Testosterone, Body Composition, and Sex

A Doctor’s Guide

Tired? Getting fat? Having issues in the bedroom? Here’s everything a man needs to know about hormones, drugs, supplements, and his willy.


Dave Can’t Get It Up

Dave is a lifter. He’s healthier than the average Westerner and he does most things right when it comes to training and diet. Sure, he drinks a little and stresses a lot. But who doesn’t, right?

But over the last year, Dave has been feeling fatigued. He’s also lacking motivation and drive, and he’s slowly been gaining weight around the middle. He’s even starting to get soft around the chest. This is fairly common in men in their mid-thirties to forties, but way less common in a lifter. But what’s really bothering Dave are his erections. Sometimes they just don’t happen, and when they do they can’t be sustained.

Dave is actually a friend of mine. When he talked to me about these issues I asked him two questions:

  1. Are you on any type of anabolic steroid or just getting off of them? 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.
  2. When’s the last time you had your testosterone levels checked?

Dave answered “no” to the first question and “never” to the second question. So what’s going on here, and what should Dave do?

A Crash Course In Erections

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 might be cuddling up with his partner or seeing his partner walking across the room naked. For others, it could require direct stimulation. The point is: the brain is the hub of erections.

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, which open the blood vessels allowing more blood to flow in. 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 it 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 contribute to this entire process? We’ll get to that in a minute. First you need to know about the three B’s.

The Three B’s

When you think of testosterone, libido, and erections, it’s helpful to have a framework: brain, biochemistry and blood flow.

1. Brain

The sexual brain can be thought of as containing sexual stimulators and sexual repressors. Emily Nakowski, PhD, 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 works like this: You’re sitting on the couch working frantically to get a proposal done for work. You’re stressed. Your girlfriend sits down next to you and starts rubbing on you. You register a “sexually relevant stimuli.” This hits the accelerators, but then the brain checks in on the context. The stress you’re under puts the brakes on. The degree to which the stimulus can amplify the accelerators, combined with the degree to which the stress is stepping on the brakes, will determine the quality of the erection and response.

Many people get this all wrong. The brain is at work here and it’s not just an automatic stimulus response apparatus. There’s much more happening. (By the way, women have far more sensitive brakes compared to men. This is why foreplay and context are so much more important for their sexual desire, arousal, and function.)

This is the same reason alcohol or a first date may result in a weak or a complete lack of erection, despite a strong desire. Every man, and likely many women, have experienced this phenomenon. The brain is critical, and relaxation with adequate nerve stimulus to the penis is required. Women, it has nothing to do with you. And guys, it’s completely normal.

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 P and S is critical. To get a boner you need adequate P, or parasympathetic outflow. Think P for “point” to remember this. To ejaculate requires adequate sympathetic outflow. Think S for “shoot.”

So, a man who ejaculates too quickly and/or has weak erections is dealing with poor parasympathetic (relaxing) outflow. Being overworked, overwhelmed, alcohol, stress, mood medications or any condition that disrupts nerve signaling could cause this, the most common being diabetes.

A man who’s unable to ejaculate, or takes forever to ejaculate, may be suffering from the opposite: poor sympathetic outflow. This too can be caused by stress, mood medications, and diabetes. This may also be a sign of the use of Viagra or another PDE5 inhibitor. For younger men who aren’t overweight, this is almost always a result of some type of stress effect or medication.

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 then coordinates other hormone-producing organs in the body.

The hypothalamus registers all the signals from the environment (site, 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 testicles, the hypothalamus releases gonadotropin-releasing hormone (GNRH), which binds in the pituitary and triggers the release of luteninizing hormone. LH then travels to the testicles, aiding sperm production 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 the drug tamoxifen is sometimes used in men.

The estrogen effect may come to be a major player here. We don’t 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: our water, leaching out of plastics, sprayed on our food as pesticides, and the accumulation 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 critical to metabolic function: we call them the HP-Axi. HPT= hypothalamus-pituitary-thyroid axis (HPT), hypothalamus-pituitary-adrenal axis (HPA) and hypothalamus-pituitary-gonadal axis (HPG, i.e. testicles and ovaries).

This is why some therapies, like HCG, can be effective in multiple ways for men. It’s 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.

2. Biochemistry

Remember, the nerve signals transfer into biochemical signals, including signaling molecules cGMP and nitric oxide. This is probably how testosterone gets involved in regulation of erection. When the brain sends nerve signals to the penis, nitric oxide 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.

cGMP is broken down by enzyme called phosphodiesterase 5 (PDE5). Since PDE5 degrades cGMP activity, if it’s overactive, blood flow into the penis is slowed and erection is either absent or incomplete.

