maze around the shape of a human head with a big red question mark in the center

Dr. Osborn Answers Your Questions

1) What constitutes low testosterone?
2) When does testosterone supplementation makes sense?
3) What are the major risks patients face?


Low testosterone is a clinical as opposed to a laboratory diagnosis. It is not simply “low testosterone” on blood testing. What constitutes “low” for one individual may be different than what is considered low for another. So-called “normal” testosterone constitutes levels that fall within a huge range (roughly between 350 ng/dL and 1,100 ng/dL). And herein lies the problem. You may have symptoms of hypogonadism (fatigue, loss of muscle mass, poor libido, etc.) and have T levels within the “normal” range. Likely you would benefit from testosterone replacement therapy regardless (provided other causative etiologies have been ruled out).  

Unfortunately, most mainstream physicians fail to recognize that a “normal” T level means relatively little in the context of symptomatic hypogonadism. Again, what be considered a “normal” value (level), may not be normal for you. Discuss T supplementation with your doctor if you suffer from any of the aforementioned symptoms (which typically begin in one’s early 30’s). If he/she is unwilling to consider HRT, well, find a new doctor.

The risks of testosterone treatment are minimal despite the media ranting. To date, not a single one of my many HRT patients has developed side effects from treatment. This is due to cautious prescribing habits. Side effects as discussed in the text include alopecia (low percentage of patients), prostatic “flare” (Testosterone does not cause prostate cancer!), polycythemia, low sperm count and in the case of injectable T, infection. These risks are far outweighed by the benefits of supplemental testosterone.

What about hypothyroidism? I’ve heard it’s quite common. What are the symptoms? How is it treated?

Hypothyroidism is the most common age-related endocrine (hormone) disorder. Who doesn’t have an “underactive thyroid,” right? 

Truth be told, this condition characterized by fatigue, weight gain, cold intolerance and hair loss to name a few affects millions of Americans. Interestingly, more than fifty percent of those affected are unaware of their condition, their treatable condition. [Source:  American Thyroid Association] As optimal thyroid levels are integral to a variety of physiologic processes (including brain function), they are routinely screened for in both baseline and follow-up laboratory testing.  Low levels (in the context of clinical symptoms) are treated with Armour Thyroid (a glandular preparation with both T3 and T4) and less often Synthroid. The treatment of hyperthyroidism is typically deferred to an endocrinologist and may require more invasive testing/treatments (ultrasound-guided biopsy, for example in the event a thyroid nodule is discovered on examination).

Treatment of the far more common hypothyroid state is usually well-tolerated. Side effects of treatment (with Armour Thyroid) include insomnia, tachycardia (rapid heart rate), headache, diarrhea and increased sweating. These are uncommon however and are typically addressed with medication dosage and timing changes.

For how long does one remain on testosterone replacement therapy (TRT)?

TRT is lifelong. Do you stop your blood pressure medication once deemed hypertensive?  Likely not.  Remember testosterone production, like progesterone, begins declining in one’s early 30’s.  Testosterone replacement therapy should be considered when a man (or woman) develops symptoms of deficiency (described elsewhere) in the context of low serum levels.  Attempts can be made to restore natural hormone production with beta (β)  or Clomid, however in the event of failure, TRT should be initiated.  And continued indefinitely (barring any unforeseen side effects).

Testosterone is not “cycled.” Does your body synthesize testosterone for 8-12 week intervals and then halt production? No. So why would periods of “on” and “off” be recommended? Cycling protocols are utilized by bodybuilders to minimize toxicity of the massive doses of hormones (most of which are dangerous synthetics) necessary to remain competitive at the professional level. These in no way mimic the body’s natural production of testosterone. 

We at the clinic aim to restore a youthful hormone profile and concomitantly minimize side effects, lifelong. This is NOT about “gearing up” for the next bodybuilding competition. It IS about health.

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As a woman, I am concerned about the potentially masculinizing effects of testosterone. Is my Adam’s apple going to get bigger if placed on TRT? Will I develop a deeper voice?

