Testosterone Replacement Therapy

At Tier1 Health & Wellness we’ll treat you if you’re experiencing symptoms of hypogonadism, regardless of your total testosterone levels. Your lab results are a guide and reference point.

What to Expect When You go on TRT

Here’s how we treat our patients at Tier1 Health & Wellness when they come to us for testosterone replacement therapy.

1. Step one: Click here to schedule a consultation with Dr. Nichols and begin your hormone optimization journey .
2. Step two is a full physical  from a healthcare provider near you and lab work with a lab near you.
3. Step three is a telemedicine appointment with Dr. Keith Nichols or Angie Nichols (for women.)
4. Step four is enrollment in our program.
5. Step five is a personalized TRT plan based on your symptoms and lab results.
6. Step six is follow-up where we’ll monitor your progress and adjust treatment if necessary.

The Elephant in the Room (Undiagnosed Low Testosterone)

All over the world men are showing up at primary care providers or specialists with symptoms of low testosterone. But instead of properly diagnosing the problem, they’re prescribed medications that only deal with the symptoms and not the root cause. For example, men will come in with high cholesterol and get prescribed statins. Or they’ll get prescribed viagra for erectile dysfunction. This happens because the majority of doctors aren’t educated about testosterone deficiency and don’t even know to look for it.

If testosterone levels are checked, in many cases the patients still go undiagnosed because their levels are “within range.” The patient could be suffering with many of the symptoms of low T but because the doctor doesn’t know any better, the patient doesn’t get the help they need.

And if by some luck a patient is both tested and diagnosed with low testosterone, he isn’t given the right treatment protocol to alleviate his symptoms because the physician has little experience treating men for testosterone deficiency and doesn’t know what works.

Following the Science: The Mountain of Evidence in Favor of TRT

Dr. Keith Nichols and Angie Nichols have both been trained by Dr. Neal Rouzier. Dr. Rouzier is an expert and a pioneer in the field  of Preventive Medicine specializing in bioidentical hormone replacement therapy. He has over 30 years of experience as a practicing physician and educator, and he has spent his life researching medical literature to support safe and effective natural therapies to provide personalized care to his patients. Dr. Rouzier is also the published author of “Natural Hormone Replacement for Men and Women: How to Achieve Healthy Aging”, which is a leading book on hormone replacement.

Along with Dr. Rouzier, Dr. Nichols has reviewed every scientific study he could find on testosterone from the 1930s to today. They were able to debunk every myth associated with testosterone therapy (more info below.) And they discovered benefits of testosterone therapy few doctors know or even talk about. The truth is, testosterone is probably the most important hormone for a man’s overall health and well being. And its importance only increases as we get older. Low testosterone is the reason why men experience rapid decline in old age.

And it is because of our extensive research and experience treating patients with hormone therapy that we are able to develop customized treatment plans that are 100% backed by science.

How Long Does it Take to Feel the Benefits of TRT?

Every patient we treat is biologically unique. There is no magic dosage we can prescribe or magic lab results we can reach to make our patients feel better. We treat every patient individually based on how they feel. Therefore, the time taken to experience the benefits of TRT is different for every patient. Our goal is symptom resolution and our treatment programs are based on this goal.

That being said, medical literature suggests the effects of TRT can be felt in these timeframes:

• Significant improvement in libido in 3-6 weeks
• Significant improvement in quality of life after 4 weeks
• Improvement in erectile dysfunction after 12 weeks; improvement in ejaculatory function may take 12 months
• Reduction in body fat, increase in muscle and strength in 12-16 weeks; effects on body weight can take up to 2 years
• Effects on depressive mood are detectable after 3-6 weeks, with maximum improvement after 18-30 weeks
• Improvements in bone density are detectable after 6 months, with the full beneficial effects taking 2-3 years

Testosterone Optimization vs Testosterone Replacement

There’s a difference between testosterone optimization therapy (TOT) and testosterone replacement therapy (TRT.) With TRT you’re only using therapeutic testosterone to achieve beneficial effects. This may be adequate for men in their 20s and early 30s who’re suffering from low testosterone/hypogonadism.

But for men in their 40s and older the ideal is hormone optimization, not just testosterone replacement. TOT is based on the understanding that each hormone has beneficial effects and we want to maximize their beneficial effects by optimizing their levels. And just like with testosterone, the better the levels of your hormones, the better the effects.

