Taurine is an organic acid found in the body that is involved in a variety of processes. It has been studied for heart failure, high cholesterol and blood pressure, fatty liver and multiple other conditions. One of the more interesting effects its ability to enhance testosterone levels and testicular function. In adult and aged rats taurine increased testosterone levels, while also increasing luteinizing hormone, nitric oxide and sexual response. Other studies show taurine provide general testicular protection from a variety of toxins like heavy metals, cancer treating drugs, and nicotine by virtue of its an antioxidant effects.
A new study shows some interesting benefits of taurine that could be specific to the user of anabolics. Rats were given nandrolone decanoate (deca) alone, or nandrolone with taurine for 8 weeks (and placebo only, and taurine only). The result was that taurine reversed several significant nandrolone induced side effects. The most important being that it normalized testosterone levels while taking nandrolone. In addition it prevented changes in sperm characteristics and in key steroid forming enzymes.
The idea of endogenous testosterone being “shut down” while on anabolics is well known, and there have been a plethora of strategies for preventing or reversing this. Usually these strategies are based on some intervention in the negative feedback loop caused by excess steroid signaling the stopping of LH production in the pituitary. This study brings to light a new idea that I haven’t seen discussed much in regards to keeping endogenous testosterone production intact while using exogenous hormones. This idea is that the decrease in T level is from oxidative damage resulting in apoptosis in the leydig cells.
So while gonadotropins are important in the production of testosterone, perhaps looking into testiculo-protective supplements could be an alternate strategy to keep endogenous T production functional, at least in the short term.
Adv Exp Med Biol. 2013;776:347-55. doi: 10.1007/978-1-4614-6093-0_32.
J Biomed Sci. 2010 Aug 24;17 Suppl 1:S9. doi: 10.1186/1423-0127-17-S1-S9.
Toxicol Appl Pharmacol. 2015 Feb 1;282(3):285-96. doi: 10.1016/j.taap.2014.12.007. Epub 2014 Dec 24.
Editors Note: The following article is a guest blog by Farmacist
When ketogenic diets came back in vogue in the 90’s, bodybuilders were looking for ways to speed up getting into ketosis. The diets were cyclic and it took several unpleasant days to get into full blown ketosis. Glucose disposal agents were typically used, but some of the more daring folks used low doses of insulin to speed the process. The idea was, the faster you get into ketosis, the more fat burning days you would get per cycle. This of course carried the risk of overdosing and becoming hypoglycemic, so this was probably not done by too many people.
Today something like Ketoforce could get your ketones raised quickly, to avoid the unpleasant shift from glucose to ketones for fuel by your brain. That said there are some interesting things that could be, in theory, done with insulin and ketosis.
Disclaimer: Insulin can kill you, do not use insulin without medical supervision. This is not a how-to guide, merely some thoughts on possible pharmacological processes.
The prospect of using insulin without carbs could be a way to reap some of the anabolic benefits of the hormone with a lower likelihood of fat gain, or it could be a way to speed “full” ketosis or ketoadaption by driving glucose levels down.
Something that may not be well known is that ketones are protective of the brain during hypoglycemia. In fact there are studies that show injecting insulin into someone with high levels of ketones will bring blood sugar into dangerously low levels, without the patient exhibiting hypoglycemic symptoms.
See this summary: http://caloriesproper.com/40-years-ago-a-group-of-researchers-turned-ketosis-into-poetry/
Insulin is known to decrease hepatic ketogenesis, so slowing ketone production may be an issue if using exogenous insulin. There is some animal data showing that ketone production from octanoate is preserved however, when insulin is administered. This is potentially important as medium chain triglycerides are about 70% octanoate.
Do humans continue to make ketones from octanoate when insulin is given? Are exogenous ketones enough to combat low blood sugar? Do you need to be ketoadapted to be protected?
While it would make interesting research, the unknowns still make this a dangerous proposition.
Oxytocin is a relatively small peptide hormone (nine amino acids) that is produced in the posterior pituitary gland. Although it is produced in both men and women, the most well known function of oxytocin is in females where it acts as a facilitator of uterine contractions during labor, and as a stimulator of milk release from the breasts in the post-partum period. More recent research has implicated oxytocin in the emotional bonding response that occurs between females and their infant offspring, and also that which occurs with adult romantic partners over time. You may have heard that oxytocin is released after sex especially in women (which may be why women tend to be more affectionate afterwards). Oxytocin is also FDA approved as a drug to facilitate labor in women and to help with post childbirth bleeding.
