Brain Blogger » Jennifer Gibson, PharmD

Aging Intelligently

Jennifer Gibson, PharmD — Thu, 09 Feb 2012 13:00:36 +0000

Human intelligence is highly variable among people, but only somewhat variable across a person’s lifespan. New research points to genes as the keys to maintaining intelligence as we age.

The study, published in Nature, analyzed the genes of nearly 2000 people to assess their intelligence in childhood and old age. The participants, all part of the Lothian Birth Cohorts, took general intelligence tests at age 11 and again at age 65, 70, or 79. The researchers simultaneously analyzed genome-wide single nucleotide polymorphisms in the individuals. Overall, genes accounted for 24% of the change in intelligence that occurred across a single person’s lifespan. The researchers also concluded that the correlation between intelligence in childhood and intelligence in adulthood was 0.62. (A similar evaluation of the same cohort reported that intelligence in childhood is actually protective of intelligence later in life.)

Differences in intelligence are related to important life outcomes: education, occupation, income, health, and lifespan. And, so far, most data has pointed to a strong heritability of intelligence. But, the individual genes that account for intelligence have not been identified, and most studies point to many small genetic influences, rather than one large one, that have an additive effect on intelligence.

This leaves lots of “wiggle room” in identifying who the intelligent people are and how they got that way. It seems that nature and nurture play a role, not only in intelligence itself, but in maintaining intelligence across the lifespan. Clearly, genetics does not explain it all; there must be environmental contributions to establishing and maintaining intelligence. Genes are not the final determinant of intelligence and mental capability, and factors such as eating a healthy diet, engaging in regular exercise, staying mentally stimulated, and maintaining an active social life can help prevent changes in intelligence as a person ages.

With this new research, the door is open for scientists to identify the actual genetic components of intelligence, and possibly develop screening tests and early interventions to combat genetically-influenced declines in cognitive abilities. But, for now, do not be defined by your genes; intelligence is what you do with your genes. In use-it-or-lose-it fashion, you will only remain as sharp as the books you read, the places you travel, or the mental challenges you accept.

References

Davies G, Tenesa A, Payton A, Yang J, Harris SE, Liewald D, Ke X, Le Hellard S, Christoforou A, Luciano M, McGhee K, Lopez L, Gow AJ, Corley J, Redmond P, Fox HC, Haggarty P, Whalley LJ, McNeill G, Goddard ME, Espeseth T, Lundervold AJ, Reinvang I, Pickles A, Steen VM, Ollier W, Porteous DJ, Horan M, Starr JM, Pendleton N, Visscher PM, & Deary IJ (2011). Genome-wide association studies establish that human intelligence is highly heritable and polygenic. Molecular psychiatry, 16 (10), 996-1005 PMID: 21826061

Deary IJ, Johnson W, & Houlihan LM (2009). Genetic foundations of human intelligence. Human genetics, 126 (1), 215-32 PMID: 19294424

McDonald PT, & Schmidt CD (1990). Differential survival of male and female partially resistant horn flies (Diptera: Muscidae) on steers treated with permethrin. Journal of economic entomology, 83 (5), 1715-7 PMID: 2258510

Gow AJ, Johnson W, Pattie A, Brett CE, Roberts B, Starr JM, & Deary IJ (2011). Stability and change in intelligence from age 11 to ages 70, 79, and 87: the Lothian Birth Cohorts of 1921 and 1936. Psychology and aging, 26 (1), 232-40 PMID: 20973608

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A Nicotine Patch a Day Keeps the Cognitive Impairment Away

Jennifer Gibson, PharmD — Mon, 06 Feb 2012 12:00:30 +0000

Normally, a nicotine patch on someone’s arm is evidence that they are trying to quit smoking. But, soon, nicotine patches may be appearing on arms of the cognitively impaired.

A study published in the journal Neurology reported that transdermal nicotine administration improved the symptoms of cognitive impairment in nonsmoking adults. In a randomized, double-blind, placebo-controlled study, 74 nonsmoking adults with mild cognitive impairment received either 15 mg of nicotine or placebo daily for 6 months. (Most smoking cessation patches deliver between 7 and 21 mg of nicotine per day.) At the end of the study period, the subjects showed significant improvement in most measures of cognitive function, including attention, memory, and psychomotor speed. There was no statistically significant improvement in clinician-rated global impression. The nicotine showed exceptional safety and tolerability.