Did you have those issues when you were an adolescent when your hormones were raging? Doubtful. 

Testosterone is produced is females as it is in males, except at lower physiologic doses. If has identical effects in both genders.  Women, like men, need testosterone (as men need both progesterone and estrogen).  It supports bone mass, augments muscular size and strength, improves mood and increases libido.

Feel 18 again? Properly dosed, testosterone is unlikely to cause any untoward side effects. Of course, the dosage in females is lesser than that of males. Why? Physiologically, women produce less! That’s to some degree what makes a female, well… a female. The stigma of women with deep voices and thickened jawlines stems from the bodybuilding arenas. Again, this is not about bodybuilding but about health.

What is the correlation between Free testosterone and Sex Hormone-Binding Globulin (SHBG)? What is the difference between the Free and Total testosterone levels?

Both free and total testosterone levels should be assayed. Why? The majority of circulating testosterone is protein-bound. Albumin binds testosterone “reversibly.” It has affinity for the molecule but freely releases into the tissues. Sex hormone-binding globulin has a higher affinity for testosterone (and other sex hormones) and binds them “irreversibly.”  

Once bound therefore, testosterone is unavailable to the tissues, as SHBG does not readily release its grip on the molecule. That said, an SHBG level must be obtained as part of your baseline lab studies. Noting all three levels, your physician will best be able to tailor your therapy. You may have high-normal Total T levels but very low Free T due to high levels of circulating SHBG. This can be remedied easily with the addition of stinging nettle root extract (and other agents potentially). Obtaining these values (Free or Total testosterone) in isolation is of little value.

There are many ways to dose injectable testosterone, some better than others. What is your practice paradigm? How do you avoid the “roller-coaster” effects of intermittent dosing?

I use testosterone cypionate in my practice and dose according to knowledge of its half-life. That said, I prescribe injections once or twice weekly (at half the dosage).

Patient feedback is paramount to optimize one’s response to HRT. If one feels better on twice weekly dosing, so be it. Levels of both T (total and free) and estradiol are checked frequently as to avoid any significant deviations from optimal levels. There tends to be a less aggressive approach in the community however. I know of many patients who, in the past, have been given prescriptions for cypionate injections once monthly. This carries with it significant risks, namely marked fluctuations in testosterone and estradiol levels in addition to dramatically stressing (and suppressing) the central nervous system’s hormonal regulation machinery (HPTA).

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What is beta-HCG? Do you believe in its usage?

Loaded question. HCG or human chorionic gonadotropin is the “pregnancy hormone” which, through the actions of progesterone, supports the placenta during the first trimester. Pregnancy tests assay for the beta (β) subunit of the HCG molecule (a so-called “glycoprotein’) in the urine (First Response, for example) or blood.  
Interestingly, there is biochemical similarity between HCG and the pituitary hormone known as “leutinizing hormone” or LH. LH stimulates testicular production of testosterone (and as stated above, progesterone in females); so does HCG. In fact, one needs only to inject the beta (β) subunit of the molecule (or approximately half of it) to elicit a significant rise in serum testosterone levels.

In my clinic, I use beta-HCG to support testicular production of testosterone in males of childbearing age on TRT. Males even considering fathering children in the future will be prescribed beta-HCG to prevent the natural shutdown of sperm production induced by testosterone (through a negative feedback loop).  That said, males of childbearing age are often prescribed beta-HCG in isolation as primary therapy. 

The purpose is two-fold: 

  1. Increase testosterone production via normal mechanisms (testicular production) as opposed to undergoing injections of the bio-identical hormone (with its potential to suppress normal testosterone and sperm production)
  2. Stimulate spermatogenesis (sperm production)

So yes, I believe in the usage of beta-HCG in the context of the above. It works! In fact, my third child Makenna was fathered without hiatus from supplemental testosterone. How? Beta-HCG.

