More about treating male testosterone deficiency
Your sex hormones (testosterone and oestrogen) along with your gonadotrophins (LH and FSH) operate naturally in a tightly regulated and automated process. The brain creates a feed back loop which regulates how much testosterone is released. There is an interplay between the signal from the hypothalamus, the pituitary gland, and your testes. When you start Testosterone Replacement Therapy the regulated process will still occur but to a lesser degree and you will then take over control. You and your doctor determine how much testosterone your body receives, when it receives it and how often it receives it. Normally this is all managed for you by the Hypothalamus, but because age related Andropause or adult hypogonadism has blunted the response and has lowered your normal output to an unsatisfactory level it is now up to you to manage your hormones by topping them up with balanced testosterone replacement therapy including HCG.
How your body regulates testosterone through the hypothalamic gonadal axis
An analogy might be to think of your heating system. The thermostat would be the hypothalmus and pituitary gland and Boiler would be your testes. The thermostat releases a signal called gonadotrophin releasing hormones, which signals your pituitary gland (think of microprocessor in your thermostat) to release gonadotrophins (LH and FSH) which signal to the testes (boiler) to produce more testosterone and sperm for reproduction. This process keeps the testes functioning and healthy. The testes produce sperm and testosterone allowing them to maintain their size. The Leydig cells are responsible for the production of testosterone and are sensitive to the signal (LH) sent from your pituitary. Without this signal which can be blunted by taking testosterone then the Leydig cells will cease functioning causing testicular atrophy. This can be prevented using HCG or recombinant LH and FSH as an adjunct whilst on male testosterone replacement therapy.
Categories of low male testosterone
Age related testosterone deficiency can be described by several different terms:
- Adult onset hypogonadism
- Male menopause
- Low T
Other Names for low male testosterone or traditional/classical hypogonadism
- Primary hypogonadism
- Secondary hypogonadism
- Idiopathic hypogonadism
Diagnosis for low testosterone
When you are being diagnosed for low male testosterone the LH will be looked at to determine if you have primary or secondary hypogonadism. In secondary hypogonadism the problem is with the Hypothalamus not signalling the Pituitary Gland to release it’s signal. The downstream effect being low LH and FSH and very little testosterone being produced. Primary hypogonadism occurs when the signal from Hypothalamus or Pituitary Gland are doing their job but when it reaches the testes it’s just not switching on production of testosterone. In this case you would have an elevated LH and FSH level with little testosterone being produced. When testosterone is produced and after a certain undetermined level is reached then enzymes known as aromatase begin to convert excess testosterone into oestrogens. These oestrogens are then sensed by the hypothalmus which then stops sending its signal to the pituitary and then the body stops sending its signal back to the testes. With no signal to produce testosterone or sperm the testes will begin to atrophy. Testosterone replacement therapy without managing oestrogen and using HCG will shrink your bollocks. The degree of atrophy depends on the individual. For some it may be hardly noticeable and body may still produce some of its own testosterone albeit at a greatly reduced level which will cause sluggishness in the whole system and eventually atrophy.
Our testosterone balancing treatments
Our doctors will order a blood test to try to determine the category of low testosterone you are suffering and come up with a bespoke treatment plan.
There have never been more options available for treating low testosterone. The goal of therapy should be to keep your body producing natural endogenous testosterone whilst topping up what you may be missing. By correctly balancing your testosterone and other hormones you will mitigate the symptoms associated with low testosterone levels. After your doctor diagnoses you for low testosterone you can set out finding the right treatment.
