T Nation

Low Test Due to Anorexia Athletica

Hey guys. Pretty hard for me to admit something like this, though I have posted on diff boards, but I am recovering from anorexia athletica. Basically over exercised and underate for my activity levels (Never starved myself, aways ate 2000-3000 calories a day, but like I said, still not enough for my activity). I cam currently under the care of Dr John Crisler and we are trying some things to get my own production back up (along with me gaining weight…already gained 6 pounds in 4 weeks so hurray lol).

I guess I just wanted advice/opinions from members on this board as well. Its always good to hear what people have to say or have seen in their lives. I have looked at various studies of anorexic males (not necessarily anorexia athletica, but the same hormonal outcomes occur) and it is the pretty much unanimous consensus that even years after weight restoration, testosterone levels never return to normal. I have found various other stories of males like me on other forums, and out of about 12 different souls like myself 1 had a successfull response to clomid therapy and restored his levels (all the others seemed to have to go on trt).

I recently got into med school and have been given a year deferral to get healthy. I am hoping in that year we can either

  1. get me up an running on my own


  1. go on trt if needed and get me optimized by the time I start up medical school

Its very sad that this has taken from me everything I enjoy. No libido, no sense of well being, tired, sad, etc. I also stopped all forms of endurance training 2 years ago and after meeting some friends who were into to bodybuilding became very passionate about it, but by then the damage had already been done and it is basically a futile attempt for me to try and put on any muscle.
I am hoping in the future though, however i turns out, it is a passion/hobby I can pursue and see results in.

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I know how you feel. I put a lot of pressure on myself to feel better/get my Test levels normal right before I started studying for my master’s degree and the CPA exams. Granted that’s not nearly as demanding as med school, but it wasn’t easy. You’re lucky in that what you are learning about your body now will definitely parlay into your medical studies. I still remember nights in the accounting library where I’d be writing furiously on a paper about accounting treatments for stock options then 10 mins later I’d change gears and go straight into endotext.

Personally: I used to eat about 2000 calories a day and also running 4x a week. I was a MLB in high school and usually was around 195-210 pounds. I got all the way down to 168 lbs. I probably weighed less at some points. I was extremely skinny and just didn’t look right. My testosterone levels dipped to about 226. When I started eating again and being “normal”, my libido came back for a little while, but it was temporary and my test levels dropped to 168! I was put on HcG and Test-Cyp for a few weeks, then I switched doctors and was taken completely off.

I am not 100% sure as to whether recovery is certain or not. I am still waiting for my “wash-out” period to end and see where my testosterone levels are. The medical profession is slowly but surely accepting exercise induced hypogonadism as a new way of determining causes of hypogonadism.

I was in sort of the same position as you for slightly different reasons. I raced bicycles for a good part of my life, and tried to maintain a low weight (145-150 lbs at 5’11") in order to climb fast up those mountains. Years of this plus some ill-advised experimentation with low fat vegetarian diets left me with very strong legs (I worked out in the gym as on a regular basis as well) but fairly emancipated from the waist up.

What I didn’t realize that this lifestyle plus low testosterone levels were having devestating effects on my bone density, to the point that I became nearly osteoperodic by the age of 48. A fracture to my vertebrea a couple of years ago while on a ride put an end to that aspect of my athletic career, and I now spend most of my time working out in the gym, eating a clean high protein diet (with plenty of red meat), and am on TRT. I am beginning to see increases in bone density, although this will take time and will never restore to the point of where it should be.

If you are young, you will probably not have lost much in the way of bone density, but as many do not know, osteoperosis is not just a woman’s disease and can affect men as well if their hormones and diet are out of balance. You might want to be safe and have a bone density scan if your insurance will pay for it.

These problems relate to what levels of nutrients and hormones exist in the blood and the effect that that has on various organ systems and resulting state of well-being. One can get into an adverse state by starvation, or eat moderately and drive nutrients and hormones to a low state by depleting them with excessive exercise levels.

In a situation like this, cholesterol levels may be way too low. DHEA and pregnenolone might have a role in recovery from low cholesterol levels. Steroid hormone production can be rate limited by low cholesterol levels.