That said, I do not believe in utilizing beta-HCG is a dietary supplement. The “HCG diet” is nothing more than a low-calorie, modified starvation protocol that results in loss of both body fat and significant muscle mass in a nutritionally depleted state. It is unsustainable. The diet, like most fitness trends, has fallen in and out of favor for the past 50+ years. Skip it.

Let’s talk about TRT and cardiovascular risk. Recent studies suggest an increased risk of cardiovascular events in males on testosterone replacement. Is this true?

A very timely question. Simply put, the studies are flawed (as are many published in peer-reviewed journals).

There are several major flaws in the 2013 JAMA study, for example:

  1. The men were not properly monitored and the dosages of T therefore were not restorative. The men enrolled in this study only boosted their mean total T to 332 ng/dL. This is low in the context of cardiac protection (testosterone levels > 500-550 ng/dL have been shown to confer protection).
  2. Estrogen levels were not routinely assayed. Likely many of the subjects, by virtue of aromatization, had high serum estradiol levels. Excess circulating estrogen predisposes individuals to thrombotic events.  It is critical therefore to not only monitor free and total testosterone, but also estradiol levels.

Bottom line: Testosterone in physiologic doses (at optimal levels) is cardio-protective. How could the resultant increased vitality (and tendency to exercise, which itself confers protection from cardiovascular disease), muscle mass and libido be associated with elevated risk of heart attack? Aren’t these entities associated with youth? That said, adolescents exhibit very high levels of T on formal testing. When did you last hear of a 16 year-old male dying of a heart attack?  

Substantiating the beneficial effects of testosterone replacement therapy are the numerous studies (with large cohorts) correlating increased mortality with low testosterone:

  1. Pye SR, Huhtaniemi IT, Finn JD, et al. Late-onset hypogonadism and mortality in aging men. J Clin Endocrinol Metab. 2014 Apr;99(4):1357-66.
  2. Yeap BB, Alfonso H, Chubb SAP, et al. In older men an optimal plasma testosterone is associated with reduced all-cause mortality and higher dihydrotestosterone with reduced ischemic heart disease mortality, while estradiol levels do not predict mortality. Journal of Clinical Endocrinology & Metabolism. 2014;99(1).
  3. Li L, Guo CY, Jia EZ, et al. Testosterone is negatively associated with the severity of coronary artery disease in men. Asian Journal of Andrology. 2012;14:875–878.
  4. Hyde Z, Norman PE, Flicker L, et al. Low free testosterone predicts mortality from cardiovascular disease but not other causes: the health in men study. Journal of Clinical Endocrinology & Metabolism. 2012;97(1):179–189.
  5. Araujo AB, Dixon JM, Suarez EA, et al. Endogenous testosterone and mortality in men: a systematic review and meta-analysis. Journal of Clinical Endocrinology & Metabolism. 2011;96(10):3007–3019.
  6. Haring R, Völzke HV, Steveling A, et al. Association of low testosterone levels with all-cause mortality by different cut-offs from recent studies. European Heart Journal. 2010;31:1494–1501.
  7. Corona G, Monami M, Boddi V, et al. Low testosterone is associated with an increased risk of MACE lethality in subjects with erectile dysfunction. Journal of Sexual Medicine. 2010;7(4):1557–1564.
  8. Malkin CJ, Pugh PJ, Morris PD, et al. Low serum testosterone and increased mortality in men with coronary heart disease. Heart. 2010;96(22):1821–1825.
  9. Tivesten Å, Vandenput L, Labrie F, et al. Low serum testosterone and estradiol predict mortality in elderly men. Journal of Clinical Endocrinology & Metabolism. 2009;94(7):2482–2488.
  10. Vikan T, Schirmer H, Njølstad I, et al. Endogenous sex hormones and the prospective association with cardiovascular disease and mortality in men: the Tromsø study. European Journal of Endocrinology. 2009;161(3):435–442.
  11. Yeap BB, Hyde Z, Almeida OP, et al. Lower testosterone levels predict incident stroke and transient ischemic attack in older men. Journal of Clinical Endocrinology & Metabolism. 2009;94(7):2353–2359.
  12. Khaw K-T, Dowsett M, Folkerd E, et al. Endogenous testosterone and mortality due to all causes, cardiovascular disease, and cancer in men: European prospective investigation into cancer in Norfolk (EPIC-Norfolk) prospective population study. Circulation. 2007;116(23):2694–2701.
  13. Maggio M, Lauretani F, Ceda GP, et al. Relationship between low levels of anabolic hormones and 6-year mortality in older men: the aging in the chianti area (InCHIANTI) study. Archives of Internal Medicine. 2007;167(20):2249–2254.
  14. Shores MM, Matsumoto AM, Sloan KL, et al. Low serum testosterone and mortality in male veterans. Archives of Internal Medicine. 2006;166(15):1660–1665.
  15. Oh J-Y, Barrett-Connor E, Wedick NM, et al. Endogenous sex hormones and the development of type 2 diabetes in older men and women: the Rancho Bernardo study. Diabetes Care. 2002;25(1):55–60.