Like many hormones in the body, science is discovering that oxytocin may have a wide variety of actions on multiple tissues – activities beyond the classical ones for which it is most well known. Most recently evidence has popped up suggesting that oxytocin is a factor in the regeneration of muscle tissue and that its levels are suppressed with age.
Researchers at UC Berkeley published a paper demonstrating that oxytocin is an indispensable factor in the healthy repair and maintenance of skeletal muscle tissue. They used young and old mice and showed that levels of oxytocin in the older mice were much lower than the younger mice. Administration of oxytocin (by subcutaneous injection) for a few days restored the ability of muscle to repair itself in these older mice to levels seen in younger mice. Conversely, mice bred with inability to produce oxytocin were born normal but quickly developed sarcopenia (muscle loss associated with aging).
The mechanism of this enhanced muscle regenerative capacity is thought to be due to increasing the proliferation and activation of muscle satellite cells. Muscle satellite cells are known to decrease with aging and they serve a key role in muscle recovery and growth. Injury (exercise induced or via trauma) causes the release of certain chemical signals which stimulate satellite cells to fuse with their parent muscle cells where they add myonuclei (the powerhouse of protein synthesis within the muscle cell).
It has been shown previously that muscle cells possess functional oxytocin receptors and that muscles themselves can manufacture oxytocin. One study in particular showed that in cattle the expression of oxytocin in muscle is increased dramatically in cattle receiving the anabolic steroid implant Revalor H, and it is speculated that oxytocin may be related to the increased muscle mass that results. The UC Berkeley study now shows that direct systemic administration of oxytocin may have positive effects upon skeletal muscle as well.
As I mentioned previously, oxytocin is an FDA approved drug so its safety profile has been examined. However its intended use is short term, and any usage to treat a condition such as sarcopenia would require more long term administration. Oxytocin is also available freely from veterinary stores and is actually not very expensive. I don’t really know what dosages might theoretically work in a human (if any dose would work at all).
Editors Note: The following article is a guest blog by Farmacist
Bioidentical hormone replacement is a popular treatment for women (and men) that uses steroids identical in structure to what the body naturally produces, instead of a nonhuman estrogen or progestin. In a certain percentage of patients, increased doses are needed to achieve a reduction in symptoms. There are patients who do not respond to increased doses, and some of these fall into a category of hormone hyperexcretors.
In these patients, a 24 urine analysis reveals metabolite level 50% to 1800% higher than what would normally be expected. For whatever reason, these patients ability to eliminate estrogen is upregulated, and they end up peeing out estrogen at too high of a rate to get the beneficial effects.
This is all great but as this blog isn’t targeted to postmenopausal women, what the significance of this?
Its very possible something similar happens with high levels of androgens. Historically, switching esters or mixing up the types of steroids used were strategies to avoid plateauing. A lot of talk about receptor sensitivity and up/down regulation has been discussed on this topic, but increased metabolism and elimination is an angle that hasn’t been covered as much. This certainly could be a factor in why response to an androgen decreases over time.
In the BHRT women, there is a strategy of using cobalt to affect steroid metabolism to essentially retain more drug in the body so it is able to stay active longer. The way this is accomplished to by taking small amounts of cobalt orally for a period of about 3 months.
There is mention of this being used in male BHRT as well and a few anecdotal experiences can be found on the web, but its far from certain that this would work. What is known is that oral cobalt can decrease the activity cytochrome p450 enzymes in the liver, and this can affect the metabolism of steroids.
Dose appears to very important in getting the desired effect from cobalt, as it may have opposing action at high doses as it does at lower doses.1 The BHRT women used in the neighborhood of 500mcg per day to restore hormone action, and this dose in humans is not expected to cause toxicity.1
In rats high doses suppress androgens and can cause testicular necrosis.2 Low doses of a cobalt compound has shown to improve the protein to fat ratio without affecting testosterone levels.3
3. US patent 4997828
Researchers at the University of South Florida recently had some very exciting research published in the International Journal of Cancer. http://www.ncbi.nlm.nih.gov/pubmed/24615175 The research team was led by Dr. Dominic D’agostino, and the goal of the study was to examine the impact of supplemental ketones and ketone precursors on metastatic cancer in mice. The research has important implications on the treatment of cancer and also possibly on the prevention of cancer.
