Motivational deficiency disorder is the name of a fake disease imagined for a health campaign to raise awareness of disease mongering.

The term “monger” has ancient roots, providing the basis for many common compound forms such as cheesemonger, fishmonger, and fleshmonger for those who peddle such wares respectively. “Disease mongering” as a label for the "invention" or promotion of diseases in order to capitalize on their treatment was first used in 1992 by health writer Lynn Payer, who applied it to the Listerine mouthwash campaign against halitosis (bad breath).

Payer defined disease mongering as a set of practices which include the following:

- Stating that normal human experiences are abnormal and in need of treatment

- Claiming to recognize suffering which is not present

- Defining a disease such that a large number of people have it

- Defining a disease's cause as some ambiguous deficiency or hormonal imbalance

- Associating a disease with a public relations spin campaign

- Directing the framing of public discussion of a disease

- Intentionally misusing statistics to exaggerate treatment benefits

- Setting a dubious clinical endpoint in research

- Advertising a treatment as without side effect

- Advertising a common symptom as a serious disease

The incidence of conditions not previously defined as illness being medicalised as "diseases" is difficult to scientifically assess due to the inherent social and political nature of the definition of what constitutes a disease, and what aspects of the human condition should be managed according to a medical model. For example, halitosis, the condition which prompted Payer to coin the phrase "disease mongering", isn't merely an imagined social stigma but can stem from any of a wide spectrum of conditions spanning from bacterial infection of the gums to kidney failure, and is recognized by the Scientific Council of the American Dental Association as "a recognizable condition which deserves professional attention".

A study on comorbidity of GAD and other depressive disorders has shown that treatment is not more or less effective when there is some sort of comorbidity of another disorder. The severity of symptoms did not affect the outcome of the treatment process in these cases.

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Disease mongering is a term for the practice of widening the diagnostic boundaries of illnesses and aggressively promoting their public awareness in order to expand the markets for treatment.

Among the entities benefiting from selling and delivering treatments are pharmaceutical companies, physicians, alternative practitioners and other professional or consumer organizations. It is distinct from the promulgation of bogus or unrecognised diagnoses.

Many different causes of aboulia have been suggested. While there is some debate about the validity of aboulia as a separate disease, experts mostly agree that aboulia is the result of frontal lesions and not with cerebellar or brainstem lesions. As a result of more and more evidence showing that the mesolimbic and the mesocortical dopamine system are key to motivation and responsiveness to reward, aboulia may be a dopamine-related dysfunction. Aboulia may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere.

In addition to coexisting with depression, research shows that GAD often coexists with conditions associated with stress, such as irritable bowel syndrome. Patients with GAD can sometimes present with symptoms such as insomnia or headaches as well as pain, cardiac events and interpersonal problems.

Further research suggests that about 20 to 40 percent of individuals with attention deficit hyperactivity disorder have comorbid anxiety disorders, with GAD being the most prevalent.

The World Health Organization's Global Burden of Disease project did not include generalized anxiety disorders. In lieu of global statistics, here are some prevalence rates from around the world:

- Australia: 3 percent of adults

- Canada: Between 3 and 5 percent of adults

- Taiwan: 0.4 percent

- United States: approx. 3.1 percent of people age 18 and over in a given year (9.5 million)

The usual age of onset is variable, from childhood to late adulthood, with the median age of onset being approximately 31 and mean age of onset is 32.7. Most studies find that GAD is associated with an earlier and more gradual onset than the other anxiety disorders. The prevalence of GAD in children is approximately 3%; the prevalence in adolescents is reported as high as 10.8%. When GAD appears in children and adolescents, it typically begins around 8 to 9 years of age.

Populations with a higher rate of diagnosis of GAD are individuals that are traditionally oppressed. This includes individuals with low and middle socio-economic status, separated, divorced, and widowed individuals. Women are twice as likely to develop GAD as men. This is primarily because women are more likely than men to live in poverty, be subject to discrimination, and be sexually and physically abused. African Americans have significantly higher odds of enduring GAD and the disorder often manifests itself in different patterns. Other populations that are more diagnosed with GAD are those who live alone, those with a low level of education, and the unemployed. GAD is also common in the elderly population.

Compared to the general population, patients with internalizing disorders such as depression, generalized anxiety disorder (GAD) and post-traumatic stress disorder (PTSD) have higher mortality rates, but die of the same age-related diseases as the population, such as heart disease, cerebrovascular disease and cancer.

Injuries to the frontal lobe and/or the basal ganglia can interfere with an individual's ability to initiate speech, movement, and social interaction. Studies have shown that 5-67% of all patients with traumatic brain injuries and 13% of patients with lesions on their basal ganglia suffer from some form of diminished motivation.

