More Testosterone Boosters: Andrographolide & Quassinoid Rich Fraction from Eurycoma Longifolia. Preview: Science Round-Up - Sesamin, Teas, Muscle Swelling & Growth...

Do you really get along without estrogen when you want to build muscle (read the answer)

You thought I would already have forgotten my promise from last week to tell you about the other potential testosterone & libido (+fertility) boosters? How dare you ;-)! I just wanted to keep thrill of anticipation and in order to prolong that a little further, I will start out - as on every Thursday - with a sneak preview on today's Science Round-Up  (airs on the Super Human Radio Network on 1PM, click here to listen live).

As you may imagine there were not all too many novel papers published since last week. Notwithstanding, I could assemble enough material for the 1h show. According to my current plan, the schedule will look like this:

• the fat burning effects of n-6 sesamin, AA and D-GLA
• the antibacterial effects of raspberry extracts
• fermented green tea and liver protection
• the optimal brewing time for tea depending on your goals
• the futility of using green tea as a "fat burner" in healthy individuals
• muscle swelling and skeletal hypertrophy & training with cuffs
• exercise will make you hungry, you will eat more and still lose weight

... and more if there is still enough time. Ok, I guess you have been waiting long enough, now. So let's take a look at the promised testosterone boosters and their individual effects:

Andrographolide - Never heard of it? The data suggests it may be wort remembering

Don't worry if you have never heard the name "Andrographolide" before, because even if you did, you are probably only aware of the effects the active agent in Andrographis paniculata (Burm. F.) is supposed to have on the gastro-intestinal tract and upper respiratory infections, fever and herpes (Ayurveda), detoxification (TCM) and the prevention and treatment of the common cold (Scandinavia; cf. Mishra. 2007).

Figure 1: Mounting frequency in male rodents receiving 50mg/kg andrographolide (HED: 8.1mg/kg) compared to sildenafi (left) and long-term effects on serum testosterone levels (right; Sattayasai. 2010)

As the data in figure 1 goes to show you it can help you find back your libido and increase your testosterone levels. With the libido effects being not as immediate, but more long-lasting than with sildenafil and the effects on testosterone only after 4 weeks of continuous use, it is yet not a 1:1 alternative for the typical Western immediate satisfaction seeker ;-)

That said, as with all the natural test-boosters the chance that they will translate into muscle gains are pretty slim - and this stuff first has to prove its efficacy in humans.

Eurycoma Longifolia may be worth taking a look at - though for a brief HTPA boost, only

I guess many of you will know "longjack" aka "Tonkat Ali" and who knows some may even have a supplement that was either based on or did at least contain some of a couple of milligrams of it. Now, in case that did not work, the underlying reason may well have been that your extract was devoid or at least low in the active quassinoids the scientists from the School of Pharmaceutical Sciences Universiti Sains Malaysia in Penang, Malaysia, administered to male rats at dosages of 25mg/kg (4mg/kg for a human).

Figure 2: Endocrine effects of different doses of quassinoids from Tonkat Ali (Low. 2012)

As the data in figure 2 goes to show you, this was actually actually the case and the mechanism appears to be mediated by direct effects on the luteinizing hormone release in the hypothalamus.

Now don't get too excited. While previous studies have shown that the change of toxic side-effects is low, the study at hand did also reveal that

Comparing natty test boosters with anabolic agents (read more)

"[...] the over stimulated effect of testosterone production by E. longifolia probably may not be an issue as the peak testosterone level recorded at the first complete spermatogenesis process of 52 days was reduced back to the normal level even though the animals were given a higher dose or prolonged treatment period, due probably to the effect of homeostasis." (Low. 2012)

That said, chances that you will actually gain some muscle mass on this stuff are (as usual with natty test boosters) zero. To give your HPTA a kickstart the LH inducing effect could come handy, though. So if you whacked your natural testosterone production by whatever means, it is worth a try (not as a standalone PCT, however).

That's it for now, so if you want more news, you better don't forget to tune in live to the SuppVersity Science Round-Up on Superhuman Radio at 1PM (EST)

References:

• Low BS, Das PK, Chan KL. Standardized quassinoid-rich Eurycoma longifolia extract improved spermatogenesis and fertility in male rats via the hypothalamic-pituitary-gonadal axis. J Ethnopharmacol. 2012 Dec 19.
• Mishra SK, Sangwan NS, Sanwan RS. Andrographis paniculata(Kalmegh): a review. Phcog. Rev. 2007; 1, 283–298.
• Sattayasai J, Srisuwan S, Arkaravichien T, Aromdee C. Effects of andrographolide on sexual functions, vascular reactivity and serum testosterone level in rodents. Food Chem Toxicol. 2010 Jul;48(7):1934-8.