The goal of TOT or hormone optimization is prevention. We want to prevent age-related disease, disability, dependence and frailty. We want to preserve our health span and retain our strength and vitality as we age. TOT is about achieving a better quality of life as a whole.

Because of this, when we treat our patients at Tier1 Health & Wellness we’re as concerned about preventing cardiovascular disease, insulin resistance, and cancer as we are about building muscle, losing fat, and increasing sex drive.

Myths About Testosterone Therapy are Due to Flawed Research

“To address widespread concerns regarding the medical condition of testosterone (T) deficiency (TD) (male hypogonadism) and its treatment with T therapy, an international expert consensus conference was convened… Nine resolutions were debated, with unanimous approval… (6) there is no scientific basis for any age-specific recommendations against the use of T therapy in men; (7) the evidence does not support increased risks of cardiovascular events with T therapy; (8) the evidence does not support increased risk of prostate cancer with T therapy…”

Morgentaler A, et al. “Fundamental concepts regarding testosterone deficiency and treatment: international expert consensus resolutions.” Mayo Clin Proc. July 2016;91(7):881.

TRT is safe and effective. There is not a single randomized controlled trial that proves that testosterone is harmful to your health. On the contrary, more and more research is suggesting the opposite.

The myths and misconceptions about testosterone today are the result of misinterpretations of poorly conducted studies. Any time testosterone has been allegedly shown to have negative effects or no effect, the experiment conducted had one of two flaws.

• In the case of negative effects, the subjects of the experiment had comorbidities.
• Not enough testosterone was administered to achieve the desired beneficial effects

Moreover, testosterone has been used clinically since 1937. If testosterone did cause men harm, we would have ample proof.

Finally, many primary care and even endocrine doctors have not educated themselves as to the truth of testosterone therapy, and merely follow the guidelines of the American Urological Association  and the Endocrine Society Guidelines that are based on these flawed studies.

As a result, the medical community’s general refusal to treat hypogonadal men with testosterone replacement and hormone optimization has caused great harm to millions of men around the world.

Testosterone Therapy and Your Prostate

The belief for over seven decades has been that high testosterone causes prostate cancer or increases a man’s risk of developing prostate cancer, that low testosterone is protective against prostate cancer and that if you raised  testosterone you would cause an  existing prostate cancer to grow rapidly…The “equivalent of pouring gasoline on a fire”.

Now where did this androgen hypothesis originate? It came from a paper written in 1941 by two urologists Drs Huggins and Hodges. Dr. Huggins was a very well-known urologist who in fact went on to win the Nobel Peace Prize in 1966 for his work with hormones and cancer.

In this paper they looked at men with metastatic prostate cancer. Back then there was not a PSA test so they looked at something called prostate acid phosphatase as a serum marker for metastatic prostate cancer. In this study Dr. Huggins reported that when men were castrated either surgically or chemically the acid phosphatase levels went down. He also gave testosterone injections to men and he reported that in every man that got testosterone injections the acid phosphatase levels went up. Now this was an important paper at the time because it was the first paper that identified a cancer to be hormonally sensitive. This paper established three things: 1. That prostate acid phosphatase could be used as a serum marker for metastatic prostate cancer. 2. Castration was effective for metastatic prostate cancer. 3. Testosterone injections given to men with metastatic prostate cancer was dangerous.

Now when you take a closer look at the paper you see that testosterone injections were only given to three men. Results were given for only two of those men and one of those men had been surgically castrated so he was no longer hormonally intact and what we would call “androgen deprived “. So the general conclusion that “cancer of the prostate is activated by testosterone injections” was based on one hormonally intact patient who received testosterone injections for only 18 days who’s acid phosphatase levels went up and down and were essentially uninterpretable.

So decades of depriving men of testosterone was based on the over interpretation of the results of one single man in one study

Now you may wonder how that can happen but the problem was that in the 1940s and 50s there weren’t many physicians with experience using testosterone so no one had an adequate knowledge to question the results so it became dogma… that testosterone was dangerous for prostate cancer

It wasn’t until the 1990s that a Harvard urologist by the name of Abraham Morgentaler began to question the validity of the Androgen hypothesis. In 1988 he began treating men with sexual dysfunction and  low testosterone levels with testosterone . At that time there wasn’t any Cialis or Viagra so treatment options were limited. What he noticed was that not only did they improve sexually but they also improved both physically and mentally. Now at this time his treatment defied standard medical practice because in the 1980s testosterone therapy was limited to three groups of men.