Aboulia has also been associated with amphetamine withdrawal. It may complicate rehabilitation when a stroke patient is uninterested in performing tasks like walking despite being capable of doing so. It should be differentiated from apraxia, when a brain injured patient has impairment in comprehending the movements necessary to perform a motor task despite not having any paralysis that prevents performing the task; that condition can also result in lack of initiation of activity.

In Europe, the rate of problem gambling is typically 0.5 to 3 percent. The "British Gambling Prevalence Survey 2007", conducted by the United Kingdom Gambling Commission, found approximately 0.6 percent of the adult population had problem gambling issues—the same percentage as in 1999. The highest prevalence of problem gambling was found among those who participated in spread betting (14.7%), fixed odds betting terminals (11.2%) and betting exchanges (9.8%). In Norway, a December 2007 study showed the amount of present problem gamblers was 0.7 percent.

In the United States, the percentage of pathological gamblers was 0.6 percent, and the percentage of problem gamblers was 2.3 percent in 2008. Studies commissioned by the National Gambling Impact Study Commission Act has shown the prevalence rate ranges from 0.1 percent to 0.6 percent. Nevada has the highest percentage of pathological gambling; a 2002 report estimated 2.2 to 3.6 percent of Nevada residents over the age of 18 could be called problem gamblers. Also, 2.7 to 4.3 percent could be called probable pathological gamblers.

According to a 1997 meta-analysis by Harvard Medical School's division on addictions, 1.1 percent of the adult population of the United States and Canada could be called pathological gamblers. A 1996 study estimated 1.2 to 1.9 percent of adults in Canada were pathological. In Ontario, a 2006 report showed 2.6 percent of residents experienced "moderate gambling problems" and 0.8 percent had "severe gambling problems". In Quebec, an estimated 0.8 percent of the adult population were pathological gamblers in 2002. Although most who gamble do so without harm, approximately 6 million American adults are addicted to gambling.

Signs of a gambling problem include:

- Using income or savings to gamble while letting bills go unpaid

- Repeated, unsuccessful attempts to stop gambling

- Chasing losses

- Losing sleep over thoughts of gambling

- Arguing with friends or family about gambling behavior

- Feeling depressed or suicidal because of gambling losses

Although disorder for written expressions skills can be difficult and an enduring problem all throughout childhood into adulthood, different types of treatment and support can help individuals who have this disorder to employ strategies and skills in the home and school environment. This includes remedial education tailored to improve specific skills, providing special academic services in the learning environment, and addressing concurrent health and mental issues. It is sometimes necessary to foster motivational techniques to maintain motivation and minimize negative thoughts or feelings. Using whatever modifications are necessary to overcome fears of failure in the early stages of writing mediation is strongly encouraged because children with learning disabilities often experience low self-esteem and confidence, which may further interfere with learning and academic success.

The disease was first described in an effort coordinated by Ray Moynihan when "BMJ" published a description of it for April Fool's Day in 2006.

Fake neurologist "Leth Argos" is said to have described the disorder, finding that "extreme laziness may have a medical basis" and that "motivational deficiency disorder can be fatal, because the condition reduces the motivation to breathe." Despite the condition being poorly understood, it is also "underdiagnosed and undertreated." A person living with the condition complained that he would spend all day at the beach.

In the original campaign medical marketers recommended treating the disease with a drug called "Indolebant". They presented a case study in which a lazy man who took the drug then got off his sofa to begin a job as an investment adviser. The original campaign also contained an advertisement for an issue of "PLOS" on disease mongering.

In 2008 Consumers International revived the campaign to draw further attention to the issue of disease mongering.

Although a spoof, some news outlets have reported the disease as if this were a real disorder. The disease was invented and presented to the public as a demonstration that some media outlets are willing to publish sensational health stories and that people respond with worry when they do.

Specific causes of this disorder are unknown. The interaction of physical, psychological, and environmental factors is thought to contribute to the disorder of written expression. In neuropsychological and neurobiological research, some studies show evidence that abnormally high testosterone levels and abnormalities in cognitive processes (visual-motor, linguistic, attentional, and memory) are thought to play a role in learning disorder cases. The impact of brain injuries in both children and adults can impair any of these cognitive processes.

Current research suggests that nearly 8% of the population has at least partial DPD deficiency. A diagnostics determination test for DPD deficiency is available and it is expected that with a potential 500,000 people in North America using 5-FU this form of testing will increase. The whole genetic events affecting the DPYD gene and possibly impacting on its function are far from being elucidated, and epigenetic regulations could probably play a major role in DPD deficiency. It seems that the actual incidence of DPD deficiency remains to be understood because it could depend on the very technique used to detect it. Screening for genetic polymorphisms affecting the "DPYD" gene usually identify less than 5% of patients bearing critical mutations, whereas functional studies suggest that up to 20% of patients could actually show various levels of DPD deficiency.

