Anxiety hormone

CCK is found in the digestive tract and the central and peripheral nervous systems. In the brain, CCK coexists with DA. In the peripheral nervous system, the two principal physiological actions of CCK are stimulation of gaU. bladder contraction and pancreatic enzyme secretion. CCK also stimulates glucose and amino acid transport, protein and DNA synthesis, and pancreatic hormone secretion. In the CNS, CCK induces hypothermia, analgesia, hyperglycemia, stimulation of pituitary hormone release, and a decrease in exploratory behavior. The CCK family of neuropeptides has been impHcated in anxiety and panic disorders, psychoses, satiety, and gastric acid and pancreatic enzyme secretions. 

CRH (Corticotropin releasing hormone) is expressed in the nucleus paraventricularis of the hypothalamus and drives the stress hormone system by activating synthesis and release of corticotropin at the pituitary and in turn corticosteroid from the adrenal cortex. CRH is also expressed at many other brain locations not involved in neuroendocrine regulation, e.g. the prefrontal cortex and the amygdala. Preclinical studies have shown that CRH also coordinates the behavioral adaptation to stress (e.g. anxiety, loss of appetite, decreased sleepiness, autonomic changes, loss of libido). 

For some conditions, a large placebo effect can be anticipated. For example, studies of hormone replacement therapies for hot flashes in postmenopausal women consistently show a 50% decline from baseline in the number of daily hot flashes in the placebo group. Therefore, in order to show significance, an active treatment must produce an effect that is substantially larger than 50%. A marked placebo response is commonly observed with any condition that has a subjective component, such as chronic pain (e.g. arthritis), episodic pain (e.g. headaches), psychological states (e.g. anxiety), and certain physiologic measurements (e.g. blood pressure). 

Several neuropeptides are under current investigation for their role in anxiety disorders. Important neuropeptides include neuropeptide Y (NPY), substance P, and cholecystokinin. NPY appears to have a role in reducing the effect of stress hormones and inhibiting activity of the LC. Both mechanisms may contribute to the anxiolytic properties seen experimentally. Substance P may have anxiolytic and antidepressant properties. This may be due in part to its effects on corticotropin-releasing hormone.21... 

SSRIs are theorized to reduce the frequency of hot flashes by increasing serotonin in the central nervous system and by decreasing LH. Of the SSRIs, citalopram, paroxetine, and sertraline all have been studied and have demonstrated a reduction in hot flashes while treating other symptomatic complaints such as depression and anxiety.33 Venlafaxine, which blocks the reuptake of serotonin and norepinephrine, has demonstrated a reduction in hot flashes primarily in the oncology population.34 Overall, these antidepressant medications offer a reasonable option for women who are unwilling or cannot take hormonal therapies, particularly those who suffer from depression or anxiety. These agents should be prescribed at the lowest effective dose to treat symptoms and may be titrated based on individual response. 

Palomba et al. (2004) have also studied the effects on cognigtion, mood, and QoL in 100 premenopausal women with symptomatic uterine leiomyomas treated with gonadotropin-releasing hormone agonist with or without raloxifene. The findings demonstrate that raloxifene is not able to prevent decreases in cognitive function and does not reduce the depresion and anxiety symptoms in women treated with GnRHa. 

Stress and stress hormones Anxiety or stress can increase energy expenditure, although the effect is small. It is caused by increased sympathetic activity and hence increased levels of the stress hormones adrenaline and noradrenaline. Injection of these hormones increases oxygen consumption, as does caffeine, which... 

Taking into account the central role of the HPA-axis for the regulation of anxiety, a variety of genetically altered mice has been developed, aimed at targeting the hormonal stress system (Muller and Keck 2002 Sillaber et al. 2002 Stenzel-Poore et al. 1992 Timpl et al. 1998). These models are described extensively in the chapter by Keck and Muller and will, therefore, be omitted here. 

Holsboer F (1999) The rationale for corticotropin-releasing hormone receptor (CRH-R) antagonists to treat depression and anxiety. J Psychiatr Res 33 181-214... 

---