Ketogenic Diet, Caloric Restiction, and Cancer
Recent research has strongly suggested that the ketogenic diet may prevent the spread of metastatic cancer (metastatic cancer is cancer that can spread from the original tumor site to other parts of the body). This research was pioneered by Dr. Thomas Seyfried from Boston College. Dr. Seyfried has used the ketogenic diet in conjunction with caloric restriction to successfully restrict metastasis, and in some cases actually shrink the size of tumors.
The concept is relatively simple. Cancer cells can generally only use glucose to energize their growth, while normal cells have the metabolic flexibility to use fatty acids and ketones in addition to glucose. So by starving tumors of glucose via calorie and/or carbohydrate restriction – while simultaneously providing abundant alternative fuels for the body and brain (the ketogenic diet) – you may halt the cancer without side effects.
The concept may be quite bold, but it is not new. A Nobel Prize physicist named Otto Warburg first conceived of the general idea back in the 1920s. Unfortunately, after the discovery of the structure and function of DNA in 1953, the popular view of cancer was that it was a disease of purely genetic origin. As a consequence, Warburg’s hypotheses were largely discarded. Hopes were high that a cure for cancer was just around the corner back then, but as we all know that was not to be. Luckily, within the last few decades some researchers have taken a second look at Warburg’s work and the “metabolic theory of cancer”.*
Using this “metabolic theory of cancer” as an inspiration, studies were undertaken examining the efficacy of caloric restriction and/or ketogenic diet in cancer survival. It was found that often the growth and spread of tumors was halted, and in some case actually reversed. These findings have garnered attention and have sparked some controversy. There are concerns with the practical applications of these dietary interventions in the patient population. One concern involves the idea of initiating caloric restriction while the threat of cachexia looms. Cachexia is the condition of lean tissue wasting that often occurs as a consequence of cancer, and it is cachexia which often kills the patient rather than the tumors themselves. Could caloric restriction exacerbate cachexia in some instances and lead to an earlier demise? In addition to the cachexia issue, how readily will patients be willing to endure the restrictive and often unappetizing aspects of the ketogenic diet?
What Dr. D’agostino and his team set out to find is whether or not metastatic cancer could be controlled via exogenous supplementation alone. He designed an experiment in which three groups of mice were inoculated with a highly metatstatic line of cancer cells that contained a luminescent tag (to enable clear imaging of the tumors). All the mice were given unrestricted access to a standard diet (60% carbohydrates). One group would have the diet alone while the other two groups would receive one of two different forms of exogenous ketone compounds in addition to the diet. The two exogenous ketone supplements used were 1,3-butanediol (BD) and RS-butanediol diacetoacetate (ketone ester or KE). Their metabolic conversions to ketone bodies is exemplified in the following diagram
The results of this experiment were remarkable. Despite being on a high carb unrestricted diet the groups taking the exogenous ketones exhibited dramatically less tumor infiltration throughout the body compared to the diet alone mice (as seen by bioluminescent imaging). Survival in the BD supplemented and KE groups were prolonged 51% and 69% respectively compared to controls as well.
These results seem to contradict much of what was assumed regarding how the ketogenic diet fights cancer. It has traditionally been thought glucose deprivation was necessary to starve the cancer. However in this study the mice were eating unrestricted amounts of a high carb diet, so glucose remained high. What could be going on here? The researchers speculate that the ketones themselves may be directly toxic to the tumor cells, via mechanisms such as disruption of energy production by glycolysis in the tumors.
This paper certainly will cause an upheaval amongst those studying dietary interventions for cancer. Now the possibility has been opened up for simple supplementation as a course of treatment using the synthetic ketone precursors used in the study, or perhaps even by using natural ketone supplements such as beta-hydroxybutyrate (BHB) salts. Supplementation would be a much simpler, convenient, and patient compliant alternative to the more drastic dietary interventions previously thought necessary.
*The metabolic theory of cancer postulates that cancer does not arise because of damage to our DNA resulting in mutated oncogenes, but rather it arises as a result to disruptions in processes of energy production in our mitochondria. The disruption of oxidative phosphorylation in the mitochondria forces a cell to rely on the less efficient glucose driven anaerobic glycolysis. It is this dysfunction in energy production which then is thought to turn on existing oncogenes in the nucleus, causing the cell to turn cancerous.
