Sugar is to testosterone what kryptonite is to Superman. Eliminating sugar is probably the single most powerful way to increase your performance, in part because sugar absolutely devastates your testosterone levels (but all carbs do not, especially under heavy training.) In one study of 74 men, a 75g dose of sugar – about the equivalent of a bottle of soda – decreased serum testosterone by 25% in under an hour, and levels stayed low for at least 2 hours [7]. On top of that, 15% of the men who started with normal testosterone dipped into the hypogonadal range after they ate sugar – that’s the range in which doctors diagnose men’s testes and women’s ovaries as failing. When you do eat carbs, stick to Bulletproof ones like sweet potatoes and squash. My recommendations for types of carbs and how often to eat them are here.

In a subsequent study of 345 men with normal PSA and low testosterone, we found the cancer rate was similar: 15%. And we had a large enough group to look at the impact of testosterone on cancer risk. For men whose total testosterone or free testosterone value was in the lowest third, the odds of having a positive biopsy were double the odds in the rest of the men. That’s the first evidence that low testosterone may be an independent predictor for the development of prostate cancer.
For example, the study published in Obesity Research tells that the scientists measured testosterone levels in two groups of middle-aged men with obesity. One group underwent a 16-week weight loss program, while the second group did nothing. Each participant of the first group lost 20 kg on the average. And these participants experienced a significant increase in testosterone levels. So, the fight against overweight is very important for those who want to overcome testosterone deficiency. But starvation is strictly forbidden because this is a stressful situation which leads to the sharp decline in T levels.
Believe it or not, free testosterone makes up only about 2% of all the testosterone in your body. This rest is bound to globulin and albumin. There are ways to increase your free testosterone though and one of them is through strenuous exercises. Strenuous exercise like lifting heavy weights and sprints will cause the body to release some of that bound testosterone making it free and it aids the body with the heavy workload.
Overall, it seems that both estrogen and testosterone are important for normal bone growth and maintenance. Deficiency or failure of action of the sex hormones is associated with osteoporosis and minimal trauma fractures. Estrogen in males is produced via metabolism of testosterone by aromatase and it is therefore important that androgens used for the treatment of hypogonadism be amenable to the action of aromatase to yield maximal positive effects on bone. There is data showing that testosterone treatment increases bone mineral density in aging males but that these benefits are confined to hypogonadal men. The magnitude of this improvement is greater in the spine than in the hip and further studies are warranted to confirm or refute any differential effects of testosterone at these important sites. Improvements seen in randomized controlled trials to date may underestimate true positive effects due to relatively short duration and/or baseline characteristics of the patients involved. There is no data as yet to confirm that the improvement in bone density with testosterone treatment reduces fractures in men and this is an important area for future study.
Pellets. Your doctor will place the testosterone pellets under the skin of your upper hip or buttocks. Your doctor will give a shot of local anesthesia to numb your skin, then make a small cut and place the pellets inside the fatty tissues underneath your skin. This medication dissolves slowly and is released over about 3-6 months, depending on the number of pellets. 
“I'm a truck driver and for 13 hours a night I sit in my truck and I drive. Out of boredom, I'd stop and eat. That was all until Andro400 – ever since then my life has changed. I started out weighing 341 pounds, and since taking Andro400 I've dropped 85 pounds! There's no cravings – I actually don't even think about food anymore. One thing that Andro400 said on the radio ad is it attacks belly fat – well let me tell you it did – the 2nd month is where I saw a drastic change in the size of my stomach. I've lost 6 inches! I'm sleeping better. My knee pain went away. I've had some lower back issues and that went away, and I can only attribute that to Andro400. It's a Life Changer for me!”
The T Trials are a set of seven clinical trials hosted at 12 sites around the country. In the aggregate, 790 men aged 65 or older with low levels of testosterone and associated symptoms participated. First, participants had to qualify for one of the main three trials: the Sexual Function Trial, the Physical Function Trial, or the Vitality Trial. Then, participants could participate in any of the other trials for which they qualified.
Jeff- I read your post and I can relate to your problem. Perhaps you’ve already received some help but I can tell you this much. I recovered from prostate cancer about 2 yrs ago. My oncologist is also a graduate of Harvard like the doc that wrote this article. He put me on Axiron about 8 months ago after I complained to him of symptoms similar to you. He has no concerns that the T will cause me to get prostate cancer again. I do my 4 month check ups and have my T tested at that time along with my PSA. Everything is normal so far. My T count was initially 50 and now I am in the low 300 range. The Axiron has gotten me back to normal and then some!! I’m 58 and I told him at my last appt that I feel like I’m 40.
