You are talking to the GMs, Dawnon. I have no qualms.
@Lugubrious, I'll fix that when I next edit the Compendium. Thank you for pointing that out.
Endocrinology said
Addiction
Addiction is the continued repetition of a behaviour despite adverse consequences, or a neurological impairment leading to such behaviours. Classic hallmarks of addiction include impaired control over substances or behaviour, preoccupation with substance or behaviour, continued use despite consequences, and denial. Habits and patterns associated with addiction are typically characterised by immediate gratification (short-term reward), coupled with delayed deleterious effects (long-term costs).
Physiological dependence occurs when the body has to adjust to the substance by incorporating the substance into its "normal" functioning. This state creates the conditions of tolerance and withdrawal. Tolerance is the process by which the body continually adapts to the substance and requires increasingly larger amounts to achieve the original effects. Withdrawal refers to physical and psychological symptoms experienced when reducing or discontinuing a substance that the body has become dependent on. Symptoms of withdrawal generally include but are not limited to anxiety, irritability, intense cravings for the substance, nausea, hallucinations, headaches, cold sweats, and tremors.
Several brain regions are also involved in the biological mechanisms of addiction. Most notably, the release of dopamine into the nucleus accumbens, which is triggered by a wide variety of drugs in a wide variety of ways, plays a role in the reinforcing qualities of stimuli. Since dopamine secretion is also characteristic of natural reinforcing stimuli such as food, water, and sex, it's evident that the addictive nature of drug involves processes that hijack these mechanisms. Research indicates that this process begins in the limbic dopaminergic system and subsequently modifies other parts of the brain that receive input from the affected neurons. Among these areas is the ventral tegmental area.
The nucleus accumbens (NAc) and the ventral tegmental area (VTA) are the primary sites where drugs of abuse act. The following are commonly considered abused drugs: heroin, cocaine, alcohol, opiates, marijuana, nicotine, amphetamine, and their synthetic analogues. These drugs alter the neuromodulatory influence of dopamine on the processing of reinforcement signals by prolonging the action of dopamine in the nucleus accumbens or by potentiating the activation of neurons in the VTA and NAc. The most common drugs of abuse stimulate the release of dopamine, which creates both their rewarding and the psychomotor effects. Compulsive drug-taking behaviours are a result of the permanent functional changes in the mesolimbic dopamine system arising from repetitive dopamine stimulation. Molecular and cellular adaptations are responsible for a sensitised dopamine activity in the VTA and along the mesolimbic dopamine projection in response to drug abuse. In the VTA of addicted individuals, the activity of the dopamine-synthesising enzyme tyrosine hydroxylase increases, as does the ability of these neurons to respond to excitatory inputs. The latter effect is secondary to increases in the activity of the transcription factor CREB and the up regulation of GluR1, an important subunit of AMPA receptors for glutamate. These alterations in neural processing could account for the waning influence of adaptive emotional signals in the operation of decision making faculties as drug-seeking and drug-taking behaviours become habitual and compulsive.
The withdrawal phenomenon occurs because the deficit in reward functioning causes the organism to enter a distress cycle wherein the drugs become necessary to restore the normal homoeostatic state. Recent research has shown that even after the final stages of withdrawal have been passed, an organism will reinstate the drug-seeking behaviour if exposed to the drug or drug-related stimuli.
Endocrinology said
Cortisol
Cortisol is a steroid hormone, more specifically a glucocorticoid, produced by the zona fasciculata of the adrenal cortex. It is released in response to stress and a low level of blood glucocorticoid. Its primary functions are to increase blood sugar through gluconeogenesis, suppress the immune system, and aid with fat, protein, and carbohydrate metabolisms. It also decreases bone formation.
Cortisol is produced in the human body by the adrenal gland in the zona fasciculata, the second of three layers comprising the adrenal cortex. The cortex forms the outer "bark" of each adrenal gland, situated atop the kidneys. The release of cortisol is controlled by the hypothalamus, a part of the brain. The secretion of corticotropin-releasing hormone (CRH) by the hypothalamus triggers cells in the neighbouring anterior pituitary to secrete another hormone, the adrenocorticotropic hormone (ACTH), into the vascular system, through which blood carries it to the adrenal cortex.
In the fasting state, cortisol stimulates gluconeogenesis (formation of glucose, in the liver, from certain amino acids, glycerol, lactate, and/or propionate), and activates anti-stress and anti-inflammatory pathways. Cortisol prevents the release of substances in the body that cause inflammation.
Cortisol is released in response to stress, sparing available glucose for the brain, generating new energy from stored reserves, and diverting energy from low-priority activities (such as the immune system) in order to survive immediate threats or prepare for the exertion of rising to a new day.