The Female(?) Athlete Triad - Part III/III: Road to Recovery! Step #2 = Accept There is No Magic Macronutrient Ratio

No need to raid another tomb, Lara, the quest for the one and only ideal macronutrient composition that will yield optimal results for the rest of your life ends here (img courtesy of Paramount)!

I am not planning to bore you with a longish summary of the previous installment(s) of this series, here. Still, I don't want to head on to the 2nd step of the "Road to Recovery", which is going to deal with the quest for the "optimal" macronutrient ratio, without a brief reminder of the central role of nutrient availability in both the etiology, as well as the recovery from the athlete triad - or, as Dr. Zanker from the Carnegie Research Institute at the Leeds Metropolitan University in the United Kingdom puts it, the simple fact that the "exercise associated reproductive dysfunction in women is attributable to deficits of readily available energy" (Zanker. 2006)

In a couple of more general remarks some of you have recently (not without good reason, by the way) criticized my excessive and in parts random use of mark-ups like bold print or underlining. In the introductory paragraph to today's post the word "readily" is however so important that the underlining is obligatory.

Your hypothalamus does not like to wait, therefore "readily" is the keyword, here!

It is after all the lack of appropriate readily available energy, primarily in the form of circulating glucose, liver glycogen, and adipose tissue triacylglycerol that precedes the low plasma insulin concentration and reductions in total body fat content and corresponding disturbance of leptin secretion, ghrelin, cortisol, thyroid and of course luteinizing hormone (see data in figure 1; the absolute levels from the healthy group may also serve as a reference to compare your own labwork to; mind the units!).

Figure 1: Hormonal and glucose metabolism (* indicates 24h values) of women with functional hypothalamic amenorrhea (not necessarily exercise induced) expressed relative to values in eumenorrheic control; values above the bars indicate the total values of the respective markers in healthy controls and may provide you with some orientation, when you are looking at your own bloodwork (data based on Loughlin. 1998)

In order to avoid / counter the reproductive and associated problems and break out of the vicious circle of the athlete's triad, Zanker proposes the following three steps (based on Zanker. 2006; yet with a couple of additions from my side): 

• Avoid abrupt and rapid weight loss and maintain an “adequate” body fat content, which may be individually specific, but coincides with regular reproductive function.
• Consume adequate amounts of energy to fuel your increased metabolic demands; never go below your resting energy expenditure, regardless of whether you  want to or even have to lose weight.
• Make sure you get an adequate amount of carbohydrates either on a continuous (low GI carbs with every meal) or in a cyclic manner as part of a low(er)* carbohydrate diet with a baseline intake of 90-120g/day and additional carbs after every workout.
  *compared to the RDA of ~60% carbs

"Carbohydrates? But aren't those just making you fat?" With this very question that's now probably on the mind of one or two (or three ;-) of you, we did eventually arrive at the topic of this episode of the Athlete's Triad Series:

Is there a ideal macronutrient ratio that will prevent the onset
and help you get rid of the athlete's triad?

To be honest, I don't know the answer to this question... and although I had almost typed the word "yet" win the place where you now see the "..." , I must admit that I am not even sure if there actually is a definitive answer to this question. What I do have to offer, though, is a couple of things to keep in mind, when it comes to the macronutrient make-up of your diet.

1. There is no such thing as a "bad" nutrient. There are about as many good arguments to vilify the overconsumption of protein, as there are arguments against the usual scapegoats, carbohydrates and fats.
2. Glucose and saturated fats can be essential, too. Just because your body can produce carbs and saturated fats on its own, this does not mean that you do not have to, let alone should not eat them.
3. The optimal macronutrient ratio will change over time - just like and in response to the way your physique, conditioning, lifestyle, training and general stress levels  will be changing. This implies that diet X, which may have worked magically for you, when you got rid of slabs of body fat is now that you are finally in the "normal range", let alone already so lean that your body's alarm bells are constantly ringing, hampering your progress.

And even if the previous comments on the importance of readily available energy and glycogen repletion would suggest that carbohydrates should make up the lion's share of the diet of any athlete trying to recover from the triad (or not to fall victim to it), an extreme high carbohydrate alone is neither guaranteed to solve the problem nor is it a sustainable way of eating you could stick to once you've "carbed" yourself out of the dark hole you have been digging over the past months.