Feed your self lots of fish oil and vit-D3. Make sure that your salt is iodized.

here are a bunch of labs I have had done

Test Name Flag Result Ref Range Units
Glucose 80 65-99 mg/dL
Uric Acid 3.2 2.4-8.2 mg/dL
BUN 26 5-26 mg/dL
Creatinine 0.92 0.76-1.27 mg/dL
eGFR >59 >59 mL/min/1.73
eGFR AfricanAmerican >59 >59 mL/min/1.73
BUN/Creatinine Ratio HIGH 28 8-27
Sodium 140 135-145 mmol/L
Potassium 4.5 3.5-5.2 mmol/L
Chloride 104 97-108 mmol/L
Calcium 9.2 8.7-10.2 mg/dL
Phosphorus 3.6 2.5-4.5 mg/dL
Protein, Total 6.4 6.0-8.5 g/dL
Albumin 4.6 3.5-5.5 g/dL
Globulin, Total 1.8 1.5-4.5 g/dL
A/G Ratio HIGH 2.6 1.1-2.5
Bilirubin, Total 0.5 0.0-1.2 mg/dL
Alkaline Phosphatase, S 83 25-150 IU/L
LDH 144 100-250 IU/L
AST (SGOT) 34 0-40 IU/L
ALT (SGPT) 52 0-55 IU/L
GGT 51 0-65 IU/L
Iron 77 40-155 ug/dL
Cholesterol, Total 159 100-199 mg/dL
Triglycerides 31 0-149 mg/dL
HDL Cholesterol 79 >39 mg/dL
VLDL Cholesterol Cal 6 5-40 mg/dL
LDL Cholesterol Calc 74 0-99 mg/dL
T. Chol/HDL Ratio 2.0 0.0-5.0 ratio units
Estimated CHD Risk < 0.5 0.0-1.0 times avg.
TSH 2.950 0.450-4.500 uIU/mL

Testosterone LOW 115 280-800 ng/dL

LH LOW 0.5 1.7-8.6 mIU/mL

Vitamin D, 25-Hydroxy 37.6 32.0-100.0 ng/mL

T4,Free(Direct) 1.23 0.82-1.77 ng/dL

Prolactin 9.5 4.0-15.2 ng/mL

Estradiol 15.0 7.6-42.6 pg/mL

DHEA-Sulfate 455.3 211.0-492.0 ug/dL

FSH 2.3 1.5-12.4 mIU/mL

Progesterone 0.9 0.2-1.4 ng/mL

Thyroid Peroxidase (TPO) Ab 17 0-34 IU/mL

Triiodothyronine,Free 2.1 2.0-4.4 pg/mL

After only two weeks of being off synthroid my TSH is already going back up, and like I suspected my freet3 is at the very bottom of its range. I am also essentially castrated testosterone wise.

We then did a more detailed testosterone workup and got the following

We got the testosterone workup back and I am worse off then we thought

Name Value Reference Range
40 13-71
1.1 6.0-27.0

8AM 6.23 ng/ml 3.5-6.3
12PM 2.47 1.4-2.8
4PM 2.25 0.8-2.4
8PM 1.32 0.6-1.6
12AM 1.19 0.3-1.2
4AM 1.49 0.3-1.7

8AM 4.7 ng/m 2.8-12.7
8PM 3.3 2.7-9.0
MIDNIGHT 2.7 1.8-8.1

T3, REVERSE 436 90-350

I recently through heavy supplementation got my vitamin D up from 32 to 60 and will try to get it higher. Cholesterol doesnt look bad does it? My triglycerides are low as shite, most likely due to depletion from years of overexercise and just not eating enough.

Pretty much all the endocrine markers of starvation lol. High rt3, low ft3, low sex hormones, elevated cortisol, yada, yada. Gosh darn cross country :frowning:

Yep. I just posted in another thread a whole thing on starvation, rt3, and t3. It sounds like it is transient, however. Endurance runners are known to have lower testosterone levels than average males.

Regardless, you need to get something going in your body. Clomid may be a good start. If your body responds, you may not need TRT.

Your adrenals aren’t shot, which is a good thing. Why did you quit the Synthroid??

