Jade Teta, ND

As a naturopath, who spends a lot of time in the gym and fitness realm, I am often asked health-related questions. Reflecting on some of these questions, I realized there is an underlying theme for many of the men who seek me out.

Recently, I had a question asked by an acquaintance who made it clear, he was uncomfortable asking. The short of it is, this guy is a lifter. He is fairly healthy, beyond healthy, compared to the average Westerner. He does mostly all the right things. Sure, he drinks a little and stresses a lot. But who doesn’t, right?

He told me he has been fatigued, lacking motivation and drive for almost a year. He has slowly been gaining weight around the middle. Not enough that anyone else would notice, but he sees it. He has also starting to get soft around the chest. This is fairly common in men in their mid-thirties to forties, but not so common in a lifter. None of this bothered him too much, and then he told me about his erections. They are incomplete, unsustainable, and sometimes don’t come at all. This was the part that is obviously the most upsetting because his tone became desperate.

I hear all of this, and I have two questions for him. First, are you on any type of anabolic steroid, or did you just get off of them? I ask this because he is a weight lifter, and steroid use is so common. A well-known symptom of anabolics is, when you come off of them, the body has difficulty picking back up its own production of testosterone. The second question is when did you last have your testosterone levels checked? He answers “no” to the first question and “never” to the second question. This tells me I am going to need to give him a crash course in both erections and testosterone.

A Crash Course in Erections

Obviously, his major concern is the erections, but there is much more going on. Let me walk you through what I am thinking, as a naturopathic physician.

The male erection is a closely orchestrated event between the nervous system and blood flow into and out of the penis.

The brain registers a “sexually relevant” cue. This could be any number of things, and the stimulus response depends on the man. It may be cuddling up with his partner, seeing his partner walking across the room naked, maybe visual pictures or porn, while others may need direct penile stimulation. The point? The brain is where erections are made and they are often context dependent.

Assuming the brain is adequately sensitized to a sexual stimulus, nerve impulses are sent to the penis. This triggers a host of biochemical events that involve chemicals like nitric oxide (NO) being released, which then trigger cellular cyclic GMP (cGMP), which opens the blood vessels in the penis allowing more blood to flow in.

The penis is a pretty remarkable piece of physiological machinery. While blood flow is increased going in, a spongy layer of the penis, rich with capillaries, becomes engorged causing pressure to build up. This hydrostatic pressure causes the penis to inflate. This is all also contingent on a separate set of blood vessels that drain the penis. These vessels start to constrict under the increasing pressure and other biochemical events. The coordinated action of the incoming blood vessels, and the building pressure is what allows blood to rush in and stay in, creating an erection.

Where does testosterone get in on the action and contribute to this entire process? We will get to that in a second. First, I want to teach you a framework that will help you triage your own erection issues (or that of your partner). When you think of testosterone, libido, and erections, it is helpful to have a framework. The framework I use is the three Bs: brain, biochemistry, and blood flow.

The Brain

The sexual brain can be thought of as containing sexual stimulators and sexual repressors. Emily Nagowski, PhD, author of Come as You Are: The Surprising New Science that Will Transform Your Sex Life, calls these “accelerators and brakes.” In order for sexual desire to occur and sexual arousal to engage, the accelerators need to be turned up while the brakes are turned down.

It kind of works like this: You are sitting on the couch working frantically to get a proposal done for work. You are stressed. Your partner sits down next to you, and starts rubbing on you. You register a “sexually relevant stimulus” in your brain. This hits the accelerators. But, before you can really get aroused, the brain checks in on the context. It says, “This is nice, but I have to get this stuff done.” The stress you are under puts the brakes on.

The degree to which the stimulus can amplify the accelerators, and the stress holds on the brakes, will determine the quality of the erection response.

Many people get this all wrong. The brain is at work here, and it is not just an automatic stimulus response apparatus. There is much more going on. By the way, men, women have far more sensitive brakes compared to men. This is why foreplay and context are so much more important to their sexual arousal, desire, and function. It is also the same reason alcohol, or a first date, may result in a weak erection or a complete lack of erection for a guy, despite his strong desire. Every man, and likely most women, has experienced this phenomenon.

