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.
In January 2004, Major League Baseball announced a new drug policy which included random, offseason testing and 10-day suspensions for first-time offenders, 30-days for second-time offenders, 60-days for third-time offenders, and one year for fourth-time offenders, all without pay, in an effort to curtail performance-enhancing drug use (PED) in professional baseball. This policy strengthened baseball's pre-existing ban on controlled substances , including steroids, which has been in effect since 1991.  The policy was to be reviewed in 2008, but under pressure from the . Congress , on November 15, 2005, players and owners agreed to tougher penalties; a 50-game suspension for a first offense, a 100-game suspension for a second, and a lifetime ban for a third.
Por sí solos ninguno de estos síntomas indica que alguien está tomando esteroides anabólicos, pero podrían alertar a los padres y a los entrenadores sobre la posibilidad de que el abuso de la droga está ocurriendo. Hay pocas enfermedades médicas en la juventud en las que la prescripción médica de testosterona es apropiada e indicada; el uso apropiado de testosterona no debe causar ninguno de los síntomas físicos enlistados arriba. El uso sin autorización médica de esteroides anabólicos plantea un peligro grave. La posesión y distribución de los esteroides anabólicos para propósitos no médicos, es ilegal bajo la ley federal, porque los esteroides están clasificados como una droga Programa III bajo el Controlled Substances Act.