Dr. Anthony’s Notes: Magnesium is best to take at night as it is relaxing. Supplemental magnesium can cause loose stools at high doses. If you experience loose stools, you'll know to back off your dose. This is a really useful supplement for overall health – not JUST for testosterone. Verdict: this is one of the natural testosterone supplements that work. Best Food Sources: pumpkin seeds, spinach, swiss chard, black beans, cashews, quinoa, quality whole gains like Ezekiel bread How To Take Magnesium: 200-400mg capsule form at night before bed.
It is important to note that you can certainly boost testosterone naturally without supplementation. Supplements are expensive now a days and a lot of people do not like taking tons of pills. Plus, a lot of these vitamins and minerals are only needed if deficient, so I recommend getting routine blood work done to see where you are short. I can almost guarantee you will come out vitamin D deficient, so while you don’t have to take these, they will certainly help.
Testosterone makes a contribution to nitric oxide formation. Nitric oxide, released from penile nerves stimulates guanylate cyclase which catalyzes the transformation of guanosine-5-triphosphate into 3′,5′-cyclic, guanosine monophosphate (cyclic GMP). Gyclic GMP causes vasodilatation and hence erection formation (Morelli et al 2005). The breakdown of cyclic GMP to GMP is mediated by the enzyme, phosphodiesterase type-5, the inhibitors of which (eg, sildenafil citrate) enhance erection formation and maintanence (Carson and Lue 2005).
This supplement contains herbal remedies to enhance the male hormone and increase a man's sexual desire. Ingredients found in the product include horney goat weed, milk thistle, tribulis terristris, wild yam, saw palmetto and maca. The manufacturer of the supplement claims that it is endorsed by a doctor for male enhancement. Recommended dosage is one capsule taken before engaging in sexual activity. Women should not take a testosterone supplement unless otherwise advised by a physician.
This supplier is located in north sumatra (but they ship from Amazon via the U.S). They harvest the tongkat ali from the sumatra jungle and use roots of trees >10 years of age. I know this supplier is the best because he used to purchase from Tongkatali.org, which if you search Google you will find is the most reputable stuff. But he tests every batch before sending it out and became unhappy with the quality of their product. He now purchases from a new supplier who get tongkat ali extract from the same jungle, with the same extraction process, but who performs chemical and microbiological analysis of every batch they produce, which brings me peace of mind.
To get a good dietary source of selenium, you can eat shellfish or Brazilian nuts. 1-2 Brazilian nuts is enough to get 200% of your daily intake. You don’t need any more than that. Read more about increasing testosterone with Brazilian nuts here. It’s a good idea to get your selenium levels checked before hand and then adjust your diet as needed to avoid selenium toxicity.
3. Beans. Beans are an excellent source of fiber, protein and zinc. If you compare beans with other vegetables, you will see that beans have the highest zinc content. This is a good thing if you’re trying to get your testosterone levels up since zinc plays an important role when it comes to testosterone production. Without an adequate amount of zinc in the body, the testosterone produced will be converted into estrogen. Likewise zinc may help convert estrogen back into testosterone. Yet another study on rats confirms this. Sorry for the rat-heavy studies in this post.
Testosterone is considered to be the "male hormone" that's produced in men by the testes. Although women's ovaries produce some testosterone, the hormone is produced in much higher concentrations in men and it is responsible for many of the secondary sex characteristics seen in men such as a deeper voice and hair on the chest, in addition to contributing to a healthy libido, building muscle mass, and maintaining energy levels.
Try a protein deprivation diet. According to "Optimum Anabolics," the body produces more testosterone in response to heavy training when there is insufficient protein in the diet. Testosterone provides a hypertrophic, or muscle-building, backup system, allowing for muscle recovery when protein is not available. To follow this diet, take in only 30 grams of high-quality, fast-digesting protein (whey protein) immediately following your weight training. The rest of the days, your calories, split into five or six meals, should be divided between low-glycemic carbohydrates (oatmeal, whole grains and sweet potatoes) and healthy fats. After three weeks of this diet, switch back to a higher-protein diet (1 gram of protein per pound of body weight), adding one extra 20 to 30 gram serving of protein before bed.
Regardless of the method of testosterone treatment chosen, patients will require regular monitoring during the first year of treatment in order to monitor clinical response to testosterone, testosterone levels and adverse effects, including prostate cancer (see Table 2). It is recommended that patients should be reviewed at least every three months during this time. Once treatment has been established, less frequent review is appropriate but the care of the patient should be the responsibility of an appropriately trained specialist with sufficient experience of managing patients treated with testosterone.
Researchers at Ball State University found that “strength training can induce growth hormone and testosterone release.” (6) Another study from the University of Nebraska Medical Center researched the acute effects of weight lifting on serum testosterone levels. (7) The results concluded that even moderate weight lifting and light weightlifting increased serum testosterone levels in participants.
In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6. 6β-Hydroxylation and to a lesser extent 16β-hydroxylation are the major transformations. The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism. In addition to 6β- and 16β-hydroxytestosterone, 1β-, 2α/β-, 11β-, and 15β-hydroxytestosterone are also formed as minor metabolites. Certain cytochrome P450 enzymes such as CYP2C9 and CYP2C19 can also oxidize testosterone at the C17 position to form androstenedione.
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.
"I went from 230 pounds down to 192. When my son got married, I went for the suit fitting, and I was a size 48. When I went back to do the final fitting, I was a 44! I want to keep getting it for the weight loss; I lost 4 inches around my belly, and I want to get rid of the rest of the weight around my belly. I’m 57, and my wife says I look like I’m back in my 30s. I have more energy for sure, and I’m going to participate in one of those Savage races where they have the obstacle courses with one of our kids."
VI-PEX or Vasodilator Ingredients with Penile Expansion is a highly-potent combination of blood flow-boosting ingredients which prolong and intensify the vasodilation properties of Male UltraCore, resulting in an undeniable improvement in size and hardness during penile erection. VI-PEX technology works hand-in-hand with STEM technology to leverage sexual arousal as a size-boosting factor during penile erection.
If you still feel the need to supplement, keep in mind that supplemental magnesium is more likely than dietary magnesium to cause adverse effects, which is why the FDA fixed at 350 mg the Tolerable Upper Intake Level for magnesium supplementation in adults. Also, you may want to avoid magnesium oxide: it has poor bioavailability (rats absorbed only 15% in one study, and humans only 4% in another) and can cause intestinal discomfort and diarrhea.
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).
"A lot of the symptoms are mirrored by other medical problems," Hedges says. "And for a long time, we were not attributing them to low testosterone, but to diabetes, depression, high blood pressure, and coronary artery disease. But awareness and appreciation of low testosterone has risen. We recognize now that low testosterone may be at the root of problems."