The nicotinic acetylcholine receptor system is believed to be a part of memory and attention processes in the brain, and, thus, is thought to be dysregulated in memory- and attention-related disorders, including amnestic cognitive impairment, schizophrenia, attention-deficit disorder, and Alzheimer’s Disease. Therefore, nicotinic agonists, like nicotine, are potential treatment options for the memory and attention impairment components of many diseases. Nicotine has already shown significant improvement in memory- and attention-related symptoms and inhibition of impulsive responses in psychiatric populations.

To date, the reports of the benefits of nicotine have come from nonsmoking populations who have some form of cognitive impairment. The same effects of nicotine are not seen in current smokers, nor are they seen in healthy individuals without cognitive impairment. In fact, in adults with no memory or attention deficits, nicotine actually decreases performance on a battery of cognitive tests.

Clinicians are far from recommending nicotine patches to every forgetful person they meet, but nicotine does represent an interesting therapeutic target in several memory- and attention-related disorders. (And explains, at least in part, attention-deficient and cognitively-impaired populations who self-medicate with a higher prevalence of cigarette smoking compared to healthy populations.) The long-term effects of chronic transdermal nicotine are not well defined and the clinical importance and significance of the cognitive improvement is yet to be determined, but larger, more comprehensive studies are underway to further investigate nicotine therapy.

References

Barr RS, Culhane MA, Jubelt LE, Mufti RS, Dyer MA, Weiss AP, Deckersbach T, Kelly JF, Freudenreich O, Goff DC, & Evins AE (2008). The effects of transdermal nicotine on cognition in nonsmokers with schizophrenia and nonpsychiatric controls. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 33 (3), 480-90 PMID: 17443126

Newhouse P, Kellar K, Aisen P, White H, Wesnes K, Coderre E, Pfaff A, Wilkins H, Howard D, & Levin ED (2012). Nicotine treatment of mild cognitive impairment: A 6-month double-blind pilot clinical trial. Neurology, 78 (2), 91-101 PMID: 22232050

Poltavski DV, & Petros T (2006). Effects of transdermal nicotine on attention in adult non-smokers with and without attentional deficits. Physiology & behavior, 87 (3), 614-24 PMID: 16466655

Potter AS, & Newhouse PA (2008). Acute nicotine improves cognitive deficits in young adults with attention-deficit/hyperactivity disorder. Pharmacology, biochemistry, and behavior, 88 (4), 407-17 PMID: 18022679

White HK, & Levin ED (2004). Chronic transdermal nicotine patch treatment effects on cognitive performance in age-associated memory impairment. Psychopharmacology, 171 (4), 465-71 PMID: 14534771

Wignall ND, & de Wit H (2011). Effects of nicotine on attention and inhibitory control in healthy nonsmokers. Experimental and clinical psychopharmacology, 19 (3), 183-91 PMID: 21480731

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Media Violence Leads to Real Violence

Jennifer Gibson, PharmD — Fri, 27 Jan 2012 12:00:31 +0000

A few short decades ago, the most violent scenes we were exposed to in the media involved Wile E. Coyote and an anvil. The nightly news did not display graphic evidence of riots or murders or even war. Movies did not market themselves based on the amount of gunfire packed into two hours. Video games were little more than a bouncing ball controlled by a joystick. But, society has changed and, now, violence is everywhere. Children and adolescents are exposed to violent images everyday and the line between reality and fiction is blurred. Now, the consequences of such exposure are becoming evident and recent studies show neurological adaptations and desensitization that lead to aggression and violence in real life.

Adolescents spend a significant amount of time watching violent television programs and movies and playing violent video games. A recent neurological evaluation of adolescent brain function reported an association between violent media exposure and decreased brain activation in response to increasingly violent images and scenes. The adaptation was primarily seen in the fronto-parietal network, an area that has been associated with decreased control of aggressive behavior. Essentially, repeated exposure to violence blunts emotional responses to violence and decreases the association of consequences with aggression, leading to more aggressive attitudes and behaviors over time.