Anabolic drugs are not dead, in fact research to develop new ones are aggressively being pursued to address medical situations such as cancer cachexia (wasting secondary to cancer) and sarcopenia (age related loss of muscle mass). Both of these categories are potentially huge money makers. Amongst the weird drugs that are being proposed for these applications is one that kind of boggles my mind. It is actually a current drug used to treat high blood pressure. Well, I guess you can say HALF of the drug is being developed as an anabolic
The drug I am referring to is called Pindolol, and the “half” that is being developed is S-pindolol. What I mean by that is that Pindolol is what is known as a racemic compound (it exists in a 50/50 ratio of right and left handed isomers) and the drug proposed as an anabolic is S-pindolol (the left handed isomer only). Many drugs are like this and often only one isomer is the active one. Take for example methamphetamine. Its active isomer is the right handed one. The left handed one is weak enough that it is allowed to be sold over the counter as a component of vicks inhalers.
Pindolol is sold to treat high blood pressure and it does so by blocking the effects of adrenaline like compounds on the heart (it’s a beta1 blocker). As such it decreases the force and frequency of heartbeats and thusly blood pressure decreases. Interestingly, pindolol also has agonist effects upon receptors of adrenaline like compounds too, specifically on skeletal muscle (it’s a beta2 agonist). You may be familiar with beta2 agonists such as clenbuterol. They are anabolic
Anyway, this compound (the S-isomer of pindolol which is the isomer that does stuff) is poised to be marketed as an anabolic for cancer cachexia and maybe sarcopenia. Studies have been done that have demonstrated muscle growth in these models. Myostatin has been shown to be suppressed amongst other things, which are effects we know happens with beta2 agonists (at least in the short term). Cool thing is that unlike most beta2 agonists (clen) this has no stimulatory effect on the heart. Not so cool thing is that it actually has a depressive effect on the heart, which means your exercise performance can suffer because your heart won’t beat fast and hard enough to support your efforts (that is if you train like a man)
Anyway, interesting stuff I suppose and expect it to appear on your banned list soon
DMAA, also known as methylhexanamine or “geranamine” is a controversial stimulant ingredient used in weight loss and energy supplements. In April of this year the FDA made a strong statement regarding its health dangers and its lack of legal standing as a nutritional supplement. Companies selling DMAA products for the most part stopped selling the stuff, and those who didn’t fully comply were subject to harsh enforcement actions by the FDA.
It took a long time for the FDA to act on DMAA, and that was in large part due to the fact that they really didn’t have clear cut evidence that the product was dangerous. Outcries by certain people that claimed the product was responsible for various adverse medical events and deaths however became louder and louder. These claims were not substantiated by any medical evidence though and so were not enough for the FDA to act upon.
The most publicized adverse health events regarding DMAA involved the US military. The deaths of four servicemen were being blamed on DMAA. As a consequence, the department of defense commissioned a safety study on the compound to determine whether it indeed was dangerous and to blame for the soldiers’ deaths (as well as other medical incidents involving soldiers). This was to be the study that the FDA could rest its hat on and justify an emergency action against DMAA.
Things started getting strange though. The study was supposed to be finished in February 2012. That date came and went and no word on the study results were announced. Then word came that the study was taking longer than expected and would be done in December 2012. Well December 2012 came around and still no word. Months passed and no one seemed to be talking about the huge DOD study that was supposed to prove once and for all that DMAA was deadly.
Then in April 2013 the FDA announced that it considered DMAA illegal to sell and warned of a whole variety of potential health risks. No mention of the DOD study which was supposed to provide the scientific validation was made – the FDA announcement was based simply on theory.
What happened to the DOD study? Well, in August the results were finally released (four months after the FDA’s arbitrary action). They were released with such lack of fanfare and media coverage that even I was not aware of the results until just today (almost two months later). Essentially they found that despite a high apparent usage of DMAA by soldiers (as much as 15 percent) the substance at doses recommended by manufacture poses a low risk of serious harm for most service members. The study basically exonerated DMAA from being responsible for the deaths of the four soldiers. They cautioned though that the “potential” of DMAA to cause harm still exists and ongoing studies would be needed to fully understand the health issues (I guess two years wasn’t enough).
Anyway, I have my own take on this situation. I think it was clear quite a while ago that the DOD study was not going to provide the smoking gun that was expected and hoped for. At that point the results were kept hush hush and the FDA decided to act anyway against DMAA. Then they waited four months to quietly announce the study results – so quietly that it took me six weeks to even be aware of them.
