A: According to the NIH, normal values for testosterone levels in men can range from 300 to 1,200ng/dL. There can be many different causes of low testosterone including age, diseases, accidents, and medications. Symptoms of low testosterone may include: loss of sex drive, erectile dysfunction, depressed mood, and difficulty concentrating. Low testosterone levels may also bring around body changes including: hair loss, decrease in blood cells possibly leading to anemia, fragile bones, and a decrease in muscle mass. There are different testosterone replacement therapies including patches, such as Androderm; gels, such as Androgel and Testim; and injections, such as testosterone cypionate. Only your health care provider can decide if and what kind of testosterone replacement therapy is appropriate for you. Testosterone replacement therapy is not right for everyone. Patient with certain prostate issues or breast cancer should not take testosterone. For more specific information, consult with your doctor for guidance based on your health status and current medications, particularly before taking any action. Kristen Dore, PharmD
I’m a 70 year old male. Here’s my brief story, I was exhausted all the time after an encounter with H-Py-Lori. After may tests it was found out that my T-count was at about 250. I was put on a testosterone cream replacement therapy. Before I knew it, at about month I was at 1500 count. This was at 4 cream applications a day. The doctor took me down to twice/two applications a day, now I was at 600. I felt great at both levels.
Two of the immediate metabolites of testosterone, 5α-DHT and estradiol, are biologically important and can be formed both in the liver and in extrahepatic tissues. Approximately 5 to 7% of testosterone is converted by 5α-reductase into 5α-DHT, with circulating levels of 5α-DHT about 10% of those of testosterone, and approximately 0.3% of testosterone is converted into estradiol by aromatase. 5α-Reductase is highly expressed in the male reproductive organs (including the prostate gland, seminal vesicles, and epididymides), skin, hair follicles, and brain and aromatase is highly expressed in adipose tissue, bone, and the brain. As much as 90% of testosterone is converted into 5α-DHT in so-called androgenic tissues with high 5α-reductase expression, and due to the several-fold greater potency of 5α-DHT as an AR agonist relative to testosterone, it has been estimated that the effects of testosterone are potentiated 2- to 3-fold in such tissues.
The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)". They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The structure was worked out by Schering's Adolf Butenandt, at the Chemisches Institut of Technical University in Gdańsk.
Much like female hormone replacement, you should never, never ever use conjugated equine estrogen and synthetic progestins. Those two coupled together are evil twins. It is not hormone replacement that is the issue in men or women. The issue is the type of hormone used and doctors not knowing what they are doing. I always use bio-identical hormones. Synthetics are not the proper administration of any hormone program.
If your need is greater though, there are other legal options to consider. DHEA is a precursor steroid hormone that is only available on prescription in the UK, but if taken under close supervision it can have dramatic effects. It must be taken under supervision though because too high a dose can cause mood changes and aggression — roid rage, in other words — as well as all the other unwanted by-products of too much testosterone.
Short bursts of timed intense activity — known as high-intensity interval training or HIIT — trigger the body to make more testosterone than less-than-intense aerobic or endurance exercise, says La Puma. Spurts of activity stimulate androgen-sensitive tissue, he explains, which tells the body to make more testosterone. Strength training has also been shown to increase testosterone.
Looking at the ingredients and we see that they used a nice dose of D-Aspartic Acid which we have already talked about how much we like that. They also used a good dose of Fenugreek which boosts testosterone and enhances libido as well as Ginseng Extract which is a natural aphrodisiac. They also use Zinc Gluconate which is a solid testosterone booster and also has shown to be a bit of an aphrodisiac itself.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
Autopsy studies have found histological prostate cancer to be very common, with one series showing a prevalence of greater than fifty percent in men over age sixty (Holund 1980). The majority of histological cancers go undetected so that the clinical incidence of the disease is much lower, but it is still the most prevalent non-skin cancer in men (Jemal et al 2003). Prostate cancer is also unusual in comparison to other adult cancers in that the majority of those with the disease will die of other causes. Treatment of prostate cancer with androgen deprivation is known to be successful and is widely practiced, indicating an important role for testosterone in modifying the behavior of prostate cancer. In view of this, testosterone treatment is absolutely contraindicated in any case of known or suspected prostate cancer. The question of whether testosterone treatment could cause new cases of prostate cancer, or more likely cause progression of undiagnosed histological prostate cancer that would otherwise have remained occult, is an important consideration when treating ageing males with testosterone.