Common Treatments for Testosterone in the UK
- Sustanon®(Aspen), testosterone propionate 30 mg, testosterone phenylpropionate 60 mg, testosterone isocaproate 60 mg, and testosterone decanoate 100 mg/mL
- Nebido®(Bayer), testosterone undecanoate 250 mg/mL in a 4ml amp or vial dosed 1gm ever 10-14 weeks by slow intramuscular injection
- Testosterone Enantate (Non-proprietary) , testosterone enantate 250 mg/mL dosed 250mg every 10-14 days
- Virormone®(Nordic), testosterone propionate 50 mg/mL, 2-mL amp Short Acting Testosterone ester dosed 2-3 times weekly
- Alcohol Gels commercially prepared
- TESTIM®(Ferring),Gel, testosterone 50 mg/5 g tube, 30-tube pack
- TESTOGEL®(Besin),Gel, testosterone 50 mg/5 g sachet, 30-sachet packs
- TOSTRAN®(ProStrakan),Gel, testosterone 2% (10 mg/metered application), 60-g multidose dispenser
- Lipoderm based Testosterone creams for scrotal applications. These are non commercially available creams that can be applied to the scrotum.
- Oral Androgens for reducing SHGB. There are times when SHGB bind too much of your total testosterone. These androgens have helped significantly reduce those levels elevate free unbound testosterone.
- HCG-Human Chorionic Gonadotrophin – used to help treat delayed puberty, undescended testes or oligospermia (low sperm count). This treatment can be used as monotherapy or as an adjunct with exogenous testosterone. Your doctor will discuss with you an individual treatment plan.
Our doctors will make every effort to focus on bespoke treatment and individualised care. There is no one size fits all or cookie cutter approach.
Your treatment could include a suitable testosterone ester or combination of esters dosed appropriately so you will need very little oestrogen control if any. HCG is on offer to maintain fertility helping with both the size and function of your testes.
When you start on TRT (testosterone replacement therapy) the body begins to sense the elevation of exogenous testosterone through it’s conversion to oestrogen and then over time begins to slow down the production of any of your endogenous testosterone.
You might not mind because the overall output of your endogenous testosterone was low or low normal to begin with. It may or may not completely shut down but it will be greatly diminished depending on how your body senses and responds to it. At the end of the day the benefit of TRT will outweigh the substandard levels and symptoms associated with it. When used in men as a therapeutic, HCG mimics the actions of gonadatrophins LH and to a lesser degree FSH. With HCG the testes are receiving a steady signal to produce more testosterone. Essentially you are bypassing the hypothalmus and the pituitary and providing a signal directly to the testes. This 3 part approach (Exogenous Testosterone, Oestrogen Control, and HCG) maintains function and size of your testes whilst also benefiting from exogenous testosterone.
What about oestrogen blockers or aromatase inhibitors, how do they make a difference?
We know that HCG signals the testes to produce keeping the circulation of testosterone flowing through signalling the testicles to “stay open for business” there will be a glut of testosterone which will most likely be converted by various tissues that contain the aromatase enzyme. To minimise the amount of oestrogen it’s important not to create an imbalance. Putting the right amount of testosterone in the right conditions will provide in most cases the right amount of oestrogen.
In some cases where dose reduction, diet and lifestyle alone doesn’t lower oestrogen, a small tablet called an aromatase inhibitor may be prescribed. This tablet was originally designed for woman undergoing breast cancer treatment to keep the levels of oestrogen in a women’s body very low and thus preventing oestrogen sensitive breast cancer for recurring.
In men aromatase inhibitors also reduce the total amount of oestrogen in the body. The challenge for men is finding the right dose of testosterone so ideally no aromatase inhibitor is needed. If an aromatase inhibitor is needed then only the least amount should be used.
Too much oestrogen, prolactin, insulin resistance, or genetic predisposition may cause increased breast growth in men known as gynaecomastia or man boobs which may require surgical excision.
Many of the side effects associated with male testosterone therapy can also be attributed to oestrogen. You may have too much or too little. Both can be an issue. There are even cases of men who have low testosterone and elevated oestrogen with symptoms. In these men it’s not possible to lower there oestrogen level by lowering the dose of exogenous testosterone. In these cases aromatase inhibitors such as anastrozole in low doses may be needed for a short period of time.
