JB et al ........
I had my annual physical today and got my blood work back. Here are the results of my hormone profile:
Result / Normal Range
FSH: 5.80 / (1.27 - 19.60 mIU/mL)
T (Free): 10.88 / (8.7 - 54.7 pg/mL)
DHEA SO4: 208 / (80 - 560 mcg/dL)
Estradiol: 26 / (20 - 75 pg/mL)
ESTRONE: 31.8 / ?
PSA: 0.4 / (0.0 - 4.0 ng/mL)
(BTW I had weight trained and ran sprints pretty hard for 2 weeks leading up to this)
I was disappointed in the Free Testosterone level. I've been supplementing with 50 - 100 mg of DHEA daily, and have been taking that for 8 years now. It seems there is some room to up my daily DHEA supplementation - to perhaps even double it given low oral bioavailability - without getting that out of range, in order increase my endo T levels. My doc thinks the T free level might be low because I am supplementing with DHEA. He thinks it could be low because of the negative feed back loop with exogenous DHEA supplementation. While he didn't tell me to stop taking it, he doesn't recommend it.
While I agree my endo DHEA is probably suppressed, Do you feel oral DHEA supplementation would be suppressing my T levels?
Thanks!
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
i really doubt it. in males, dhea does not really effect t levels that much and certainly does not effet free t by suppression. there is a general (in my observation) predjudice against dhea supplementation by the medical field. so what is your dose, 50 or 100mg/day?
jb
==============
J Appl Physiol. 1999 Dec;87(6):2274-83. Links
Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men.Brown GA, Vukovich MD, Sharp RL, Reifenrath TA, Parsons KA, King DS.
Exercise Biochemistry Laboratory, Department of Health and Human Performance, Iowa State University, Ames, Iowa 50011, USA.
This study examined the effects of acute dehydroepiandrosterone (DHEA) ingestion on serum steroid hormones and the effect of chronic DHEA intake on the adaptations to resistance training. In 10 young men (23 +/- 4 yr old), ingestion of 50 mg of DHEA increased serum androstenedione concentrations 150% within 60 min (P < 0.05) but did not affect serum testosterone and estrogen concentrations. An additional 19 men (23 +/- 1 yr old) participated in an 8-wk whole body resistance-training program and ingested DHEA (150 mg/day, n = 9) or placebo (n = 10) during weeks 1, 2, 4, 5, 7, and 8. Serum androstenedione concentrations were significantly (P < 0.05) increased in the DHEA-treated group after 2 and 5 wk. Serum concentrations of free and total testosterone, estrone, estradiol, estriol, lipids, and liver transaminases were unaffected by supplementation and training, while strength and lean body mass increased significantly and similarly (P < 0.05) in the men treated with placebo and DHEA. These results suggest that DHEA ingestion does not enhance serum testosterone concentrations or adaptations associated with resistance training in young men.
Thanks for that JB............
I probably average 75 mg/daily, sometimes I take (1) 50 mg tab at night, sometimes (2).
Insofar as the above study goes, I think that generally speaking we've known that dhea supplementation for young men in their early 20's conveys little to no benefit. But I'm 48.
Based on your research, would increasing my dosage to say, 150 mg each night help increase my free T levels?
If not, are there any supplements you know of that would do so without suppressing something in the hpta chain?
Thanks!
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
i would definitely try 150. you need to be consistent. you might also want to give micronized dhea a try at 100mg. there have been few studies that have tried larger doses and those i have read are not that encouraging wrt increasing test.
jb
Thanks JB
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
did you take the day off from exercise before the blood work? T levels are affected by exercise.
And we'll collect the moments one by one. I guess that's how the future's done. Feist, "Mushaboom", 2005
Headdoc,
No, I was alternating training days with running sprints.
Thanks,
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
Headdoc,No, I was alternating training days with running sprints.
Thanks,
no workout, no sex on the day before blood tests.
And we'll collect the moments one by one. I guess that's how the future's done. Feist, "Mushaboom", 2005
argh! no sex? just as an interesting aside, here is an interesting study that bears some more investigation:
jb
===================
J Endocrinol. 2008 May;197(2):315-23.Click here to read
Chrysin, a natural flavonoid enhances steroidogenesis and steroidogenic acute regulatory protein gene expression in mouse Leydig cells.
Jana K, Yin X, Schiffer RB, Chen JJ, Pandey AK, Stocco DM, Grammas P, Wang X.
Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, Texas 79430, USA.
