However, its addition was contested with claims that this diagnostic model of caffeine addiction is not supported by evidence. The American Psychiatric Associations DSM-5 does not include the diagnosis of a caffeine addiction but proposes criteria for the disorder for more study. Dependence and withdrawal
Withdrawal can cause mild to clinically significant distress or impairment in daily functioning. The frequency at which this occurs is self-reported at 11%, but in lab tests only half of the people who report withdrawal actually experience it, casting doubt on many claims of dependence. Mild physical dependence and withdrawal symptoms may occur upon abstinence, with greater than 100 mg caffeine per day, although these symptoms last no longer than a day. Some symptoms associated with psychological dependence may also occur during withdrawal. The diagnostic criteria for caffeine withdrawal require a previous prolonged daily use of caffeine. Following 24 hours of a marked reduction in consumption, a minimum of 3 of these signs or symptoms is required to meet withdrawal criteria: difficulty concentrating, depressed mood/irritability, flu-like symptoms, headache, and fatigue. Additionally, the signs and symptoms must disrupt important areas of functioning and are not associated with effects of another condition.The ICD-11 includes caffeine dependence as a distinct diagnostic category, which closely mirrors the DSM-5s proposed set of criteria for "caffeine-use disorder". Caffeine use disorder refers to dependence on caffeine characterized by failure to control caffeine consumption despite negative physiological consequences.
Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis, is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty. Signs of puberty can develop as early as an age of 1 year.The spinal length in boys may be short due to a rapid advance in epiphyseal maturation. It is an autosomal dominant condition with a mutation of the luteinizing hormone (LH) receptor. As FMPP is a gonadotropin-independent form of precocious puberty, gonadotropin-releasing hormone agonists (GnRH agonists) are ineffective. Treatment is with drugs that suppress or block the effects of gonadal steroidogenesis, such as cyproterone acetate, ketoconazole, spironolactone, and testolactone. Alternatively, the combination of the androgen receptor antagonist bicalutamide and the aromatase inhibitor anastrozole may be used.Robert King Stone, personal physician to American president Abraham Lincoln, described the first case of FMPP in 1852. See also
Follicle-stimulating hormone insensitivity
Gonadotropin-releasing hormone insensitivity
Hypergonadism, hyperandrogenism, and precocious puberty
Inborn errors of steroid metabolism
Leydig cell hypoplasia (or LH insensitivity)

References
External links
Testotoxicosis at NIHs Office of Rare Diseases