In the womb the human fetus has a low level of SHBG allowing increased activity of sex hormones. After birth, the SHBG level rises and remains at a high level throughout childhood. At puberty the SHBG level halves in girls and goes down to a quarter in boys.  The change at puberty is triggered by growth hormone , and its pulsatility differs in boys and girls. In pregnant women in the last two thirds of pregnancy the SHBG level escalates to five to ten times the usual level for a woman. A hypothesis is that this protects against the effect of hormone produced by the fetus. 
As men age, their serum testosterone concentrations decrease, as do their bone densities. Because bone density is also low in hypogonadal men, we hypothesized that increasing the serum testosterone concentrations of men over 65 yr to those found in young men would increase their bone densities. We randomized 108 men over 65 yr of age to wear either a testosterone patch or a placebo patch double blindly for 36 months. We measured bone mineral density by dual energy x-ray absorptiometry before and during treatment. Ninety-six men completed the entire 36-month protocol. The mean serum testosterone concentration in the men treated with testosterone increased from 367 +/- 79 ng/dL (+/-SD; +/- nmol/L) before treatment to 625 +/- 249 ng/dL ( +/- nmol/L; P < ) at 6 months of treatment and remained at that level for the duration of the study. The mean bone mineral density of the lumbar spine increased (P < ) in both the placebo-treated ( +/- %) and testosterone-treated ( +/- %) groups, but the mean changes did not differ between the groups. Linear regression analysis, however, demonstrated that the lower the pretreatment serum testosterone concentration, the greater the effect of testosterone treatment on lumbar spine bone density from 0-36 months (P = ). This analysis showed a minimal effect ( +/- %) of testosterone treatment on bone mineral density for a pretreatment serum testosterone concentration of 400 ng/dL ( nmol/L), but an increase of +/- % for a pretreatment testosterone concentration of 200 ng/dL ( nmol/L). Increasing the serum testosterone concentrations of normal men over 65 yr of age to the midnormal range for young men did not increase lumbar spine bone density overall, but did increase it in those men with low pretreatment serum testosterone concentrations.
The primary focus on serotonin deficiency as the main cause of depression has created treatment failure in many depressed and addicted patients. Other happy (excitatory) neurotransmitters are often ignored and some patients become more depressed when treated with medication. The classic depressive disorder patient who presents to Florida Detox ® is Susan, a 42-year-old professional female who seeks medical attention for depression from her local physician. Dr. Jones immediately assumes that she would benefit from a serotonin enhancer such as Paxil, Prozac, or Lexapro. If indeed this patient suffers from low serotonin levels, her depression should respond within 2-4 weeks of treatment with the serotonin enhancer. Typically, prescribed a medication like Paxil (20 mg per day), she returns one month later insisting her depression is worse. Dr. Jones raises the Paxil to 40 mg per day. Frequently these patients are prescribed extremely high doses (60 mg to 80 mg per day) in the physician’s effort to conquer the problem. Unfortunately Dr. Jones disregards the continuous report from the patient that they are not feeling any better and may actually feel more depressed. What is the problem? If serotonin is unilaterally elevated above normal levels with the mediation, the brain will down regulate production of dopamine. This makes the patient with dopamine deficiency even more dopamine deficient. These patients will typically begin to self medicate with dopaminergic drugs like Percocet, Vicodin, or OxyContin to counteract the decreased production. All of these drugs produce increased dopamine activity in the brain’s pleasure center (nucleus accumbens). When these patients are accurately diagnosed with their genetic dopamine/glutamate deficiency and treated with appropriate dopamine/glutamate enhancing medication, they quickly experience cessation of their depression and lose the craving (psychological and biochemical) for drugs and alcohol. Treatment results in better relapse statistics with the application of this scientific approach to addiction and depression. Unilateral elevation of serotonin without dopamine level protection will result in markedly elevated prolactin levels. Prolactin will increase appetite and decrease sex drive. When dopamine levels are enhanced to normal levels, sex drive will return as will better appetite control.