The brain is critical. Relaxation and adequate nerve stimulus to the penis is required. Women, it has nothing to do with you. And, guys, it is completely normal to occur on occasion.

To understand this brain effect better, think “Point and Shoot.” The two branches of the nervous system are P, parasympathetic, and S, sympathetic. Parasympathetic is relaxing, and sympathetic is stimulating. The balance of the P and S is critical. To get an erection, you need adequate P, or parasympathetic outflow. Think P, for Point, to remember this. To ejaculate requires adequate sympathetic outflow. Think S, for Shoot, to remember this.

A man who ejaculates too quickly and/or has weak erections may be dealing with poor parasympathetic (relaxing) outflow. This may be due to being overworked, overwhelmed, alcohol, stress, mood, medications, or any condition that disrupts nerve signaling—the most common being diabetes.

A man who is unable to ejaculate or takes longer to ejaculate may be suffering from the opposite: Poor sympathetic outflow. This, too, can be caused by stress, overwork, overwhelm, mood medications, and diabetes. This also may be a sign of the use of Viagra or another PDE5 inhibitor. For younger men, who are not overweight, this is almost always a result of some type of stress effect or medication since most are not dealing with diabetes. My friend was an example. We could assume the brain piece of this was fine.

Another brain concern has to do with the command and control center of the metabolism. The hypothalamus is an area of the brain that receives signals from other hormones and coordinates other hormone-producing organs in the body. The hypothalamus registers all the signals from the environment (sight, sound, temperature, etc.) and signals from inside the body (exogenous hormones) then adjusts the metabolism as needed, much like a thermostat.

As it pertains to the testes, the hypothalamus releases gonadotropin releasing hormone (GnRH), which binds in the pituitary and triggers the release of luteinizing hormone (LH). LH then travels to the testicles, aiding sperm production (mostly the job of FSH), and turning up testosterone production.   

If this hypothalamus-pituitary-gonad communication link is compromised, it can dramatically impact testicular function and testosterone. Testosterone inhibits feedback at the hypothalamus and can also be converted to estrogen via the enzyme aromatase. That estrogen plays a role in feedback to the pituitary, which is why SERMs (selective estrogen receptor modulators) like tamoxifen, are sometimes used in men.

The estrogen effect may come to be a major player here. We do not yet have proof, but many natural medicine practitioners, like myself, believe the sharp rise of low testosterone in young men may be connected with the estrogen saturation in our environment. Estrogen-like compounds are everywhere now. They are in our water, leach out of plastics, sprayed on our food as pesticides, and accumulate in the fat and milk of the animals we eat.

So, when we think “brain,” we also want to be thinking hypothalamus. The other interesting thing here is that the hypothalamus and pituitary are also responsible for thyroid and adrenal function. These are so critical to metabolic function; they are referred to as HP-axis (hypothalamus-pituitary-thyroid axis (HPT), hypothalamus-pituitary-adrenal axis (HPA), and hypothalamus-pituitary-gonadal axis (HPG, i.e. testicles and ovaries)). This will become important later.

This is why some therapies, like human chorionic gonadotropin (HCG), can be effective in multiple ways for men. It is also why low libido and low testosterone issues, coming from the brain, usually result in fatigue, sleep disruption, mood issues, weight gain, cold intolerance, etc. When the hypothalamus “takes a hit,” it negatively impacts multiple downstream processes in the thyroid, adrenals, and gonads.

The Biochemistry

Given my friend is younger and fit, I am thinking his issue is biochemical, not brain or blood flow related. I have already covered some of the biochemistry of erection, but there is a ton more.  Let’s just stick with some of the more relevant material.

I already explained how the nerve signals transfer into biochemical signals, including signaling molecule cGMP and NO (nitric oxide). Let’s cover this in a little more detail, as this is probably how testosterone gets involved in regulation of erection. When the brain sends nerve signals to the penis, NO is released and signals cGMP. This, then, dilates blood vessels and sets the erection cascade in motion with increased blood flow in and decreased blood flow out.

Cyclic guanosine monophosphate (cGMP) is broken down by an enzyme called phosphodiesterase 5 (PDE5). Since PDE5 degrades cGMP activity, if this enzyme is overactive, blood flow into the penis is slowed, and erection is either absent or incomplete.