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The data are clear:

“Men with low testosterone usually present with bothersome symptoms, particularly ED, and require treatment to address those problems, not simply for cardiovascular prevention purposes. The benefits of conventional cardiovascular risk reduction with exercise and weight reduction are fundamental to management but are frequently unsuccessful. There is a considerable body of evidence that low testosterone is associated with increased cardiovascular and cancer mortality. A policy of taking little or no action for these men based on concerns of increased cardiovascular and cancer risk associated with physiological replacement would seem illogical. There is considerable evidence of modest cardiac and metabolic benefits that are shown to reduce cardiovascular risk plus sexual, mood, and quality of life changes associated with restoring testosterone levels. These may add up to substantial benefit to many patients. These benefits may potentially denied to patients by fears over prostate and cardiac risk that is not currently supported by evidence.”  

[Source:  G. Hackett, M. Kirby and A. J. Sinclair. Testosterone Deficiency, Cardiac Health, and Older Men. Int J Endocrinol. 2014.]

Numerous studies support the benefits of restoring of a youthful hormone profile while only a few negate this. These studies too were of poor design. As with many evolving medical treatments, there will always be resistance to their acceptance and integration into mainstream. In my mind, and in the minds of those currently reaping the benefits of a well-designed HRT regimen, this is truly a no-brainer…

The fact that estradiol (an estrogen subtype) levels were not routinely assayed (nor controlled) is a purported flaw in the 2013 JAMA study that vilified TRT. Why is this important? What bearing does estradiol have on one’s health?

Circulating testosterone is subject to “aromatization” and biochemical conversion to estradiol (E2). Estradiol maintains bone mineral density (post-menopausal women are predisposed to osteoporosis, right?), is cardioprotective and supports sexual function.  Bottom line?  Both men and women need estradiol. It is not a gender-specific sex hormone, although levels in females are higher than those in males. Estradiol is also a growth factor and has been implicated in tumor progression in various hormone-sensitive cancers (i.e., breast). Control of estradiol levels is therefore important. More importantly in women, a balance between estradiol and progesterone is critical. 

Simply put, progesterone keeps the growth-promoting effects of estradiol in check. Therefore, female HRT candidates are always placed on combination therapy with both estrogen and progesterone.

Back to the JAMA study… Elevated levels of estradiol in men are not only associated with obesity, sexual dysfunction and gynecomastia, but also with thrombotic events (blood clotting within a vessel and resultant stroke, heart attack, mesenteric thrombosis or pulmonary embolism).  Undoubtedly, a percentage of patients in the JAMA study cohort had elevated levels of estradiol due to aromatization of the exogenous (supplemental) testosterone, predisposing them to coronary events.  Estradiol levels were not routinely assayed however and contribute to the spurious nature of the study conclusions.

It is imperative to control estradiol levels in male patients on TRT. Akin to the necessary balance between progesterone and estradiol in females, there is a critical balancing act between testosterone and estradiol in males. Typically, males fare well with estradiol levels approximating 20 pg/mL. 