During the aging process of males, testosterone biosynthesis declines in testicular Leydig cells resulting in decreases in various physiological functions. To explore the possibility of delaying the decline using food supplements, we have studied steroidogenic effects of a natural flavonoid, chrysin, in mouse Leydig cells. Chrysin dramatically increased cyclic AMP (cAMP)-induced steroidogenesis in MA-10 mouse Leydig tumor cells. This result was confirmed using Leydig cells isolated from mouse testes. The steroidogenic effect of chrysin is not associated with an increase in expression of the P450 side-chain cleavage enzyme, required for the conversion of cholesterol to pregnenolone. In addition, when 22(R)hydroxylcholesterol was used as a substrate, chrysin induced a non-significant increase in steroid hormone, suggesting that the majority of the observed increase in steroidogenesis was due to the increased supply of substrate cholesterol. These observations were corroborated by showing that chrysin induced a marked increase in the expression of steroidogenic acute regulatory (StAR) protein, the factor that controls mitochondrial cholesterol transfer. Also, chrysin significantly increased StAR promoter activity and StAR mRNA level. Further studies indicated that this compound depressed expression of DAX-1, a repressor in StAR gene transcription. In the absence of cAMP, chrysin did not increase steroidogenesis. However, when a sub-threshold level of cAMP was used, StAR protein and steroid hormone were increased by chrysin to the levels seen with maximal stimulation of cAMP. These results suggest that while chrysin itself is unable to induce StAR gene expression and steroidogenesis, it appears to function by increasing the sensitivity of Leydig cells to cAMP stimulation.
Thanks guys.
My doc wants me to do some follow up blood work in 6 weeks due to the high liver enzymes. I'm going to bump my dhea to 150 mg each evening, and I picked up some some Activate Extreme. It'll be interesting to see if I can get that Free Testosterone up to a more acceptable level.
I'll also look into Chrysin.
Thanks again,
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
go to himalyas website and pickup some liv 52 fo rthe liver enzymes.
jb
Just wanted to give a follow up report on my before/after blood work results. Diet, training and times of day of blood work were all largely the same. The 2 changes were:
1. I increased dhea supplementation from 75 mg/day to about 100 mg/day;
2. I started supplementing with Activate Extreme, which is supposed to increase free test levels as it has ingredients with a supposed higher affinity for SHBG. Here are the results, after 4 weeks of increased dhea and taking 4 pills / day of Activate Extreme (label recommends 4-6 pills/day, for a duration of 4 to 8 weeks):
Before / After / Normal Range:
T (Free): 10.88 / 6.57 / (8.7 - 54.7 pg/mL)
DHEA SO4: 208 / 282 / (80 - 560 mcg/dL)
A few things:
1. My doc suspects dhea supplementation is causing a suppression in endo test levels;
2. I'm scheduled for a follow up exam / blood work in 3 months. If the low trend continues, he also is talking about me having an MRI on my testicles;
3. My wife reminded me, after my doctor's appointment of course so I didn't get to ask him specifically about it, that I have a vericoseal (like a vericose vein) in my left testicle. I know that usually causes a decrease in sperm count,
Do any of you know if that may also cause a decrease in endo testosterone production? I can't seem to find any info on it specifically?
4. Activate Extreme, for me, evidently is worthless. I am not inexperienced in exogenous testosterone supplementation, so I know what increased blood levels feels like. After 4 weeks of this product, there was zero accompanying strength gain, size, muscular pumps during work out, libido, etc. Disappointing, as I had high hopes for this product.
Thanks,
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
i am not familiar with any research that concludes dhea will suppress endo test, if anything much larger doses eg 250mg may significantly increase it.
jb
JB,
Thanks. But I was more interested specifically in whether a Varicocele would limit endo test production? What I've seen on the internet so far is inconclusive....... some think so, others say no.
Thanks
Be well.
PC1
"You still got the tools, but they're different" (Angelo Dundee => Muhammad Ali)
6'4"
242 lbs.
leaning out a bit
"One guy thinks he can, another guy thinks he can't. Both are right. Which one are you son?" (Nike commercial football coach)
Elevation of serum testosterone and free testosterone after embolization of the internal spermatic vein for the treatment of
there does not seem to be much doubt about varicocele affecting test level. treatment seems to be an option along with HCG. sorry i did not have time to highlight.
jb
=-================
varicocele in infertile men.Gat Y, Gornish M, Belenky A, Bachar GN.