Readily available energy? Does that mean I have to eat sugar all day?

Figure 2: Cortisol (left) and testosterone (right) levels in healthy men after 10 days on high protein vs. high carbohydrate diets (based on Anderson. 1987). Tegelman et al. report similar results from Swedish elite male Ice Hockey players after a reduction of fat and an increase in carbs (Tegelman. 2007)

On the one hand, we've known for over two decades that a high carbohydrate diet based on bread, vegetables, fruit, juices, pastry, and candy having a protein / carb / fat ratio of 10% / 70% / 20% will result in lower cortisol and higher testosterone levels (in men) than a high protein diet with a protein / carb / fat ratio of 44% / 35% / 21% that's based on lots of meat, fish, poultry, egg whites, and a liquid dietary supplement protein supplement (Anderson. 1987; see figure 2). On the other hand, a closer analysis of the data I compiled based on the tabular overview of pertinent studies on amenorrheic from the review by Manore (see figure 3 in the last installment) suggests that real.world advantage of carbohydrates depends on the deepness of the whole you already dug (the deeper the more advantageous) and your willingness / ability to cover or even surpass your daily energy requirements (the more you eat on a daily basis and in at least three square meals spread equally across the day, the less you will depend on the readily available energy from carbs).

Against that background, the high carbohydrate intake (62% of total energy from carbohydrates; nutrient ratio in grams 16% protein, 71% carbs, 14% fats) was probably necessary for the women in the eumenorrheic group with an energy intake of slightly less than 30g/kg body weight (figure 3, R5).

Figure 3: Macronutrient compositions (in kcal!) of amenorrheic and eumenorrheic women from 15 different studies (based on an overview in Manore. 2002)

For the eumenorrheic female athletes who were at, or way above the average mean energy intake of 35g/kg body weight, the "high" carbohydrate intake of 265g/day probably wasn't detrimental. On the other hand, it appears questionable, whether an increase in protein intake from 1.2g protein per kg of body weight to 1.5-2.0g/kg and a corresponding protein to carbohydrate ratio of 25% / 62% would not have been more facilitative to their goals (specifically if those include strength training). The same goes for both, the replacement of yet another part of the carbohydrate ration with an isocaloric amount of fats and the overall role of fats in the etiology of and the recovery from the athlete's triad.

The fat-phobia still loomed large, when the majority of studies was conducted

Part of the problem of reconciling theoretical considerations, such as the "availability advantage" of carbohydrates and the scarce and almost exclusively observational data based on which I compiled the overview in figure 3 of this, as well as the last installment of this series, is that eating patterns of both the eumenorrheic, as well as the amennorheic athletes was geared towards the dietary paradigm of the day. With "the day" being the late 1980s and 1990s, i.e. those years in which the fat-phobia literally climaxed, it should be obvious that the baseline diet was low in fat and high in carbs.

Against that background it should also be clear that anyone trying to "cut calories" would reduce the amount of fats, the "bad energy dense heart killers" and keep the intake of carbohydrates constant (=high). This is probably also, the reason that the ostensible disproportionate lack of fats in the diets of the amenorrheic women vanished, once I weighted the data with the number of participants.

Figure 4: Total dietary intake of protein, carbohydrates and fats (in g; left) and differences between women with and without regular menses (right); data expressed either as simple group averages or weighed for the number of study participants (same sources as figure 3)

The picture that emerges after this adjustment has been done (figure 4, right, light bars) is clear and stands in line with my initial remarks on the primary of readily available energy in the form of circulating glucose, liver glycogen, and adipose tissue triacylglycerol, of which at least the former are way more readily derived from carbohydrates than fats.

And even the triacylglycers do, as the name implies, require a certain amount of glucose for the glycerol backbone (could be produced in the liver from amino acids and/or fats, though) and a minimal amount insulin to be stored in the fat cells (can be secreted in response to high amounts of protein and fat, as well, though).

So no fats? Just carbs and some protein?

Yet though carbohydrates have the availability bonus and proteins are necessary to maintain, better even build muscle mass, you would be ill-advised to steer clear of all dietary fats and, even more so the many good foods that contain them. Not so much because of the "essential" polyunsaturated fatty acid, though. According to a study by Tomten and Høstmark the dietary intake of PUFAs in 20 female runners with regular (n=10) and irregular (n=10) menses (LH levels of 7.6 vs. 2.9 IU/l!) was not statistically different. The intake saturated fats (-28%) and even more the intake of MUFAs (-38%), on the other hand was (Tomten. 2009) and the corresponding total fat-intake of 1.1g/kg body weight was obviously not sufficient to maintain optimal hormonal levels in the presence of a training volume of 7.5h per week.