Your story reminds me of a case study I read about a guy who was a boxer and ran his testosterone into the ground. I think they gave him some Clomid. It didn’t work at first but they tried it again and I think it got him to at least the eugonadal range, which for the researchers was a “success”. I am really interested to see how your treatment helps. Please keep up and make sure you follow up because undoubtedly so many guys will read this thread years from now!

Please do not cite these clomid stories without also stating that clomid has nasty side effects and that nolvadex would be a better approach.

A SERM can tell you if the top end of the HPTA is broken if there is no increase in LH.

hCG will tell you if the testes are willing and able. In either case, T level increases may be delayed by the testes needing to recover size and function when LH has been very low for a longer time.

Clomid does have some nasty sides, but still appears to hold a place over Nolvadex in the medical world
for treatment of hypogonadism. Nolvadex is still used with letrozole and anastrazole to combat gynecomastia if I’m not mistaken.

Medical practice is also driven by the fact that the earlier SERM got all of the research. But the clomid research does not disclose the negative side effects for some. I have not seen anything to indicated that nolvadex does not increase LH. In this case, medical practice is probably a simple case of not changing, even when there are other effective SERMs that do not have severe estrogen side effects.

You cannot say that nolvadex is ineffective.
“”“In one study the administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). Treatment of patients with “idiopathic” oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. “””

I stand neutral on the SERM debate. My main conclusion was that clomiphene citrate appears highly favored by the medical practice for treatment of hypogonadism over tamoxifen, which is still mainly thought of as an anti-gynecomastia agent. I wonder whether this is due to their indications in females, where Clomid is used to induce ovulation while Nolvadex is used in the treatment of breast cancer.

I think Nolvadex is probably just as effective as Clomid, but through another mechanism. Some speculation exists as to whether it may actually re-sensitize the testicles’ Leydig cells to the LH signal.

P.S. I thought that Nolvadex was invented in the 1950’s while Clomid arrived in the 1970’s…I’m guessing you meant as a SERM in males?

Would eugonadal ranges just be low normal? Doubt anyone wants to feel low normal lol :confused:

Yep. Hence why I said “success”.

BTW: I was wrong. They actually didn’t administer clomiphene citrate in the boxer case I thought I was talking about. It was actually in another case. I will post both abstracts below for your reference:

Association of carotene rich diet with hypogonadism in a male athlete.
Adamopoulos D, Venaki E, Koukkou E, Billa E, Kapolla N, Nicopoulou S.

AIM: To report on a unique case of hypogonadism associated with excessive carotene intake in a young male athlete. CASE REPORT: A 20-year-old patient presented with a gradual decline in muscular and physical activity, sexual interest and erectile ability associated with a high in carotene and low in animal fat diet of his own design a year prior to the clinical manifestations. Clinically, he presented with very overt signs of carotene excess: his palms and soles were yellow. Moreover, 2 weeks after normalization of his diet, carotene B levels were at the upper end of the normal range. METHODS: Repeated stimulation tests of hypothalamic, pituitary and testicular function were performed before and at 3, 6 and 12 months after the introduction of a balanced diet. RESULTS: Very low basal and stimulated values for gonadotropins and gonadal steroids were found at the initial evaluation with a progressive recovery shown after months of a balanced diet and carotene B restoration. Complete androgen secretion and sexual response recovery were observed only after 9-12 months from diagnosis. CONCLUSION: This is the first report associating excessive carotene intake with a hypothalamic form of hypogonadism in a young man.

Long-Distance Runner and Clomid

Idiopathic hypogonadotropic hypogonadism in a male runner is reversed by clomiphene citrate.
Burge MR, Lanzi RA, Skarda ST, Eaton RP.

OBJECTIVE: To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism. DESIGN: An uncontrolled case study. SETTING: The outpatient endocrinology clinic of a university tertiary referral center. PATIENT(S): A 29-year-old male who has run 50 to 90 miles per week since 15 years of age and who presented with a pelvic stress fracture, markedly decreased bone mineral density, and symptomatic hypogonadotropic hypogonadism. INTERVENTION(S): Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period. MAIN OUTCOME MEASURE(S): Serum concentrations of LH, FSH, and T before and after CC therapy, as well as clinical indicators of gonadal function. RESULT(S): Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being. CONCLUSION(S): Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with debilitating hypogonadism related to endurance exercise.