Andrology Unit, Department of Obstetrics & Gynecology, Rabin Medical Center, Beilinson Campus, Petah Tiqva and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
BACKGROUND: To evaluate the effect of internal spermatic vein (ISV) embolization on levels of serum testosterone and free testosterone and on spermatogenesis. METHODS: The files of 83 infertile men treated for varicocele were reviewed for changes in serum testosterone, free testosterone and spermatogenesis after ISV embolization. RESULTS: Mean serum testosterone concentration rose after embolization by 43%, from 12.07 +/- 6.07 nmol/l to 17.22 +/- 8.43 nmol/l (P<0.001). Mean serum free testosterone concentration rose by 72%, from 5.93 +/- 2.44 nmol/l to 10.21 +/- 7.69 nmol/l (P<0.001). Mean sperm concentration increased from 7.49 +/- 1.73 x 10(6)/ml to 18.14 +/- 2.36 x 10(6)/ml (P<0.001); mean sperm motility increased from 21.74 +/- 2.47 to 34.47 +/- 2.27% (P<0.001); and mean sperm morphology increased from 6.63 +/- 1.07 to 13.08 +/- 1.44% (P<0.001). CONCLUSIONS: ISV embolization apparently induces an increase in both serum testosterone and free testosterone concentrations and in sperm parameters in infertile patient with varicocele, regardless of the size of the varicocele.
Varicocele ligation on free testosterone levels in infertile men with varicocele.Ishikawa T, Fujisawa M.
The Population Council, New York, NY, USA.
We have analyzed the effects of varicocele ligation on free testosterone levels, and investigated the interrelationships between free testosterone and fertility. The records were retrospectively evaluated for 42 infertile patients who underwent varicocele ligation, with serum free testosterone levels, follicle stimulating hormone (FSH), lutenizing hormone (LH), testosterone, estradiol, prolactin, ejaculated volume, sperm concentration and motility before and after surgery. Serum free testosterone levels increased from 12.97+/-4.16 to 13.59+/-3.93 pg/mL, but the difference was insignificant. The differences before and after surgery of patients in sperm concentration and motility were also insignificant. However, in free testosterone increasing group, the sperm concentration and motility increased significantly, from 4.05+/-4.35 to 7.90+/-8.19 million/mL (P=0.01) and from 30.64+/-21.87% to 41.00+/-22.00%, respectively (P=0.03). The increase in serum free testosterone level by varicocele ligation results in a significant improvement in sperm concentration and motility.
Low plasma testosterone in varicocele patients with impotence and male infertility.Younes AK.
Department of Andrology, Al Azhar University, Cairo, Egypt.
To study the affect of bilateral varicocele (grade 3) on impotence and male infertility patients, 29 patients were selected from an outpatient clinic during 15 May 1998 to 15 August 1999 (the mean age was 33.9 +/- 6.3), 15 patients complaining of erectile dysfunction and 14 patients complaining of male infertility. The mean duration of impotence was 3 +/- 2.3 years and for male infertility was 6 +/- 2.5. All organic and psychogenic causes related to impotence and male infertility except bilateral varicocele (grade 3) and low plasma testosterone were excluded by clinical and laboratory investigations. Twenty males with normal erection and fertility were included as controls. Detailed medical history and complete physical examination included measurement of testicular size by orchiometer; semen and hormonal parameters were measured for all patients and control. In impotent patients left and right testicular volume was significantly decreased (p < .05), while in male infertility patients left and right testicular volume was highly significantly and, significantly decreased (p < .005, p < .05) compared to controls. In male infertility patients, left testicular volume was highly significantly decreased compared to impotent patients (p < .005). The sperm count and semen volume in impotent patients was significantly decreased (p < .05, p < .01), but no significant differences were found in sperm motility and abnormal forms, while in male infertility the sperm count was highly significantly decreased (p < .005), the sperm motility was significantly decreased (p < .05), the abnormal form was significantly increased (p) < .05), but in the semen volume there was no significant difference compared to controls. In impotent patients the sperm count was significantly increased and abnormal form was significantly decreased compared to male infertility (p < .05). The mean serum testosterone was significantly decreased in impotent patients (p < .01), and highly significantly decreased in male infertility (p < .005) compared to controls. The mean serum FSH was significantly increased in male infertility (p < .05) and nonsignificant in impotent patients compared to controls. The mean serum LH and prolactin levels were nonsignificant in both impotent and male infertility patients compared to controls, but LH was significantly increased in impotence compared to male infertility patients (p < .025). Therefore, bilateral varicocele (grade 3) is associated with significant reduction in testicular function with significant increase in serum levels of FSH and LH, which may cause erectile dysfunction and male infertility.
