|The cover of the Vogue is usually not the place to turn to, if you are looking for role-models, but let's be honest: Do you believe Hope Solo or Serena Williams suffer from amenorrhea or their fellow Olympian Brian Lochte from low testosterone? I don't think so. So, there must be something "real" athletes do that way too many weekend warriors, who are in it, often to look just like their stars don't do - and in this multi-part SuppVersity Special, we are going to figure out what this may be.|
The main reason I decided to split things up is that I did not want you to simply skip on the fundamental information you will get today and fast forward to the potential solutions to the problem, I will present in the next installment.
After all, the idea of the SuppVersity is not to present cookie-cutter guru advice that may or may not work for you, but rather to put you into a position, where you do at least understand, at best have the skills to question, modify and tweak any exemplary "plans of attack" I will be outlining in upcoming the second part of this series... and if my past efforts to provide you with a basic understanding of your own metabolism have not totally failed, I would suspect that many of you will be able to come up with their own preliminary conclusions after reading this lengthy, but as I hope informative and not overtly complicated first part of the series.
"Female athlete triad:" How the problems start with a false label, already
But my bones are still strong! Specifically the inclusion of osteoporosis as an obligatory criteria for the diagnosis of the female athlete triad is nonsensical and was repeatedly criticized (e.g. Kahn. 2002), as it excludes a large, if not the major part of women (and men) who suffer from a syndrome the prevalence and consequences of which are thus largely underestimated. Moreover, in weight bearing sports, for example the load alone will counter the occurrence of osteoporosis, while other consequences like musculoskeletal injuries will be more prevalent.So, let's initially take a look at what we are actually talking about here. The phenomenon itself is often somewhat misleadingly labeled as the "female athlete triad" (FAT; or AT w/out the sex-specificity), a term which falsely implies that it was sex-specific and men were immune to it and, what may be even worse, that it would be quite easy to diagnose as it comprises a "triad" of
- low energy availability / disordered eating
- amenorrhea, and
How prevalent is this misery?
Even if we don't extend our definition to include overall exhaustion and stagnating performance on the "harmless" and "heart disease" and "sudden cardiac death" on the other "life-threatening" end of the continuum, but simply include low testosterone levels and minor menstrual irregularities into our definition of AT (athlete triad), the answer to the above question is "It is rampant!" So rampant in fact that Luigi Di Florence chose the title "Does the high performance athlete need hormone replacement?" for a talk he held at a recent conference. In the respective abstract (a paper has not yet been published), he states:
"Exercise per se is associated to the release of different hormones: acute exercise stimulates an acute hormones secretion (e.g. catecholamines, growth hormone, CRH-ACTH-cortisol, testosterone) while chronic exercise (training) is able to modify hormones secretion at rest and their activation during acute exercise. [...] besides symptomatic classical diseases or conditions that may reduce/alter the qualitative/quantitative hormones secretion, serious clinical concerns exist for asymptomatic endocrine hypo-function (e.g. sub-clinical hypogonadism, growth hormone deficit and hypothyroidism), particularly in adult athletes. For example, in master athletes we observed an high prevalence of undiagnosed severe (12%) and mild (18%) hypo-testosteronemia frequently in the absence of clinical symptoms. [...] Unfortunately, few studies evaluated the prevalence of reduced hormones secretion in athletes and the concept of adapted hormone replacement in high competitive athletes." (Di Luigi. 2012; my emphases)The absence of a clearcut definition of "the female athlete triad", the ignorance towards the existence of corresponding problems in male athletes (of all age groups!) and the vast differences within different study populations makes it very difficult to quantify, how many men and women actually suffer from AT. The little data we have is obviously sex-specific and of rather qualitative nature, as the following citation from Hobart 2000 goes to show you:
Although the exact prevalence of the female athlete triad is unknown, studies have reported disordered eating behavior in 15 to 62 percent of female college athletes. Amenorrhea occurs in 3.4 to 66 percent of female athletes, compared with only 2 to 5 percent of women in the general population. (Hobart. 2000)If we take the latest NCAA numbers as a baseline (191,131 female athletes in the year 2011) and multiply them by 2x to include those lonesome gymrats and crossfitters out there who are often even more likely to overdo it than their co-ed peers who usually work with a more or less qualified coach, of whom you would expect that he or she is able to call a halt before it is too late, we are talking about ~13,000-252,000 young women and an undisclosed number of young men, here!