On my last blog I promised I would show you some data on my KetoForce product (BHB mixed salts). I have two sets of data – the first showing blood beta-hydroxybutyrate (BHB) responses and the second showing specific changes in physiological parameters during a controlled exercise experiment.
The blood data was done at a university on a set of subjects and the average changes in BHB levels are what this graph shows
These subjects drank a diluted version of the KetoForce product that was essentially equivalent to 36mL of KetoForce.* The product was consumed on an empty stomach and as you can see blood BHB levels rose pretty quickly. Levels appear to stay decently elevated until round the 180 minute (3 hour) mark. 30-60 minutes seems to be the sweet spot for maximum blood levels, so for pre-exercise use one should probably time the ingestion accordingly.
The exercise data I have was done using a 20% solution of the BHB salts which was equivalent to 40 mL of the KetoForce product. The data was done by an independent individual that does such research for a non-profit organization. Out of respect for this fact – and the fact that the data is only preliminary (more research is going to be performed) – I won’t report the full data here. I will give a glimpse into the most interesting thing he found though.
First of all this individual was ketoadapted. Ketoadapated means he had been on a ketogenic diet for a period of time long enough so that he was in full ketosis and had developed a good ability to utilize ketones. He did a bike exercise that was set up so the workload was maintained at a constant level roughly equal to 60% of his VO2 max. During the first stage he did the exercise for twenty minutes without the salts, and during the second stage he consumed the salts 60 minutes prior to the exercise bout.
One of the things that was measured was the amount of oxygen consumed during the exercise bouts. Theoretically, ketones should reduce oxygen consumption because they are known to generate more cellular energy per unit oxygen burned compared to glucose and other energy sources. The data he got with the BHB salts strongly suggested that this theory was at work during the experiment. Below is the difference in oxygen consumption reported as a percentage between a bout without the salts and a bout with the salts.
Last 5 minutes – minus 8.8%
Last 10 minutes – minus 7.7%
Last 15 minutes – minus 6.6%
Apparently there was a substantial decrease in the amount of oxygen he needed to maintain the workload after taking the salts. Very interestingly, this decrease in oxygen demand got more prominent as the session went on as well.
BHB salts are natural products that mimic the nutritional state of ketosis and have been studied in the past for medical applications as well. KetoForce is the first introduction of these salts to supplement and fitness industry so we are very early on in regards to figuring out how best to use them. This preliminary data does give us some clues on how they may be used (timing wise) and what benefits they may offer. We are very hopeful that our collaborations will enable us to generate a lot more research on the product (such as what performance benefits might be seen in non ketoadapted people) in the very near future.
* The KetoForce label suggests a serving size of 30mL instead of 36mL. Since I don’t expect all my customers to own graduated cylinders many will have to use the cap for measuring, and the cap holds 10mL . For this reason I rounded the serving size off to 30mL.
In late 2010 a professor from a university in Florida approached me to see if I could synthesize a compound that he wanted to use in his research. This compound was what is known as a “ketone ester”. This ketone ester is a synthetic prodrug which, after ingestion, your body naturally breaks down into the ketone bodies beta-hydroxybutyrate (BHB) and acetoacetate (AcAc).
Ketone bodies are energy sources that your body naturally produce and burn under special metabolic conditions. These conditions include starvation and a very high fat / low carbohydrate diet (known as the ketogenic diet). Ketones are the end products of fatty acid metabolism, and compared to your body’s major source of caloric energy (glucose), they are pretty amazing. Unlike glucose, ketones do not require insulin to enter cells and be incorporated into the metabolic cycles that generate the cellular fuel ATP. They cannot be converted to body fat. Also, unlike most fats, ketones can freely enter the brain where they are an excellent fuel for brain cells. On top of all that, ketones generate more ATP per unit oxygen consumed than any other energy source. Ketones are essentially your body’s super fuel.
I ended up successfully synthesizing this ketone ester for the professor, and he ended up performing some pretty cool studies utilizing the product. For instance in one study he made rats resistant to the toxic effects of high pressure oxygen upon the central nervous system (this has major implications for deep sea divers such as navy seals, as well as indirectly on folks suffering from epilepsy). In another study he almost completely halted the growth of cancerous tumors in rats by giving them the ketone ester. The professor also showed in a more informal study that rats taking the ketone ester could exercise quite a bit longer than control rats.
