Tag: Psychiatric Disorders

What is MindFreedom International?

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Introduction

MindFreedom International is an international coalition of over one hundred grassroots groups and thousands of individual members from fourteen nations.

Based in the United States, it was founded in 1990 to advocate against forced medication, medical restraints, and involuntary electroconvulsive therapy. Its stated mission is to protect the rights of people who have been labelled with psychiatric disorders. Membership is open to anyone who supports human rights, including mental health professionals, advocates, activists, and family members. MindFreedom has been recognised by the United Nations Economic and Social Council as a human rights non-governmental organisation (NGO) with Consultative Roster Status.

Origins and Purpose

MindFreedom International is rooted in the psychiatric survivors movement, which arose out of the civil rights ferment of the late 1960s and early 1970s and the personal histories of psychiatric abuse experienced by some ex-patients rather than the intradisciplinary discourse of antipsychiatry. The precursors of MFI include ex-patient groups of the 1970s such as the Portland, Oregon-based Insane Liberation Front and the Mental Patients’ Liberation Front in New York. The key text in the intellectual development of the survivor movement, at least in the US, was Judi Chamberlin’s 1978 text, On Our Own: Patient Controlled Alternatives to the Mental Health System. Chamberlin was an ex-patient and co-founder of the Mental Patients’ Liberation Front. Coalescing around the ex-patient newsletter Dendron, in late 1988 leaders from several of the main national and grassroots psychiatric survivor groups felt that an independent, human rights coalition focused on problems in the mental health system was needed. That year the Support Coalition International (SCI) was formed. In 2005 the SCI changed its name to MFI with David W. Oaks as its director. SCI’s first public action was to stage a counter-conference and protest in May 1990 in New York City at the same time as (and directly outside of) the American Psychiatric Association’s annual meeting.

Many of the members of MFI, who feel that their human rights were violated by the mental health system, refer to themselves as ‘psychiatric survivors’. MFI is a contemporary and active coalition of grassroots groups which are carrying forward the historical tradition of survivor opposition to coercive psychiatry. It does not define itself as an antipsychiatry organisation and its members point to the role which ‘compassionate’ psychiatrists have played in MFI. Activists within the coalition have been drawn from both left and right wing of politics.

MFI functions as a forum for its thousands of members to express their views and experiences, to form support networks and to organise activist campaigns in support of human rights in psychiatry. The coalition regards the psychiatric practices of ‘unscientific labelling, forced drugging, solitary confinement, restraints, involuntary commitment, electroshock’ as human rights violations.

In 2003, eight Mindfreedom members, led by then-executive director David Oaks, went on a hunger strike to publicise a series of “challenges” they had put forth to the American Psychiatric Association (APA), the US Surgeon General and the National Alliance on Mental Illness (NAMI). The eight MFI members challenged the APA, US Surgeon General and NAMI to present MFI with “unambiguous proof that mental illness is brain disorder.” By sustaining the hunger-strike for more than one month, MFI forced the APA and NAMI to enter into a debate with them on this and other issues.

MindFreedom describes their Shield Programme as “an all for one and one for all” network of members. When a registered member is receiving (or is being considered for) involuntary psychiatric treatment, an alert is sent to the MindFreedom Solidarity Network on that person’s behalf. Members of the network are then expected to participate in organised, constructive, nonviolent actions—e.g. political action, publicity and media alerts, passive resistance, etc. – to stop or prevent the forced treatment.

What is Amotivational Syndrome?

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Introduction

Amotivational syndrome is a chronic psychiatric disorder characterised by signs that are linked to cognitive and emotional states such as detachment, blunted emotion and drives, executive functions like memory and attention, disinterest, passivity, apathy, and a general lack of motivation. This syndrome can be branched into two subtypes – marijuana amotivational syndrome, interchangeably known as cannabis induced amotivational syndrome which is caused by usage and/or dependency of the substance and is primarily associated with long-term effects of cannabis use, and SSRI-induced amotivational syndrome or SSRI-induced apathy caused by the intake of SSRI medication dosage. According to the Handbook of Clinical Psychopharmacology for Therapists, amotivational syndrome is listed as a possible side effect of SSRIs in the treatment of clinical depression.

Refer to Avolition.

Signs and Symptoms

Amotivational syndrome has been suspected to affect the frontal cortex or frontal lobe of the brain by the impairment of that region which monitors cognitive functions and skills that revolve around emotional expression, decision making, prioritisation, and internal, purposeful mental action. It is most often detected through signs that are linked to apathy such as disinhibited presentations, short and long term memory deficit or amnesia, a lack of emotional display also known as emotional blunting, relative disinterest, passivity, and reluctance to participate in prolonged activities that require attention or tenacity. Common symptoms that may also be experienced include incoherence, an inability to concentrate on tasks, emotional distress, a diminished level of consciousness, selective attention or attentional control, and being withdrawn and asocial. These symptoms are also generally linked to cannabis consumption and abuse, as well as SSRI medication that are often used as forms of antidepressant medication.

Subtypes

Cannabis Amotivational Syndrome

The term amotivational syndrome was first devised to understand and explain the diminished drive and desire to work or compete among the population of youth who are frequent consumers of cannabis and has since been researched through various methodological studies with this focus on cannabis, or marijuana. Cannabis amotivational syndrome is often used interchangeably with marijuana amotivational syndrome and marijuana or cannabis induced or related amotivational syndrome. Cannabis related amotivational syndrome is closely tied with cannabis use disorder which is recognised in the fifth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and has similar conditions such as withdrawing and giving up from daily activities and neglecting major roles and responsibilities. It is one of the major complications of chronic exposure to cannabis as it includes the effects and elements of cognitive deficit or cognitive impairment that are similar to what appears in schizophrenia and depression. It is characterised by a gradual detachment and disconnect from the outer world due to a loss of emotional reactivity, drives, and aims. Responsiveness to any stimuli is limited, and those affected are unable to experience or anticipate any pleasure except through the use of cannabis. Marijuana amotivational syndrome has been looked at within the context of how motivation-related constructs influence the young adult in the context of the school or workplace as those affected have poor levels of school-related functioning, are unable to focus on schoolwork due to their lack of motivation, are less satisfied with participating in educational activities, and easily enter into conflict with scholastic authorities. Additionally, marijuana amotivational syndrome is closely linked to self-efficacy, a psychological concept which encapsulates how one values their capabilities and the amount of confidence they hold in their capabilities to persevere – this is related to motivation as people who hold a high amount of self-efficacy are more likely to make efforts to complete a task and persist longer in those efforts compared to those with lower self-efficacy.

SSRI-Induced Amotivational Syndrome

Amotivational syndrome caused or related to SSRI dosage is also commonly known as apathy syndrome, SSRI-induced apathy syndrome, SSRI-induced apathy, and antidepressant apathy syndrome. “Apathy is defined as the presence of diminished motivation in an individual – a development that is not attributable to a reduced level of consciousness, cognitive impairment (e.g. dementia), or emotional distress (i.e. depression)”. This syndrome is linked to the consumption and dosage of selective serotonin reuptake inhibitors (SSRIs), which are typically used as antidepressants, and has been reported in patients undergoing SSRI treatment as SSRIs may modulate and alter the activity occurring in the frontal lobe of the brain, one of the four major lobes in the brain that contains most of the dopaminergic pathways that are associated with reward, attention, short-term memory tasks, planning, and motivation. This syndrome may be related to serotonergic effects on the frontal lobes and/or serotonergic modulation of mid-brain dopaminergic systems which project to the prefrontal cortex, both suggesting the possibility of frontal lobe dysfunction due to the alteration of serotonin levels. This brings on a number of similar symptoms that lead to dose dependency and apathy, however, it has often been unrecognized and undiagnosed due to the lack of prevalent data and its subtle and delayed onset.

When looking at SSRI-induced amotivational syndrome as a clinical side effect, it can be looked at through a behavioural perspective as well as an emotional perspective. When looked at as a behavioural syndrome the association between apathy or low motivation and SSRI prescription has been recognised as a potential side effect, for example, behavioural apathy has been noted in several case reports. Aside from a behavioural perspective, an emotional perspective emphasizes the emotional aspects of indifference such as a lack of emotional responsiveness, a reduction in emotional sensitivity such as numbing or blunting emotion, affected patients often describe having a restricted range of emotions including those emotions that are a part of everyday life, and distinct emotional themes in affected patience that include a general reduction in the intensity or experience of all emotions, both positive and negative, and feeling emotionally detached and “just not caring”, diminishing emotionality in both personal and professional interpersonal relationships.

Treatment and Evaluation

Cannabis Amotivational Syndrome

Treatment of cannabis amotivational syndrome is like the treatment for cannabis dependence in which there should be careful evaluation for any signs of depression that predate the development of the amotivational syndrome and may be the basis for cannabis dependence and usage. The user is slowly weaned off usage through urine monitoring, self-help groups, education, and therapy in different treatment settings such as group, family, and individual therapy in order to separate themselves from cannabis consumption and any cannabis-related environment as both contribute to the cognitive aspects of amotivational syndrome.

SSRI-Induced Amotivational Syndrome

Treatments include gradually reducing or discontinuing the SSRI, changing the SSRI to another antidepressant class, or co-prescribing with the SSRI a medication that boosts dopamine, such as the antidepressant bupropion.

Current Research and Discourse

Cannabis Amotivational Syndrome

Though there is a prevalent relationship between cannabis consumption and amotivational syndrome, there is still some considerable debate that exists around cannabis consumption causing amotivational syndrome meaning that it may not be a single entity but rather a collection of behaviours that form the result of a combination of effects of an already existent or reactive depression that occurs alongside cannabis’s ability to facilitate a unique attention state. Trait absorption is often mentioned within discourses surrounding cannabis-induced amotivational syndrome and it states that the traits associated with a large majority of marijuana users, which are similar to traits found in those who have amotivational syndrome, such as boredom and a general feeling of disconnect, are absorbed and taken up by the cannabis user. It is used as a common argument against cannabis potentially being able to cause amotivational syndrome, instead, many cannabis users have stated that users often absorb what is often thought of as the typical set of traits marijuana consumers possess, which overlap with some of the traits found in amotivational syndrome. As a result, many have proposed that rather than cannabis being thought of as a psychologically harmful substance, it is instead thought of as an active placebo in which its effects on the mind are placebo effects in response to minimal physiological action rather than being a direct cause of the psychological changes seen in users.

Additionally, though research has been conducted, it is recognized that there is not enough substantial empirical research to conclude that the use of cannabis leads to amotivational syndrome. Anecdotal information such as statements taken from cannabis users includes feeling listless and lethargic. Amotivational syndrome still ranks high among the key problems associated with the drug, with researchers having adopted the phrase “amotivational” to describe lethargic cannabis users. The US Department of Health and Human Services also warns that usage in youth may result in amotivational symptoms such as an apathetic approach to life, fatigue, and poor academic and work performance. However, empirical research on the effects of cannabis on users’ motivation implies that there is no strong correlation and that there are numerous alternative explanations of these negative outcomes as a review of laboratory performance research, education data, and employment statistics fail to offer consistent evidence that directly link cannabis to any symptoms associated with amotivational syndrome. Though several studies contain data in which heavy cannabis users have reported feeling a lack of motivation, it has also been acknowledged that other variables such as comorbid drug use and baselines for low motivation may not be examined.

SSRI-Induced Amotivational Syndrome

Most research in psychological fields regarding amotivational syndrome caused by SSRI treatment has revolved around case studies and anecdotal reports to understand how SSRI medication influences levels of motivation and apathy in patients. There is considerable overlap in the clinical presentations of apathy and motivation and depression. Many patients with amotivational or apathy syndrome reported that they felt a lack of motivation that was unlike what they had sometimes experienced during previous episodes or depression, or that their feelings of apathy had no link to depression. Apathy syndrome has also been reported in a number of patients that have received or are receiving SSRI treatment over the last decade, which has also been linked to a deficit in the performance and activities of daily living, signalling a functional decline. It is a common behavioural problem that often goes undiagnosed and untreated, which is why it is considered to be clinical significant. Neuropsychological research has shown that a common feature of amotivational syndrome involves the presence of lesions and other abnormalities in the circulation of the frontal lobe. Neuroimaging studies of clinical populations have also reported correlations between apathy and structural and functional changes in the frontal lobe in the anterior cingulate gyrus and subregions of the basal ganglia. Recent case-control studies have also reported that apathy has appeared to be greater in patients who were treated with SSRI medication compared to patients who were not. Current findings are consistent with other findings supporting the correlation of SSRI and apathy due to the occurrence of abnormalities found within various regions of the frontal lobe. Though amotivational syndrome has been an emerging concern for pharmacotherapeutic industries to consider, there is still a growing body of empirical investigations that need to continue in order for the development of novel therapeutic interventions to improve, as well as treatment. Currently, empirical studies are limited and there is not a substantial enough amount of research to fully understand the link between frontal lobe abnormalities caused by SSRIs and thus resulting in amotivational syndrome. There is a lack of large-scale clinical studies that focus on the prevalence of SSRI-induced amotivational syndrome with regards to emotional blunting and apathy in both psychiatric or primary care populations, despite the high prescription rates for SSRI medication. There are also no current clinically popular scales to measure and assess SSRI-induced apathy. The Oxford Questionnaire of Emotional Side Effects of Antidepressants (OQESA) is a scale under development and presents a 26-item, Likert-style, self-report scale that aims to understand respondents’ emotional experiences such as a general reduction in emotions, a reduction in positive emotions, emotional detachment and blunting, and feelings of not caring. Respondents are also asked to what extent they believe their antidepressant is responsible for these emotional symptoms.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Amotivational_syndrome >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is the Epidemiology of Child Psychiatric Disorders?

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Introduction

The epidemiology of child psychiatric disorders is the study of the incidence, prevalence, and distribution of conditions in child and adolescent psychiatry.

Subfields of paediatric psychiatric epidemiology include developmental epidemiology, which focuses on the genetic and environmental causes of child psychiatric disorders. The field of paediatric psychiatric epidemiology finds widely varying rates of childhood psychiatric disorders, depending on study population, diagnostic method, and cultural setting.

Prevalence of Mental Illness

Epidemiological research has shown that between 3% and 18% of children have a psychiatric disorder causing significant functional impairment (reasons for these widely divergent prevalence rates are discussed below) and Costello and colleagues have proposed a median prevalence estimate of 12%. Using a different statistical method, Waddell and colleagues propose a prevalence rate for all mental disorders in children of 14.2%.

Developmental Epidemiology

Developmental epidemiology seeks to “disentangle how the trajectories of symptoms, environment, and individual development intertwine to produce psychopathology”.

Socio-Economic Influences

Mental illness in childhood and adolescence is associated with parental unemployment, low family income, being on family income assistance, lower parental educational level, and single-parent, blended or stepparent families.

Methodological Issues

Epidemiological research has produced widely divergent estimates, depending on the nature of the diagnostic method (e.g. structured clinical interview, unstructured clinical interview, self-report or parent-report questionnaire), but more recent studies using DSM-IV-based structured interviews produce more reliable estimates of clinical “caseness”. Past research has also been limited by inconsistent definitions of clinical disorders, and differing upper and lower age limits of the study population. Changing definitions over time have given rise to spurious evidence of changing prevalence of disorders. Furthermore, almost all epidemiological surveys have been carried out in Europe, North America and Australia, and the cross-cultural validity of DSM criteria have been questioned, so it is not clear to what extent the published data can be generalised to developing countries.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Epidemiology_of_child_psychiatric_disorders >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

On This Day … 17 May [2022]

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Events

  • 1990 – The General Assembly of the World Health Organisation (WHO) eliminates homosexuality from the list of psychiatric diseases.

People (Deaths)

  • 1964 – Nandor Fodor, Hungarian-American psychologist and parapsychologist (b. 1895).

Nandor Fodor

Nandor Fodor (13 May 1895 to 17 May 1964) was a British and American parapsychologist, psychoanalyst, author and journalist of Hungarian origin.

Fodor was born in Beregszász, Hungary. He received a doctorate in law from the Royal Hungarian University of Science in Budapest. He moved to New York to work as a journalist and to Britain in 1929 where he worked for a newspaper company.

Fodor was one of the leading authorities on poltergeists, haunting and paranormal phenomena usually associated with mediumship. Fodor, who was at one time Sigmund Freud’s associate, wrote on subjects like prenatal development and dream interpretation, but is credited mostly for his magnum opus, Encyclopaedia of Psychic Science, first published in 1934. Fodor was the London correspondent for the American Society for Psychical Research (1935-1939). He worked as an editor for the Psychoanalytic Review and was a member of the New York Academy of Sciences.

Fodor in the 1930s embraced paranormal phenomena but by the 1940s took a break from his previous work and advocated a psychoanalytic approach to psychic phenomena. He published sceptical newspaper articles on mediumship, which caused opposition from spiritualists.

Among the subjects he closely studied was the case of Gef the talking mongoose.

What is Logorrhoea?

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Introduction

In psychology, logorrhea or logorrhoea (from Ancient Greek λόγος logos “word” and ῥέω rheo “to flow”), is a communication disorder that causes excessive wordiness and repetitiveness, which can cause incoherency.

Logorrhoea is sometimes classified as a mental illness, though it is more commonly classified as a symptom of mental illness or brain injury. This ailment is often reported as a symptom of Wernicke’s aphasia, where damage to the language processing centre of the brain creates difficulty in self-centred speech.

Refer to Tangential Speech.

Characteristics

Logorrhoea is characterised by the constant need to talk. Occasionally, patients suffering from logorrhoea may produce speech with normal prosody and a slightly fast speech rate. Other related symptoms include the use of neologisms (new words without clear derivation, e.g. hipidomateous for hippopotamus), words that bear no apparent meaning, and, in some extreme cases, the creation of new words and morphosyntactic constructions. From the “stream of unchecked nonsense often under pressure and the lack of self-correction” that the patient may exhibit, and their circumlocution (the ability to talk around missing words) we may conclude that they are unaware of the grammatical errors they are making.

Examples of Logorrhoea

When a clinician said, “Tell me what you do with a comb”, to a patient suffering from mild Wernicke’s aphasia (which produces the symptom of logorrhoea), the patient responded:

“What do I do with a comb … what I do with a comb. Well a comb is a utensil or some such thing that can be used for arranging and rearranging the hair on the head both by men and by women. One could also make music with it by putting a piece of paper behind and blowing through it. Sometimes it could be used in art – in sculpture, for example, to make a series of lines in soft clay. It’s usually made of plastic and usually black, although it comes in other colors. It is carried in the pocket or until it’s needed, when it is taken out and used, then put back in the pocket. Is that what you had in mind?”

In this case, the patient maintained proper grammar and did not exhibit any signs of neologisms. However, the patient did use an overabundance of speech in responding to the clinician, as most people would simply respond, “I use a comb to comb my hair.”

In a more extreme version of logorrhoea aphasia, a clinician asked a male patient, also with Wernicke’s aphasia, what brought him to the hospital. The patient responded:

“Is this some of the work that we work as we did before? … All right … From when wine [why] I’m here. What’s wrong with me because I … was myself until the taenz took something about the time between me and my regular time in that time and they took the time in that time here and that’s when the time took around here and saw me around in it’s started with me no time and I bekan [began] work of nothing else that’s the way the doctor find me that way…”

In this example, the patient’s aphasia was much more severe. Not only was this a case of logorrhoea, but this included neologisms (such as “taenz” for “stroke” and “regular time” for “regular bath”) and a loss of proper sentence structure.

Causes

Logorrhoea has been shown to be associated with traumatic brain injuries in the frontal lobe[7] as well as with lesions in the thalamus] and the ascending reticular inhibitory system and has been associated with aphasia. Logorrhoea can also result from a variety of psychiatric and neurological disorders including tachypsychia, mania, hyperactivity, catatonia, ADHD and schizophrenia.

Aphasias

Wernicke’s Aphasia, amongst other aphasias, are often associated with logorrhoea. Aphasia refers to the neurological disruption of language that occurs as a consequence of brain dysfunction. For a patient to truly have an aphasia, they cannot have been diagnosed with any other medical condition that may affect their cognition. Logorrhoea is a common symptom of Wernicke’s Aphasia, along with circumlocution, paraphasias, and neologisms. Often a patient with aphasia may present all of these symptoms at one time.

Treatment

Excessive talking may be a symptom of an underlying illness and should be addressed by a medical provider if combined with hyperactivity or symptoms of mental illness, such as hallucinations. Treatment of logorrhoea depends on its underlying disorder, if any. Antipsychotics are often used, and lithium is a common supplement given to manic patients. For patients with lesions of the brain, attempting to correct their errors may upset and anger the patients, since the language centre of their brain may not be able to process that what they are saying is incorrect and wordy.

This page is based on the copyrighted Wikipedia article <https://en.wikipedia.org/wiki/Logorrhea_(psychology)&gt;; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

Creatine and Exercise

A Quick Overview of Creatine

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Introduction

Creatine is a chemical found naturally in the body, and also in red meat and seafood. It is often used to improve exercise performance and muscle mass.

Creatine and Exercise

Creatine is involved in making energy for muscles, with approximately 95% of it being found in skeletal muscle. The majority of sports supplements in the US contain creatine. Individuals who have lower creatine levels when they start taking creatine seem to get more benefit than individuals who start with higher levels.

People commonly use creatine for improving exercise performance and increasing muscle mass, but it is also used for muscle cramps, fatigue, multiple sclerosis (MS), depression, and many other conditions – although there is no good scientific evidence to support most of these uses.

Creatine use is allowed by the International Olympic Committee (IOC) and the US National Collegiate Athletic Association (NCAA).

What is Creatine?

It is a combination of three different amino acids:

  • Glycine;
  • Arginine; and
  • Methionine.

Creatine is involved in a vast number of processes in the body. For example, it is a fundamental component in how your body creates its primary form of energy in muscle cells, the compound adenosine triphosphate (ATP). When muscles contract explosively, or for brief, intense work lasting no longer than 8-12 seconds, creatine (bonded with phosphoric acid as creatine phosphate) is how the muscle creates the energy necessary to do it.

  • It exists in a steady state with a similar compound named creatinine that can be measured in lab tests as a marker of kidney function.
  • It is passed out of your body in your urine.
  • This means your body must release stored creatine each day to keep normal levels, the amount depending on your muscle mass.
  • Although creatine is created naturally in your body, you must keep up your levels and do so through your daily diet.

What is the Role of Creatine?

  • Creatine is a fuel source.
  • Simply put, creatine helps to maintain a continuous supply of energy to working muscles by keep production up in working muscles.
  • Small amounts are also found in your heart, brain and other tissues.
  • The phosphate-bonded form of creatine is your body’s energy of first choice when performing anaerobic activity, for example lifting weights.
  • When your body is trying to create the compound that powers quick muscle contractions, ATP, it does so by ‘borrowing’ a phosphate molecule from phosphocreatine and combining it with another compound, adenosine diphosphate (ADP).
  • Only after a muscle has largely used up its store of phosphocreatine does it start to produce ATP from other sources, like glucose or fats.
  • A secondary function of creatine is to draw water into muscle cells, making them more hydrated.

What are our Sources of Creatine?

  • Most of the creatine in your body is created in the liver and kidneys, but the majority of it is stored in muscle tissue (approximately 95%).
  • As a healthy human body is capable of creating its own creatine – and it can also be easily obtained through a diet that contains animal products – it is not considered an ‘essential’ nutrient.
  • In a normal omnivorous /carnivorous diet, you consume one to two grams/day of creatine.
  • However, as dietary creatine generally comes from animal products, vegan and vegetarian fitness enthusiasts and professional athletes may not get as much creatine in their diet as those who eat dairy products, eggs, and/or meat.
  • This is one reason why creatine is often recommended as an important supplement for vegans and vegetarians.
Sources of Creatine

What is it Used For?

  • Possibly Effective for:
    • Athletic Performance: Taking creatine by mouth seems to somewhat improve rowing, jumping, and soccer performance. It is not clear if it helps with sprinting, cycling, swimming, or tennis.
    • Disorders of Creatine Metabolism or Transport: Taking creatine by mouth daily can increase creatine levels in the brain in children and young adults with conditions called GAMT deficiency or AGAT deficiency. But taking creatine does not seem to improve brain creatine levels in children who have a disorder in which creatine is not transported properly.
      • Guanidinoacetate Methyltransferase (GMAT) deficiency is an inherited disorder that primarily affects the brain and muscles.
      • Arginine: Glycine Amidinotransferase (AGAT) deficiency is an inherited disorder that primarily affects the brain.
    • Muscle Strength: Taking creatine by mouth seems to somewhat improve muscle strength in both younger and older adults. It is not clear if applying creatine to the skin helps.
    • Sarcopenia (Age-Related Muscle Loss): Taking creatine by mouth for up to 12 weeks seems to improve muscle strength in older adults. It seems to work best when used along with exercise to build muscles.
  • Possibly Ineffective for:
    • Lou Gehrig Disease (Amyotrophic Lateral Sclerosis or ALS): Taking creatine by mouth does not seem to slow disease progression or improve survival in people with ALS.
    • An inherited brain disorder that affects movements, emotions, and thinking (Huntington Disease): Taking creatine by mouth does not improve symptoms in people with Huntington disease.
    • Osteopenia (Low Bone Mass): Taking creatine by mouth does not seem to slow or reduce bone loss in people with osteopenia.

There is interest in using creatine for a number of other purposes, but there is not enough reliable information to say whether it might be helpful.

What are the Side Effects?

  • When taken by mouth:
    • Creatine is likely safe for most people.
    • Doses up to 25 grams daily for up to 14 days have been safely used.
    • Lower doses up to 4-5 grams daily for up to 18 months have also been safely used.
    • Creatine is possibly safe when taken long-term.
    • Doses up to 10 grams daily for up to 5 years have been safely used.
    • Side effects might include dehydration, upset stomach, and muscle cramps.
  • When applied to the skin:
    • There is not enough reliable information to know if creatine is safe.
    • It might cause side effects such as redness and itching.

The majority of reported side effects (mild to moderate) are of weight gain, gastrointestinal distress, altered insulin production, inhibition of endogenous creatine synthesis, renal dysfunction, or dehydration in study participants.

Experts generally agree that there is sufficient evidence to be confident that 5 g/day of creatine is generally harmless to healthy adults, but there is not enough evidence to make an informed recommendation in favour or against doses higher than 5 g/day (Shao et al., 2006).

Are There Any Special Precautions or Warnings to Consider?

  • Pregnancy and breast-feeding:
    • Creatine is used as a dietary supplement to increase muscle mass and improve exercise performance.
    • Creatine is a normal component of human milk, supplying about 9% of the infant’s daily requirements.
    • Milk levels of creatine have not been measured after exogenous administration in humans.
    • Creatine is converted into creatinine in the mother’s and infant’s bodies.
    • It may increase the infant’s serum creatinine, which may alter estimations of the infant’s kidney function.
    • Some authors speculate that creatine supplementation of nursing mothers might help avoid creatine deficiency syndromes, but no studies are available that test this hypothesis.
    • Until more data are available, it is probably best to avoid creatine supplementation unless it is prescribed by a healthcare professional.
  • Children:
    • Creatine is possibly safe when taken by mouth, short-term.
    • Creatine 3-5 grams daily for 2-6 months has been taken safely in children 5-18 years of age.
    • Creatine 2 grams daily for 6 months has been taken safely in children 2-5 years of age.
    • Creatine 0.1-0.4 grams/kg daily for up to 6 months has been taken safely in both infants and children.
  • Bipolar disorder:
  • Kidney disease:
    • Creatine might make kidney disease worse in people who already have kidney disease.
    • If you have kidney disease, speak with a healthcare professional before using creatine.
  • Parkinson disease:
    • Caffeine and creatine taken together may make symptoms of Parkinson disease worse.
    • If you have Parkinson disease and take creatine, use caffeine with caution.

What about Dosage?

  • Creatine is found in foods such as meat and seafood. Creatine is also found in many different types of sports supplements.
  • In supplements (discussed below), creatine has most often been used by adults in a one-time loading dose of up to 20 grams by mouth daily for up to 7 days, followed by a maintenance dose of 2.25-10 grams daily for up to 16 weeks.
  • Speak with a healthcare provider to find out what type of product and dose might be best for a specific condition.

Interactions

A total of five (5) drugs are known to interact with creatine:

  • Minor:
    • Cimetidine.
    • Probenecid.
    • Trimethoprim.
    • These are all known to interfere with the kidney’s secretion of creatinine.
  • Moderate:
    • Entecavir: Using entecavir together with creatine may increase the blood levels of one or both medications.
    • Pemetrexed: Creatine may increase the blood levels of Pemetrexed. You may be more likely to develop serious side effects such as anaemia, bleeding problems, infections, and nerve damage when these medications are used together.

What about Creatine Monohydrate?

  • Creatine monohydrate, the most popular form of creatine supplements, is simply creatine with one molecule of water attached to it – hence the name monohydrate.
  • It is usually around 88-90% creatine by weight.
  • It is not a steroid, it is totally different and works in a different manner.
  • Its not a stimulant, although it is sometimes combined with stimulant ingredients (such as caffeine) in pre-workout formulas.

Supplementation and Fitness

  • More Work:
    • Supplementation with creatine serves to increase creatine stores and phosphocreatine availability in the body, resulting in faster ATP formation.
    • The understanding being that the more phosphocreatine you have, the more work you can accomplish before fatigue sets it.
  • Cell Hydration:
    • A secondary function of creatine is to draw water into muscle cells, making them more hydrated.
    • When muscle cells are hydrated a few things happen, the most notable being an increase in protein synthesis. Muscle protein synthesis (MPS) is the driving force behind adaptive responses to exercise and represents a widely adopted proxy for gauging chronic efficacy of acute interventions (i.e. exercise/nutrition).
    • This action of drawing water into the cell can make muscles look bigger or fuller (think weightlifters/bodybuilders).

Supplementation and Bipolar Disorder

  • Negative changes in mood or anxiety following supplementation with creatine have been documented in two human trials (Roitman et al., 2007; Volek et al., 2000) and one animal experiment (Allen et al., 2010).
  • Specifically, in an open-label clinical trial of creatine, Roitman et al. (2007) reported that two patients diagnosed with bipolar disorder exhibited hypomania or mania following daily supplementation with 3-5 g creatine.
  • In a clinical trial examining the effectiveness of creatine to enhance heavy resistance training, Volek et al. (2000) noted that two subjects reported feeling more aggressive and nervous after 1 week of creatine supplementation (25 g/day).
  • In rodents, Allen et al. (2010) observed increased depression-like behaviour in male rats supplemented with 4% creatine for five weeks, although this effect was not replicated in male rats in a follow-up study (Allen et al., in press).
  • Taken together, there remains the possibility that creatine can increase risk of mania or depression in susceptible individuals.
  • It is also possible that long-term high dosing of creatine alters creatine transporter function or creatine kinase activity in a manner that adversely affects emotional regulation.
  • Further research is required before definitive conclusions are drawn, but caution is warranted in at-risk individuals.

For a good outline of creatine metabolism and psychiatric disorders read Patricia Allen’s article here.

What is a Mental Health Consumer?

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Introduction

A mental health consumer (or mental health patient) is a person who is obtaining treatment or support for a mental disorder, also known as psychiatric or mental illness.

The term was coined by people who use mental health services in an attempt to empower those with mental health issues, historically considered a marginalised segment of society. The term suggests that there is a reciprocal contract between those who provide a service and those who use a service and that individuals have a choice in their treatment and that without them there could not exist mental health providers.

Brief History

In the 1970s the term “patient” was most commonly used. Mental Health activists of the civil rights times recognised, as did many other groups seeking self-definition, that such labels are metaphors that reflect how identities are perceived and constructed. In particular, in the mental health field they shape the nature of the relationship between the giver and receiver of psychiatric services, be it one with an emphasis on reciprocity or hierarchy. Users of psychiatric services repulsed the efforts of experts to define them and sought to develop ways to define themselves. In Australia, informal support groups of people who had recovered from episodes of mental ill health were formed during the first wave of moving patients out of psychiatric hospitals into the community in the 1960s. In the USA and other countries, radical movements to change service delivery and legislation began to be driven by consumers during the 1980s. Activists, such as Judi Chamberlain, pressed for alternatives to psychiatrist dominated and controlled systems of mental health provision. Chamberlain’s On Our Own: Patient Controlled Alternatives to the Mental Health System helped guide others intent on a more collaborative form of mental health healing.

In the 1980s with some funding from NIMH, small experimental groups flourished. In 1985 at the First Alternatives Conference attendees agreed upon the term “consumer” reflecting the patients’ choice of services. The term also implied assumptions of rationality and ability to make choices in one’s own best interests rather than be a passive incapacitated recipient of “expert” attention. In the 1990s many consumer groups were formed, such as Self Help Clearing House and the National Empowerment Centre. They continued to press for more peer involvement in alternatives treatments, pointing out that peers support and comfort, which may be in contrast to some therapists who just attempt to change the behaviour and thinking patterns.

Contemporary Usage

Today, the word mental health consumer has expanded in the popular usage of consumers themselves to include anyone who has received mental health services in the past, anyone who has a behavioural health diagnosis, or simply anyone who has experienced a mental or behavioural disorder. Other terms sometimes used by members of this community for empowerment through positive self-identification include “peers,” “people with mental health disabilities,” “psychiatric survivors,” “users,” individuals with “lived experience” and “ex-patients.” The term “service users,” is commonly used in the UK. In the US “consumer” is most frequently used by ex-patients and users of psychiatric and alternative services.

One can view this term, “consumer,” neutrally as a person who receives psychological services, perhaps from a psychologist, a psychiatrist or a social worker. It can be impersonal term relating to the use in the health sector of a large economy. It suggests that the consumer expects to have some influence on service delivery and provides feedback to the provider. Used in its more activist sense, consumer groups aim to correct perceived problems in mental health services and to promote consultation with consumers. Consumer theory was devised to interpret the special relationship between a service provider and service user in the context of mental health. Consumer theory examines the consequences and sociological meaning of the relationship.

What is Impulse-Control Disorder?

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Introduction

Impulse-control disorder (ICD) is a class of psychiatric disorders characterised by impulsivity – failure to resist a temptation, an urge, or an impulse; or having the inability to not speak on a thought.

Many psychiatric disorders feature impulsivity, including substance-related disorders, behavioural addictions, attention deficit hyperactivity disorder, foetal alcohol spectrum disorders, antisocial personality disorder, borderline personality disorder, conduct disorder and some mood disorders.

The fifth edition of the American Psychiatric Association’s Diagnostic and statistical manual of mental disorders (DSM-5) that was published in 2013 includes a new chapter (not in DSM-IV-TR) on disruptive, impulse-control, and conduct disorders covering disorders “characterized by problems in emotional and behavioral self-control”. Five behavioural stages characterise impulsivity:

  • An impulse;
  • Growing tension;
  • Pleasure on acting;
  • Relief from the urge; and
  • Finally guilt (which may or may not arise).

Types

Disorders characterised by impulsivity that were not categorised elsewhere in the DSM-IV-TR were also included in the category “Impulse-control disorders not elsewhere classified”. Trichotillomania (hair-pulling) and skin-picking were moved in DSM-5 to the obsessive-compulsive chapter. Additionally, other disorders not specifically listed in this category are often classed as impulsivity disorders. Terminology was changed in the DSM-V from “Not Otherwise Classified” to “Not Elsewhere Classified”.

Sexual Compulsion

Sexual compulsion includes an increased urge in sexual behaviour and thoughts. This compulsion may also lead to several consequences in the individual’s life, including risky partner selection, increased chance for STIs and depression, as well as unwanted pregnancy. There has not yet been a determined estimate of its prevalence due to the secretiveness of the disorder. However, research conducted in the early 1990s in the United States gave prevalence estimates between 5-6% in the US population, with male cases being higher than female.

Internet Addiction

The disorder of Internet addiction has only recently been taken into consideration and has been added as a form of ICD. It is characterised by excessive and damaging usage of Internet with increased amount of time spent chatting, web surfing, gambling, shopping or consuming pornography. Excessive and problematic Internet use has been reported across all age, social, economic, and educational ranges. Although initially thought to occur mostly in males, increasing rates have been also observed in females. However, no epidemiological study has been conducted yet to understand its prevalence.

Compulsive Shopping

Compulsive shopping or buying is characterised by a frequent irresistible urge to shop even if the purchases are not needed or cannot be afforded. The prevalence of compulsive buying in the US has been estimated to be 2-8% of the general adult population, with 80-95% of these cases being females. The onset is believed to occur in late teens or early twenties and the disorder is considered to be generally chronic.

Pyromania

Pyromania is characterised by impulsive and repetitive urges to deliberately start fires. Because of its nature, the number of studies performed for fire-setting are understandably very few. However, studies done on children and adolescents suffering from pyromania have reported its prevalence to be between 2.4 and 3.5% in the United States. It has also been observed that the incidence of fire-setting is more common in juvenile and teenage boys than girls of the same age.

Intermittent Explosive Disorder

Intermittent explosive disorder or IED is a clinical condition of experiencing recurrent aggressive episodes that are out of proportion of any given stressor. Earlier studies reported a prevalence rate between 1-2% in a clinical setting, however a study done by Coccaro and colleagues in 2004 had reported about 11.1% lifetime prevalence and 3.2% one month prevalence in a sample of a moderate number of individuals (n=253). Based on the study, Coccaro and colleagues estimated the prevalence of IED in 1.4 million individuals in the US and 10 million with lifetime IED.

Kleptomania

Kleptomania is characterised by an impulsive urge to steal purely for the sake of gratification. In the US the presence of kleptomania is unknown but has been estimated at 6 per 1000 individuals. Kleptomania is also thought to be the cause of 5% of annual shoplifting in the US If true, 100,000 arrests are made in the US annually due to kleptomaniac behaviour.

Signs and Symptoms

The signs and symptoms of impulse-control disorders vary based on the age of the persons suffering from them, the actual type of impulse-control that they are struggling with, the environment in which they are living, and whether they are male or female.

Co-Morbidity

Complications of late Parkinson’s disease may include a range of impulse-control disorders, including eating, buying, compulsive gambling, sexual behaviour, and related behaviours (punding, hobbyism and walkabout). Prevalence studies suggest that ICDs occur in 13.6-36.0% of Parkinson’s patients exhibited at least one form of ICD. There is a significant co-occurrence of pathological gambling and personality disorder, and is suggested to be caused partly by their common “genetic vulnerability”. The degree of heritability to ICD is similar to other psychiatric disorders including substance use disorder. There has also been found a genetic factor to the development of ICD just as there is for substance use disorder. The risk for subclinical PG in a population is accounted for by the risk of alcohol dependence by about 12-20% genetic and 3-8% environmental factors. There is a high rate of co-morbidity between ADHD and other impulse-control disorders.

Mechanism

Dysfunction of the striatum may prove to be the link between OCD, ICD and SUD. According to research, the ‘impulsiveness’ that occurs in the later stages of OCD is caused by progressive dysfunction of the ventral striatal circuit. Whereas in case of ICD and SUD, the increased dysfunction of dorsal striatal circuit increases the “ICD and SUD behaviours that are driven by the compulsive processes”. OCD and ICD have traditionally been viewed as two very different disorders, the former one is generally driven by the desire to avoid harm whereas the latter one driven “by reward-seeking behaviour”. Still, there are certain behaviours similar in both, for example the compulsive actions of ICD patients and the behaviour of reward-seeking (for example hoarding) in OCD patients.

Treatment

Impulse-control disorders have two treatment options: psychosocial and pharmacological. Treatment methodology is informed by the presence of comorbid conditions.

Medication

In the case of pathological gambling, along with fluvoxamine, clomipramine has been shown effective in the treatment, with reducing the problems of pathological gambling in a subject by up to 90%. Whereas in trichotillomania, the use of clomipramine has again been found to be effective, fluoxetine has not produced consistent positive results. Fluoxetine, however, has produced positive results in the treatment of pathological skin picking disorder, although more research is needed to conclude this information. Fluoxetine has also been evaluated in treating IED and demonstrated significant improvement in reducing frequency and severity of impulsive aggression and irritability in a sample of 100 subjects who were randomised into a 14-week, double-blind study. Despite a large decrease in impulsive aggression behaviour from baseline, only 44% of fluoxetine responders and 29% of all fluoxetine subjects were considered to be in full remission at the end of the study. Paroxetine has shown to be somewhat effective although the results are inconsistent. Another medication, escitalopram, has shown to improve the condition of the subjects of pathological gambling with anxiety symptoms. The results suggest that although SSRIs have shown positive results in the treatment of pathological gambling, inconsistent results with the use of SSRIs have been obtained which might suggest a neurological heterogeneity in the ICD spectrum.

Psychosocial

The psychosocial approach to the treatment of ICDs includes cognitive behavioural therapy (CBT) which has been reported to have positive results in the case of treatment of pathological gambling and sexual addiction. There is general consensus that cognitive-behavioural therapies offer an effective intervention model.

TypeDescription
Pathological GamblingSystematic desensitisation, aversive therapy, covert sensitisation, imaginal desensitisation, and stimulus control have been proven to be successful in the treatments to the problems of pathological gambling. Also, “cognitive techniques such as psychoeducation, cognitive-restructuring, and relapse prevention” have proven to be effective in the treatments of such cases.
PyromaniaPyromania is harder to control in adults due to lack of co-operation; however, CBT is effective in treating child pyromaniacs.
Intermittent Explosive DisorderAlong with several other methods of treatments, cognitive behavioural therapy has also shown to be effective in the case of Intermittent explosive disorder as well. Cognitive Relaxation and Coping Skills Therapy (CRCST), which consists of 12 sessions starting first with the relaxation training followed by cognitive restructuring, then exposure therapy is taken. Later, the focus is on resisting aggressive impulses and taking other preventative measures.
KleptomaniaIn the case of kleptomania, the cognitive behaviour techniques used in these cases consists of covert sensitisation, imaginal desensitisation, systematic desensitisation, aversion therapy, relaxation training, and “alternative sources of satisfaction”.
Compulsive BuyingAlthough compulsive buying falls under the category of Impulse-control disorder – Not Otherwise Specified in the DSM-IV-TR, some researchers have suggested that it consists of core features that represent impulse-control disorders which includes preceding tension, difficult to resist urges and relief or pleasure after action. The efficiency of cognitive behaviour therapy for compulsive buying is not truly determined yet; however, common techniques for the treatment include exposure and response prevention, relapse prevention, cognitive restructuring, covert sensitization, and stimulus control.

What are Racing Thoughts?

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Introduction

Racing thoughts refers to the rapid thought patterns that often occur in manic, hypomanic, or mixed episodes.

While racing thoughts are most commonly described in people with bipolar disorder and sleep apnoea, they are also common with anxiety disorders, OCD, and other psychiatric disorders such as attention deficit hyperactivity disorder. Racing thoughts are also associated with sleep deprivation, hyperthyroidism and the use of amphetamines.

Description

Racing thoughts may be experienced as background or take over a person’s consciousness. Thoughts, music, and voices might be zooming through one’s mind as they jump tangentially from one to the next. There also might be a repetitive pattern of voice or of pressure without any associated “sound”. It is a very overwhelming and irritating feeling, and can result in losing track of time. In some cases, it may also be frightening to the person experiencing it, as there is a loss of control. If one is experiencing these thoughts at night when going to sleep, they may suddenly awaken, startled and confused by the very random and sudden nature of the thoughts.

Racing thoughts differ in manifestation according to the individual’s perspective. These manifestations can vary from unnoticed or minor distractions to debilitating stress, preventing the sufferer from maintaining a thought.

Generally, racing thoughts are described by an individual who has had an episode where the mind uncontrollably brings up random thoughts and memories and switches between them very quickly. Sometimes they are related, as one thought leads to another; other times they seem completely random. A person suffering from an episode of racing thoughts has no control over their train of thought, and it stops them from focusing on one topic or prevents sleeping.

Associated Conditions

The causes of racing thoughts are most often associated with anxiety disorders, but many influences can cause these rapid, racing thoughts. There are also many associated conditions, in addition to anxiety disorders, which can be classified as having secondary relationships with causing racing thoughts. The conditions most commonly linked to racing thoughts are bipolar disorder, anxiety disorder, attention deficit hyperactivity disorder, sleep deprivation, amphetamine dependence, and hyperthyroidism.

Anxiety Disorders

Racing thoughts associated with anxiety disorders can be caused by many different conditions, such as obsessive-compulsive disorder (OCD), panic disorder, generalised anxiety disorder, or posttraumatic stress disorder.

In people with OCD, racing thoughts can be brought on by stressors, or triggers, causing disturbing thoughts in the individual. These disturbing thoughts, then, result in compulsions characterising OCD in order to lower the stress and gain some sort of control over these stressful, racing thoughts.

Panic disorder is an anxiety disorder characterised by repeated panic attacks of fear or nervousness, lasting several minutes. During these panic attacks, the response is out of proportion to the situation. The racing thoughts may feel catastrophic and intense, but they are a symptom of the panic attack and must be controlled in order to soothe the panic and minimise the panic attack.

Generalised anxiety disorder (GAD) is a neurological anxiety disorder that involves uncontrollable and excessive worrying about irrational topics or problems. These stressful thoughts must be present for at least six months in order to be diagnosed as GAD. Along with other symptoms, racing thoughts is one of the most common ones. With GAD, there is an inability to relax or let thoughts or worries go, persistent worrying and obsessions about small concerns that are out of proportion to the result, and even worrying about their excessive worrying.

Bipolar Disorder

Racing thoughts can be brought on by bipolar disorder, defined by mood instability that range from extreme emotional highs, mania, to severe depression. During the manic phase of bipolar disorder is when racing thoughts usually occur. Disjointed, constantly changing thoughts with no underlying theme can be a sign of the manic phase of bipolar disorder. Manic thoughts can prevent performance of daily routines due to their rapid, unfocused and overwhelming nature. Racing thoughts in people with bipolar disorder are generally accompanied with other symptoms associated with this disorder.

Amphetamines

Amphetamines are used as a stimulant to trigger the central nervous system, increasing heart rate and blood pressure while decreasing appetite. Since amphetamines are a stimulant, use of these drugs result in a state that resembles the manic phase of bipolar disorder and also produces similar symptoms, as stated above.

Attention Deficit Hyperactivity Disorder

Racing thoughts associated with ADHD is most common in adults. With ADHD, racing thoughts can occur and tend to cause insomnia. Racing thoughts in people with ADHD tend to be rapid, unstable thoughts which do not follow any sort of pattern, similar to racing thoughts in people with bipolar disorder. Medications used to treat ADHD, such as Adderall or Methylphenidate, can be prescribed to patients with ADHD to calm these racing thoughts, most commonly in the morning when people wake up but just as well in the evening before sleep.

Lack of Sleep

Racing thoughts, also referred to as “racing mind”, may prevent a person from falling asleep. Chronic sleep apnoea and prolonged disturbed sleep patterns may also induce racing thoughts. Treatment for sleep apnoea and obstructive airway disorder can improve airflow and improve sleep resulting in improved brain and REM (rapid eye movement) function and reduced racing thought patterns.

Hyperthyroidism

Hyperthyroidism is a condition in which the thyroid gland produces too much thyroid hormone, thyroxin. This overabundance of thyroxin causes irregular and rapid heartbeat, irritability, weight loss, nervousness, anxiety and racing thoughts. The anxiety and inability to focus is very common in hyperthyroidism and leads to racing thoughts, as well as panic attacks and difficulty concentrating.

Frequency

Anxiety disorder, the most common mental illness in the United States, affects 40 million people, ages 10 and older; this accounts for 18% of the US population. Most people suffering from anxiety disorder report some form of racing thoughts symptom.

The prevalence of OCD in every culture studied is at least 2% of the population, and the majority of those have obsessions, or racing thoughts. With these reports, estimates of more than 2 million people in the United States (as of 2000) suffer from racing thoughts.

Treatment

There are various treatments available to calm racing thoughts, some of which involve medication. One type of treatment involves writing out the thoughts onto paper. Some treatments suggest using activities, such as painting, cooking, and other hobbies, to keep the mind busy and distract from the racing thoughts. Exercise may be used to tire the person, thereby calming their mind. When racing thoughts are anxiety induced during panic or anxiety attacks, it is recommended that the person wait it out. Using breathing and meditation techniques to calm the breath and mind simultaneously is another tool for handling racing thoughts induced by anxiety attacks. Mindfulness meditation has also shown to help with racing thoughts by allowing practitioners to face their thoughts head-on, without reacting.

While all of these techniques can be useful to cope with racing thoughts, it may prove necessary to seek medical attention and counsel. Since racing thoughts are associated with many other underlying mental illnesses, such as bipolar disorder, anxiety disorder, and ADHD, medications used commonly to treat these disorders will help calm racing thoughts in patients.

Treatment for the underlying causes of racing thoughts is helpful and useful in order to calm the racing thoughts more permanently. For example, in people with ADHD, medications used to promote focus and calm distracting thoughts, will help them with their ADHD.

Some obstructive airway disorders may be relieved with nasal septoplasty which can improve sleep and lead to a reduction of racing mind. Insomnia may increase racing thoughts and those effected will find sleep apnoea treatment and nasal surgery helpful to eliminate their racing thoughts.

It is important to look at the underlying defect that may be causing racing thoughts in order to prevent them in the long-term.

Book: Doctoring the Mind: Why Psychiatric Treatments Fail

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Book Title:

Doctoring the Mind: Why Psychiatric Treatments Fail.

Author(s): Richard P. Bentall.

Year: 2010.

Edition: First (1st).

Publisher: Penguin.

Type(s): Hardcover, Paperback and Kindle.

Synopsis:

Why is the Western world’s treatment of mental illness so flawed? Who really benefits from psychiatry? And why would a patient in Nigeria have a much greater chance of recovery than one in the UK?

In Doctoring the Mind, leading clinical psychologist Richard Bentall reveals the shocking truths behind the system of mental health care in the West. With a heavy dependence on pills and the profit they bring, psychiatry has been relying on myths and misunderstandings of madness for too long, and builds on methods which can often hinder rather than help the patient.

Bentall argues passionately for a new future of mental health, one that considers the patient as an individual and redefines our understanding and treatment of madness for the twenty-first century.