^ Jump up to: a b Lazaridis I, Charalampopoulos I, Alexaki VI, Avlonitis N, Pediaditakis I, Efstathopoulos P, Calogeropoulou T, Castanas E, Gravanis A (2011). "Neurosteroid dehydroepiandrosterone interacts with nerve growth factor (NGF) receptors, preventing neuronal apoptosis". PLoS Biol. 9 (4): e1001051. doi:10.1371/journal.pbio.1001051. PMC 3082517. PMID 21541365.
during therapy. It is very hard to find a local endo who is thinking with his head vs complying with old trt programs. I tool clomid in the past to see what it would do and it elevated my t level to 520 in 2 weeks from low 220. Aromason will do same but clomid is more potent. Not sure what the long effect would be since you tend to get bit moody on clomid after 2 months. LH is also being affected in negative way since the lh receptors can burn out to a degree. I will contact the trt clinic in order to start my trt as they have much more experience with these things.
I know many of you are clamoring for the “how-to” part of this series (which will go up on Thursday), but before we get to that, it’s important to cover why you should even care about your testosterone levels in the first place, what T is and how it’s made, and how to get properly tested for it. Building a sound foundation before we dive into the nitty gritty details will be highly beneficial.
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).
Gary Womble… Get out of here with your quackery nonsense. No one likes trolls that want to push diet and weight loss pills as a serious solution to low t and ED. Anyone who reads your comment will waste at least 20 seconds of their life. What’s worse, they might listen to you instead of getting real medical advice that might actually help with an issue that is devastating to their lifestyle. And btw, before you decide to respond to this with more quackery, testimonials or fake research, know that I am a pharmaceutical scientist and won’t fall for your bogus statements
There’s a significant failure rate of the PDE5 inhibitors for erectile dysfunction, something on the order of 25% to 50%, depending on the underlying condition. It turns out that a third of those men will have adequate erections with testosterone-replacement therapy alone and another third will have adequate erections with the pills and testosterone combined. There’s still a third who don’t respond, but normalizing their testosterone level has definitely rescued many men who had failed on PDE5 inhibitors.
46 year old whose suffered with low libido and all the related symptoms for over a decade. Finally had the courage to have a frank talk with dr. and urologist. Testosterone level 165, free testos level 3.6. Re-doing blood work again just to be sure in the next week or so, and will post updates then as things progress. Normal ranges are 300-1200 and 6 to 12.
I definitely enjoyed an increase in muscle mass during my experiment. Despite dropping six percentage points in body fat in three months, my weight stayed about the same; I began the experiment weighing 185 pounds and I ended it weighing the same. The body fat I lost was replaced with muscle. It was fun to see and hear Kate’s reaction when I’d take off my shirt to get into the shower. “Whoa! Your muscles have gotten huge!”
Of course, testosterone’s primary function is to bring about secondary sexual characteristics in men. A healthy dose of testosterone is shown to treat conditions such as impotence. Men with fertility issues benefit from increased levels of testosterone in the body. The aging process slows down the rate of testosterone production by the adrenals and testes. It is irreversible and one of the only means to mediate the effects of low testosterone concentration is to include testosterone boosting agents in your regimen.
Testosterone therapy improves body composition (increase in lean body mass, decrease in fat mass) in men with hypogonadism.1 There is a supplementary improvement in muscle strength and physical function. The benefits of testosterone treatment on body composition have consistently been demonstrated in clinical studies of testosterone therapy in hypogonadal men or men with borderline low testosterone levels,1,6,8,12,13 and confirmed by systematic reviews or meta-analyses of randomized controlled trials.4,5,6,13

Studies have shown that testosterone-replacement therapy may offer a wide range of benefits for men with hypogonadism, including improved libido, mood, cognition, muscle mass, bone density, and red blood cell production. But little consensus exists on what constitutes low testosterone, when testosterone supplementation makes sense, or what risks patients face. Much of the current debate focuses on the long-held belief that testosterone may stimulate prostate cancer.


The regulation of testosterone production is tightly controlled to maintain normal levels in blood, although levels are usually highest in the morning and fall after that. The hypothalamus and the pituitary gland are important in controlling the amount of testosterone produced by the testes. In response to gonadotrophin-releasing hormone from the hypothalamus, the pituitary gland produces luteinising hormone which travels in the bloodstream to the gonads and stimulates the production and release of testosterone.
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