1. Men who had congenital or genetic disorders like Klinefelter’s

2. Pituitary disorders

3. Those with absent testes.

He became concerned because some of his colleagues warned him that he could potentially be causing harm based on the work of Dr. Huggins.

So in 1992 he began performing biopsies prior to initiating testosterone therapy in symptomatic testosterone deficient men who had normal PSA’s and digital rectal exams in an effort to rule out an existing prostate cancer.  What he found was 11 out of the first 77 men that he biopsied had prostate cancer. Now remember low testosterone was supposed to be protective against  prostate cancer and what he found was that approximately 14% of men with low testosterone levels had prostate cancer. Now this percentage was almost the same as the percentage of men that have prostate cancer with increased risk factors such as an elevated PSA or a positive digital rectal exam. 

So low testosterone was found not to be protective and these findings were published in the Journal of the American medical Association in 1996.

So now that he knew that low testosterone was not protective , what about high testosterone being harmful?

In 2004 Dr. Morgentaler published the paper “risks of testosterone replacement therapy and recommendations for monitoring” in the New England Journal of medicine.  For that paper he performed a review of the World literature between 1985 to 2004 looking for any worrisome relationship between testosterone and prostate cancer or testosterone therapy and prostate cancer.

He was unable to find a single article that testosterone increased a man’s risk of getting prostate cancer or that testosterone therapy caused prostate cancer progression.

He also made the observation that with a 10 fold increase in testosterone prescriptions after the release of Androgel in 2001  there was not an epidemic of prostate cancer. We know that 50% of men more than 50 years old have micro foci of prostate cancer in their prostates.  If Increasing levels of androgens cause cancer to grow more rapidly then we should see more cancer growth in these men but we don’t. The observation has  also been right  in front of us for decades that younger men with high testosterone levels don’t get prostate cancer but instead it is a disease of aging when testosterone levels decline.

So in 2007  Dr. Morgentaler developed the saturation model to make sense of two opposite observations that the data reported. Castration decreases testosterone and the PSA goes down. If you increase testosterone levels out of the castrate range the PSA also increases. But the data also shows that for most of the range of testosterone levels including supraphysiologic levels there’s no change in PSA level or prostate size.

This is because androgens have a limited ability to stimulate prostate tissue. In order for androgens to exert an effect on prostate tissue they must first  bind to the androgen receptor. Once the androgen receptors are fully saturated with androgen any increase in androgen will simply be excess.  This saturation of the androgen receptors occurs at a very low level which is around 250 ng/dL.  Above this level androgens have no further effect on benign or cancerous prostate tissue growth.

Think of the prostate like a house plant. If you deprive the plant of water it will shrink.  If you give it water at this point it will grow. Giving it any additional water past this point will have no effect on  growth. You could give it a constant water supply and it will never grow into a tree. Once it’s thirst has been quenched giving it any additional water will have no effect on growth and the same goes for testosterone and the prostate.

So what does the modern data show us?

1. In hypogonadal men testosterone therapy does not increase the risk of developing prostate cancer even in high-risk individuals. It may in fact have a protective role against high-grade cancer and Studies have shown that higher levels of testosterone can suppress prostate cancer growth. There is an inverted U with regard to prostate cancer cell proliferation and testosterone levels. At low Testosterone levels there is suppression of prostate cancer cell proliferation, between castrate levels and the saturation level (hypogonadal) there is growth, and with high levels of testosterone there is  once again suppression of prostate cancer cell proliferation. The unfortunate reality is that about 1 in 6  men have prostate cancer and if you are in a clinic and you’re seeing at least 60 patients then you are most likely treating at least 10 men with active prostate cancer.  So all of these clinics are in effect treating men on active surveillance with prostate cancer without any detrimental effects.

2. Testosterone therapy does not increase the risk of progression in men on active surveillance

3. Testosterone therapy does not increase the risk of biochemical recurrence after treatment of prostate cancer by radiation therapy or radical prostatectomy. Some studies have shown decreased recurrence rates in men on testosterone therapy.