"Sh..Sh.. let's not talk about it!"
female exercisers (age 18-40 yr), engaging in ≥2 hr/wk of strenuous activity, Miller et al. questioned for their 2012 study on "the knowledge, attitudes, and behaviors of regularly exercising adult women in Australia", could name the initially mentioned three components of the female athlete triad:.
"Regardless of reported history of stress fracture, 45% of the respondents did not think that amenorrhea (absence of menses for ≥3 months) could affect bone health, and 22% of those involved in lean-build sports would do nothing if experiencing amenorrhea (vs. 3.2% in non-lean-build sports, p = .005)." (Miller. 2012; my emphases)This lack of knowledge and - in parts - even downright ignorance towards the problem certainly raises the question:
"How do I actually realize I am about to develop the (female) athlete triad (AT)?"
I guess, we can derive a (not the!) answer to this question if we take a closer look at an overview of the etiology that has been part of a 2002 analysis by Melinda M. Manore from the Department of Nutrition and Food Management at the Oregon State University in Corvallis, Oregon, USA (see figure 2).
There is hope - even after the horse has bolted
"Men can't be anorexic?!" False! According to the latest data from the South Carolina Department of Mental Health there are currently 1,000,000 male US citizens suffering from eating disorders. Their estimated stake among anorexics and bulemics is between 10-15%. Among adolescents, anorexia is the 3rd most common chronic illness, and many of it's physical features are identical to those of the "female" athlete triad - not the least due to the fact that excessive exercise is often part of the pathology. The boundaries between them are fluid. The mortality rate associated with anorexia nervosa is 12x higher than the death rate of ALL causes of death: 5 – 10% of anorexics die within 10 years after contracting the disease; 18-20% of anorexics will be dead after 20 years and only 30 – 40% ever fully recover.The good news is that our bodies (male and female) are self-repairing machines, evolutionary designed to take beating after beating - esp. if those "beatings" resemble periods of famine. From studies in anorexic men(!) and women we know that many of the pathological features of self-cannibalism (this, and nothing else is what your body is doing, when you constantly deprive it of an adequate supply of energy, as it is the case in the accute phases of the athlete triad) are reversible.
Mont et al. who have been following 31 severely underweight anorexic adolescents with body mass indexes of 15.2 +/- 2 kg/m², sinus bradycardia (=abnormally slow heart beat), decreased left ventricular mass, and diminished thickness of cardiac walls in 35%, 93% and 70%, respectively, report for example:
"After refeeding, a significant decrease in QT interval (p <.05) and QT dispersion (p <.01) was observed. Echocardiograms showed an increase in cardiac diameters (p <.01), left ventricular mass (p <.001), and cardiac output (p <.001). There was also an improvement in the exercise capacity (p <.05) and a normalization of the heart rate and heart rate variability (p <.05)." (Mont. 2012)Allegedly, few athletes will maneuver themselves into a situation, where they are actually so weak that they can barely walk (which is unfortunately the case for way too many young anorexic patients), their susceptibility to sudden cardiac death and other CVD-related diseases is probably even higher, due to the exercise induced chronic overload of their cardiovascular system.
With the athlete's triad an evolutionary advantage is turning is turning against us
Athlete or not, even these severe physical abnormalities usually disappear with adequate rest, lots of patience and, most importantly, a progressive increase in energy intake (the increases in lean mass, i.e. muscle, organ and bone!, wants to be fed and the the metabolic switch from "energy save" to "normal" mode will increase the energetic demands even more). In fact, even in severely anorexic patients, where most of these pathologies are more severe than in athletes, renal abnormalities (Boag. 1985), atrophy of the bone marrow (Steinberg. 1987; Orlandi. 2000), cognitive impairment (Mikos. 2008) and most of the other functions that are related to survival (not reproduction!) usually recover with adequate energy intake, alone.
|Without the evolutionary preserved, catecholamine and glucocorticoid driven "hunger high" our ancestors needed to keep going until they finally found something to eat, neither anorexia (AN), nor the athlete triad (AT) would "work".|
For many, it does in fact feel, as if they had just been hit by a truck, but in fact very truck has rolling right over them for years now and the person behind the steering wheel, was nobody else than the patient him-/herself.