This is how the erectile drugs Viagra, Cialis, Levitra, and others work. They each act as inhibitors to PDE5, prolonging action of cGMP activity, and therefore, allowing harder, longer lasting erections. Depending on the strength, their effects are short acting like Viagra (takes 30 min to kick-in and lasts 2-4 hours), or long acting like Cialis (takes a few hours to kick-in and lasts 18-36 hours). This may also be where low testosterone comes in.¹ Testosterone treatment increases NO activity and may stimulate healthy promotion of erectile tissue. Testosterone may also play a role in PDE5 inhibition because adequate testosterone levels are required for these drugs to work.

The brain is also impacted by testosterone. All the mechanisms as to how testosterone promotes libido and sexual function are not completely understood, but one of the hallmarks of any hormone is its ability to impact many enzymes and other hormone receptors involved in multiple areas.

Testosterone is likely acting as a priming apparatus for the male sexual brain and penile function.  Without this primer, the entire cascade is disrupted.

Blood Flow

Ultimately, erectile function is really about a blood flow problem. If nervous system function is good and testosterone levels are adequate but blood flow is compromised, then erections are compromised.

For younger guys who are fit and not overweight, blood flow is likely not the primary issue. However, it will always be involved, which is why erection drugs work.

Erection issues in older men, overweight men, and those with metabolic syndrome or diabetes, however, are almost always about blood vessel issues. High blood sugar, high blood pressure, and inflammatory mechanisms are highly damaging to the cells lining the blood vessels. These are the same cells that are functioning through NO and cGMP.

This is why lifestyle effects are so critical to men. Most men jump to testosterone and erection drugs, but studies show complete restoration of erections in men as old as eighty when lifestyle is corrected.²

Erection issues are early warning signs of cardiovascular disease. Fixing the issue at this stage requires a complete overhaul of diet and lifestyle, including weight loss, decreased sugar and carb intake, weight training, stress reduction, and more.

Unless you want to be reliant on erection drugs the rest of your life (which become less effective over time if you don’t correct the underlying issue) and you don’t want to die of a heart attack or stroke, then change your lifestyle: eat right and manage stress.

Taking testosterone therapy in the context of an unhealthy lifestyle won’t produce the expected results.

Lifestyle, Testosterone, and Erections

For most men under the age of fifty, not overweight, and no high blood pressure, the issue is likely brain or biochemistry related and NOT blood flow related. This is exactly what I was suspecting with my friend. One of the first things you will see in men with low testosterone is a lack of morning erections. Testosterone is usually at play here, as this is often a first warning something is up and a great biofeedback tool to measure progress with therapies. If the morning erections come back, this is a good sign.

I realize most men will want to jump right to testosterone replacement therapy, but not so fast. The thing you need to understand about hormones is that they work in symphony. You can’t simply throw testosterone into the mix and expect it to fix the issues. Hormones work in context. They are like people and behave differently depending on the environment they are in. Make sure the overall biochemistry is optimized through lifestyle if you want testosterone to work correctly.

In other words, the first step is to live a testosterone supportive lifestyle. The things that raise testosterone are the following:

• Adequate macronutrient intake—in other words, enough but not too much protein, fat, and carbohydrate.
• Adequate calorie intake—not too much and not too little.
• Adequate intake of micronutrients. The three most important for testosterone may be zinc, magnesium, and vitamin D. Being low in any of these will compromise testosterone levels. Adding these in, if you already have adequate amounts, will likely do nothing but correcting deficiencies will.
• Weight training and intense exercise. Lifting weights reliably stimulates testosterone. Intense exercise, that is high volume and heavy loads, is best.
• Enough, but not too much, exercise.
• Lots of walking, since this sensitizes the body to insulin and lowers the stress hormone cortisol—both of which, indirectly and negatively, impact testosterone.

Diet and Exercise

Since the hypothalamus is essentially a stress barometer, you do not want to train too hard, too often, or for too long. You also don’t want to go to dietary extremes by cutting calories and/or carbs too low. Do enough, but not too much; otherwise you risk downstream, negative effects flowing from a dysfunctional hypothalamus, which is severely and negatively impacted by insulin resistance and excess cortisol.