What about vegetarianism? I know a few of you won't like this, but unless you are at least ovo-lacto vegetarian, i.e. a person who eats dairy and eggs, you are going to have a hard time fueling your athletic endeavors appropriately. After all, vegetarianism is associated with hormonal and menstrual abnormalities even in the non-athletic population, when they are dieting (Pirke. 1986). If you combine a mild energy deficit, as it is often seen in vegetarian, let alone vegan athletes, simply because it's harder for them to cover their energy and specifically protein and fat requirements without guzzling omega-6 oils and soy shakes all day (both not advisable, by the way), it is actually not surprising that Benson et al. mention vegetarianism right along low calorie intakes, nutritional inadequacies and low body fat stores as one of the main contributers to the (female) athlete triad (Benson. 1996).

Now you can certainly argue that all this comes down to the energy density and the correspondingly lower overall energy intake and could have been compensated for, if the women with menstrual irregularities had simply eaten more carbohydrates. In view of the fact that they didn't do so, I can hardly refute this argument. On the other hand, we have seen in the previous installment that an overexpression of GH and ghrelin is in as much part of the problem as too little insulin and a pathologically high insulin sensitivity. And some more fat in the diet (alongside carbs / not as the sole energy source!) couId in fact come handy to get that back in check.

Moreover, having a carb to fat ratio of ~2:1 (in energy equivalents) and a baseline fat intake in the range  of 80-100g (total) as the female runners with regular menses in the Tomton sudy had, has the beauty of never having to throw away the egg yolks, being able to get your share of fatty fish, full fat dairy, Kerrygold butter, virgin coconut and olive oil and beef or better calf liver as well as nuts once in a while. This in turn will allow you not just to stay sane and flexible with your diet, but also to satisfy your need for all those vital micronutrients you won't find in any of E-number laden fat-reduced garbage from the "low fat" shelves at the supermarket.

You see, in the end it all comes back eating simply more of the usual suspects, many people would probably file under "a paleo diet with lots of (safe) starches & fruit to fuel the energetic demands of a hard working athlete", these days.

If we think of the hypothetical daily energy requirement of 2000kcal/day which is often used as a reference for the nutrition information on those products of which you are going to buy less in the future (most real foods don't have nutritional information printed on them, you know ;-), the corresponding "numbers" could be anywhere on a continuum

• from 110g protein / 190g carbs / 100g fats, for someone without an endurance component in his workouts*, 
• to 100g protein / 240g carbs / 80g fats for someone who has a major endurance component and / or follows a high volume lifting routine*
  *pre- and post workout nutrition are not included, here!

This approach would ensure that you get enough protein, appropriate amounts of readily available energy, mainly in the form of safe starches and fruit, quasi unlimited amounts of vegetables and so much fat that you don't have to resort to the devastating "chicken breast, rice and broccoli diet", which will only worsen your situation.


References:

• Anderson KE, Rosner W, Khan MS, New MI, Pang SY, Wissel PS, Kappas A. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sci. 1987 May 4;40(18):1761-8.
• Benson JE, Engelbert-Fenton KA, Eisenman PA. Nutritional aspects of amenorrhea in the female athlete triad. Int J Sport Nutr. 1996 Jun;6(2):134-45.
• Laughlin GA, Dominguez CE, Yen SS. Nutritional and endocrine-metabolic aberrations in women with functional hypothalamic amenorrhea. J Clin Endocrinol Metab. 1998 Jan;83(1):25-32.
• Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med. 2002;32(14):887-901.
• Pirke KM, Schweiger U, Laessle R, Dickhaut B, Schweiger M, Waechtler M. Dieting influences the menstrual cycle: vegetarian versus nonvegetarian diet. Fertil Steril. 1986 Dec;46(6):1083-8.
• Tegelman R, Aberg T, Pousette A, Carlström K. Effects of a diet regimen on pituitary and steroid hormones in male ice hockey players. Int J Sports Med. 1992 Jul;13(5):424-30.
• Tomten SE, Høstmark AT. Serum vitamin E concentration and osmotic fragility in female long-distance runners. J Sports Sci. 2009 Jan 1;27(1):69-76.
• Zanker CL. Regulation of reproductive function in athletic women: an investigation of the roles of energy availability and body composition. Br J Sports Med. 2006 Jun;40(6):489-90; discussion 490.

