Pearls and Pitfalls of Testosterone Boosting Modalities

Eugene Shippen, M.D.

Medical Consultant for Lead Toxicology, Exide Technologies, Inc

The primary reason for low testosterone in younger aging males, and for some older aging males as well, is low gonadotrophin output, particularly LH. Leydig cells decline with aging and persistently low gonadotrophins and some diseases, i.e., hemochromatosis, hypothyroidism, etc. If boosting methods fail, then primary hypogonadism is present and replacement modalities are required. Reasons for low gonadotrophins today may be related to xeno-estrogens in diet and environmental intake. Additionally, obesity with increased endogenous estrogens, drugs and poor health or co-morbid diseases add to the long list that requires investigation. In this regard, we can do much to change negative patterns, but along with these changes we can add great benefits through boosting testosterone through increasing gonadotrophins or giving them directly. In my experience, boosting should be the first diagnostic and treatment intervention before direct replacement of testosterone is initiated, particularly under the age of 65. The three most common methods are: (1) Through the use of SERMS, such as clomiphene or analogues; (2) Suppression of endogenous conversion of androgens into estrogens within the hypothalamus with reversible aromatase inhibitors like anastrozole or femara; and (3) hCG Chorionic Gonadotrophin, a direct LH containing natural compound with a very long history of safe, effective uses. My discussion will cover the background literature and my long use of all three modalities and some observations on potential problems and benefits of these approaches. Some of the unique benefits are poorly known and, sadly, under-utilized. Questions and answers will be welcomed depending on time constraints.