A similar study did report that the presence of innate aggressive personality traits or tendencies does moderate brain responses to media violence. Adolescents with diagnoses of aggressive behavior disorders with repeated exposure to media violence showed decreased brain activation in response to emotional stimuli compared to healthy controls with low violence exposure and compared to aggressive adolescents with low violence exposure. Still, another examination of adolescents showed that brain activation and emotional responses to violence were similar between healthy, non-aggressive adolescents with high exposure to media violence and adolescents diagnosed with aggressive behavior disorders.

Violence is everywhere. As a society, we are desensitized to viewing aggressive and brutal scenes every day. But, is it as simple as desensitization or does exposure to violence really change who we are? The findings of the neurological studies suggest that brain function is actually altered in response to violence and, as a result, individuals are less able to react emotionally to violence and control their own aggressive behavior. Our choices in entertainment are becoming self-fulfilling prophecies, of sorts, and the more violence we see, the more violent we are.

References

Kalnin AJ, Edwards CR, Wang Y, Kronenberger WG, Hummer TA, Mosier KM, Dunn DW, & Mathews VP (2011). The interacting role of media violence exposure and aggressive-disruptive behavior in adolescent brain activation during an emotional Stroop task. Psychiatry research, 192 (1), 12-9 PMID: 21376543

Kelly CR, Grinband J, & Hirsch J (2007). Repeated exposure to media violence is associated with diminished response in an inhibitory frontolimbic network. PloS one, 2 (12) PMID: 18060062

Mathews VP, Kronenberger WG, Wang Y, Lurito JT, Lowe MJ, & Dunn DW (2005). Media violence exposure and frontal lobe activation measured by functional magnetic resonance imaging in aggressive and nonaggressive adolescents. Journal of computer assisted tomography, 29 (3), 287-92 PMID: 15891492

Strenziok M, Krueger F, Deshpande G, Lenroot RK, van der Meer E, & Grafman J (2011). Fronto-parietal regulation of media violence exposure in adolescents: a multi-method study. Social cognitive and affective neuroscience, 6 (5), 537-47 PMID: 20934985

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Childhood Aggression Predicts Health Care Use Later in Life

Jennifer Gibson, PharmD — Sat, 21 Jan 2012 12:00:03 +0000

Young children can be physically aggressive, owing to a combination of instinct, temperament, cultural and social influences, and (sometimes) not getting what they want. But, by the time most kids reach preschool age, they have learned to control their aggression with coping skills and relational techniques. However, children who do not learn to regulate aggressive behavior are at risk for physical and mental health issues, as well as serious patterns of aggression and violence, as adults. A new study, published in the Canadian Medical Association Journal, shows that the more aggressive a young child is the more likely he or she is to use health care services as an adult.

The 15-year longitudinal cohort study examined nearly 4000 children who were in grades 1, 4, and 7 in the mid-1980s. Children were ranked by their peers on three attributes: aggression, withdrawal, and likeability. Researchers used Canadian databases to assess health care use when the subjects were, on average, 39 years old. They adjusted their results for socioeconomic status of the children in 1986 and educational level.

Overall, results indicate that each standard deviation in peer-rated childhood aggression accounted for an 8% increase in overall medical visits during the follow-up period. Additionally, aggressive children showed an 11% increase in medical visits for injuries, a 44% increase for lifestyle-related illnesses, which included obesity, type 2 diabetes, ulcers, alcohol dependence, and drug use, a 6% increase in visits to specialists, a 24% increase in visits to dentists, a 12% increase in visits to emergency rooms, and an 11% increase in hospital admissions. Childhood aggression was not associated with an increase in infections.

Children who were judged to be more socially withdrawn than their peers had a 15% increase in visits to dentists. Alternatively, likeable children had a 4% decrease in overall health care use, a 9% decrease in medical visits due to injuries, and an 11% decrease in visits to dentists.

