Sunday, June 2, 2013

Overtraining, Undereating & Self-Inflicted Hypothyrodism: Thresholds for Low T3 and High Reverse T3 Levels at 8% & 15% Reduced Energy Intake + Exercise After Only 4 Days!

This is not a "woman thing" only and your T3 levels are not the only thing that's going to "fall flat" if you starve yourself through your workouts! Yep, low libido => low total testosterone => low free testosterone => hypogonadism, that's what we are talking about, guys.
While I did promise to summarize some of the things, I said about creatine kinase, ALT, AST & Co on the last installment of the SuppVersity Science Round-Up on the Super Human Radio Network (I will do that in a future blogpost), today's SuppVersity article will focus on a single and in my experience often misinterpreted and / or overlooked symptom of overtraining that I personally have encountered numerous times in both male and female trainees: Self-induced hypothyrodism, low T3- or the euthyroid sick syndrome are just a couple of names that have been used in the science and laypress to describe this peculiar result of the way trainees deliberately ruin their metabolism by training for hours day in and day out, while following a diet that would hardly nourish a sedentary person, let alone the athlete or fitness model whose physique they are aspiring to achieve.

Pertinent studies are scarce, but they exist

I don't know if the shortage of scientific evidence is a result of the general ignorance of professional athletes, trainers and above all the "average gymrat" that he or she has an organically  healthy thyroid that's just shut off by your body in order not to waste precious muscle and organ weight in a state of constant catabolism.

Despite the scarcity of research, there are two pertinent studies from the Department  of  Biological  Sciences at the College  of  Osteopathic  Medicine of the Ohio  University. Both studies were published in the early 1990s and deal - as you would expect it with female subjects (with no recent history of dieting or weight loss were recruited from the university and surrounding community) who were randomly assigned to a 3x2 experimental design of aerobic exercise and energy availability treatments. The subjects had kept detailed food logs (including weighing and measuring all their foods) before the intervention to have a baseline reading for their energy intake and their heart rates and VO2 max were established during testing seasons before the first workout day.
  • Table 1: Detailed information about the participants in the 1993 (Study A) and 1994 (Study B) studies by Loucks et al. (Loucks. 1993 & 1994)
    participants in study A (Loucks. 1993): 51 volunteers 18-29 years of age
  • participants in study B (Loucks. 1994): 28 volunteers 18-29 years of age 
  • none of the participant was using medication including oral contraceptives, no history of heart, liver, or renal disease, diabetes, menstrual or thyroid disorders, or a history of severe dieting; all had  at least 3 mo of documented menstrual cycles 26-32 days in length and had exercised for only ~60 min per week in the previous 3 months 
Since the basic design of the studies did vary, we are now going to look at the studies separately and in the order in which they've been conducted. This does obviously mean that we'll start with study A the subjects were randomized to groups
  • exercising not at all (Z; zero exercise group), 
  • expending 1,300kcal/day on low (40% VO2max) intensity exercise (LO)
  • expending 1,300kcal/day on high (70% VO2max) intensity exercise (HI)
The exercise was performed under continuous supervision on treadmill and cycle ergometers in 30min and 60min bouts for the high and low intensity groups, respectively.

"So what did happen? Did they drop dead?" Not exactly, no...

Figure 1: Experimental design: dietary energy intake (I), energy expenditure during exercise (E), and net energy availability (A) in the 3 x 2 (exercise X energy availability) experimental design; note: B indicates adequate energy intake, D indicated reduced energy intake (Loucks, 1993)
On the 4 subsequent treatment days the women consumed a liquid clinical dietary product (Ensure, Ross Laboratories, Columbus, OH) was consumed by all subjects as their only food source. The latter contained either
  • 30kcal/kg body weight per day (~1,750kcal/day of available energy) in the normal energy group (B) and
  • 8kcal/kg body weight per day (~500kcal/day of available energy) in the low energy group (D)
According to the protocol of study A, no effort was made to compensate for the daily energy expenditure and other than the liquid meal replacement Ensure (250 kcal/can, 15% protein, 30% fat, and 55% carbohydrate) the subjects were allowed to consume only plain water.

The blood was sampled for 8 days beginning on the day before the intervention began, in order to track (a) the time course of the development and (b) the persistence of the hormonal changes in the subjects.
Figure 2: Thyroid hormones at the end of the 4-day intervention expressed relative to baseline (Loucks. 1993)
Now, while there were no differences in baseline thyroid status for the participants a brief glance at the data in figure 2 will suffice to see that those were present during and after the intervention. And while the scientists state that ...
"[w]hen dietary energy intake was increased in exact compensation for the energy cost of exercise (LB, HB) [...] even the large volume of exercise performed in this study (similar to running a half marathon each day) had no effect on T3 levels." (Loucks. 1993)
I have my doubts whether "training in the zone" for hours everyday will not shut down the thyroid after 3 weeks and thus 5x the duration of the study. I mean -10% T3 & 5%+ increase in reverse T3 are certainly boding ill (see my comment in figure 2). The data from the two-way ANOVA plotted in figure 3, on the other hand, confirm that the scarcity of energy and thus your bodies' desire to conserve energy is the main factor, here. 

"You're thyroid function is fine - rather high than low!", says the Dr. to the patient

The experiment Loucks et al. conducted does also shows why most patients don't receive adequate counseling (there is no need for treatment) by their doctors and statements like the one above are rather the rule than the exception.