Natural Hormone Optimization Made Simple & Cheap: Avoid These 10 Anti-Androgens to Boost Testosterone & DHT

Image 1: I am not aware of the effect the process of making yourself up has on androgen levels, but the PCPs in many cosmetics could in fact lead to hormonal imbalances.

One of the things you hear and read increasingly often, when it comes to topics such as detoxification, the use of anti-inflammatory supplements or simply increased intakes of omega-3 fatty acids to counter the "hazardous omega-6 overload in your diet", is the analogy of somebody banging his head against a wall asking for a helmet, instead of simply stopping this stupid practice. Likewise, it does not really make sense to invest $50 into an already more or less worthless natural testosterone booster, when, at the same time, you are eating or even supplementing one of the items on the following list of proven anti-androgens:

• anti-androgenic drugs - cyproterone acetate, spirolonactone, flutamide, ketoconazole, finasteride & co.: It stands to reason that your doctor will have had good reason to prescribe you one or the other of the aforementioned drugs; and at least as far as the DHT blocker dustasteride is concerned, diligent SuppVersity students will be aware that it does not compromise testosterone-replacement-therapy induced changes in body composition. In this regard, it should however be mentioned that the pertinent study, I discussed on March 12, 2012 (cf. "Dustasteride Does Not Hamper Changes in Body Composition on Supraphysiological Doses of Testosterone") was not a training study and that, given DHT's hitherto not fully elucidated role in satellite cell recruitment and proliferation, it is well possible that we would have seen differences in weight training athletes.To use these drugs as a means to bolster up your testosterone levels is therefore not just risky and irresponsible, but plain out stupid.
• ATD (1,4,6-androstatriene-3,17-dione): Yes, surprisingly the potent anti-estrogen (aromatase inhibitor) and much-touted testosterone-booster ATD is a relatively potent anti-androgen. You can read all about ATD's anti-androgenic effects in an older blogpost here at the SuppVersity: "Anti-androgenic effect of ATD"
   
• Chaste tree (Vitex agnus-castus): Also sold to help your testosterone levels along, yet even more to counter the scientifically hitherto non-established phenomenon of "progesterone gyno", Vitex is another relatively commonly used supplement of which a 2007 study by Nasri et al. shows that it will probably reduce, not increase your luteinizing hormone (LH) and testosterone levels in parts, but not exclusively via dopaminergic pathways (Nasri. 2007)
• Green Tea (Camellia sinensis): As a diligent student of the SuppVersity you will already be aware of the differential effects of green tea and its catechins on serum testosterone levels; if you are interested, in the details you can read them up in "5 Cups of Green Tea Can Reduce Testosterone by Up to -20%"
• Licorice (Glycyrrhiza glabra): The phytoestrogens in licorice have been shown to reduce testosterone levels in women; glycyrrhizin and glycrrhetic acid exhibit anti-androgen effects in healthy (Armanini. 2003) and diabetic men (Fukui. 2003)  - there is yet also counter-evidence coming from Josephs et al., who were "unable to reproduce" previous results showing a licorice reduced reduction in the conversion of androstenedione to testosterone (Josephs. 2001), since the latter does yet reference a previous study by Armanini et al. the results of which the latter were able to repdroduce in 2003 (Armanini. 2003), it is save to assume that licorice does in fact reduce testosterone levels in diabetic and healthy men and women; and that despite the fact, that a more recent study shows that its corticosteroid (cortisol) modulating effects are probably of greater relevance than its impact on the androgens and other sex steroids (Sigurjonsdottir. 2006)
• Red clover: Extracts from red clover exhibit potent binding affinity to the androgen and progesterone receptor and "theoretical estrogenic activity expressed as equivalent E2 concentration is in the same range as recommended for synthetic estrogen" (Beck. 2003)
• Reishi (LinghZi): Red reishi is supposed to be the mushroom with the greatest anti-androgenic activity. A methanol extract from Ganoderma lucidum has been found to decrease testosterone-to-DHT conversion by up to 80% in a 2005 study by Fujita et al. (Fujita. 2005)
• Spearmint (M. spicata): At least in women spearmint tea has been shown to increase estrogen and luteinizing hormone in the follicular phase of their menstrual cycle (Aktodgan. 2007). In a 2004 study that was conducted on male rodents, on the other hand, the daily administration of peppermint tea (M. spicata) for a period of 30days lead to significant increases in luteinizing and follicle stimulating hormone and increases in serum testosterone, yet with the serious downside of "extensive degenerative changes in the germinal epithelium and spermatogenesis arrest compared with the findings in the testicular biopsies of the control group" (Aktogan. 2003)
• Soy and soy phytoestrogens: It goes without saying that you won't take your girlfriends pill, right? So why do you even remotely consider eating soy, let alone supplementing soy phytoestrogens? "I've seen soy consumption cause impotency in numerous patients." - Dr. John Crisler (male hormone expert) on my facebook wall in response to Jefferson. 2012; avoid feeding soy to your male offspring at all costs (Sherill. 2010; Leraiki. 2011; Siepmann. 2011)
• White Peony (Paeonia lactiflora): Also known as Chinese Peony, the ornamental plant has been shown to contain at least two compounds, 6'-O-galloylalbiflorin and pentagalloylglucos, which bind to the androgen receptor and thusly inhibit its activation by testosterone, DHT and weaker androgens (Washida. 2009).
• Xenoestrogens & Co - BPA (Bisphenol A as in plastics), PCPs (as in cosmetics), etc.: Can inhibit testosterone production by reducing the conversion of cholesterol to androgens (Feng. 2012) and estrogen-like effects (Nakamura. 2010); similar effects have been reported for all sorts of so-called "xenoestrogens", these are synthetic compounds that act as (mostly weak) estrogens in the human body and can induce permanent damage to the endocrine system and resproductive system, specifically in young boys and adolescents. In grown up men and women they have been linked to the development of various forms of cancer (Donovan. 2007).