Multiple studies have revealed that low testosterone is associated with:

1. Higher grades of cancer

2. A more advanced stage of cancer at surgery

3. A increased rate of recurrence after surgery

4. Decreased survival

It is not high testosterone levels that are associated with poor prognostic factors but it appears to be low testosterone levels.

Testosterone and Hematocrit (Red Blood Cell Count)

The most common side effect of testosterone therapy, and the one that causes the most concern for the patient and their family physician, is a secondary erythrocytosis which is an increase in red blood cells.  It is often described by the patient and their physician as “thick blood” requiring a blood donation because they  fear it could possibly lead to a heart attack, stroke, or blood clot.

Where does this fear originate?  When the family physician or internist sees an increase in red blood cells along with hemoglobin and hematocrit, it is frequently misinterpreted as the patient having Polycythemia Vera which is a myeloproliferative neoplasm of the bone marrow (bone marrow cancer). Thrombosis (blood clots) are a leading cause of morbidity and mortality in this disorder. Polycythemia vera is known as a primary erythrocytosis where there is an unregulated proliferation of hematopoietic clonal stem cells which leads to over production of red blood cells, white blood cells, and platelets.  In Polycythemia Vera, in contrast to the secondary erythrocytosis from testosterone therapy, not only is there a quantitative change in the number of circulating blood cells, but there is also a qualitative change that leads to the expression of procoagulant characteristics. In addition there are abnormalities involving the vascular endothelial cells which become procoagulant in response to inflammatory stimuli. These abnormalities result in a hypercoagulable state leading to an increase in arterial thrombosis and venous thrombosis.  Therefore part of the recommended treatment is blood donation to reduce the risk of thrombosis. The risk of elevated hematocrit seen in patients with polycythemia vera cannot be extrapolated to hematocrit elevation seen during testosterone therapy.  They are not the same and should not be treated as such.

The secondary erythrocytosis from testosterone therapy is an increase in red blood cells only leading to an increase in hemoglobin and hematocrit. The mechanisms behind testosterone stimulating red blood cell production is not completely understood but is thought to occur through stimulation of erythropoietin, stimulation of hematopoietic progenitor cells, and reduced hepcidin.  A secondary erythrocytosis is also seen in other conditions such as smoking, obstructive sleep apnea, chronic obstructive pulmonary disease, and living at high altitude.  While a primary erythrocytosis has been well established as a risk factor for thromboembolic disease the risk of a  secondary erythrocytosis has not been shown to cause an increase in thromboembolic events in any randomized control trial or prospective study to date. Most guidelines recommend following hematocrit after initiating testosterone therapy and if the Hct exceeds 54% clinicians should either adjust testosterone dosage, stop therapy, order phlebotomy, or recommend a combination of these.  These recommendations are based on assumptions and the Hct cut off of 54% was arbitrarily chosen and not based on any study showing harm when this value is exceeded with testosterone therapy. The upper limit of normal for hematocrit in most laboratory reference ranges for healthy adult males is 54% which is where this value is likely derived. 

This normal hct range for men is for those without a secondary erythrocytosis and not for men on testosterone or living at high altitude for instance.  There are over 80 million people that live higher than 2,500 meters and they develop a secondary erythrocytosis. Men in parts of Bolivia for instance have a normal range of Hct from 45-61%. These men are not at an increased risk of thrombotic events nor do they have to undergo phlebotomies to manage their hematocrit.  One also cannot ignore the observation that literally tens of thousands of men presently use and abuse testosterone in this country and have done so for decades. A large percentage of these men are not under the supervision of a physician or getting lab work and yet we have not seen an epidemic of heart attacks, strokes, or blood clots in these men. Almost all previously reported cases of testosterone treatment related venous thromboembolism were seen in patients with a previously undiagnosed thrombophilia like factor five Leiden deficiency.

The other concern with increasing hematocrit is that it will increase viscosity and decrease blood flow resulting in thrombotic events.  In experimental studies using rigid glass viscometers or cone-plate viscometers there is a logarithmic increase in viscosity with increasing hematocrit. It is inappropriate to correlate these in vitro viscosity readings to what occurs to flowing blood through tiny distensible vessels in vivo. In other words, viscometer measures in these experiments do not translate to human blood vessels.  Firstly, the flow through these narrow blood vessels is rapid (high shear rate), which in a non-Newtonian fluid such as blood causes a marked decrease in viscosity. Second, blood flowing through these narrow channels is axial with a central core of packed red blood cells sliding over a peripheral layer of lubricating low viscosity plasma. With a secondary  erythrocytosis there is an increase in blood volume which enlarges the vascular bed, decreases peripheral resistance and increases cardiac output. Therefore, in a secondary erythrocytosis optimal oxygen transport with increased blood volume occurs at a higher hematocrit value than with a normal blood volume. A moderate increase in hematocrit may be beneficial despite the increased viscosity.

