Pine Pollen is an androgen, meaning in theory it can raise testosterone levels – effectively making it a naturally derived source of testosterone. Read more about this on the links below. But like I said I started taking it for a few weeks and did notice a bit more ‘up and go’ so to speak, but it did only last a few weeks. I have tried cycling it but haven’t noticed the same effects as I had when I initially started with it. I’m still experimenting and will keep this page updated. Therefore I recommend doing your own research.
Among the changes which occur with aging are those that affect several aspects of the endocrine system which reduces its secretions to varying degrees in different individuals. These reductions in secretions are identified by a poor but widely recognized appellation, the “pauses”: menopause (decreased ovarian function), adrenopause (decreased adrenal function, especially with regard to dehydroepiandrosterone secretion), somatopause (decreased growth hormone production), andropause (decreased hypothalamic-pituitary testicular function with diminished testosterone availability and impaired spermatogenesis) (Lamberts 1997).
Acne and Allergic Reactions: The testosterone is universally regarded as one of the triggering factors for acne. It stimulates the activity of oil glands making the skin more oily and vulnerable to acne. This body hormone might also cause allergic reactions, such as hives, rash, difficulty breathing, itching, chest tightness, and big swelling of the facial parts.
The largest amounts of testosterone (>95%) are produced by the testes in men,[2] while the adrenal glands account for most of the remainder. Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta.[126] In the testes, testosterone is produced by the Leydig cells.[127] The male generative glands also contain Sertoli cells, which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein, sex hormone-binding globulin (SHBG).
14. Volek JS, Volk BM, Gómez AL, Kunces LJ, Kupchak BR, Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C, Ballard KD, Quann EE, Kawiecki DL, Flanagan SD, Comstock BA, Fragala MS, Earp JE, Fernandez ML, Bruno RS, Ptolemy AS, Kellogg MD, Maresh CM, Kraemer WJ. Whey protein supplementation during resistance training augments lean body mass. J Am Coll Nutr. 2013;32(2):122-35. PMID: 24015719

A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).


TT may help you but it may have adverse (harmful) results. (See discussion of these side effects below.) The Federal Drug Administration (FDA) has said that testosterone drug labels should state that there is a risk for heart disease and stroke for some men using testosterone products. All men should be checked for heart disease and stroke before, and periodically while on, TT. The AUA however, on careful review of evidence-based peer review literature, has stated that there is no strong evidence that TT either increases or decreases the risk of cardiovascular events.
Ashwagandha is shown to be effective at reducing cortisol which in turn helps with testosterone production. There are also numerous studies showing the effects on improving testosterone in infertile men (ref 80).  If you are using the Aggressive Strength product you don't need to supplement with ashwagandha as it's included in the test booster formula. Likewise if you're using Tian Chi (my daily herb drink).
A recent study compared total and bioavailable testosterone levels with inflammatory cytokines in men aged 65 and over. There was an inverse correlation with the pro-inflammatory soluble interleukin-6 receptor, but no association with interleukin-6 (IL-6), highly sensitive CRP (hsCRP), tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β (Maggio et al 2006). Another trial found that young men with idiopathic hypogonadotrophic hypogonadism had higher levels of proinflammatory factors interleukin-2 (IL-2), interleukin-4 (IL-4), complement C3c and total immunoglobulin in comparison to controls (Yesilova et al 2000). Testosterone treatment in a group of hypogonadal men, mostly with known coronary artery disease, induced anti-inflammatory changes in the cytokine profile of reduced IL-1β and TNF-α and increased IL-10 (Malkin, Pugh, Jones et al 2004).
How do you boost testosterone naturally? Testosterone is a male sex hormone. Low levels can cause changes to the distribution of body fat and muscle strength. Testosterone reduces with age, but people can boost it with lifestyle changes, including diet and exercise. Adequate sleep, nutritional supplements, and stress reduction may also help. Learn more here. Read now
Infertility in men and women Infertility or a couple being unable to conceive a child can cause significant stress and unhappiness. There are numerous reasons for both male and female infertility but many ways in which medical assistance can overcome problems that people may face. Everything concerning infertility is discussed and explained here. Read now
Dr. Anthony's Notes: I like Tribulus. It is a VERY common herb in almost all testosterone boosting products – again though, it may be more of a libido enhancer than anything. From my personal experience, it's effective when stacked with the other libido enhancing supplements in this guide. How To Take Tribulus: Take 200-400mg once per day of a 45-60% saponin extract product.