I know, "avoid this... avoid that..." does not sound half as sexy as "with just three caps of our product you can boost your testosterone levels by up to 123.741%!... but you know what? Other than those red gren, blue, yellow, red and white caps in their mostly black, as of late yet often white (probably to suggest "drug-like" effects) boxes, it's totally free and, more importantly, it works!

Overtraining Research: New Insights into Athlete Triad. Plus: Depression, Palpitations, Urination, Injuries and Weight & Performance Plateaus, the Many Faces of Overtraining

Chronic overtraining is one of the main contributers to the occurrence of often likewise chronic injuries, which persist even, when you finally realized that your own ambition is about to ruin your health.

It's the last day of the SuppVersity Exercise Science Week with a topic of which you actually have read as an aside, or "read up on" note in the previous installments, already: Overtraining and the infamous athlete's triad (read the whole SuppVersity Special here). Since I know that especially the male SuppVersity readers tend to believe they were bullet, or rather overtraining proof by nature, I decided to add a more general follow up to the results of a tightly controlled rodent experiment from the Graduate School of Sport Sciences at the Waseda University and the National Institute of Health and Nutrition University in Japan (Yanaka. 2012), which provide insights into the etiology of the (female) athlete triad phenomenon. A follow up with a potpourrie of studies pertaining to hard to diagnose pathology that goes by the name "overtraining" and is something I guess every training has experienced at least once in his or her career.

The female athlete triad - female only by definition

While Kaoru Yanaka, Mitsuru Higuchi and Yoshiko Ishimi follow the current scientific paradigm and discuss the problem in a female specific context, I want to remind everyone that the athlete triad, which is defined as the triad of eating disorders, amenorrhea, and osteoporosis is in fact female specific (at least I have not yet seen a guy with amenorrhea), but will - in a very different, much more subtle form featuring orthorexic eating patterns, loss of libido and general fatigue - also occur in men.

Figure 1: Time effect of restricted feeding on body weight, food intake and voluntary wheel running in sedentary + ad libitum diet (full filled rhombus; obviously not present in the running distance graph), vol. exercising + ad libitum diet (filled circles) and dietary restricet + ad libitum exercised rats (Yanaka. 2012)

As the data in figure 1 goes to show you, the ergolytic effect on endurance exercise performance was very short-lived and compensated for, when the body weight levels reached a new steady state (see figure 1, left). In other words, once you're caught in the spiral, you will probably not even notice this due to further weight loss and/or noticeable performance declines - specifically if you are not strength training or put an (over-)emphasis on volume training.

Weakening bones and infertility in the presence of (in parts) normal hormonal status

What's even nastier and actually different to human studies, where the "voluntary" exercise is actually compulsive and thus probably way more demanding, is the fact that even some of the hormonal you would expect to be good indicators of the athlete triad, namely estrogen (E2 and osteocalcin (OC), don't differ between the ad libitum and the restricted feeding group.

