Looking for ingredients that work in the realm of supplements can be like finding a needle in a haystack. Testosterone boosters, like all dietary supplements, are not approved by the Food and Drug Administration prior to marketing. This lack of oversight dates back to the 1994 Dietary Supplement Health and Education Act (DSHEA), which stipulated that purveyors of supplements weren’t required to prove the safety of their products or the veracity of what’s on the labels to the FDA before listing them for sale. Often, there isn’t a lot of scientific backing behind an ingredient, or research has been done solely on animals, not humans.
Early infancy androgen effects are the least understood. In the first weeks of life for male infants, testosterone levels rise. The levels remain in a pubertal range for a few months, but usually reach the barely detectable levels of childhood by 4–7 months of age. The function of this rise in humans is unknown. It has been theorized that brain masculinization is occurring since no significant changes have been identified in other parts of the body. The male brain is masculinized by the aromatization of testosterone into estrogen, which crosses the blood–brain barrier and enters the male brain, whereas female fetuses have α-fetoprotein, which binds the estrogen so that female brains are not affected.
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The science backs up the soldier’s self discovery, in fact, exposure to radiation (whether it’s from an army radar or the cell phone in your pocket, or the wifi router in your house) has been shown to lower sperm quality, fertility and testosterone. This is true not only for military personnel (88, 89,90) but all males living in a modern world (91).
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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.
If in a 46 XY individual testosterone is either not produced in adequate concentrations as in gonadal dysgenesis (MacLaughlin and Donahue 2004), or in the absence of the enzyme 17 alpha-hydroxylase so that testosterone is not produced (Ergun-Longmire et al 2006), or testosterone androgen receptors are absent as in the androgen insensitivity syndrome (Hughes and Deeb 2006), phenotypic females will result.