As a supplement manufacturer I found the potential health and performance implications for raising ketones through the administration of a “ketone supplement” very exciting. Unfortunately the ketone ester I made for the professor is both synthetic and extremely expensive, so it was wholly unsuitable for sale as a supplement. My collaboration with the professor did get me thinking though, and I set out to see if I could develop a way to raise ketone levels by administering a natural product alternative.
My focus was on the ketones themselves. As I mentioned previously, there are two major endogenous ketones: beta-hydroxybutyrate (BHB) and acetoacetate (AcAc). AcAc I had to eliminate right off the bat because it is too unstable (it breaks down relatively quickly to acetone and carbon dioxide). BHB on the other hand was a possibility – particularly in the form of one or more of its salts. The problem was the only BHB salt which is commercially available is sodium BHB and it’s just too expensive. So I had to embark on my own R&D project to figure out how to make BHB salts at a price that is not completely out of reach.
I ended up perfecting a proprietary manufacturing method for sodium and potassium mixed BHB salts. Why mixed sodium and potassium salts? The reason for that is because at the level of intake of BHB required for benefits you would have to ingest a substantial amount of cation (positively charged mineral such as sodium or potassium). At such levels of cation ingestion it made sense that a balance of sodium and potassium salts would be the healthiest thing to do.
Additionally, I discovered that the product had to be delivered as a concentrated liquid because potassium BHB is simply too hygroscopic to isolate as a powder (it picks up water from the atmosphere and turns into mush at an astonishing rate, whether by itself or mixed with sodium BHB).
So, just to make things clear, is I have developed a supplement product that raises blood ketone levels. This product does not require a ketogenic diet to raise ketone levels as it is essentially providing an external source of ketones. As such, it will raise ketones even if you eat a plate of spaghetti before taking it (still, its benefits are maximized when combined with either a ketogenic or other sort of low carb diet).
This kind of thing is a lot of work. For instance it involved developing novel analytical testing methodologies (which as an organic synthesis guy isn’t second nature by any means!) But after about a year of work this weekend I am proud to announce the introduction my sodium and potassium mixed BHB salts on my prototypenutrition.com website.
I hope to continue this topic next week and introduce you to some blood data and exercise performance data on my BHB salts that I think you will find very exciting. Also I will give some tips on how to possibly best uitilize this product for whatever health or fitness goals you may have.
So stay tuned!
I was recently asked a question about a very strange new prohormone product. What makes it strange is that is actually based on a female hormone – specifically it is based upon a hormone called 17alpha-hydroxyprogesterone.
17a-hydroxyprogesterone (or 17-HP) is a hormone intermediate in the steroidogenic pathway between progesterone and androstenedione. 17-HP is present in the blood of women in varying amounts during their monthly cycle and is present in particularly high amounts during pregnancy. It has similar actions to progesterone (albeit somewhat weaker), and is thought to serve a complimentary role to progesterone as an endogenous progestogen.
The prohormone in question here is not actually 17-HP however, but a close structural derivative to 17-HP that I will call Dehydro 17-HP. For all intents and purposes however, the metabolism of the derivative should be analogous to 17-HP. Specifically, here are the potential pathways of the two
17-HP ——– Androstenedione —– Testosterone
Dehydro 17-HP ——— Boldione ——– Boldenone
So it is definite that the potential for 17-HP and Dehydro 17-HP to convert to active anabolic/androgenic hormones is there. There are two questions though. How much do they convert and is there any HPTA suppression from the progestational action of the parent compounds?
Perusing the research on 17-HP I did find a little bit of information on the first question. Apparently at least one study found that given to humans and to rats the compound results in a substantial increase in urinary 17-ketosteroids (androgenic metabolites). This indicates that it does convert to a significant extent to androstenedione at least. Furthermore, a study where 17-HP was given orally to cockerels (immature roosters) showed it to have one half the androgenic activity of methyltestosterone. It is important however to note that androgenic activity in a cockerel is measured by the size of that red comb on their heads, which is not necessarily easily translatable to anything in a human.
The answer to the second question – involving whether the compound is HPTA suppressive – is harder to answer. Data on women show varying effects on 17-HP at different times throughout the cycle, but this data is irrelevant to men. I couldn’t find anything on men and LH/FSH levels. So that part of the equation remains unanswered.
I guess I don’t really know what to say about this stuff. If it works at all I would expect one to have to take many hundreds of milligrams before an effect is seen (due to it being a two step conversion via an intermediary dione). Whatever the case, it is sort of amusing how creative companies will get in an attempt to fulfill customers’ demands while trying to minimize legal exposure.