Blood sugar management and insulin sensitivity are critical to testosterone. There is a hormone called SHBG (steroid hormone binding globulin) that binds very strongly to testosterone, effectively removing it from the usable pool of hormones. Insulin resistance and excess cortisol both elevate SHBG. The end result is a reduction in usable testosterone, even when you are making enough. Also, excess cortisol and insulin have many other negative effects that disrupt metabolic function.

There are two dietary regimes I find useful as “off the shelf” advice for testosterone management: the 40-30-30 dietary regime for heavy exercisers and athletes and the 30-40-30 regime for everyone else. These formulas dictate the carb-protein-fat macronutrient ratios that I start most men out with. If men are overweight, I suggest a calorie intake that can be calculated by multiplying your body weight times 10. For those training heavily, the bodyweight multiplied times 15 is a good starting point. So, to reiterate:

• Calorie intake equal to 10 times body weight and a 30-40-30 diet for overweight less active men; and
• Calorie intake equal to 15 times body weight and 40-30-30 ratio for all men engaged in frequent, intense exercise.

All guys dealing with this issue should be walking daily (best insulin sensitizer and cortisol lowering behavior) and lifting weights at least three times per week (testosterone promoter).

Remember, it is a mistake to take these kinds of rules as gospel. Use these as a starting place only. Adjust based on three factors:

1. Are your hunger, energy, cravings and other hormonal feedback (i.e. libido and erection quality) improving?
2. Is your body composition achieving the V-Shape? (See http://www.metaboliceffect.com/me-shape-calculator/ )
3. Are your blood labs (especially free testosterone, total testosterone and SHBG levels) improving?

If all the above is true, then you are on the right track.

Testing and Labs

Once you get the diet and exercise under control, you want to make sure you get baseline labs. The labs recommended are the following:

• Testosterone (total and free),
• SHBG (if this is high to start with, diet and stress will need to be priority),
• High sensitivity estrogen (to rule out high aromatase. Some men aromatize testosterone to estrogen),

• Hemoglobin A1C (rule out high blood sugar and diabetes),
• Fasting Insulin (rule out insulin resistance),
• DHEA Sulfate (if low, supplementing can restore erectile function in 80%), and
• Vitamin D.

These should be done in addition to the general screening of lipids, CBC, and chem panel a doctor will do. Zinc and magnesium are also worth noting here; but since so many people are deficient and their supplementation has little risk, taking the supplement, ZMA, is likely wise and precludes the need for testing.

Research on things like horny goat weed, Longjax, and ForsLean, as well as other herbs and compounds, have little research supporting their use; and I personally have seen them as essentially useless clinically.

You can have these labs done directly at https://www.directlabs.com/.

Some supplements you may want to consider include the following:

• DHEA, if DHEA sulfate is low. In one study, 50 mg DHEA restored erectile function in upwards of 80% of males who were low.³
• Vitamin D.   Low vitamin D has been shown to impact testosterone, and restoring Vitamin D to levels between 50-100 ng/ml may raise testosterone; and it may help erections.⁴
• Citrulline malate. This is an amino acid that is a NO precursor and can act as a weak Viagra, assuring NO is abundant; 1.5g/day improved erections in men within one month.⁵
• Rhodiola Rosea.  This one is controversial, but I have personally seen it be effective. There are also, supposedly, some old Russian studies showing its benefit. I was never able to find the actual article/book that outlines these studies, but the reference is Rhodiola rosea is a valuable medicinal plant (Golden Root) (Saratikov, et al. Tomsk, Russia: Tomsk State University Press; 1987). I have seen people reporting that rhodiola increased testosterone, libido, and erection quality. Given rhodiola’s favorable effects on the hypothalamus, this makes sense. Although most of the people I have seen respond were doing other things too, I can’t say for sure this is effective; but, if you were my good friend, I would encourage you to take it (200-400 mg a day). It may also help premature ejaculation (makes sense given it is an adaptogen balancing the parasympathetic and sympathetic nervous system).⁶

Hormonal Approaches to Raising Testosterone

Okay, we are finally here. What happens if, when you test your levels, they are low? And, what is considered low? Most standard references for testosterone ranges are the following:

• Total testosterone normal = 300-1200 ng/dl (Many practitioners will treat if levels are below 500, and you have symptoms.)
• Free testosterone = 5-21 ng/dl

My recommendation is that a free testosterone below 10 and a total testosterone below 500 with testosterone-related symptoms, especially loss of morning erection, should be managed with the lifestyle changes and supplements listed above.