BCAA peptides are the building blocks of muscle. Your body cannot make BCAA’s. You have to eat them. One easy way of course is food and things like whey protein powder. That is why whey protein works so well because it contains BCAA’s at high levels. Advanced BCAA is 50% BCAA in peptide form!! Peptides are digested faster and more efficiently than whole foods and normal protein powders. This means more muscle building and recovery support!!
Low Testosterone has a big impact on men. Some males suffer debilitating symptoms when their bodies produce insufficient levels of testosterone, resulting in a condition called hypogonadism. Hypogonadism is the decreased functionality of the testes in producing an adequate amount of testosterone. Hypogonadism is not permanent, and can be treated with hormone replacement therapy, specifically Low Testosterone Therapy.
According to a study in the International Journal of Reproductive BioMedicine, D-Aspartic acid increases testosterone levels in some animals. However, studies that have looked at its effects on humans are inconclusive and mainly of poor quality. The paper says there is an urgent need for more research on this chemical, which occurs naturally in some human tissues.
Joe Costello is a Nutrition & Wellness Consultant, certified by the American Fitness Professionals & Associates (AFPA), author, and internet blogger. Joe has more than 9 years of experience in the sports nutrition industry and over 3 years of experience as a supplement and nutrition blogger. As a certified NWC who specializes in dietary supplements, Joe strives to deliver accurate, comprehensive, and research-backed information to his readers. You can find more of Joe’s work including his E-Books about fitness and nutrition at his official website joecostellonwc.com, or connect with him on LinkedIn, Facebook, Instagram, Vimeo, or YouTube.
The hypogonadal-obesity-adipocytokine cycle hypothesis. Adipose tissue contains the enzyme aromatase which metabolises testosterone to oestrogen. This results in reduced testosterone levels, which increase the action of lipoprotein lipase and increase fat mass, thus increasing aromatisation of testosterone and completing the cycle. Visceral fat also promotes lower testosterone levels by reducing pituitary LH pulse amplitude via leptin and/or other factors. In vitro studies have shown that leptin also inhibits testosterone production directly at the testes. Visceral adiposity could also provide the link between testosterone and insulin resistance (Jones 2007).
In high-fat high-furctose fed rats, ginger neutralized diet induced impairment in glucose regulation, dyslipidemia, and oxidative stress . This observed anti-diabetic activity of ginger powder is credited to two active components: 6-paradol and 6-shogaol . They both exhibit potent activity in stimulating glucose utilization by 3T3-L1 adipocytes and C2C12 myotubes. In the high-fat diet mouse model, 6-paradol decreased blood glucose, cholesterol and body weight.
As mentioned earlier, too much protein can negate testosterone production quite a bit. If your protein intake is over 0.85g/lb of body weight a day, then you may not be making full use of each of the nutrients. Consuming these high amounts of protein can cause your cortisol and SHBG levels to increase, which in turn lowers testosterone production. What do you get out of this deal? Increased fat gain and lower testosterone levels.
Falling in love decreases men's testosterone levels while increasing women's testosterone levels. There has been speculation that these changes in testosterone result in the temporary reduction of differences in behavior between the sexes. However, it is suggested that after the "honeymoon phase" ends—about four years into a relationship—this change in testosterone levels is no longer apparent. Men who produce less testosterone are more likely to be in a relationship or married, and men who produce more testosterone are more likely to divorce; however, causality cannot be determined in this correlation. Marriage or commitment could cause a decrease in testosterone levels. Single men who have not had relationship experience have lower testosterone levels than single men with experience. It is suggested that these single men with prior experience are in a more competitive state than their non-experienced counterparts. Married men who engage in bond-maintenance activities such as spending the day with their spouse/and or child have no different testosterone levels compared to times when they do not engage in such activities. Collectively, these results suggest that the presence of competitive activities rather than bond-maintenance activities are more relevant to changes in testosterone levels.
Results from the clinical trial demonstrated that there were significant increases in hemoglobin in both men with unexplained anemia as well as men with anemia from known causes who used the testosterone gel. These results may be of clinical value, and testosterone treatment could be used to boost hemoglobin levels in men more than 65 who have unexplained anemia and low testosterone. However, more research needs to be done.