The effect of microsurgical varicocelectomy on serum follicle stimulating hormone, testosterone and free testosterone levels in infertile men with varicocele.Cayan S, Kadioglu A, Orhan I, Kandirali E, Tefekli A, Tellaloglu S.
Department of Urology, Faculty of Medicine, Mersin University, Mersin, Istanbul, Turkey. [email protected]
OBJECTIVES: To analyse the effects of varicocelectomy on serum follicle-stimulating hormone (FSH), testosterone and free testosterone levels, and to investigate the interrelationships between seminal and hormonal variables. PATIENTS AND METHODS: The records were retrospectively evaluated for 78 infertile patients who underwent microsurgical inguinal varicocelectomy, with documented serum FSH, testosterone, free testosterone levels, sperm concentration and sperm motility before and after surgery. Left and bilateral varicoceles were detected in 40 and 38 patients, respectively. In addition, serum hormonal values of 10 fertile men in whom physical examinations and Doppler ultrasonography revealed no evidence of varicocele were recorded and used as a control group. RESULTS: The mean (sd) serum FSH levels of all patients decreased from 15.21 (3.34) before surgery to 10.82 (2.93) mIU/mL afterward (P=0.01), and serum testosterone levels increased from 5.63 (1.40) to 8.37 (2.2) ng/mL (P=0.01), whereas free testosterone levels increased from 23.13 (3.19) to 32.83 (4.37) pg/mL (P<0.001). In contrast to the significant difference in sperm motility before and after surgery of all patients (P<0.01), the difference in sperm count was insignificant (P>0.05). Thirty-six patients with high serum FSH levels before surgery had significantly lower levels afterward (P=0.001). In this group, the sperm concentration and motility also increased, from 17.66 (4.35) to 20.76 (4.37) million/mL (P=0.05) and from 30.9 (4.4)% to 37.5 (4.34)%, respectively (P=0.01). In the remaining 42 patients who had normal preoperative serum FSH levels, there was a slight decrease after surgery (P=0.02). Their sperm concentration increased slightly (P=0. 04), and motility also increased (P=0.001). Sixty patients had a significantly higher testosterone level after surgery; in this group the sperm concentration and motility increased (P=0.01). CONCLUSION: Varicocelectomy promotes Sertoli and Leydig cell function. The significant increase in serum free testosterone level results in a significant improvement in sperm concentration and motility.
Andrologia. 1983 Nov-Dec;15(6):637-41.Links
Testosterone in peripheral plasma, spermatic vein and in testicular tissue under basal conditions and after HCG-stimulation in patients with varicocele.Pirke KM, Vogt HJ, Sintermann R, Spyra B.
The incretory testicular function was tested in 21 patient with varicocele aged 19 to 39 years. In one group baseline testosterone was measured, while a second group received a single injection of 5000 IU HCG. Testosterone was studied in peripheral plasma in the spermatic vein and in testicular tissue. Baseline values after stimulation were not different from those of normal controls. Testosterone in the spermatic vein rose, and in testicular tissue was greatly increased after HCG. The data provide further evidence that Leydig cell function is normal in patients with varicocele. In varicocele spermatogenesis is not impaired by low intratesticular testosterone concentrations.
Plasma testosterone in patients with varicocele and sexual inadequacy.Comhaire F, Vermeulen A.
Plasma testosterone concentration was decreased in 10 patients combining varicocele with sexual inadequacy (mean 346.2 ng/100 ml) against normal concentration observed in 23 men with varicocele without sexual disturbances (mean 567.8 ng/100 ml) and in 31 patients with pure psychogenic impotence (mean 581.6 ng/100 ml). There was a significant inverse linear correlation between age and plasma testosterone concentration in the varicocele patients (r= minus 0.56, P smaller than 0.01) in contrast to the absence of such correlation in normal men or in patients with psychogenic impotence of the same age range. The secretion products of the secondary sex glands were more often in the lower range in the ejaculates of men combining varicocele with sexual disturbance (P smaller than 0.02), proving the decreased testosterone level to induce a deficient function of these glands. Plasma testosterone levels normalized after surgical correction in varicocele patients with a low preoperative concentration. Since adequate surgical or hormonal treatment resulted in complete recovery of sexual potency in the majority of patients with varicocele and sexual inadequacy, it is suggested that the decreased testosterone production might have contributed to the impairment of sexual function.