Women could be more at risk than men. It is more common among African-Americans than it is among Caucasians.

PNP-deficiency is extremely rare. Only 33 patients with the disorder in the United States have been documented. In the United Kingdom only one child has been diagnosed with this disorder.

Based on the results of worldwide screening of biotinidase deficiency in 1991, the incidence of the disorder is:

5 in 137,401 for profound biotinidase deficiency

- One in 109,921 for partial biotinidase deficiency

- One in 61,067 for the combined incidence of profound and partial biotinidase deficiency

- Carrier frequency in the general population is approximately one in 120.

This disorder, epidemiologically speaking, is thought to affect approximately 1 in 50,000 newborns according to Jethva, et al. While in the U.S. state of California there seems to be a ratio of 1 in 35,000.

Human findings provide insufficient data for developing treatments due to differences in the patients physiological and metabolic disorders thus, a suitable alternative animal model is essential in obtaining a better understanding of the SR deficiency. In this particular case, researchers used silkworms to identify and characterize mutations relating to SPR activity from an initial purified state created in the larvae of the silkworm. The researchers used genetic and biochemical approaches to demonstrate oral administration of BH and dopamine which increased the survival rates of the silkworm larvae. The results indicate that BH deficiency in silkworms leads to death in response to the lack of dopamine. This shows that silkworms can be useful insect models in additional SR deficiency research and study.

As demonstrated by the chart below, numerous studies have examined factors which mediate substance abuse or dependence. In these examples, the predictor variables lead to the mediator which in turn leads to the outcome, which is always substance abuse or dependence. For example, research has found that being raised in a single-parent home can lead to increased exposure to stress and that increased exposure to stress, not being raised in a single-parent home, leads to substance abuse or dependence. The following are some, but by no means all, of the possible mediators of substance abuse.

As demonstrated by the chart below, numerous studies have examined factors which moderate substance abuse or dependence. In these examples, the moderator variable impacts the level to which the strength of the relationship varies between a given predictor variable and the outcome of substance abuse or dependence. For example, there is a significant relationship between psychobehavioral risk factors, such as tolerance of deviance, rebelliousness, achievement, perceived drug risk, familism, family church attendance and other factors, and substance abuse and dependence. That relationship is moderated by familism which means that the strength of the relationship is increased or decreased based on the level of familism present in a given individual.

Examples of mediators and moderators can be found in several empirical studies. For example, Pilgrim et al.’s hypothesized mediation model posited that school success and time spent with friends mediated the relationship between parental involvement and risk-taking behavior with substance use (2006). More specifically, the relationship between parental involvement and risk-taking behavior is explained via the interaction with third variables, school success and time spent with friends. In this example, increased parental involvement led to increased school success and decreased time with friends, both of which were associated with decreased drug use. Another example of mediation involved risk-taking behaviors. As risk-taking behaviors increased, school success decreased and time with friends increased, both of which were associated with increased drug use.

A second example of a mediating variable is depression. In a study by Lo and Cheng (2007), depression was found to mediate the relationship between childhood maltreatment and subsequent substance abuse in adulthood. In other words, childhood physical abuse is associated with increased depression, which in turn, in associated with increased drug and alcohol use in young adulthood. More specifically, depression helps to explain how childhood abuse is related to subsequent substance abuse in young adulthood.

A third example of a mediating variable is an increase of externalizing symptoms. King and Chassin (2008) conducted research examining the relationship between stressful life events and drug dependence in young adulthood. Their findings identified problematic externalizing behavior on subsequent substance dependency. In other words, stressful life events are associated with externalizing symptoms, such as aggression or hostility, which can lead to peer alienation or acceptance by socially deviant peers, which could lead to increased drug use. The relationship between stressful life events and subsequent drug dependence however exists via the presence of the mediation effects of externalizing behaviors.

An example of a moderating variable is level of cognitive distortion. An individual with high levels of cognitive distortion might react adversely to potentially innocuous events, and may have increased difficulty reacting to them in an adaptive manner (Shoal & Giancola, 2005). In their study, Shoal and Giancola investigated the moderating effects of cognitive distortion on adolescent substance use. Individuals with low levels of cognitive distortion may be more apt to choose more adaptive methods of coping with social problems, thereby potentially reducing the risk of drug use. Individuals with high levels of cognitive distortions, because of their increased misperceptions and misattributions, are at increased risk for social difficulties. Individuals may be more likely to react aggressively or inappropriately, potentially alienating themselves from their peers, thereby putting them at greater risk for delinquent behaviors, including substance use and abuse. In this study, social problems are a significant risk factor for drug use when moderated by high levels of cognitive distortions.