Without the hilarious amounts of glucocorticoids (cortisol) and excitatory neurotransmitters their bodies seize producing, now that they are no longer necessary to keep the brain from dying a hypoglycemic death and the patients able and motivated to "seek for food" (another evolutionary preserved mechanism, by the way), all the weight of years of over-training and under-eating hits them all at once. In conjunction with the unwanted, but inevitable weight gain, of which Golden et al. state that it comes - specifically in this early phase - almost exclusively from increases in body water, organ, bone and muscle mass (Golden. 2004), this often triggers a relapse into the old "cosy" stress pattern of under-eating and over-exercising. And what's really nasty, here, is that this will provide (felt) "relief" within days, if not hours and via the exact same mechanism that has kept the patients going (and later alive!) over the past months and years: HUNGER (not workout) STRESS!
Not BMI, not fat, not exercise, but simply a constant state of energy deprivation is the culprit
Since we are all aware that weight gain does not happen over night, but the aforementioned perceived aggravation of fatigue can, it should be obvious that neither a low body weight, let alone the amount of body fat a person, man or women, is carrying on his/her frame (scientists refer to this as the "body composition hypothesis), nor the exercise induced stress ("stress hypothesis"), of which I have just outlined that it is a necessary and life-saving reaction to starvation, are at the root of the poblem. The true causative factor is (at least according to the current paradigm) the lack of a sufficient and constant supply of readily available energy (we are not talking about leafy greens and chicken breast, here!).
|Evidence against the "body composition" hypothesis: After a surgical reduction of the stomach volume even obese women can develop amenorrhea|
In this context, Anne B. Loucks who worked in the Department of Biological Sciences of the Ohio University in Athens, back in 2005, points out:
"Interest in the body composition hypothesis was rejuvenated several years ago by the discovery of leptin. Because leptin is secreted by adipose tissue cells, it was originally thought to signal information about the size of body fat stores. Rapid and profound declines in leptin were soon observed in response to fasting and dietary restriction, how-ever, and similarly extreme increases were observed in response to overfeeding and refeeding after energy restriction, all before changes in adiposity could occur. These observa-tions led to the revised hypothesis that leptin actually signals information about dietary energy intake. Since then, however, we have shown that the level and diurnal rhythm of leptin actually depend on energy availability (defined as dietary energy intake minus exercise energy expenditure) and that exercise itself has no suppressive effect on leptin beyond the impact of its energy cost on energy availability." (Loucks. 2005; my emphases)In other words, the same hypothesis that initially pointed towards the amount of leptin secreting adipose tissue as a regulator of the hormonal balance in amenorrhetic women (the "body composition hypothesis"), does now, that it appears clear that energy availability and not body fat stores determine the secretion of leptin, clearly indicate that body fatness is a subordinate (as being the consequence of constant dieting) indicator of a persons susceptibility to suffer from hormonal imbalances, at best.
For similar reasons, the "stress hypothesis" which points with a finger at the exercise induced increases in cortisol is bullocks, as well. After all, those increases in cortisol and catecholamine expression are - just like low leptin levels - a necessary and healthy adaptation to the absence of a constant and adequate supply of energy. Without the glucocorticoids (just in case you still don't get it: "gluco" as in "glucose" <= the stuff everybody is scared about these days) no athlete or anorexic patient would be able to maintain normal blood glucose - without any cortisol, they would simply die.
Evidence for the "energy availability hypothesis"
|Figure 4: 24h-LH profile in healthy women after 5 days of normal (top) as well as calorically restricted (-33, -66, -87%) nutrient intake (arrows indicate meals, the black bar indicates sleep).|
In this regard, the profound disturbances in the pulsatile release of luteinizing hormone (LH) from the gonadotroph cells in the anterior pituitary gland, Loucks et al. observed after only 5 days of
- 33% - lower LH amplitude
- 66% - increased amplitude decreased frequency
- 77% - further decrease in frequency + increase in amplitude
Don't forget to come back next week for part II!
In other words, if you want more about the role of the thyroid gland, of adiponectin and insulin sensitivity, of ghrelin and growth hormone, of insulin and IGF-1 and the circadian clock and intermittent fasting in the etiology of the athlete triad and which tweaks to your nutrition, exercise and supplementation regimen can help you not end up in a viscous circle that will not just hamper your perfomance, but compromise your physique and physical and psychological well-being, come back next Sunday for part II of the SuppVersity Athlete's Triad Special.
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