Figure 2: Levels of estrogen (E2), the bonebuilding protein osteocalcin (OC) and luteinizing hormone (LH) in the sendentary (SED) and voluntary wheel running ad-libitum (RC) and restrictedly fed (RR) rodents (Yanaka. 2012)

That being said, LH remains as the sole, reliable marker of the athlete's triad in response to insufficient food intakes. Whether it is similarly sensitive to overtraining and how the interaction between these two aspects of the athlete triad actually are (beyond increased energy needs in response to exercise) would yet have required a different study protocol, which the rodents being dumped into a container full of water to have them swim to exhaustion on a daily basis. What? That's animal abuse? True. It is however the perfect model for what I see people do at the gym day in and out - the same people who will then tell me that they cannot get rid of their belly fat, although they are "on a calorie deficit, avoid carbs like a plague, eat 100% clean and never miss a workout". My reply in these cases usually is: "You see, and that's why!"

A couple of additional findings on overtraining

Since I know that many of you will simply ignore the above post, because they feel that it does not affect them (don't tell me that's not you, guys ;-), I will summarize a handful of significant findings from general studies revolving around "overtraining" in general.

Table 1: Symptoms of overtraining (Fry. 1992)

• 10 days of 2x daily HIIT induce fatigue and compromise immune system for longer than 5 days (Fry. 1994) -- The five well-trained men (mean(s.d.) age 31.6(3.5) years; members of the Special Air Services Regiment of the Australian Army) who performed 15x 1 min HIIT protocols (2min rest between sprints) and 10 "sets " of the same protocol in the PM for ten days were unable to fully recover from this intermediate overexertion within the following 5 days of active recover.
  
  And while the overall mood disturbance index was remained only nonsignificantly 15% elevtet (p > 0.05), the soldiers felt still 7x more confused, 5x more depressed, 6x more angry.
  
  The exercise performance, on the other hand was restored to normal levels and that despite persistent immune system deficits. This is in line with the findings of the above rodent studies, where the volume of voluntary wheel running was not a reliable criterion to identify overtraining / undereating. So you better be careful about the "well, I did my 10 squats with 250lbs as usual"-mentality that lulls us into the believe that we are fully recovered and just did not sleep long enough and therefore feel fatigued.

• 

  It's not in table 1, but not just in the case report by Uusitalo et al. from 2004, frequent urination (especially nightly) is one of the classic features of severe overtraining.

  Overtraining induced depressive mood state is not related to depressed 5-HT reuptake, but tinnitus, palpitations & frequent urination are additional symptoms of OT (Uusital. 2004 & 2006) -- Contrary to what you could assume the OT induced depressive mood states are not mediated by decreased serotonin reuptake, which means that they will be resistant to the standard treatment with serotonin-reuptake inhibitors (SSRIs). With this study the scientists did by the way refute a hypothesis they themselves had proposed in a study 2 years earlies, where single-photon emission computed tomography (SPECT) of a single patient had suggested that it was a decreased 5-HT uptake that was behind the major depression he had in addition to continuous fatigue, tinnitus in his left ear, disturbing palpitation and pollacisuria (frequent urination) he had developed after upping his training volume by 100% (Uusitalo. 2004)

• High intensity + low rest times = increased risk of overtraining (Szivak. 2012) -- In Szivak et al.'s 2012 study, the 18 trained men (age: 23.5±3.5 years, height: 172.4±4.0cm, weight: 77.8±8.8kg) and women  (age: 22.9±2.0 years, height: 168.4±9.4cm, weight: 68.5±10.4kg) completed high intensity short rest protocol (HI/SR) participated consisting of a descending pyramid scheme (from 10 down to 1 rep) of back squats, bench presses, and deadlifts. The ensuing increases in lactate (IP men: 17.3 mmol·L, IP women: 13.8 mmol·L) and cortisol (+15 men: 1860.2 nmol·L; +15 women: 1831.7 nmol·L) were considerably greater than those produced in typical resistance exercise programs. The scientist interpret this absorvation as indicative of the fact that coaches should implement HI/SR protocols only sporadically, and prefer a gradual reduction in rest interval length with concurrent gradual increase in intensity to minimize potential negative effects such as non-functional overreaching.

• 

  The self-perpetuation viscous cycle of upping your efforts, decreasing your returns and reupping your efforts again is actually the real danger - and I don't care if you call it overtraining or athlete triad + suggest you don' either (learn more)

  Mental exhaustion and vigorous-intensity training are significant correlates of the occurrence of injuries (Vetter. 2010) -- While mental exhaustion during and outside of the competitive season is a risk for chronic injuries in women, in men, only intra-seasonal mental exhaustion correlates with acute injuries, the occurrence of which is likewise increased with the number of vigorous-intensity training days per week, which in turn is a reliable predictor of mental fatigue in the off and on-season. You see, we are going round in circles once more.