If there is no change after three months of concerted effort, then, and only then, consider testosterone replacement therapy (TRT). Keep in mind at this point that there is a difference between replacing testosterone and enhancing with testosterone.

When you do TRT, you are restoring normal levels, not trying to exceed them. Replacing to normal levels is not only beneficial for symptoms but, likely, one of the healthier things you can do.

Enhancing with testosterone by going over 1200 ng/dl is not necessary and may cause some issues. Remember, what you want when restoring testosterone is to bring your levels back to optimal and help the hypothalamus-pituitary-gonadal axis become healthier. Raising testosterone to levels beyond physiological works against this goal.

If levels are low right out of the gate, you have two options: (1) HCG monotherapy (and/or Clomid) and (2) testosterone replacement. One I prefer over the other.

HCG Monotherapy

Human chorionic gonadotropin (HCG) is an LH analog. Meaning, it is biochemically similar enough to the LH hormone that it interacts with the same receptors. This means it can be used to turn on the testicular machinery, sperm, and testosterone production.

There are stories about HCG increasing ejaculation volume (this is true), and increasing penis size (this is true too, but it may only be the case for those with hypogonadism or “micro-penis”). The internet chat boards certainly are not without their stories of slight enlargement with HCG in normal men.

In the two studies^7,8 I found on micro-penis, the gains were three-quarters of an inch in length and girth. Anyone who has normal penis size and has gained these effects with HCG, I am sure all of us men would be eager to hear.

HCG is a great option because, unlike testosterone, it may actually help the hypothalamus gonadal axis as opposed to suppressing it. It also seems to have less impact on estrogen, prostate mass, and cardiovascular parameters compared to the more traditional TRT, being equal or better than traditional TRT in raising testosterone.

I realize this information may contradict other information around the internet as it pertains to HCG, but this assessment is evidence based and taken from a well-done study on men aged 45-53 with low T.⁹ The study compared HCG against transdermal test, and two different injectables. 

In fact, many doctors give HCG along with their testosterone therapies to keep the hypothalamus working and the testicles from shrinking.¹⁰

Why would the testicles shrink, you wonder? Testosterone from an outside source turns off the hypothalamus/pituitary secretion of LH; and therefore, the testicles stop producing sperm and testosterone. This is why ejaculate volume and testicles can shrink in men taking testosterone. This, usually, is not a huge issue if the drug is not abused. HCG helps keep this from happening.

As an aside, steroids do not shrink the size of the glans penis (i.e. the shaft), just the testicles, and only if used in very high amounts for too long.

Using HCG alone is a reliable promoter of testosterone and may be the safer, more natural option to start with, in those with HPG issues. It also may be the best approach for those of you who have been on testosterone for a long period of time.

Based on the studies, there are a few approaches. If using TRT, then 250 IU of HCG taken as an intramuscular injection (IM) daily is the approach recommended. If you are using HCG alone, according to the study above where it was directly compared to TRT, the dose was 2000 IU per week.

Most doctors don’t like giving such a high dose of HCG all at once for fear of excess estrogen production and desensitization of LH receptors. Although this study did not show that, it may be a consideration.

Keeping any daily dose to 500 IU or less seems wise, which means you would be injecting 500 IU one to four times per week (500 IU – 2000 IU) for HCG monotherapy.

Clomid is another option in this regard. Clomid works by blocking estrogen hormone feedback at the hypothalamus. This increases natural LH production, which then stimulates testosterone production.

The dose for Clomid, at 25 mg per day or 50 mg every other day, has been shown effective in restoration of the HPG axis in men and very safe as well.  At least in one study, Clomid compared directly to TRT outperformed testosterone treatment with no side effects from long-term use (up to 40 months).¹¹

For those with secondary testosterone deficiency coming from the hypothalamus-pituitary axis, which is usually the case for younger men (<50 years), HCG and Clomid MAY be superior to TRT. As an aside, the cost of Clomid is vastly cheaper compared to TRT.