Testosterone also exerts multiple beneficial effects on the vasculature and its components which may protect against thrombosis. In other words testosterone has positive effects on vascular reactivity.

• Testosterone is a vasodilator and increases nitric oxide
• T decreases plasma concentrations of pro coagulatory substances
• T improves erythrocyte membrane lipid composition and fluidity
• T increases red blood cell deformability
• T reduces levels of lipoprotein a

Donating blood to reduce hematocrit may also provide men with a false sense of security.

In a study done over a two-year period of time they looked at men who donated blood that were on testosterone therapy at least 25% of them had a hematocrit about 54% and when  they came back for repeat donations 44% of them had a persistent elevation of hematocrit above 54%. So it essentially showed that repeat donations were insufficient to maintain a hematocrit below 54%.

Testosterone therapy was first used clinically 1937 and it has been used in thousands of randomized control trials.  There is not a single  randomized control trial to date that shows an increased risk of major adverse cardiac events with testosterone therapy.

There is No Need to Control Estrogen While on TRT

Studies utilizing aromatase inhibitors in men with testosterone deficiency is limited and of poor quality. There is not one randomized controlled trial to date that shows benefits to men on TRT when they blocked estradiol (estrogen.) In all of the studies where testosterone was used in men and showed beneficial effects none of these studies utilized an aromatase inhibitor to block estradiol.

The practice of using aromatase inhibitors comes from the bodybuilding world. Bodybuilders want to add as much lean mass as possible. So they use AIs to block estradiol to have more free testosterone available to grow muscle tissue, but this comes at the expense of decreasing overall health.

Testosterone exerts its beneficial effects in many tissues through its conversion into its active metabolites DHT and Estradiol.  When a man produces his own testosterone or utilizes testosterone therapy, testosterone travels down three pathways.  The direct pathway where  testosterone acts directly as testosterone such as in skeletal muscle. The amplification pathway where  testosterone is converted into DHT such as in the skin and prostate. And the diversification pathway where testosterone is converted into estradiol such as in the brain, bone, blood vessels,heart, and the liver.  When we block testosterones conversion into estradiol then we block testosterones beneficial effects at the target tissues were testosterone acts through its active metabolite estradiol.

When testosterone therapy is provided appropriately there should be no need to utilize an aromatase inhibitor. Estrogens are vitally important players in many physiologic functions in men including bone metabolism, cardiovascular health, spermatogenesis, cognition and sexual function . In addition, the use of these preparations for TD is off-label. Hence, we recommended against the use of these drugs in men with TD.

Testosterone and Cardiovascular Disease (TRT does not cause heart attacks)

There is no evidence showing increased cardio- vascular (CV) mortality or morbidity with TThThis fear is due to media scaremongering after two studies reporting increased cardiovascular risks. Both of these studies had major flaws. One misreported results, the other had no control group.

Low testosterone increases the risk of atherosclerosis and coronary artery disease. This is due to plaque buildup in the arteries, which causes thickening and results in reduced blood flow to the heart. And the largest meta-analysis of medical literature showed there is no increased risk of cardiovascular disease with testosterone therapy. It also showed lower risk in men with metabolic conditions.

A large body of evidence suggests higher testosterone levels are cardioprotective. Men who receive testosterone therapy and achieve normal testosterone levels had a lower rate of cardiovascular events and mortality versus men with persistently low testosterone levels.

How Long Will I Have to Be on TRT?

Once you start testosterone therapy and feel its benefits, you won’t want to stop. It’s important to note that TRT is a long-term decision, because its beneficial effects are realized over several years.

What’s More Important, Total Testosterone or Free Testosterone?

In normal men, only 1- 3% of total testosterone circulates freely in blood, while 40-50% is bound to SHBG and 50-60% to albumin.  It is the free testosterone that acts  at the cellular level and exerts the beneficial effects of testosterone. Therefore, Free testosterone is the most important measure for diagnosing testosterone deficiency as well as for following  treatment.