The diagnosis of sepiapterin reductase deficiency in a patient at the age of 14 years was delayed by an earlier diagnosis of an initially unclassified form of methylmalonic aciduria at the age of 2. At that time the hypotonia and delayed development were not considered to be suggestive of a neurotransmitter defect. The clinically relevant diagnosis was only made following the onset of dystonia with diurnal variation, when the patient was a teenager. Variability in occurrence and severity of other symptoms of the condition, such as hypotonia, ataxia, tremors, spasticity, bulbar involvement, oculogyric crises, and cognitive impairment, is comparable with autosomal dominant GTPCH and tyrosine hydroxylase deficiency, which are both classified as forms of DOPA-responsive dystonia.

A 2001 study followed up on 50 patients. Of these 38% died in childhood while the rest suffered from problems with morbidity.

A 1999 retrospective study of 74 cases of neonatal onset found that 32 (43%) patients died during their first hyperammonemic episode. Of those who survived, less than 20% survived to age 14. Few of these patients received liver transplants.

Several scientists have developed murine models of SSADH (Aldh5a1-/-) by typical gene methodology to create a uniform absence of the SSADH enzyme activity as well as accumulations of GHB and GABA in tissues and physiological fluids. The mice are born at the expected Mendelian frequencies for an autosomal recessive disorder. Most of the models include distinctive neurological phenotypes and exhibit hypotonia, truncal ataxia, generalized tonic-clonic seizures associated with 100% mortality. The mice uniformly die at 3-4 postnatal weeks. While this model is considered to be more severe than the phenotypes seen in humans, currently, it is the most highly regarded, valid, metabolic model to study potential therapeutic interventions for the disorder.

Studies have shown that alterations of both the GABA receptor and the GABA receptor early in the life of the Aldh5a1-/- mice can increase levels of GHB and enhance GABA release. Besides these effects, it has also been shown that "...a developmental down-regulation of GABA receptor mediated neurotransmission in Aldh5a1-/- mice likely contributes to the progression of generalized convulsive seizures seen in mutant animals." Other studies have confirmed the relationship between elevated levels of GHB and MAP kinase in mutant animals contribute to profound myelin abnormalities.

Psychological dependence is a form of dependence that involves emotional–motivational withdrawal symptoms (e.g., a state of unease or dissatisfaction, a reduced capacity to experience pleasure, or anxiety) upon cessation of drug use or engagement in certain behaviors. Physical and psychological dependence are sometimes classified as a facet or component of addiction, such as in the DSM-IV-TR; however, some drugs which produce dependence syndromes do not produce addiction, and vice versa, in humans. Addiction and psychological dependence are both mediated through reinforcement, a form of operant conditioning, but are associated with different forms of reinforcement. Addiction is a compulsion for rewarding stimuli that is mediated through positive reinforcement. Psychological dependence, which is mediated through negative reinforcement, involves a desire to use a drug or perform a behavior to avoid the unpleasant withdrawal syndrome that results from cessation of exposure to it.

Psychological dependence develops through consistent and frequent exposure to a stimulus. Behaviors which can produce observable psychological withdrawal symptoms (i.e., cause psychological dependence) include physical exercise, shopping, sex and self-stimulation using pornography, and eating food with high sugar or fat content, among others. Behavioral therapy is typically employed to help individuals overcome psychological dependence upon drugs or maladaptive behaviors that produce psychological dependence.

While SSADH deficiency has been studied for nearly 30 years, knowledge of the disorder and its pathophysiology remains unclear. However, the progress that has been made with both murine and human models of the disorder have provided a lot of insights into how the disease manifests itself and what more can be done in terms of therapeutic interventions. Much of the current research into SSADH has been led by a dedicated team of physicians and scientists, including Phillip L. Pearl, MD of the Boston Children's Hospital at Harvard Medical School and K. Michael Gibson, PhD of Washington State University College of Pharmacy. Both have contributed significant efforts to finding appropriate therapies for SSADH deficiency and have specifically spent most of their recent efforts into understanding the efficacy of the ketogenic diet for patients with SSADH deficiency. In addition, a lot of the research that was published in 2007 examined the pathogenesis for the disorder by examining the role of oxidative stress on tissues in various cerebral structures of Aldh5a1-/- mice.

Ultimately, the metabolic pathway of SSADH deficiency is known, but how the enzyme deficiency and accumulation of GABA and GHB contribute to the clinical phenotype is not. For the future however, treatment strategies should focus on both decreasing the total production of GHB and increasing the total concentration of GABA and further assessing whether the effects of these changes influences the neurological manifestations seen in patients afflicted with SSADH deficiency.

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Guanidinoacetate methyltransferase deficiency, also called GAMT deficiency, is an autosomal recessive metabolic disorder that primarily affects the nervous system and muscles. It is the first observed disorder of creatine metabolism.