It is difficult to clarify precisely what causes aggression, but associations have been identified between childhood aggression and poor peer relationships, having young siblings, mothers with antisocial behavior, young mothers, families with low income, mothers who smoked during pregnancy, mothers who exhibit coercive parenting behavior, and family dysfunction. Still, no matter the cause, aggressive children can grow into aggressive adults. And, aggressive adults can impose a burden on public health services owing to increased physical, mental, and emotional violence toward victims, increased violent crimes, and increased spouse and child abuse. And, perpetrators themselves are at increased risk for depression, suicide, alcohol and drug use, and injuries.

The authors do not go so far as to calculate the total monetary costs associated with health care use within this cohort, but the implication is that the increased use of health care imposes a significant economic burden on public health services. They claim that decreasing the aggression will lead to decreased expenditures and overall health care cost savings. Identifying problematic and aggressive childhood behavior, and teaching corrective or preventive strategies, might mitigate long-term health risks and economic burdens to the children themselves and the public at large.

References

Temcheff CE, Serbin LA, Martin-Storey A, Stack DM, Hastings P, Ledingham J, & Schwartzman AE (2011). Childhood aggression, withdrawal and likeability, and the use of health care later: a longitudinal study. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 183 (18), 2095-101 PMID: 22083681

Temcheff CE, Serbin LA, Martin-Storey A, Stack DM, Ledingham J, & Schwartzman AE (2011). Predicting adult physical health outcomes from childhood aggression, social withdrawal and likeability: a 30-year prospective, longitudinal study. International journal of behavioral medicine, 18 (1), 5-12 PMID: 20383621

Tremblay RE, Nagin DS, Séguin JR, Zoccolillo M, Zelazo PD, Boivin M, Pérusse D, & Japel C (2004). Physical aggression during early childhood: trajectories and predictors. Pediatrics, 114 (1) PMID: 15231972

Yamasaki K, & Nishida N (2009). The relationship between three types of aggression and peer relations in elementary school children. International journal of psychology : Journal international de psychologie, 44 (3), 179-86 PMID: 22029493

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Risks of Personalized Medicine

Jennifer Gibson, PharmD — Sun, 15 Jan 2012 12:00:53 +0000

Anyone who has taken high school biology has probably heard one of the corniest biology jokes around: How do you tell a girl chromosome from a boy chromosome? Pull down its genes. While this has been a useful (if not really funny) mnemonic for teaching students about life science, now individuals are beginning to play genetic versions of I’ll-show-you-mine-if-you-show-me-yours by actually examining their genes. Not much more than a decade has passed since the completion of the Human Genome Project, but, already, direct-to-consumer (DTC) genome mapping and genetic testing are available with little more than a cotton swab and an envelope between you and your DNA.

Personalized genomic information is used to individualize prevention, diagnosis, and treatment of diseases. Genetic variants can now be relatively easily identified and used as markers for diagnosis and prognosis and targets for treatment. But, the clinical functionality of this information is limited, and many questions are unanswered regarding the role of behavior and ethics as related to genetic testing. Proponents of ubiquitous genome mapping claim that identifying genetic information (and, therefore, risks) will lead to improved public health by motivating lifestyle changes. But, DTC testing occurs at the discretion of an individual alone, often without the input of a healthcare provider, prompting opponents of the tests to claim increased health risks — physical, mental, and emotional — as a consequence of the test results.

In a recent review of several studies that evaluated behavioral responses to DTC genetic testing, very few studies identified significant changes in individual behavior as a result of disease-specific genetic testing. The sample of consumers was, as a whole, healthier than average Americans, reporting daily consumption of fruits and vegetables and physical activity. The authors report that this group was already motivated to adopt a healthy lifestyle, and there was little room for improvement, regardless of the genetic predispositions revealed by the tests.

Also noteworthy was the finding that most of the DTC tests reported results in terms of relative risk instead of actual risk. Without an understanding of statistics or risk analysis, a report of relative risk might make individuals unnecessarily anxious or worried about their risk of disease. Further, many tests evaluate many gene variants at once, so individuals are able to retrieve risk information regarding tens – up to, potentially, hundreds — of diseases and conditions at once. Again, this information overload, without the training or knowledge to sort through what is important and what is not, can cause unwarranted concern, and possibly inappropriate interventions. Additionally, a large number of diseases and conditions for which DTC genetic tests check are largely associated with environmental and lifestyle factors and family history – risks that a consumer likely already understands.