This is not always the case however. More important than the absolute value is the ratio between testosterone and estradiol. And there is no “one size, fits all.” We are all biochemically distinct. An optimal T:E ratio for you is likely to be different from that of your sibling, for example. You may function well with an estradiol level of 20 pg/mL, while he may experience hot flashes or erectile dysfunction (symptoms of low estradiol). He may function optimally with an estradiol level of 35 pg/mL, while you may experience nipple sensitivity (from relatively high estradiol). This is precisely why there must open communication lines between physician and patient. Treatment will at times require tailoring to meet the needs of the individual.  

To manipulate circulating estradiol levels in males on TRT, I routinely prescribe anastrozole, a so-called “aromatase inhibitor.” The chemotherapy drug? Yes, the same compound utilized to temper the growth-promoting effects of estrogen in breast cancer patients. Other estrogen modulators include tamoxifen, chrysin and zinc, the latter two being non-pharmaceutical in nature.

Is therapeutic phlebotomy a treatment for testosterone-induced polycythemia? How many times a year should a man on TRT have his hemoglobin and hematocrit tested?

Many of my patients are routinely phlebotomized. I tolerate hematocrit levels of 50. Anything above warrants concern. I tend to be aggressive about phlebotomy to avoid any potential issues due to “sludging.” That said, patients undergo laboratory testing at 3-month intervals initially. After optimizing their hormone levels, I will typically see patients (and obtain labs) every 6 months. In the interim, they are being phlebotomized per schedule (which ultimately depends upon their response to the prescribed blood draws: a STAT hematocrit is obtained prior to every phlebotomy session).

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Do you believe patients with an elevated PSA but otherwise presenting in healthy/normal condition avoid TRT?

It is not unreasonable to utilize TRT in patients with elevated PSA provided the patient has a normal digital rectal exam (as documented by a urologist) and lacks urinary symptoms.  I typically discuss these patients with the treating urologist who may opt to perform a biopsy prior to the initiation of TRT. Again, testosterone does not cause prostate cancer, but prostate cancer is hormone-responsive. Therefore, testosterone therapy should be avoided in individuals harboring untreated prostate cancer.

A patient with treated prostate cancer however may be treated with the consent and under the supervision of his urologist. [Morgentaler A, Conners WP. Testosterone therapy in men with prostate cancer: literature review, clinical experience, and recommendations. Asian J Androl 2015;17:206-11]

The evidence-based guidelines on the evaluation and treatment of androgen deficiency syndromes in adult men updated in 2010 by The Endocrine Society are the most current recommendations available to guide practitioners. In addition to recommending serial testosterone measurements, the Task Force suggests that clinicians consider case detection by measurement of total testosterone levels in men with certain clinical disorders (i.e., type II diabetes) in which the prevalence of low testosterone levels is high. What is your take on aging and low testosterone?

Chicken or the egg controversy reiterated. At this point, we as scientists are unsure whether hormonal decline “causes” aging or whether the converse is true. Regardless, as posed in the question, there are environmental factors to which the “disease” of aging (and age-related disease) may be attributed. 

In fact, there is indirect evidence that aging is 75-80% environmental in etiology. Keep in mind that “environment” encompasses ALL factors to which the body is exposed: nutrition, physical and psychological stressors and toxins to name a few. That said, many conditions such as type II diabetes and obesity, both of which have their underpinnings in insulin resistance, could cause hypogonadism. The proverbial “quick fix” is to place a patient on restorative testosterone therapy, thereby correcting one’s lab values. This however is a short-sighted approach, in essence addressing the epiphenomenon, as opposed to the phenomenon (type II diabetes in this case), or treating the effect and not the cause. I wholeheartedly agree with the Task Force’s in this regard and routinely screen my patients for disease risk factors. In this context, I address BOTH the low testosterone AND said risk factors concomitantly. This is my practice paradigm. One is not addressed without the other.

