Fertility and Infertility

Thyroid hormone was recognized as the fundamental fertility hormone for both sexes by the 1940s, making infertility a standard sign of hypothyroidism. 2 Peat argued that a TSH level even as high as 2.0 is associated with serious symptoms, and that correcting thyroid function, often alongside dietary improvements, has allowed women infertile for over a decade to conceive within weeks. 1 He noted that pregnenolone alone was sufficient to greatly increase sperm quality, and that polyunsaturated fats interfere with both steroid production and thyroid function, acting as a major villain in male fertility. 2 In his teaching, women regularly regained fertility simply through dietary changes that increased progesterone and thyroid while bringing estrogen under control. 3

The central hormonal dynamic in fertility is the balance between progesterone and estrogen. 5 Progesterone increases oxygen availability, while estrogen lowers it, and a decreased ratio of progesterone to estrogen is characteristic of both normal menstruation and the heightened miscarriage risk seen around the ninth week of pregnancy. 5 Peat explained that the onset of menopause corresponds to a failure to produce progesterone while estrogen remains at normal levels, creating a functional excess. 7 He detailed how estrogen kills embryos at any stage of pregnancy and causes premature infertility by desensitizing and killing brain cells through an excitotoxic process, which progesterone and pregnenolone inhibit. 7 Dinkov has observed that in women with unexplained infertility, the often-ignored estrogen estrone and prolactin are frequently elevated, even when estradiol is undetectable. 6

Beyond the primary sex steroids, a network of supportive factors is critical. Peat identified insufficient cholesterol, too much carotene, too little vitamin A, inadequate magnesium or sodium, and excessive cortisol as commonly overlooked causes of infertility. 5 He traced the historical recognition of vitamin E as a fertility nutrient that protects against the oxidative damage caused by polyunsaturated fats and estrogen. 4 Dinkov has extended this framework, citing studies where vitamin D improved ovarian reserves in infertile women more effectively and with less risk than megadosing DHEA, which can massively raise estrogen. 11 He also described a case where a man with a clinically "normal" testosterone level of 350 ng/dL saw his fertility restored and testosterone rise after using aspirin and vitamin E, underscoring that standard lab ranges often miss profound metabolic dysfunction. 8

The bioenergetic state of the organism is the ultimate foundation of fertility. Dinkov has pointed to research showing that both red light exposure and niacinamide restore female fertility by increasing ATP production and lowering nitric oxide. 9 Roddy and Dinkov have emphasized that low metabolic rate, often masked by stress hormones, is the core issue, and that fertility should be viewed as a barometer of systemic health rather than an isolated genital problem. 2 Emma Sgourakis noted that for many women with prior long-term oral contraceptive use, simply improving sleep, eating more food, and ceasing restrictive diets was sufficient to restore fertility, without any medical intervention ever having addressed these fundamentals. 9 Peat maintained that because both parents contribute to reproduction, the health of both must be optimized, with thyroid, pregnenolone, and vitamin E being as crucial for male fertility as thyroid, progesterone, and vitamin E are for female fertility. 5