Puberty occurs when there is an “awakening” of the hypothalamic-pituitary axis. The hypothalamus increases its secretion of gonadotropin releasing hormone (GnRH) which in turn stimulates the release of luteinizing hormone (LH) and follicle stimulating hormone (FSH). This leads to a significant increase in the production of testicular testosterone and the induction of the well-known secondary sex characteristics associated with puberty: growth spurt, increased libido, increased erectile function, acne, increased body hair, increased muscle mass, deepening of the voice, spermatogenesis, gynecomastia (usually transient).
Exercise boosts testosterone in two important ways. First, specific types of exercise actually cause our body to produce more testosterone. We’ll talk more about those in a bit. Second, exercise helps to increase muscle mass and decrease body fat. As we’ve discussed previously, adipose tissue converts testosterone into estrogen. The less fat we get, the more T we have.
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.
The definition of the metabolic syndrome continues to be a work in progress. Within the last decade a number of definitions have emerged each with its own set of criteria although there is considerable overlap among them. The most recent definition seems to enjoy considerable consensus. It requires central adiposity (>94 cm waist circumference) plus two of, increased triglycerides, decreased HDL cholesterol, hypertension, insulin resistance as evidenced by impaired glucose tolerance, or frank diabetes (Alberti 2005). Almost immediately on the heels of this consensus, came a number of specific chemical markers which have been proposed to complement the basic definition of the metabolic syndrome (Eckel et al 2005).
Grape seed extract is another ingredient with not enough research to suggest a dosage. Grape seed extract can interact with drugs like “blood thinners, NSAID painkillers (like aspirin, Advil, and Aleve), certain heart medicines, cancer treatments, and others.” If this sounds like you (or if you ever pop an Advil to clear off a headache), you’ll need to speak with a doctor to make sure this supplement is safe to take.
The unsexy truth is that increasing T naturally simply comes down to making some long-term changes in your diet and lifestyle. As you’ll see, what I did to increase T largely boils down to eating better, exercising smarter, and getting more sleep. That’s pretty much it. But as with most things in life, the devil is in the details, so I’ll share with you exactly what I did and provide research that explains why the things I did helped boost my testosterone.
^ 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.
Like other steroid hormones, testosterone is derived from cholesterol (see figure). The first step in the biosynthesis involves the oxidative cleavage of the side-chain of cholesterol by cholesterol side-chain cleavage enzyme (P450scc, CYP11A1), a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to give pregnenolone. In the next step, two additional carbon atoms are removed by the CYP17A1 (17α-hydroxylase/17,20-lyase) enzyme in the endoplasmic reticulum to yield a variety of C19 steroids. In addition, the 3β-hydroxyl group is oxidized by 3β-hydroxysteroid dehydrogenase to produce androstenedione. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone.