<unk>  may include disinhibition, impaired concentration and memory, depression, as well as sexual dysfunction. The<unk> -term effects of<unk> s may differ from the adverse effects seen after acute administration of<unk> s. An analysis of cancer patients found that those who took tranquillisers or sleeping tablets had a substantially poorer quality of life on all measurements conducted, as well as a worse clinical picture of symptomatology. Worsening of symptoms such as fatigue, insomnia, pain, dyspnea and constipation was found when compared against those who did not take tranquillisers or sleeping tablets. Most individuals who successfully discontinue hypnotic therapy after a gradual taper and do not take<unk> s for 6 months have less severe sleep and anxiety problems, are less distressed and have a general feeling of improved health at 6-month follow-up. The<unk>  of<unk> s for the treatment of anxiety has been found to lead to a significant increase in healthcare costs due to accidents and other adverse effects associated with the<unk> -term<unk>  of<unk> s. Cognitive status<unk> -term<unk> <unk>  can lead to a generalised impairment of cognition, including sustained attention, verbal learning and memory and psychomotor, visuo-motor and visuo-conceptual abilities. Transient changes in the brain have been found using neuroimaging studies, but no brain abnormalities have been found in patients treated<unk>  term with<unk> s. When<unk> <unk> rs cease<unk> -term<unk>  therapy, their cognitive function improves in the first six months, although deficits may be permanent or take<unk> er than six months to return to baseline. In the elderly,<unk> -term<unk>  therapy is a risk factor for amplifying cognitive decline, although gradual withdrawal is associated with improved cognitive status. A study of alprazolam found that 8 weeks administration of alprazolam resulted in deficits that were detectable after several weeks but not after 3.5 years. Effect on sleep Sleep architecture can be adversely affected by<unk>  dependence. Possible adverse effects on sleep include induction or worsening of sleep disordered breathing. Like alcohol,<unk> s are commonly<unk> d to treat insomnia in the short term (both prescribed and self-medicated), but worsen sleep in the<unk>  term. Although<unk> s can put people to sleep, while asleep, the drugs disrupt sleep architecture, decreasing sleep time, delayed and decreased REM sleep, increased alpha and beta activity, decreased K complexes and delta activity, and decreased deep slow-wave sleep (i.e., NREM stages 3 and 4, the most restorative part of sleep for both energy and mood). Mental and physical health The<unk> -term<unk>  of<unk> s may have a similar effect on the brain as alcohol, and is also implicated in depression, anxiety, post-traumatic stress disorder (PTSD), mania, psychosis, sleep disorders, sexual dysfunction, delirium, and neurocognitive disorders. However a 2016 study found no association between<unk> -term usage and dementia. As with alcohol, the effects of<unk>  on neurochemistry, such as decreased levels of serotonin and norepinephrine, are believed to be responsible for their effects on mood and anxiety. Additionally,<unk> s can indirectly cause or worsen other psychiatric symptoms (e.g., mood, anxiety, psychosis, irritability) by worsening sleep (i.e.,<unk> -induced sleep disorder).<unk> -term<unk> <unk>  may lead to the creation or exacerbation of physical and mental health conditions, which improve after six or more months of abstinence. After a period of about 3 to 6 months of abstinence after completion of a gradual-reduction regimen, marked improvements in mental and physical wellbeing become apparent. For example, one study of hypnotic<unk> rs gradually withdrawn from their hypnotic medication reported after six months of abstinence that they had less severe sleep and anxiety problems, were less distressed, and had a general feeling of improved health. Those who remained on hypnotic medication had no improvements in their insomnia, anxiety, or general health ratings. A study found that individuals having withdrawn from<unk> s showed a marked reduction in<unk>  of medical and mental health services. Approximately half of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia may be the result of alcohol or<unk>  dependence. Sometimes anxiety disorders precede alcohol or<unk>  dependence but the alcohol or<unk>  dependence often acts to keep the anxiety disorders going and often progressively makes them worse. Many people who are addicted to alcohol or prescribed<unk> s decide to quit when it is explained to them they have a choice between ongoing ill mental health or quitting and recovering from their symptoms. It was noted that because every individual has an individual sensitivity level to alcohol or sedative hypnotic drugs, what one person can tolerate without ill health will cause another to suffer very ill health, and that even moderate drinking in sensitive individuals can cause rebound anxiety syndromes and sleep disorders. A person who is suffering