Thursday, November 20, 2014

global surge in ADHD diagnosis has more to do with marketing than with medicine

sciencedaily |  You can't catch attention deficit hyperactivity disorder (ADHD). Yet the diagnosis and treatment of this behavioral condition is spreading like a contagion -- surging as much as tenfold in some countries.

Call it an economic and cultural plague, but not necessarily a medical one, says Brandeis professor Peter Conrad. In a recent paper in the journal Social Science and Medicine, Conrad and coauthor Meredith Bergey examined the growth of ADHD in the United Kingdom, Germany, France, Italy and Brazil.

Until recently, North America tallied by far the most ADHD diagnoses, and the United States consumed 90 percent of all Ritalin, one of the most common ADHD drugs. ADHD diagnoses continue to grow in the U.S., but Americans account for only 75 percent of Ritalin users today.

Conrad and Bergey attribute ADHD's growth to five trends. Drug companies are effective lobbyists, and have spurred some countries to relax marketing restrictions on stimulants. Psychoanalytic treatment with talk therapy is giving way to biological psychiatry -- treating psychological problems with drugs. More European and South American psychologists and psychiatrists are adopting the American-based Diagnostic and Statistical Manual (DSM) standards, which are broader and have a lower threshold for diagnosing ADHD. Vocal ADHD advocacy groups work closely with drug companies to promote pharmaceutical treatment. Lastly, the easy availability of ADHD information and self-diagnosis via the Internet empowers consumers to ask for prescription treatment.
Many websites promoting ADHD drugs offer checklists with questions like these:
  • Do you fidget a lot?
  • Is it hard for you to concentrate?
  • Are you disorganized at work and home?
  • Do you start projects and then abandon them?
"These checklists turn all kinds of different behaviors into medical problems," Conrad says. "The checklists don't distinguish what is part of the human condition and what is a disease."

According to the study, in the U.K., diagnosis of the disorder in school-age children grew from less than one percent in the 1990s to about five percent today. In Germany, prescription ADHD drugs rose from 10 million daily doses in 1998 to 53 million in 2008.

Growth in Italy and France has been slower, in part due to those countries' more restrictive pharmaceutical drug laws. However, even those nations are becoming more lax, says Conrad. In Brazil, a rising number of ADHD advocacy groups, many with close ties to the pharmaceutical industry, are raising awareness of the disorder.

suicide epidemic in utah and one neuroscientist thinks he knows why

mic |  Renshaw believes that oxygen-poor air tampers with brain chemistry, leading to a drop in serotonin and an uptick in dopamine. Serotonin and dopamine are neurotransmitters, brain chemicals that relay signals between neurons and other cells. 

Serotonin, an inhibitory neurotransmitter, helps stabilize emotions. Antidepressants — SSRIs, (selective serotonin reuptake inhibitor), which include Prozac and Lexapro — work by blocking the transport of serotonin back to the neurons, thereby increasing its supply in the brain.

Dopamine, an excitatory neurotransmitter, plays a vital role in our ability to focus. Too little dopamine can make us scatterbrained, whereas a dopamine increase causes hyper-concentration and feelings of euphoria. Caffeine, prescription drugs, including some ADD/ADHD medications, and illegal stimulants like cocaine and methamphetamine, work by increasing the availability of dopamine in our brains.

So why do some people enjoy the benefits of the Utah air's impact on increased dopamine levels, which should make us happier, and some fall victim to the impact on decreased levels of serotonin, which would make us more depressed?

The answer lies in how changes in neurotransmitter levels affect our individual brain chemistry.
As Renshaw's theory goes, serotonin deficiency exacerbates symptoms of pre-existing anxiety and depression, increasing the likelihood of becoming suicidal (mental illness is a factor in about 90% of suicides). People with an existing mood disorder, or a predisposition to mental illness, would be more sensitive to the effects of waning serotonin levels.

Women, who naturally have half as much serotonin as men, Renshaw said, are more likely to develop a mood disorder as a result of living in the mountains (about 24% of middle-aged women in Utah take an SSRI — double the national rate. The various anecdotes about anxious Utah women, Renshaw believes, bolster his theory).