Anastrozole has a half life of around 3 days which means you can can dose less frequently and with smaller doses around 0.25 to 0.5 once per week or every 5 days if this is absolutely needed.
This is key as too much reduction of oestrogen or too little oestrogen will dampen a man’s sex drive, cause the penis to loose sensitivity, and potentially affect mood, affect insulin sensitivity, decrease fat loss, and may cause bone loss if levels are too low for too long. It comes down to creating the right balance.
Supporting Studies in the scientific literature
- An update on male hypogonadism therapy Expert Opin Pharmacother. 2014 Jun; 15(9): 1247–1264. Published online 2014 Apr23.doi: PMCID: PMC4168024. NIHMSID: NIHMS627664 Prasanth Surampudi, MD,1 Ronald S Swerdloff, MD,2 and Christina Wang, MD‡†,3
- Testosterone Therapies. Urol Clin North Am. 2016 May;43(2):185-93. doi: 10.1016/j.ucl.2016.01.004. Epub 2016 Mar 18. Khera M1.
- Low testosterone associated with obesity and the metabolic syndrome contributes to sexual dysfunction and cardiovascular disease risk in men with type 2 diabetes.Wang C, Jackson G, Jones TH, Matsumoto AM, Nehra A, Perelman MA, Swerdloff RS, Traish A, Zitzmann M, Cunningham G.Diabetes Care. 2011 Jul;34(7):1669-75. doi: 10.2337/dc10-2339. Review. No abstract available.
- Changes in testosterone related to body composition in late midlife: Findings from the 1946 British birth cohort study David Bann, Frederick C. W. Wu, Brian Keevil, Hany Lashen, Judith Adams, Rebecca Hardy, Graciela Muniz, Diana Kuh, Yoav Ben‐Shlomo, Ken K. Ong Obesity (Silver Spring) 2015 July; 23(7): 1486–1492. Published online 2015 June 5. doi: 10.1002/oby.21092 PMCID: PMC4744737
- Testosterone and weight loss: the evidence Abdulmaged M. Traish Curr Opin Endocrinol Diabetes Obes. 2014 October; 21(5): 313–322. Published online 2014 August 28. doi: 10.1097/MED.0000000000000086 PMCID:PMC4154787
- Effects of testosterone on spatial learning and memory in adult male rats Mark D. Spritzer, Emily D. Daviau, Meagan K. Coneeny, Shannon M. Engelman, W. Tyler Prince, Karlye N. Rodriguez-Wisdom Horm Behav. Author manuscript; available in PMC 2012 April 1. Published in final edited form as: Horm Behav. 2011 April; 59(4): 484–496. Published online 2011 February 2. doi: 10.1016/j.yhbeh.2011.01.009 PMCID: PMC3081396
- Protective role of testosterone in ischemia-reperfusion-induced acute kidney injury Andrea Soljancic, Arnaldo Lopez Ruiz, Kiran Chandrashekar, Rodrigo Maranon, Ruisheng Liu, Jane F. Reckelhoff, Luis A. Juncos Am J Physiol Regul Integr Comp Physiol. 2013 June 1; 304(11): R951–R958. Published online 2013 April 3. doi: 10.1152/ajpregu.00360.2012 PMCID: PMC4074000
- Diagnosis and management of testosterone deficiency James A McBride, Culley C Carson, Robert M Coward Asian J Androl. 2015 Mar-Apr; 17(2): 177–186. Published online 2014 December 5. doi: 10.4103/1008-682X.143317 PMCID: PMC4650468
- Endocrinology of the Aging Male Andre B. Araujo, Gary A. Wittert Best Pract Res Clin Endocrinol Metab. Author manuscript; available in PMC 2012 April 1.Published in final edited form as: Best Pract Res Clin Endocrinol Metab. 2011 April; 25(2): 303–319. doi: 10.1016/j.beem.2010.11.004 PMCID: PMC3073592