Patients are started on a rigorous exercise program (as per the protocol outlined in Get Serious), advised as to proper nutrition and supplementation, placed on medication (I utilize metformin, aspirin and antihypertensives aggressively) and counseled on the management of stress. Restorative hormonal therapy is often initiated concomitantly. The effects of the above are synergistic. Lowering disease risk factors (inflammation and insulin resistance) increases testosterone levels. Supplemental testosterone, in a reciprocal manner, reduces risk factors for disease. It’s a double whammy!      

In the wake of the FDA’s recent ruling mandating "black box" label warnings on all testosterone products, is the climate for men seeking to optimize their hormones becoming better or worse?

Answer: Neutral. I believe the FDA is simply looking out for the pharmaceutical industry and the populace at large.  By virtue of their labeling, the FDA is exonerating itself as a governing body by indirectly publicizing the resultsof the recent TRT study, albeit flawed.  This should be held in the same regard as commercial-embedded warnings issued by pharmaceutical companies.  And while attorneys may be chomping at the bit to vilify prescribing physicians in the wake of such labeling, this is by no means proof of danger (and likely is the opposite in fact).  Answering your question, sometimes perceived “negative” publicity serves an antithetic function, and hopefully in this case will raise awareness of the health-promoting benefits of TRT in select individuals.   

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Is “bio-identical” better than pharmaceutical grade testosterone?

The term ‘bio-identical’ is misconstrued. It is often claimed that bio-identical testosterone is “better” or more “natural” than pharmaceutical-grade testosterone. Case in point: “Bio-identical preparations are better because they’re synthesized to be exactly like human testosterone circulating in the blood.” Untrue. Pharmaceutical grade injectable testosterone is bio-identical. It is an “esterified” form of testosterone (Testosterone Cypionate or Enanthate for example). 

In other words, testosterone is attached to a carrier molecule or ester (i.e. Cypionate) that is enzymatically cleaved (broken off), leaving… testosterone, the “identical” molecule that your gonads produce.  

The fact that a testosterone preparation is pharmaceutical grade, does not equate to it being a potentially dangerous “synthetic,” the all-too-often abused substance of bodybuilders. “Synthetics” are NON-bio-identical testosterone-like substances, synthesized in the lab (or potentially in someone’s garage) that promote anabolism. Foreign to the body, synthetics put the user at risk for a whole host of dangerous side effects (liver dysfunction and cancer, for example). Dr. Osborn does not advocate the usage of synthetics. The risks simply outweigh the benefits. This is about health after all, right? This is NOT about bodybuilding.

How are the hormone treatments administered, orally or are they injected? How often?

Hormones may be administered in a variety of ways. Some routes are better than others however. Bio-identical testosterone may be safely delivered transdermally, via pellet or via intramuscular injection. There are pros and cons of each route. Dr. Osborn does not recommend oral testosterone. Similar to those of oral estrogen, the breakdown products (metabolites) of oral testosterone are potentially carcinogenic. That said, transdermal estrogen is typically prescribed as a compounded dual estradiol/estriol preparation (BiEst). Progesterone may be compounded into a cream as well or taken orally.

Dr. Osborn will determine the specific route of administration. Dosage and frequency will be tailored to your symptoms (and may be altered amidst treatment for optimization purposes) in the context of serum levels.

Where can I give an intramuscular (IM) injection? What are the risks? Does it hurt? How is it administered?

The skin and muscles cover nerves, blood vessels and bones. IM injections are given in specific sites to minimize danger to these vital structures. These include the shoulder (deltoid), thigh (vastus lateralis) and buttock (gluteus). The chosen site is a matter of personal preference.

Risks of an IM injection aside from the above are infection and hematoma formation (bleeding within the injected muscle). In the context of the latter, care must be exercised if you are on antiplatelet or anticoagulant agent. Overall, the risks of an IM injection are extremely low.