Wednesday, November 19, 2014

don't do it: drugs are not the answer for incompetent parenting...,

NYTimes |  Every time Matthias is kicked out of a school or day camp for defying adults and clashing with other children, his mother, Joelle Kendle, inches closer to a decision she dreads. With each morning of arm-twisting and leg-flailing as she tries to get him dressed and out the door for first grade, the temptation intensifies.

Ms. Kendle is torn over whether to have Matthias, just 6 and already taking the stimulant Adderall for attention deficit hyperactivity disorder, go on a second and more potent medication: the antipsychotic Risperdal.

Her dilemma is shared by a steadily rising number of American families who are using multiple psychotropic drugs — stimulants, antipsychotics, antidepressants and others — to temper their children’s troublesome behavior, even though many doctors who mix such medications acknowledge that little is known about the overall benefits and risks for children.

In 2012 about one in 54 youngsters ages 6 through 17 covered by private insurance was taking at least two psychotropic medications — a rise of 44 percent in four years, according to Express Scripts, which processes prescriptions for 85 million Americans. Academic studies of children covered by Medicaid have also found higher rates and growth. Combined, the data suggest that about one million children are currently taking various combinations of psychotropics.

Risks of antipsychotics alone, for example, are known to include substantial weight gain and diabetes. Stimulants can cause appetite suppression, insomnia and, far more infrequently, hallucinations. Some combinations of medication classes, like antipsychotics and antidepressants, have shown improved benefits (for psychotic depression) but also heightened risks (for heart rhythm disturbances).

But this knowledge has been derived substantially from studies in adults — children are rarely studied because of concerns about safety and ethics — leaving many experts worried that the use of multiple psychotropics in youngsters has not been explored fully. There is also debate over whether the United States Food and Drug Administration’s database of patients’ adverse drug reactions reliably monitors the hazards of psychotropic drug combinations, primarily because only a small fraction of cases are ever reported. Some clinicians are left somewhat queasy about relying mostly on anecdotal reports of benefit and harm.

Tuesday, November 18, 2014

dopamine hegemony can be disrupted by... fatty acids?

Science Daily | Taking omega-3 supplements reduces craving for nicotine and even reduces the number of cigarettes that people smoke a day, according to a new study conducted at the University of Haifa. "The substances and medications used currently to help people reduce and quit smoking are not very effective and cause adverse effects that are not easy to cope with. The findings of this study indicated that omega-3, an inexpensive and easily available dietary supplement with almost no side effects, reduces smoking significantly," said Dr. Sharon Rabinovitz Shenkar, head of the addictions program at the University of Haifa's school of criminology department and of the psychopharmacology laboratory at Bar-Ilan, who conducted this study.

Chronic exposure to smoke-derived toxicants is the primary cause of progressive pulmonary and immune dysfunctions, as well as carcinogenesis Cigarette smoking is connected not only to cardiovascular dysfunction, immune system dysfunction and cancer, it also reduces the levels of essential fatty acids in the brain, especially that of omega-3. A deficiency in omega-3 damages the cellular structure of nerve cells and interrupts neurotransmission in areas of the brain involved with feeling pleasure and satisfaction. These areas are essential in reward and decision-making, and are very important in the process of the development, maintenance and relapseof the addiction and to the inability to stop smoking. In simpler terms, omega-3 deficiency makes it harder for the smoker's body to deal with its craving for another cigarette. "Earlier studies have proven that an imbalance in omega-3 is also related to mental health, depression and the ability to cope with pressure and stress. Pressure and stress, in turn, are associated with the urge to smoke. It is also known that stress and tension levels rise among people who quit smoking. Despite all this, the connection between all these factors had not been studied until now," Dr. Rabinovitz Shenkar said


Monday, November 17, 2014

you are what you eat

pnas | Significance

Human mucosal surfaces contain a wide range of microorganisms. The biological effects of these organisms are largely unknown. Large-scale metagenomic sequencing is emerging as a method to identify novel microbes. Unexpectedly, we identified DNA sequences homologous to virus ATCV-1, an algal virus not previously known to infect humans, in oropharyngeal samples obtained from healthy adults. The presence of ATCV-1 was associated with a modest but measurable decrease in cognitive functioning. A relationship between ATCV-1 and cognitive functioning was confirmed in a mouse model, which also indicated that exposure to ATCV-1 resulted in changes in gene expression within the brain. Our study indicates that viruses in the environment not thought to infect humans can have biological effects.

