The DSM-5 eliminated the “subjective fear-based distress” criterion because research indicates that not all individuals with PTSD respond with a fear-based reaction. Some individuals instead respond with anhedonic, dysphoric, aggressive, phobic, or dissociative reactions to the trauma-causing event. This change in the diagnostic criteria helps us to be more sensitive to the diverse PTSD presentations that we may see in our clients. According to Dr. Matthew J. Friedman, a member of the DSM-5 Anxiety, Obsessive-Compulsive Spectrum, Posttraumatic and Dissociative Disorders Work Group: “When PTSD was first proposed in 1980 for DSM-III, the major scientific model was that it was a fear-based anxiety disorder. So, the A2 criteria in DSM-IV called for a fear-based reaction of fear, helplessness or horror. But a lot of research now indicates that for many people who have intense emotional reactions to a traumatic event and go on to develop PTSD, their reaction is not fear based, but more likely to be dysphoria or anhedonia.”
Multiple mechanisms contribute to individuals’ vulnerability to obesity, including genetic, developmental, and environmental factors that are likely to interact in diverse ways to produce the behavioral phenotype of overeating. A growing body of evidence from epidemiologic and community samples has documented a relationship between obesity and psychiatric disorders, including mood and anxiety disorders, as well as personality disorders. Moreover, developing evidence suggests a relationship between obesity and attention-deficit/hyperactivity disorder and posttraumatic stress disorder. Obesity also has a number of correlates in common with eating disorders and substance use disorders, including hypothalamic-pituitary-adrenal axis dysregulation and environmental precipitants such as childhood trauma. It further shares a number of symptomatic features with mood disorders, including increased appetite, decreased activity levels, and sleep disturbance.
Most notable is her inclination to act thoughtlessly and irresponsibly in peer and family matters and to be generally careless and imprudent, failing to plan ahead or to consider the consequences of her behavior. She may be prone to taking undue chances and seeking thrills, acting as if she were immune from danger. She tends to jump from one risky and momentarily gratifying escapade to another with little or no care for potentially detrimental consequences. Also salient are her failure to constrain or postpone the expression of offensive thoughts or malevolent actions, a deficit in guilt feelings, and a consequent disinclination to refashion repugnant impulses in sublimated form. She may perceive herself as a victim, a youthful bystander subjected to unjust family persecution and school hostility. Through this psychic maneuver, she not only disowns her malicious impulses but attributes 'acts of evil' to others. As a persecuted victim, she then feels free to counterattack and gain restitution and vindication.
Language was added to Criterion B that expands the disturbance in behavior to include “distress in the individual or others in his or her immediate social context (e.g., family, peer group, work colleagues).” Criterion C contains new language excluding diagnosis of oppositional defiant disorder during the course of a substance use disorder or disruptive mood dysregulation disorder.
The distribution of selenium in tissues was markedly different when rats were fed a diet deficient in selenium: the testes, brain, thymus gland, and spleen took up the greatest concentrations of selenium from a tracer dose of selenite (Burk et al., 1972).
For example, Scott & Thompson (1971) demonstrated that chicks receiving 100 mg vitamin E/kg diet needed only 0.01 mg selenium/kg diet to prevent exudative diathesis, whereas chicks not receiving any added vitamin E needed 0.05 mg/kg.
Thompson & Scott (1969) found that administration of 0.02 - 0.05 mg selenium/kg, as selenite, prevented death and exudative diathesis in chicks fed diets containing typical levels of vitamin E (sections 184.108.40.206 and 220.127.116.11 include discussions on the nutritional interrelationship of selenium and vitamin E).
Diseases such as white muscle disease in sheep and cattle, hepatosis dietetica in swine, and exudative diathesis in poultry are economically significant problems in areas of the world where the soil levels of selenium available for uptake by plants are low.
The degree of protection against exudative diathesis and the level of plasma glutathione peroxidase activity were highly correlated, suggesting that nutritional potency depended on the ability of the chick to convert various selenium compounds to the enzymatically active form.
Among these are the age and sex of the animal, starvation, exposure to certain oxidant stressors, toxicants, or heavy metals, and deficiency in iron and vitamin B12.
(1975a) found that while selenite and selenocystine were equally effective in preventing exudative diathesis in vitamin E- and selenium-deficient chicks, seleno-methionine was less effective.
Conversion of selenium compounds to nutritionally-active forms of selenium The pioneering studies of Schwarz & Foltz (1958) demonstrated that a variety of selenium compounds could protect against dietary liver necrosis in vitamin E- and selenium-deficient rats.
For those clinicians needing a diagnosis to account for sexually addictive behavior in clients, I suggest ruling out borderline personality disorder and histrionic personality disorder even though hypersexuality is characteristic of both disorders. Clinicians must also remember that hypersexuality is core to manic and hypomanic episodes, so proficient ruling out for bipolar I or II disorders is strongly encouraged. For example, as detailed in the DSM-5, manic/hypomanic episodes are characterized by:
Baird, G. (2013). Classification of diseases and the neurodevelopmental disorders: The challenge for DSM-5 and ICD-11. Developmental Medicine & Child Neurology, 55(3), 200-201. doi:10.1111/ dmcn.12087Batstra, L., & Frances, A. (2012). DSM-5 further inflates attention deficit hyperactivity disorder. , 200(6), 486-488.