Testosterone Replacement Therapy (TRT)

The first consideration to be aware of is that steroids do not equal testosterone. Many men I have worked with will assume that, if they are taking anabolic steroids, they are taking testosterone.  This is not the case, and an important distinction.

Anabolic steroids can be testosterone or androgen derivatives. Drugs like Anavar, Trenbolone, Winstrol, Primobolan, etc. have anabolic and androgenic effects similar to testosterone, but they are not testosterone. This means they are NOT suitable for TRT. Such drugs are also frequently the culprit for erection issues and low testosterone, especially after stopping them. These “non-testosterone steroids” will shut down the body’s own production of testosterone, like any other steroid, but will not be able to replace testosterone’s full effects in the body. These are best left to bodybuilding circles.

Another consideration is the creams, gels, and orals of the pharmaceutical world. You can’t patent testosterone; so to make money off of the therapy, drug companies tinker around with different delivery systems. These approaches are far inferior to injectable testosterone, and I would not use them, unless you are completely averse to injections.

The main drugs to consider are testosterone cypionate, testosterone enanthate, and testosterone propionate. The different compounds bound to the testosterone determine its half-life and, therefore, the dosing frequency. Cypionate (50-100 mg) is usually dosed one to two times per week, as is enanthate (50-100 mg). Propionate dosage is every other day at 25-100 mg per day.

There are two others: testosterone suspension and Sustanon. Testosterone suspension is 100% testosterone, while the three above are testosterone bound to esters that increase the half-life of the drug and make for a slower absorption. Suspension is rarely used due to the need for daily dosing and the rapid spikes and falls that occur with its use. Sustanon, too, is rarely used in medical circles, mostly because it is not as widely available. It is a mix of the different testosterones and is a great option if you can find it.

Everyone has a favorite.  For my taste, I like propionate more than enanthate, and enanthate more than cypionate. For some reason, propionate causes me to hold less water and just gives me a “cleaner look” and more even effects.  But this is very much an individual thing.

Other Considerations

Of course, the biochemical pathways involved with testosterone therapy should be considered. Testosterone can be converted to estrogen via the enzyme aromatase. The use of aromatase inhibitors is beneficial in this regard, which is why many people will use Arimidex (anastrozole) along with their TRT.

Testosterone can also be converted into DHT, which may contribute to some side effects, including hair loss and acne; although, DHT may be a major libido enhancer.¹² This occurs via the enzyme 5-alpha reductase, which is why finasteride is often used with TRT as well.

The herbal world is filled with great aromatase and 5-alpha reductase inhibitors, often having both actions in one herb. I have found the use of products containing nettles, saw palmetto, pygeum, chrysin, and DIM a reliable way to control these two biochemical pathways without pharmaceuticals. The supplement I use is Androgen Complex (Metabolic Effect). The dose is six capsules daily.

Final Considerations

The final things to know when it comes to TRT are regarding testing and retesting. With TRT, we want to make sure we are not elevating prostate cancer and cardiovascular disease risks or other complications. You may want to consider monitoring PSA. This is a test, becoming more and more controversial, but still, may be the best we have to assess prostate changes over time.

You will also want to make sure hemoglobin and hematocrit levels are not going up while on therapy. This can increase the risk for blood clots.

Finally, watch estrogen levels and the liver enzymes ALT and AST to make sure you are not over aromatizing, and the liver is handling the therapy respectively.

Always take a close look at the free (direct), and total testosterone levels.

If you are doing things correctly, you should see favorable changes in your blood labs on TRT. Cholesterol, triglycerides, blood sugar, and inflammatory markers usually fall.

Obviously, testosterone is a requirement for male health, and proper TRT should be improving energy, mood, libido, erections, and body composition while also making you healthier.

This article was originally published in Townsend Letter (December 2017).