Saturday, November 8, 2014

dopaminergic foundations of personality and individual difference

frontiersin |  The dopamine system can be divided into several anatomically defined branches or pathways. The nigrostriatal pathway (projecting from the substantia nigra to the striatum) is involved in motor control, and has long been of interest in the context of Parkinson's Disease and its therapeutic management via dopamine replacement (see Cenci, 2007). It was initially thought that motor control was the primary or even sole function of dopamine (e.g., Koob, 1982). However, this perspective has given way to a reward-processing interpretation of dopamine, focussed primarily on the mesolimbic pathway (projecting from the ventral tegmental area to limbic and forebrain areas including the striatum) (Robbins and Everitt, 1996; Wise, 2004; Schultz, 2007). One early theory helped integrate these diverging perspectives by proposing that the ventral striatum, a target of both nigrostriatal and mesolimbic dopamine, was responsible for converting motivation (i.e., to approach desire goal states) into action (Mogenson et al., 1980).
The reward-processing functions of dopamine have been discussed in terms of motivation by reward, enjoyment of reward, and learning from reward—or “wanting,” “liking” and “learning” (Berridge et al., 2009). Initially it was theorized that dopamine mediated reward “liking”—the hedonic impact of rewarding stimuli (Wise, 1982), and that these pleasure responses sustained reward-directed behavior. This theory enjoyed widespread influence for some time, and explains why dopamine was popularly dubbed “the pleasure chemical,” but has now been abandoned (Wise, 2004). One critique came from the addiction literature, which showed that dopamine-mediated escalation of drug dependence is accompanied by decreased pleasurable responses to those drugs (Robinson and Berridge, 2003). This favors the theory that dopamine mediates motivational “wanting” of reward by conferring stimuli with “incentive salience”—the process through which stimuli become motivationally attractive (Robinson and Berridge, 2003; Berridge et al., 2009). Dopamine is also thought to be responsible for reward learning, with phasic dopamine activity providing the “teacher” signal hypothesized in reinforcement learning models (Schultz et al., 1997; Schultz, 2007). Although reward wanting theories appear compatible with reward learning theories, they have not yet been integrated into a cohesive theoretical framework (see Alcaro et al., 2007).
Dopamine also has a major role in cognitive function and dysfunction. The mesocortical dopamine pathway (projecting from the ventral tegmental area to the dorsolateral prefrontal cortex and the anterior cingulate cortex) is implicated in higher cognitive functions such as working memory and decision-making (Robbins et al., 1996; Arnsten, 1998; Floresco and Magyar, 2006). Although these appear strikingly different to the motivational functions of the mesolimbic dopamine system, mental representations and operations seem likely to facilitate motivated action. That is, the mesocorticolimbic dopamine pathways may jointly coordinate the “anticipation of reward and activation of representations in the PFC needed to achieve it” (Miller and Cohen, 2001, p. 182). The higher cognitive functions of dopamine have implications for creative behavior, which is typically operationalized using tests of cognitive flexibility and divergent thinking. Ashby et al. (1999) suggest that this may explain the apparent impact of induced positive affect on creativity; positive affect is often preceded by reward delivery, which will often stimulate dopamine release. Finally, an enduring theory has posited a central role for dopamine in the cognitive disturbances seen in schizophrenia (e.g., Gray et al., 1991). A later iteration of this theory has related mesocortical dopamine to cognitive deficits (e.g., executive dysfunction) and negative symptoms (e.g., anhedonia), and mesolimbicdopamine to positive symptoms (e.g., hallucinations and delusions) (Lindenmayer et al., 2013).
This brief overview is only intended to orient the reader, illustrate the breadth of processes to which dopamine has been linked, and thereby foreshadow the diversity of topics addressed in this special issue. For more in-depth perspectives on dopamine function the interested reader is encouraged to consult the references cited here.