Why is Estrogen Important?

Estrogens are vitally important players in many physiologic functions in men including bone metabolism, cardiovascular health, spermatogenesis, cognition and sexual function. Estradiol also  appears to prevent fat gain

For a more detailed discussion of estradiol and its importance, click here.

Why is Dihydrotestosterone (DHT) important for men?

Increases in DHT as a result of testosterone therapy do not lead to an increased risk of prostate cancer or cardiovascular disease. Clinical studies have shown that intracellular concentrations of androgens like DHT are independent of circulating levels. Furthermore, DHT is important for maintaining healthy libido and sexual function. Multiple studies have reported sexual dysfunction in men who inhibit DHT by taking drugs like finasteride and dutasteride.

How Long Does TRT Take to Work?

Each patient responds to TRT differently. Some feel better in weeks, while others take months. The symptoms of testosterone deficiency resolve on different timelines. The key is to understand we’re running a marathon, not a sprint. It is a process not an event.  Expect to feel the benefits of TRT over months and years, not days or weeks. If a patient has been suffering from testosterone deficiency for years, it isn’t reasonable to expect an overnight fix. In addition to this, lifestyle factors like nutrition, exercise, sleep, and stress play an important role in the speed with which the benefits of TRT are experienced.

What is a Good Starting Dose for TRT?

There is no such thing. We don’t take a cookie-cutter/one-size-fits-all approach to treating our patients. Our treatments  are personalized for every individual based on their symptoms/signs and lab results, and adjusted when necessary based on follow-up observations.

The Best Way to Take Testosterone

At Tier 1 health and wellness Dr. Nichols utilizes two methods of delivery. Patients are given the option of utilizing injectable testosterone or a trans scrotal cream. There are other methods of delivery but Dr. Nichols has not found them as efficacious as the injections or trans scrotal cream in his clinical experience and personal experience. . Dr. Nichols is on TRT himself for hypognadism (pre treatment level of 254 ng/dl) and has tried every possible delivery system.

Dr. Nichols states there is no single method of delivery that everyone likes. The majority of men on injections will like it but there will be a certain percentage that do not. The same holds true for the trans scrotal cream.  If one method of delivery doesn’t work or the patient is not pleased then he can simply switch to the other mechanism of delivery. The most important factor no matter what delivery system is utilized is to maintain stable optimal levels and avoid significant peaks and troughs.  Dr. Nichols discusses each method of delivery along with the pros and cons of each and the patient can then decide which method best fits their lifestyle.

Dr. Nichols is known for his use of the trans scrotal method of delivery for testosterone and has more experience with this method of delivery than most any other physician in the country/world. Injections have been used for decades and are an excellent option for testosterone therapy but Dr. Nichols provides another option that works just as well if not better in many men for testosterone therapy.

TRT, “Feel-Good” Effects and Beneficial Effects

Testosterone has “feel-good” effects as well as beneficial effects. With testosterone, for example, you’ll most likely experience increased energy and libido. Most hormones do not have “feel good” effects, even if they do all have beneficial effects. You won’t feel any better while taking them, even though they do improve your health. Like Vitamin D, for example.

Some doctors advise men to use testosterone in isolation, and if they “feel better,” don’t recommend using any other hormones. This is a mistake because as we said earlier, not all hormones have “feel good” effects. That doesn’t mean we should ignore these hormone levels and we shouldn’t optimize them. When we treat our patients we apply the same rationale for using testosterone to all hormones.

Why Testosterone Boosting Supplements Don’t Work

The fitness industry uses false advertising to prey on men who’re looking for a quick fix. But the truth is that testosterone boosters don’t work. Even pharmaceutical-grade products only raise your levels a little. If you’re suffering from low testosterone there is no supplement that can raise your testosterone to therapeutic levels such that you’ll receive its beneficial effects. Furthermore, since the supplement industry is not regulated by the FDA, you have no guarantee of purity or potency. Buyer beware.

The only way you can raise your testosterone levels enough to achieve its benefits is by taking bioidentical testosterone. Not only that but working with an experienced doctor and getting bioidentical hormones prescribed is cheaper than purchasing testosterone boosting supplements that do nothing for you.