: 8 min, 3x daily) or both (H+CS) on oxidative stress markers from rat testis (Mohamed. 2011).

Accordingly, the Leydig cell sections from the "smoking rats" that received supplemental honey (H+CS; -15% Leydig Cell count), did not show similarly pronounced degenerations as their standard fed peers in the CS (8min 3x daily exposure to cigarette smoke; -23% Leydig cell count) group (cf. figure 3).

Figure 3: Representative photomicrographs of testicular sections showing Leydig cells in intertubular space from the control, the cigarette smoke and the honey + cigarette smoke groups (graphic is based on photos from Mohamed. 2011).

Even if, as I would hope, you have not yet seen how "damaged" Leydig cells look like, the photomicrographs in figure 3 leave no doubt that even with the protective effect of honey, 13 weeks of only 24 minutes cigarette smoke exposure wreak havoc on the morphology of those cells of your best parts that are responsible for the production of testosterone.

Image 2: Believe it or not, despite the fact that it has carbs (you could also argue that it is pure sugar!) honey is not only good for your testis, but for your blood sugar levels as well (photo from readmyreview.com)

Just a quick note to all you sugar-haters out there who are afraid that the one tablespoon of honey will give you diabetes, heart attacks and strokes (let alone all those unaesthetic body fat you will gain ;-): A very recent review on the health effects of honey consumptions comes to the conclusion that (Cortes. 2011)

compared to glucose and sucrose, the consumption of honey decreases glycemic levels and blood lipids in healthy, diabetic and hyperlipidemic individuals. Moreover, long periods of honey intake seem to reduce fasting glucose levels in humans, suggesting that honey consumption influences plasma glucose regulation, mainly through a normo- or hypoglycemic effect.

Digest this before you pass on the honey, because "it has carbs in it!" *scary*

So, while we all know that testosterone won't make you aggressive (ScienceDaily. 2009), there is another sort of "testosterone-related" issue that always has me close to freaking out: Male and female tobacco junkies who dare to light their weeds right next to their own kids... and I bet you, those poor little buggers won't be fed a teaspoon (that should be enough given their smaller body weight) of Malaysian Tulang honey a day.