Your first step should be to see your doctor. If you think you have low testosterone, we cannot stress enough that you should proceed with caution and talk to a medical professional — taking a booster can definitely do more harm than good. Low testosterone can be a symptom of more serious problems, like a pituitary disorder or a side-effect of medication, and a booster can mask the root cause. A doctor will be able to evaluate your testosterone levels with a simple blood test, and if you both decide a booster is the way to go, give the ingredients of any supplement a once-over to make sure that they’re not at risk of making your personal health situation worse.
The reason I started the experiment at that point is because I know a lot of guys who live my last-August lifestyle all the time, and I wanted to see what would happen to an “average” guy who turned things around. At the same time, there was no “normal” time in my life which would have been better for me to start the experiment. My stress level and diet fluctuates throughout the year anyway, so at any point, factors in my current lifestyle would have influenced the results. I wanted to begin at “ground zero.”
As a urologist, I tend to see men because they have sexual complaints. The primary hallmark of low testosterone is low sexual desire or libido, but another can be erectile dysfunction, and any man who complains of erectile dysfunction should get his testosterone level checked. Men may experience other symptoms, such as more difficulty achieving an orgasm, less-intense orgasms, a smaller amount of fluid from ejaculation, and a feeling of numbness in the penis when they see or experience something that would normally be arousing.
There is a negative correlation of testosterone levels with plasminogen activator inhibitor-1 (PAI-1) (Glueck et al 1993; Phillips 1993), which is a major prothrombotic factor and known to be associated with progression of atherosclerosis, as well as other prothrombotic factors fibrinogen, α2-antiplasmin and factor VII (Bonithon-Kopp et al 1988; Glueck et al 1993; Phillips 1993; De Pergola et al 1997). There is a positive correlation with tissue plasminogen activator (tPA) which is one of the major fibrinolytic agents (Glueck et al 1993). Interventional trials have shown a neutral effect of physiological testosterone replacement on the major clotting factors (Smith et al 2005) but supraphysiological androgen administration can produce a temporary mild pro-coagulant effect (Anderson et al 1995).
The other component of that study is that the subjects ate much less saturated fat. Saturated fats are common in meat, butter, and coconut products, and they’re crucial for your body to function. Saturated fats keep the integrity of your cell membranes, and if you limit carbs and/or do Bulletproof Intermittent Fasting, saturated fats become a phenomenal source of energy for your brain.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
I am generally dubious about supplement claims & have tried a few other Testosterone boosters which had no effect I could tell. Being desperate to find something to help me feel better, I ordered Dr Martin's T Booster. It arrived on May 14th and after the first day I felt better & noticeably had more energy. I don't have that tired dead feeling every morning now when trying to get out of bed. I am able to do some work & physical activities without being exhausted to the point of being sick. I have been taking Dr Martin's T-Booster for 8 days now. While I am not out running marathons yet, I am feeling much better & hope to continue getting better as I keep taking it
Also, for those with abnormal fatigue. It’s being found too often that hypogonadism is pared with another abnormality of the endocrine system called Hypothyroidism which causes intense fatigue and even alzheimer like cognitive disruption. Both the Testis and Thyroid need to receive signaling hormones from the Pituitary to function correctly and the Pituitary relies heavily on the Hypothalamus. Simple blood tests can check all of those. It is important you find out the reason you have low Testosterone!
Andy – If you take testosterone, your hypothalamus will notice an abundance of testosterone in your system and will instruct your pituitary gland not to send LH and FSH to your testicles. If you’re testicles are not receiving these two hormones, they will stop making testosterone. If you quit testosterone call turkey, you will likely fall back to your baseline level fairly quickly. There is a protocol however to get back to your normal production much quicker should you choose to quit therapy.
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
Hello there Abraham. My doc and you know each other well. We reside in Richmond, VA. Doc told me to inject my weekly Cypionate into sub fat for longer absorption, with reference you shared this info him with him. I have been his TRT patient for 10 years now. He is the best. I wont mention names. Please point me to a study showing the results of testosterone absorption from fat.
Testosterone levels generally peak during adolescence and early adulthood. As you get older, your testosterone level gradually declines — typically about 1 percent a year after age 30 or 40. It is important to determine in older men if a low testosterone level is simply due to the decline of normal aging or if it is due to a disease (hypogonadism).