This is how Viagra, Cialis, Levitra and other erectile dysfunction drugs work. They each act as inhibitors to PDE5, prolonging action of cGMP activity, therefore allowing harder, longer lasting erections (yay science!).

This may also be where low testosterone comes in. Testosterone treatment increases nitric oxide activity and may stimulate healthy promotion of erectile tissue. Testosterone also may play a role in PDE5 inhibition because adequate testosterone levels are required for these drugs to work.

Testosterone is also having an impact on the brain. It’s not completely understood how testosterone promotes libido and sexual function, 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.

3. Blood Flow

Erectile dysfunction is really a blood flow problem. If nervous system function is good and testosterone levels are adequate, but blood flow is compromised, this is “no bueno” for erections.

For younger guys who are 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 nitric oxide and cGMP.

This is why lifestyle corrections are so critical for 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.

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, and stress reduction. In other words, stop living and acting like an imbecile when it comes to your erections. If you want to sit on the couch crushing Cokes and crunching Doritos, then your penis is going to rebel at some point!

Unless you want to be reliant on enhancement 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 get it together: eat right and manage stress. Taking testosterone in the context of an unhealthy lifestyle won’t do a thing for you.

Lifestyle, Testosterone, and Erections

For most healthy men under the age of fifty, the issue is likely going to be brain or biochemistry related and NOT blood flow related. One of the first things you’ll see with low testosterone is a lack of morning wood.

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 context. You can’t simply throw testosterone into the mix and expect it to fix the issues. Hormones are like people and behave differently depending on the environment they’re in. Make sure the overall biochemistry is the proper setup to have testosterone work correctly.

The first step is to live a testosterone-supportive lifestyle. The things that raise testosterone are:

  • Adequate macronutrient intake. Get 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 – 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.

Insulin, Cortisol & Testosterone

Since the hypothalamus is essentially a stress barometer, you don’t 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 negatively impacted by insulin resistance and excess cortisol.

Blood sugar management and insulin sensitivity are critical to testosterone. There’s 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’re making enough. Not to mention, excess cortisol and insulin have many other negative effects that disrupt metabolic function.

Diet

There are two dietary regimens I find useful as “off the shelf” advice for testosterone management: the 40-30-30 dietary strategy for heavy exercisers and athletes, and 30-40-30 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, then bodyweight multiplied times 15 is a good starting point.

So, to reiterate:

  • 10 x bodyweight and a 30-40-30 (carbs, protein, fat) diet for overweight less active men.
  • 15 x bodyweight and 40-30-30 (carbs, protein, fat) ratio for all men engaged in frequent, intense exercise.

All guys dealing with this issue should be walking daily (the best insulin sensitizer and cortisol-lowering behavior), and lifting weights at least three time per week (testosterone promoter). Remember, it’s 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 (like libido and erection quality) improving?
  2. Is your body composition achieving the V-shape?
  3. Are your blood labs – free testosterone, total testosterone, and SHBG levels – improving?

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

Testing and Labs

Once you get diet and exercise taken care of you’ll want to get a baseline of labs:

  • Testosterone, total and free
  • SHBG
  • Hemoglobin A1C (to rule out high blood sugar and diabetes)
  • Fasting Insulin (to rule out insulin resistance)
  • DHEA Sulfate
  • Vitamin D
  • High sensitivity estrogen (to rule out high aromatase since some men aromatize testosterone to estrogen)

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, it’s safe and wise to supplement with Elitepro (on Amazon).

ElitePro Minerals at Amazon

It’s worth noting here that things like horny goat weed, longjax, forslean and other herbs and compounds have little research supporting their use and I’ve seen them as essentially useless clinically.

You can have these labs done directly at DirectLabs and CHEKD. Just google them.

Some things you may want to consider:

  1. DHEA, if DHEA sulfate is low. In one study, 50mg DHEA restores erectile function in 80% of males who were low.
  2. Vitamin D. Low vitamin D has been shown to impact testosterone, and restoring Vitamin D to levels between 50-100ng/ml may raise testosterone to help with erections.
  3. Citrulline malate (on Amazon). This is an amino acid that’s a nitric oxide precursor. It can act as a weak Viagra, assuring nitric oxide is abundant. 1.5g per day improved erections in men within one month.
  4. Rhodiola. This one is controversial but I’ve personally seen it to be effective. I’ve seen people reporting that rhodiola increased testosterone, libido, and erection quality. Given rhodiola’s favorable effects on the hypothalamus, this makes sense. Take 200-400mg a day. It may also help premature ejaculation. That makes sense given it’s an adaptogen balancing the parasympathetic and sympathetic nervous system.