How do you boost testosterone naturally? Testosterone is a male sex hormone. Low levels can cause changes to the distribution of body fat and muscle strength. Testosterone reduces with age, but people can boost it with lifestyle changes, including diet and exercise. Adequate sleep, nutritional supplements, and stress reduction may also help. Learn more here. Read now


This is natural amino acid and can boost testosterone levels. According to research, it increases the production of luteinizing hormone which triggers the production of testosterone from Leydig cells. It also helps in improving sperm quality and quantity. The men who take this have increased testosterone production which allows them to perform better in athletic activity. It helps to increase muscle mass and strength.
And remember, saturated fats work best (along with monounsaturated fats – olive oil, almonds, avocados etc.). In fact higher intakes of polyunsaturated fats (canola oil, sunflower oil, soybean oil, safflower oil, margarine etc.) are linked to LOWER testosterone levels (14 & 15). I explore the dangers of PUFA's in a lot more detail in this article - PUFA's: The Worst Thing For Your Health That You Eat Everyday.

In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
In addition to weight training, combining this with interval training like burst training is the best overall combo to increase HGH. In fact, Burst training has been proven to not only boost T-levels, it helps keeps your testosterone elevated and can prevent its decline. Burst training involves exercising at 90–100 percent of your maximum effort for a short interval in order to burn your body’s stored sugar (glycogen), followed by a period of low impact for recovery.
With the exception of increasing my fat and cholesterol intake, my diet wasn’t that unconventional. I didn’t follow a strictly low-carb or Paleo diet because recent research has suggested that a diet high in protein and low in carbs actually causes T levels to decrease. With that said, I was judicious with the carbs. I tried to get most of my carbs from veggies and fruit, but I didn’t freak out if my wife made us spaghetti for dinner.
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).
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.
Individuals with metabolic syndrome are at increased risk for developing coronary artery disease and diabetes mellitus. Predicting who might develop the metabolic syndrome would allow preventive measures to be taken in addition to weight control and other lifestyle modifications such as cessation of smoking and increased exercise. It is known that with decreasing testosterone availability in aging males there is an increase in fat mass and decrease in lean body mass (van den Beld et al 2000), there are disorders of insulin and glucose metabolism (Haffner et al 1996) and dyslipidemia (Tsai et al 2004). Kupelian and colleagues (2006) in analyzing data from the Massachusetts Male Aging Study demonstrated that men with low levels of testosterone, sex hormone-binding globulin, or clinical androgen deficiency, especially men with a BMI of greater than 25, were at increased risk of developing the metabolic syndrome and hence, diabetes mellitus and/or coronary artery disease.
^ David KG, Dingemanse E, Freud JL (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron" [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 233 (5–6): 281–83. doi:10.1515/bchm2.1935.233.5-6.281.
To get your levels into the healthy range, sun exposure is the BEST way to optimize your vitamin D levels; exposing a large amount of your skin until it turns the lightest shade of pink, as near to solar noon as possible, is typically necessary to achieve adequate vitamin D production. If sun exposure is not an option, a safe tanning bed (with electronic ballasts rather than magnetic ballasts, to avoid unnecessary exposure to EMF fields) can be used.
Low testosterone levels can cause mood disturbances, increased body fat, loss of muscle tone, inadequate erections and poor sexual performance, osteoporosis, difficulty with concentration, memory loss and sleep difficulties. Current research suggests that this effect occurs in only a minority (about 2%) of ageing men. However, there is a lot of research currently in progress to find out more about the effects of testosterone in older men and also whether the use of testosterone replacement therapy would have any benefits.
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