• Hitting it hard to frequently will downregulate the beta-2 adrenergic receptor (Fry. 2006) -- If you are fatiqued and stims have long seized working for you, you are likely to be chronically overtraining. That's the practical implication of a 2006 study by Fry et al. who found that subjects who performed 10 x 1 at 100% 1 RM daily for 2 weeks on a squat simulating machine, ended up suffering from a -8kg decrease in their 1-RM max, as well as a -36.3% decrease in mean power at 100% 1-RM loads. While this was to be expected and not actually new, the -37% reduced muscle beta(2)-adrenergic receptor density and 49% increases in nocturnal urinary epinephrine in the overtraining group suggest a
  

  "decreased beta(2)-AR sensitivity for the OT group (2.4-fold increase) [suggesting] that this may be an important contributor to performance decrements due to excessive use of maximal resistance exercise." (Fry. 2006)

  That this will likewise compromise your efforts to lose weight and blunt many of the beneficial fat loss effects you may have in mind, when thinking about brief, hard and frequent training, is not mentioned in the paper and should yet be as obvious as the cardio-protective effect of this adaptations. After all, the beta-adrenergic receptors, which are targeted by endogenous catecholamines and stimulated either directly or indirectly by many stims (most prominently clenbuterol and ephedrine) are responsible for the activation of the sympathetic nervous system, which mobilize the body's nervous system fight-or-flight response, increase the heart rate, widens the pupils, kicks the fat out of the adipocytes to have it available as additional fuel etc.

That's not the breakfast of a champion, that's the breakfast of a complete moron and if that's even remotely to what your breakfast looks like, it's high time to learn about the 3 Simple Rules of Sensible Supplementation

I guess you would like to have some supplement recommendations now, but I won't give you any - aside from the advise to abstain from cortisol blockers and the abuse of stimulants, which are only going to deepen the whole you have been digging (on a related note: I suggest you check out the recent facebook post on the -80% risk reduction for obesity in women with high morning cortisol; Manesh. 2012).

Adequate rest and nutrition cannot be compensated for by any supplements and if you allow yourself both, you won't be overtraining in the first place.

Once you have established that baseline, you are obviously free to use the Three Simple Rules of Sensible Supplementation to optimize your results.

References:

• Fry RW, Morton AR, Garcia-Webb P. Craford GPM, Keast D. Biological responses to overload training in endurance sports. Eur J Appi Physiol 1992; 64: 335-44.
• Fry RW, Grove JR, Morton AR, Zeroni PM, Gaudieri S, Keast D. Psychological and immunological correlates of acute overtraining. Br J Sports Med. 1994 Dec;28(4):241-6.
• Fry AC, Schilling BK, Weiss LW, Chiu LZ. beta2-Adrenergic receptor downregulation and performance decrements during high-intensity resistance exercise overtraining. J Appl Physiol. 2006 Dec;101(6):1664-72.
• Uusitalo AL, Valkonen-Korhonen M, Helenius P, Vanninen E, Bergström KA, Kuikka JT. Abnormal serotonin reuptake in an overtrained, insomnic and depressed team athlete. Int J Sports Med. 2004 Feb;25(2):150-3.
• Szivak TK, Hooper DR, Kupchak BK, Apicella JM, Saenz C, Maresh CM, Denegar CR, Kraemer WJ. Adrenal Cortical Responses to High Intensity, Short Rest, Resistance Exercise in Men and Women. J Strength Cond Res. 2012 May 3.
• Uusitalo AL, Vanninen E, Valkonen-Korhonen M, Kuikka JT. Brain serotonin reuptake did not change during one year in overtrained athletes. Int J Sports Med. 2006 Sep;27(9):702-8.
• Vetter RE, Symonds ML. Correlations between injury, training intensity, and physical and mental exhaustion among college athletes. J Strength Cond Res. 2010 Mar;24(3):587-96. 
• Sedaghat F, Rabiei S, Rastmanesh R. Bassak Nejad S, Poloi Shahpor Abadi F, Davoudi I. The Relationship between Serum Cortisol and Vitamin C Levels with Obesity. Jundishapur Sci Med J. 2012;11(4):341-353 
• Yanaka K, Higuchi M, Ishimi Y. Effect of long-term voluntary exercise and energy restriction on bone mineral density in mature female rats. J Phys Fitness Sports Med . 2012; 1(4): 695-702.