If you don;t mind i will probably use it as a testimonial in my tongkat ali extract article which I am not sure if you checked out. But something tells me you may be interested in it haha. I don’t know much about the medicinal tongkat ali you speak of, but I have a supplier from a Sumatra jungle in indonesia, Herbolab.com who’s product I know is 100% legit. Maybe not as powerful as medicinal but I do not know. He also tests every batch himself after the supper performs a performs chemical and microbiological analysis of every batch they product.
Take 1 teaspoon. Incredibly dense in nutrients and feed by bees to the larvae who grows on to be the queen bee. I found one human study where a 4g daily serving led to an small increase in testosterone in older men (ref 78). There are also numerous animal studies (ref 79) showing positive effects. Personally I source NZ manuka royal jelly from Manuka Health.
Dr. Anthony’s Notes: Here's a funny little effect – fenugreek can make you sweet and your urine smell sweet like Maple Syrup. Hell, this could be a good thing for you! This supplement is commonly used for good reasons – it's quite effective for enhancing libido when stacked with the other herbs on this list. Medical Note: Fenugreek may interact with blood thinning medications (Warfarin, Coumadin, Xarleto). Check with your doctor before taking any of these supplements. How To Take Fenugreek: Take 400-600mg (capsule) with food; it's best to take a product standardized for fenuside.
Use natural grooming products. Most grooming products these days contain parabens, another type of xenoestrogen. And by most, I mean more than 75% of all products. To reduce my exposure as much as possible, I became a hippy during my experiment and started using all natural, paraben-free grooming products. You can find most of these items at most health food stores:
Here’s a scary thought: You may be less of a man than your father was—at least hormonally. A study in the Journal of Clinical Endocrinology and Metabolism found that, on average, testosterone levels were higher in men of the same age in the ’80s than they were in the 2000s (due, researchers speculate, to higher rates of obesity and the wider use of medication these days).  
The effects of testosterone in humans and other vertebrates occur by way of multiple mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors.[109][110] Androgens such as testosterone have also been found to bind to and activate membrane androgen receptors.[111][112][113]

Lets touch on these individually. Gluten has been shown to increase prolactin levels in male mice (48 & 49). Increased prolactin levels in males leads to all sorts of horrible things: Man Boobs (50), High inflammation (51), and most importantly, higher prolactin levels have been shown to be testosterone lowering and lead to shrinking of the testicle (52).
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).
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.
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