P.S. Clomid has bad side effects and Nolvadex is better (For you, KSMan hahaha).

Study #1: Clomid was used as toxic levels of were washing out of subjects system. No surprise that clomid would increase T, simply proved that the HPTA was estrogen repressed. [Subject may have had repressed hormone levels from very low cholesterol as well.] What is the point of talking about this Abstract? There is nothing reported that indicates that the condition would not have resolved without clomid. The solution was a normal diet, not clomid.

Study #2: What is the long term outcome after discontinuing clomid? How did the subject feel in terms of estrogen side effects? The stated objective was to study the function of the HPTA. This report is substantially otherwise useless and definitely misleading.

As for “may provide a safe and effective treatment”, you need to not confuse “may” with “is”. When such things are stated that way, as they often are, the motive is really trolling for grant money to do a proper $tudy.

Bumping to provide interesting Nolvadex studies I found on Dr. Crisler’s board RE: Nolvadex. (Pro Nolvadex). Just for everyones info.

Int J Sports Med. 1995 Aug;16(6):413-7.
Hypogonadism as a cause of recurrent muscle injury in a high level soccer player. A case report.

Naessens G, De Slypere JP, Dijs H, Driessens M.

Department of Physical Medicine and Rehabilitation, University Hospital Antwerp, Edegem, Belgium.

Hypogonadotropic hypogonadism is a well known entity in highly trained female athletes. In male sportsmen, resting testosterone levels may be lowered especially in well endurance trained athletes and during high intensity training periods, frequently in combination with excessive weight reduction. However, only few reports illustrate a clinical pathology related to this state. In this report, where we present a case of a high level soccer player with recurrent muscle injuries over several years, hypogonadism was caused by sports activity together with an impaired testicular function (cryptorchidy). Clinical findings included testicular maldevelopment, decreased libido, infertility and a high incidence of muscle strains and delayed post-exercise soreness in mainly eccentric exercised muscle groups. Laboratory findings showed abnormally lowered resting testosterone values, most prominent during training periods, and an unfavourable testosterone/cortisol ratio during recuperation after exercise. With respect to treatment of the problem, neither any form of physical therapy nor rehabilitation program could give long lasting benefit. Using tamoxifen, an anti-oestrogenic drug, which stimulates LH and FSH production, we not only observed normal physiological resting testosterone values and a restoration of the testosterone/cortisol ratio after exercise, but our patient also experienced a higher sexual drive, well being and a spectacular decrease in the muscle injury rate. Although this patient was not a highly endurance trained athlete, we assume that a chronic anabolic/catabolic hormone imbalance may be of greater clinical importance in sports activity based on eccentric and explosive muscle work.

Andrologia. 1985 Jul-Aug;17(4):369-78.
Effect of lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men.

Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.

Administration of the antiestrogen tamoxifen for one month to 12 patients with idiopathic oligozoospermia significantly increased the mean basal testosterone (T) level and the responses of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to constant luteinizing hormone releasing hormone (LHRH) infusion but did not significantly influence the mean oestradiol (E2) levels or the E2 over testosterone ratio. Mean sperm concentration and total sperm output increased by about 70% after a mean treatment period of 5.5 +/- 0.4 months. No statistically significant difference was found between the two subgroups of patients treated with either the lower (5 or 10 mg once daily) or higher dose of tamoxifen (10 mg twice daily) with respect to basal or LHRH stimulated gonadotropin and testosterone response or the E2/T ratio and the effect on sperm density and total sperm output. In both subgroups the sperm motility and morphology remained unchanged. In conclusion higher doses of tamoxifen in this study prove not to be superior to lower doses in improving mean sperm density and total sperm output. The relative small percentage of patients achieving normalisation of only these sperm parameters pleads for further search for more effective selection of patients and other more effective treatment modalities in patients with idiopathic oligozoospermia.

Conclusion: SERMs increase LH which increases T, SERMs also increase FSH which supports sperm production, SERM dosing may be too high.

Nolvadex gets the job done, clomid not the king.

Note that these responses are not going to happen with primary hypogonadism and with aged men, aged testes are also simply less responsive to gonadotropins.

More studies on toremifene needed as well.