Figure 3: Treatment effects on the changes of total T3 (in nmol/l) in the study particpants of study A (Loucks. 1993)
With normal or low TSH levels (not measured in the study at hand; generally indicating normal or even high thyroid function) and normal or increased T4 levels (this is an exclusive feature of the earlier stages of the overtraining + undereating syndrome) usually being the only additional value you may be able to convince your medical practitioners to measure this appears like an adequate diagnosis. The lowered T3 and even more so the increasing rT3 levels, on the other hand, will go unnoticed by the majority of GPs whose text-book tells them that even a mere TSH test should suffice to determine your thyroid health (in fact that's true, because your thyroid is perfectly healthy).

In a way this is yet better than a Dr. prescribing T4 in these situations. The latter will only be converted to rT3 and can aggrevate the sluggishness and apathy that comes with the low metabolic function due to "low T3 syndrome".

We need more data: Study B (Loucks. 1994)

"How did I let this happen again?", asks Oprah in her own magazine  - the answer is simple, Oprah! Your "diet" programmed the YoYo effect! It happened not after, but right while you were starving... ah, pardon "dieting"! Learn more about the benefits of dieting down slowly.
It goes without saying that the results of study A (Loucks. 1993) of which the scientists themselves point out that it had a "limited purpose" which was to determine (Study B; Loucks. 1994)
  1. whether exercise training is capable of altering thyroid metabolism in women, and, if so, 
  2. whether this alteration can be wholly explained by the impact of exercise on energy availability, with all other physiological processes occurring during exercise training (i.e., “exercise stress”) having no influence on thyroid metabolism. 
are of low practical relevance, as I would hope that even the most notorious masochists out there won't try to cut on a "8kcal/kg per day" diet... well, I got to qualify this statement, I suppose. In the obese "diets" like that are actually common practice - the "biggest loser" diets often contain 800kcal per day, as does the HCG diet and if you take into account that almost all obese men and a significant amount of obese women weigh more than 100kg, the protocol does no longer seem to be that unrealistic.

Still, I and I would guess, you, as well, will appreciate that Loucks & Heath conducted a follow up study, in the course of which they wanted to elucidate how important the dietary compensation of the exercise induced energy expenditure is, if you want to keep your thyroid hormone metabolism intact. To this ends the subjects were randomly allocated to four groups (ordered from lowest to highest energy intake):
  • 10.8kcal/kg LBM available energy -- this is what's left from a baseline intake of 39.5kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet with a caloric deficit of ~23% below the participants' habitual intake
  • 19.0kcal/kg LBM available energy -- this is what's left from a baseline intake of 48.6kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet with a caloric deficit of ~6% below the participants' habitual intake
  • 25.0kcal/kg LBM available energy -- this is what's left from a baseline intake of 53.4kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet that had an identical energy content as the participant's habitual diets
  • 40.4kcal/kg LBM available energy -- this is what's left from a baseline intake of 68.4kcal/kg LBM, after the energy expended during the workouts is subtracted from a diet with a caloric content that was ~32% above the participants' habitual diets (typo in kcal values corrected)
All subjects performed the high intensity protocol of the previous study (70% VO2max) and expended 30 kcal kg LBM of energy in daily exercise for four consecutive days beginning on day 2, 3,4, or 5 of the menstrual cycle (this is important, because the energy expenditure during the workouts was obviously not compensated for in the habitual diet). Just as in the previous study the exercise sessions were performed on treadmill or cycle ergomenter, and in 30 min bouts with 10min breaks in between (obviously until the target calorie expenditure was met).
Figure 4: Effects of training at 70% VO2max aiming for a total energy expenditure of 30kcal/kg LBM at different levels of available energy (intake - expenditure in kcal/LBM) on thyroid hormones; values expressed rel. to baseline (Loucks. 1994)
As the literal "blind man" should see, the combination of what most people would not even necessarily call overtraining (after all it's just 4 days and "only" 70% VO2max) reduces the T3 reserves (total T3) to zero and reduce the purportedly active T3 levels by 28% - a reduction that will have a significant impact on how you feel and how your metabolism will function.
Figure 5: The changes in thyroid hormones come "stepwise" with thresholds at 22.5kcal/LBM body weight for FT3 and  ~14kcal/LBM available energy for FT4 and rT3 (Loucks. 1994)
As the text boxes in figure 5 already tell you, we are dealing with a general 2-step mechanism, here, and it it is fully dependent on the extent of the calorie deficit. For a ~8% reduced total energy intake that corresponds to an available energy level of  ~22kcal/LBM, we see "nothing" but a drop in active thyroid hormones FT3, when the energy deficit increases (and I assume when it persists for longer than 4 days), this reduction is no longer enough to minimize the energy expenditure so that your body resorts to what you may term an STRM, a selective thyroid hormone receptor modulator that goes by the telling name reverse T3. Since rT3 is produced from T4 and the other metabolic pathway, the conversion of T4 to T3 is already shutting down, we see an increase in free T4 levels, which will serve as a substrate for the production of rT3 to further slow down the metabolism (in the days/weeks to come TSH will probably go further down so that you will end up with all levels being suppressed and only rT3 high - if anything).

As you can see, your body is smarter the average starvation dieter thinks he is. So the bottom line is easily formulated: Don't starve yourself if you don't want do feel and look like miserable, hold water, get fat from whatever you eat and end up as a physiological and psychological wrack.

  • Loucks AB, Callister R. Induction and prevention of low-T3 syndrome in exercising women. Am J Physiol. 1993 May;264(5 Pt 2):R924-30.
  • Loucks AB, Heath EM. Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability. Am J Physiol. 1994 Mar;266(3 Pt 2):R817-23.