References

1. Castela A, et al. Testosterone, Endothelial Health, and Erectile Function. ISRN Endocrinol. 2011: 839149.
2. Martin SA, et al. Predictors of Sexual Dysfunction Incidence and Remission in Med. J Sex Med. 2014; 11: 1136–1147.
3. Reiter WJ, et al. Dehydroepiandrosterone in the treatment of erectile dysfunction: a prospective, double-blind, randomized, placebo-controlled study. Urology. 1999 Mar;53(3):590-4.
4. Sorenson M, Grant WB. Does vitamin D deficiency contribute to erectile dysfunction? Dermatoendocrinol. 2012 Apr 1;4(2):128-36.
5. Cormio L, et al. Oral L-citrulline supplementation improves erection hardness in men with mild erectile dysfunction. Urology. 2011 Jan;77(1):119-22.
6. Cai T, et al. Rhodiola rosea, folic acid, zinc and biotin (EndEP^®) is able to improve ejaculatory control in patients affected by lifelong premature ejaculation: Results from a phase I-II study. Exp Ther Med. 2016 Oct;12(4):2083-2087
7. Kim S-O, et al. Penile Growth in Response to Human Chorionic Gonadotropin (hCG) Treatment in Patients with Idiopathic Hypogonadotrophic Hypogonadism. Chonnam Med J. 2011 Apr; 47(1): 39–42.
8. Burgués S, et al. Subcutaneous self-administration of highly purified follicle stimulating hormone and human chorionic gonadotrophin for the treatment of male hypogonadotrophic hypogonadism. Human Reproduction. 1997;12(5): 980-986.
9. La Vignera S, et al. Late-onset hypogonadism: the advantages of treatment with human chorionic gonadotropin rather than testosterone. Aging Male. 2016;19(1):34-9.
10. Hsieh TC, et al. Concomitant intramuscular human chorionic gonadotropin preserves spermatogenesis in men undergoing testosterone replacement therapy. J Urol. 2013 Feb;189(2):647-50.
11. Taylor F, Levine L. Clomiphene citrate and testosterone gel replacement therapy for male hypogonadism: efficacy and treatment cost. J Sex Med. 2010 Jan;7(1 Pt 1): 269-76.
12.  Traish AM, et al. The dark side of 5α-reductase inhibitors’ therapy: sexual dysfunction, high Gleason grade prostate cancer and depression. Korean J Urol. 2014 June;55(6):367-79.

Other Resources

Cunningham SK, et al. The relationship between sex steroids and sex-hormone-binding globulin in plasma in physiological and pathological conditions. Ann Clin Biochem. 1985; 22: 489-497. 

Hormone Replacement with Dr. Aaron Grossman (TRT and HRT) (podcast). October 13. 2016.

Kim ED, et al. The treatment of hypogonadism in men of reproductive age. Fertil Steril. 2013 Mar 1;99(3):718-24.

Moss JL, et al. Effect of rejuvenation hormones on spermatogenesis. Fertil Steril. 2013 Jun;99(7):1814-20.

Stanworth RD, Jones TH. Testosterone for the Aging Male. Clin Interv Aging. 2008 Mar; 3(1): 25–44.

Published January 13, 2024

About the Author

Jade Teta, ND, is an integrative physician specializing in natural health, fitness, and body transformation. He is the co-author of The Metabolic Effect Diet and Lose Weight Here. He completed his undergraduate training at North Carolina State University, earning a bachelor of science degree in biochemistry. He then went on to study at Bastyr University in Seattle, Washington, completing his doctorate in naturopathic medicine. Dr. Teta has worked in the fitness and weight loss fields for over 20 years, and is the co-developer of the rest-based training system for personal training and group exercise. He is also the co-founder of the Naturopathic Health Clinic of North Carolina and of the health, fitness and international fat-loss company, Metabolic Effect.

Dr. Teta writes and lectures extensively on the subjects of lifestyle medicine, natural health, fitness and weight loss to both health care professionals and the public. He has been a contributing expert on Lifetime TV, Fox News, Onfitness magazine, Oxygen, Delicious and many more. He blogs extensively on the topics of hormonal approaches to building muscle and burning fat, the science of exercise and supplementation, sleep and stress management, the psychology of change and happiness, and that one size does not fit all when it comes to leading a healthy lifestyle.