Hormonal Approaches to Raising Testosterone

Let’s say you get your testosterone tested. What’s considered low? Most standard reference ranges are:

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

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 are no changes after three months of concerted effort, then and only then, consider testosterone replacement therapy or TRT. Keep in mind, there’s a difference between replacing testosterone and enhancing with testosterone. When you do TRT you’re seeking to restore normal levels, NOT trying to exceed them. Replacing to normal levels is not only beneficial for symptoms, but likely one of the healthiest things you can do.

Enhancing with testosterone by going up 1200 ng/dl isn’t 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 potential works against this goal.

If levels are low right out of the gate, you have two options: HCG monotherapy (and/or clomid) or testosterone replacement.

HCG Monotherapy

Human chorionic gonadotropin (HCG) is an LH analog. Meaning, it’s biochemically similar enough to the LH hormone to interact 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 aren’t without their stories of slight enlargement with HCG in normal men. In the two studies I found on micro-penis, gains were three-fourths of an inch in length and girth.

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, while being equal or better than TRT in raising testosterone.

This assessment is evidence-based and taken from a well done study on men aged 45-53 with low T. The study compared HCG against transdermal testosterone and two different injectables.

Many doctors give HCG along with their testosterone therapies to keep the hypothalamus working and the testicles from shrinking. Why would the testicles shrink? Testosterone from an outside source turns off the hypothalamus’ 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 isn’t a huge issue if the drug isn’t abused, but 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 may also be the best approach for those who’ve been on testosterone for a long period of time.

Based on the studies, there are a few approaches here. If using TRT, then the approach recommended is 250IU of HCG taken as an intramuscular injection (IM) daily. If you’re using HCG alone, according to the study above where it was directly compared to TRT, the dose is 2000IU 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 didn’t show that, it may be a consideration.

Keeping a once daily dose to 500IU or less seems wise, which means you’d be injecting 500IU 1-4 times per week (500IU – 2000IU) for HCG monotherapy.

Clomid

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

For those with secondary testosterone deficiency coming from the hypothalamus-pituitary axis, which is usually the case for younger men, HCG and Clomid may be superior to TRT. Plus, the cost of Clomid is vastly cheaper compared to TRT.

Testosterone Replacement Therapy (TRT)

First off, steroids do not equal testosterone. Many will assume that if they’re taking anabolic steroids they’re taking testosterone. This isn’t 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 won’t 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 wouldn’t use them unless you’re completely averse to injections.

The main drugs to consider:

  • Testosterone Cypionate
  • Testosterone Enanthate
  • Testosterone Propionate

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’s not as widely available. It’s a mix of the different testosterones and is a great option if you can find it.

The different compounds bound to the testosterone determine its half-life and therefore the dosing frequency. Cypionate is usually dosed 1-2 times per week (50-100mg) as is Enanthate (50-100mg 1 to 2 times per week). Propionate dosage is every-other-day at 25-100mg per day.

Everyone has their favorites. For my taste, I like propionate > enanthate > 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.

Estrogen, DHT and Hair Loss

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. 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’ve found the use of products containing nettles, saw palmetto, pygeum chrysin and DIM a reliable way to control these two biochemical pathways without pharmaceuticals.

Testing and Health

With TRT, we want to make sure we’re 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’ll also want to make sure hemoglobin and hematocrit levels aren’t 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’re 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’re 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.

SURGEAMZ

References

References

  1. Stanworth RD et al. Testosterone For The Aging Male. Clin Interv Aging. 2008 Mar;3(1):25–44. PMC.
  2. 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 Sep;22 ( Pt 5):489-97. PubMed.
  3. Burgués S et al. Subcutaneous self-administration of highly purified follicle stimulating hormone and human chorionic gonadotrophin for the treatment of male hypogonadotrophic hypogonadism. Hum Reprod. 1997 May;12(5):980-6. PubMed.
  4. 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. PubMed.
  5. Kim Ed et al. The treatment of hypogonadism in men of reproductive age. Fertil Steril. 2013 Mar 1;99(3):718-24. PubMed.
  6. Moss JL et al. Effect of rejuvenation hormones on spermatogenesis. Fertil Steril. 2013 Jun;99(7):1814-20. PubMed.
  7. Martin SA et al. Predictors of sexual dysfunction incidence and remission in men. J Sex Med. 2014 May;11(5):1136-47. PubMed.
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