the toxic effects of alcohol or<unk> s will not benefit from other therapies or medications as they do not address the root cause of the symptoms. Recovery from<unk>  dependence tends to take a lot<unk> er than recovery from alcohol, but people can regain their previous good health. A review of the literature regarding<unk>  hypnotic drugs concluded that these drugs cause an unjustifiable risk to the individual and to public health. The risks include dependence, accidents and other adverse effects. Gradual discontinuation of hypnotics leads to improved health without worsening of sleep. Daily<unk> rs of<unk> s are also at a higher risk of experiencing psychotic symptomatology such as delusions and hallucinations. A study found that of 42 patients treated with alprazolam, up to a third of<unk> -term<unk> rs of the<unk>  drug alprazolam (Xanax) develop depression. Studies have shown that<unk> -term<unk>  of<unk> s and the<unk>  receptor agonist nonbenzodiazepine Z drugs are associated with causing depression as well as a markedly raised suicide risk and an overall increased mortality risk. A study of 50 patients who attended a<unk>  withdrawal clinic found that, after several years of chronic<unk> <unk> , a large portion of patients developed health problems including agoraphobia, irritable bowel syndrome, paraesthesiae, increasing anxiety, and panic attacks, which were not preexisting. The mental health and physical health symptoms induced by<unk> -term<unk> <unk>  gradually improved significantly over a period of a year following completion of a slow withdrawal. Three of the 50 patients had wrongly been given a preliminary diagnosis of multiple sclerosis when the symptoms were actually due to chronic<unk> <unk> . Ten of the patients had taken drug overdoses whilst on<unk> s, despite the fact that only two of the patients had any prior history of depressive symptomatology. After withdrawal, no patients took any further overdoses after one year post-withdrawal. The cause of the deteriorating mental and physical health in a significant proportion of patients was hypothesised to be caused by increasing tolerance where withdrawal-type symptoms emerged, despite the administration of stable prescribed doses. Another theory is that chronic<unk> <unk>  causes subtle increasing toxicity, which in turn leads to increasing psychopathology in<unk> -term<unk> rs of<unk> s.<unk> -term<unk>  of<unk> s can induce perceptual disturbances and depersonalisation in some people, even in those taking a stable daily dosage, and it can also become a protracted withdrawal feature of the<unk>  withdrawal syndrome. In addition, chronic<unk>  of<unk> s is a risk factor for blepharospasm. Drug-induced symptoms that resemble withdrawal-like effects can occur on a set dosage as a result of prolonged<unk> , also documented with barbiturate-like substances, as well as alcohol and<unk> s. This demonstrates that the effects from chronic<unk>  of<unk>  drugs are not unique but occur with other GABAergic sedative hypnotic drugs, i.e., alcohol and barbiturates. Immune system Chronic<unk>  of<unk> s seemed to cause significant immunological disorders in a study of selected outpatients attending a psychopharmacology department. Diazepam and clonazepam have been found to have<unk> -lasting, but not permanent, immunotoxic effects in fetuses of rats. However, single very high doses of diazepam have been found to cause lifelong immunosuppression in neonatal rats. No studies have been done to assess the immunotoxic effects of diazepam in humans; however, high prescribed doses of diazepam, in humans, have been found to be a major risk of pneumonia, based on a study of people with tetanus. It has been proposed that diazepam may cause<unk> -lasting changes to the GABAA receptors with resultant<unk> -lasting disturbances to behaviour, endocrine function and immune function. Suicide and self-harm<unk>  of prescribed<unk> s is associated with an increased rate of suicide or attempted suicide. The prosuicidal effects of<unk> s are suspected to be due to a psychiatric disturbance caused by side effects or withdrawal symptoms. Because<unk> s in general may be associated with increased suicide risk, care should be taken when prescribing, especially to at-risk patients. Depressed adolescents who were taking<unk> s were found to have a greatly increased risk of self-harm or suicide, although the sample size was small. The effects of<unk> s in individuals under the age of 18 requires further research. Additional caution is required in using<unk> s in depressed adolescents.<unk>  dependence often results in an increasingly deteriorating clinical picture, which includes social deterioration leading to comorbid alcohol<unk>  disorder and substance<unk>  disorder.
Effects of long-term benzodiazepine use
Short-term effects of alcohol consumption
Long-term effects of cannabis
Acute behavioural disturbance
Sleeping disorders following traumatic brain injury
Headache attributed to a substance or its withdrawal
Alcohol-related brain damage
Opioid-induced endocrinopathy