The trivial “pain” associated with an intramuscular injection is mostly due to apprehension and the anxiety of self-administration. One quickly becomes habituated to this practice and the perceived pain diminishes. This is provided proper injection techniques are utilized:

  1. Wash your hands thoroughly with soap and dry them completely.
  2. Uncap the needle by holding the syringe (preloaded with medication) with your writing hand and pulling on the cover with your other hand.
  3. Hold the syringe in your dominant hand. Place the syringe under your thumb and first finger. Let the barrel of the syringe rest on your second finger.
  4. Swab the target skin area with an alcohol wipe and allow it to dry.  [Ideally, IM injections should be performed after a shower for antiseptic reasons.]
  5. Depress and pull the skin taut with your free hand (using your thumb and first finger).
  6. Use your wrist to inject the needle at a 90-degree angle (straight in). Do not slowly push the needle in nor jab the skin. The action should be deliberate. The needle should be advanced into the muscle nearly to the hub. The depth of needle insertion is unrelated to the perceived pain. It is rather a function of insertion technique (site selection and continuous insertion pressure).
  7. Release the skin. As you let go of the skin, hold the syringe so it stays pointed straight in.
  8. Pull back on the plunger slightly to assure you are not in a blood vessel. [In the event of blood return into the needle, remove the needle, and discard it.  The procedure should be repeated on the opposite side.]
  9. Push down on the plunger to inject the medication. Sometimes this will cause subtle twitching of the muscle into which the medication is being injected.
  10. Remove the needle and apply pressure to the injection site for 1 minute.
  11. Discard the needle in a Sharps container.

This technique will be demonstrated during your clinic appointment if requested.

The staff is available to assist you virtually (via a HIPAA-compliant videoconferencing platform) should the need arise. You will gain confidence in no time!

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How are subcutaneous (SQ) injections performed? Aren’t those similar to the injections that diabetics self-administer?

Insulin is administered subcutaneously, yes.  So is beta-HCG.  SQ injections are relatively painless injections into the fatty layer of tissue just under the skin. As the medication is injected superficially, a tuberculin or insulin syringe (with a short needle) is used. The procedure, like the intramuscular injection, is straightforward:

  1. Wash your hands thoroughly with soap and dry them completely.
  2. Uncap the needle (of the preloaded tuberculin or insulin syringe).
  3. Hold the syringe in your dominant hand. Place the syringe under your thumb and first finger. Let the barrel of the syringe rest on your second finger.
  4. Swab the target skin area with an alcohol wipe and allow it to dry.  
  5. Grasp the skin with the hand your free hand.
  6. Holding the syringe barrel tightly with your writing hand, use your wrist to insert the needle through the skin at a 45-degree angle. Remember, this injection is superficial.
  7. Once the needle is all the way in, push the plunger down slowly to inject the syringe’s contents. If a small bubble if fluid is noted beneath the skin or the injection was painful, do not become alarmed. Inject slightly deeper the next time (the needle should enter the skin at > 45-degree angle).
  8. Remove the needle and apply gentle pressure with a cotton swab for 1 minute or less.
  9. Discard the needle in a Sharps container.

Subcutaneous injections are typically performed in the lower quadrants of the abdomen. Other potential sites are the upper arm and thigh. Again this is patient-dependent and a matter of comfort.

How do I store the medication?

Transdermal hormone preparations are typically refrigerated. Injectable testosterone (Cypionate and Enanthate for example) is stored at room temperature and should be shielded from light (to prevent oxidation).  Reconstituted beta-HCG is to be refrigerated.

 When will I feel the medication starting to work?

The effects of HRT are typically experienced within the first several weeks in both males and females.  In females on dual estrogen/progesterone therapy (+/- testosterone), sleep patterns tend to improve, as does vitality.  Males on TRT typically experience similar effects and often notice return of morning erections.  

If started on thyroid replacement (typically Armour thyroid), you will likely notice an increase in energy levels in a similar time frame.

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What should I do if I miss my injection date?

[This answer applies to those prescribed injectable testosterone or beta-HCG.] Firstly, do not panic! This is not an emergency nor is it necessary to contact the doctor. Simply take your usual dosage and continue your current schedule. Do not revise your current injection schedule based upon your missed dosage, as this will likely confuse matters. Become habituated to a certain dosing regimen and stick to it.  Intermittent variations will not affect your response to HRT.

This applies to those of you on HRT who are travelling. If you are scheduled to be away from home for more than a week, plan to take your medications with you. This obviously includes needles and syringes as well.  Reconstituted beta-HCG is to be kept on ice in a smaller cooler.  Injectable testosterone (also in a small vial) should be maintained at room temperature.  If you are travelling by plane, be prepared to present copies of your prescriptions to the TSA agents if asked. Remember, testosterone is a schedule III drug.

At what intervals are follow-up labs drawn?

Good question. Follow-up labs are typically drawn 12 weeks after initiation of an HRT regimen. Of course this is barring any unforeseen issue that would warrant an earlier reassessment. A premenopausal woman for example may not experience a substantial reduction in hot flashes initially. Dr. Osborn may order a repeat estradiol level therefore to assure adequate serum levels. A male may similarly develop nipple sensitivity after several weeks of TRT. This may prompt a repeat lab draw earlier than scheduled.

Those patients who require “biochemical tweaking” based upon symptoms and serology (lab results) will undergo repeat testing quarterly. Those who appear to be optimized will present to the clinic semiannually having undergone repeat labs.

A Couple of Rules:

  1. MEN on injectable TRT should schedule their follow-up labs 6 days post-injection. Drawing labs any other time (in the wake of an in injection) will result in erroneous values (and mandate a repeat draw). Males on compounded testosterone cream (transdermal) should apply the medication in the AM and several hours later present for their blood draw. The blood is to be drawn from the arm opposite to that upon which the testosterone was applied.
  2. FEMALES on HRT are to have their labs drawn during the first 25 days of the month, as Dr. Osborn typically withholds progesterone on days 26-31. As per the above, the compounded transdermal preparation(s) should be applied in the AM prior to the scheduled blood draw. The blood is to be drawn from the arm opposite to that upon which the preparations were applied.
How much does Hormone Replacement Therapy (HRT) cost?

Hormone replacement therapy (medications only) costs $100-150 per month. This does not include clinic visits, laboratory studies and other diagnostic tests, nor the recommended supplements. Ultimately, the level of commitment to your heath is a personal decision. You and you alone have a choice, a choice to be healthy or…

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What changes do you see taking place on the TRT front over the next five years?

The acceptance of TRT will continue to lag behind the robust manifestations of its life-changing effects. Millions of men and women are successfully utilizing TRT currently and regaining their vitality and lust (pun intended) for life. And without side effects. Properly prescribed, TRT is safe. Its acceptance is simply a matter of its gaining momentum through documented treatment successes. A revolution of thought is in order. We are fast moving more towards a preventive health care paradigm and ultimately into one of human optimization. The treatment of disease post-facto will soon be of days of yesteryear.

Talk about your practice—where is it going relative to all of the TRT clinics springing up across the country.  

Firstly, this not a “TRT clinic.” The mainstay of my practice is Neurosurgery albeit with a holistic slant. I make concerted efforts to treat all patients conservatively unless there are pressing neurologic issues that mandate surgery. Anti-inflammatory agents (high-dose omega-3 fatty acids and pharmaceuticals) are utilized, as are exercise and nutritional strategies.

Degenerative disease of the spine (affecting a large percentage of my patients) is an age-related disease. And herein lies the tie-in to Anti-Aging and Regenerative medicine. Treating degenerative disease of the spine is nearly identical to the treatment of all other degenerative diseases: coronary artery and cerebrovascular disease, diabetes and Alzheimer’s dementia. It’s just different geography. And the aging process itself is a degenerative disease, right? 

This notion will drive the expansion of my practice ultimately. Many physicians have taken this leap of faith already, as the rewards of primary care medicine have become virtually non-existent. And while it is unlikely that I will forego Neurosurgery (patients will still fall ill), I plan on making every effort, through the looking glass of anti-aging physician, to alert the masses that we are simply doing it backwards.

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