Many organizations and groups that evaluate genetic testing and genomic applications do not support routine genetic testing, DTC or under the supervision of a healthcare provider. The biological mechanisms underlying diseases’ connections to genetic markers are largely undefined and the level of intervention that alters risk is unknown in most cases. And, for many disease states, there is no long-term data that shows improved health or disease outcomes related to genetic testing results. Traditional risk factors are more precise, measureable indicators of disease progression and/or treatment effectiveness.

Thanks, at least in part, to crime scene and medical dramas (real-life and fictional), the study of genomics and genetic risk analysis has been met with understandable enthusiasm, even from outside of the scientific world. But, the enthusiasm should not be without hesitation. The burden of having information, but not understanding how to interpret it or apply it clinically, can cause tremendous challenges to individuals and their families. And, it calls into question the ethics of DTC testing and the truthfulness of advertising and information provided by DTC tests. Further, the risk to future health care provision that may come as a consequence of personalized genotyping and phenotyping is left out of many discussions. Insurance coverage could be altered or denied due to supposed genetic risks. Discrimination could result owing to assumed predispositions. Judgments could be concluded based on incomplete information.

In a medical test-for-everything age (even if we don’t know what to do with the results), individuals are sometimes asked to make choices about their future health, the life of a developing fetus, or treatment options for a family member based on genetic testing. If there is not a trained counselor or healthcare provider available to deliver the correct and relevant information, people may not be able to make the most informed decision. Personalized medicine will likely revolutionize the way medicine is practiced, and likely lead to improved overall public health, but personalization includes much more than just genes; individuals, time, circumstances, and social norms dictate how and when information should be obtained and interpreted.

References

Bloss CS, Madlensky L, Schork NJ, & Topol EJ (2011). Genomic information as a behavioral health intervention: can it work? Personalized medicine, 8 (6), 659-667 PMID: 22199991

Henrikson NB, Bowen D, & Burke W (2009). Does genomic risk information motivate people to change their behavior? Genome medicine, 1 (4) PMID: 19341508

Offit K (2011). Personalized medicine: new genomics, old lessons. Human genetics, 130 (1), 3-14 PMID: 21706342

Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group (2010). Recommendations from the EGAPP Working Group: genomic profiling to assess cardiovascular risk to improve cardiovascular health. Genetics in medicine : official journal of the American College of Medical Genetics, 12 (12), 839-43 PMID: 21042222

Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group (2011). Recommendations from the EGAPP Working Group: routine testing for Factor V Leiden (R506Q) and prothrombin (20210GA) mutations in adults with a history of idiopathic venous thromboembolism and their adult family members. Genetics in medicine : official journal of the American College of Medical Genetics, 13 (1), 67-76 PMID: 21150787

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Economic Burden of Poor Mental Health

Jennifer Gibson, PharmD — Sat, 31 Dec 2011 12:00:53 +0000

In today’s economy, workers across all sectors are seeking steady, gainful employment. Likewise, employers are seeking productive, consistent workers. For individuals with mental illness, this may be an impossible job description to fill. A recent report published by the Organization for Economic Cooperation and Development (OECD) claims that common mental health conditions lead to decreased workplace productivity and substantial economic losses.

The OECD is an organization of approximately three dozen developed nations that seeks to improve the economic and social well-being of people around the world. The OECD recommends policies and business practices to address long-term challenges in worldwide productivity, innovation, and economic growth. In its latest report, the OECD addresses the substantial economic burden of mental illness around the world. According to data compiled from multiple sources, the OECD reports that, at any point in time, 20% of the population suffers from a mental illness and these conditions negatively affect workplace productivity. Primarily, people with mental illness are more likely than healthier coworkers to be absent from work, and each absence is longer for those with mental illness. Additionally, even when workers with mental illness are present at work, they struggle to be highly productive.

The total monetary cost associated with mental health is hundreds of billions of dollars annually in developed countries. Yet, most of these dollars are not spent in the health care sector. Most of the costs are incurred through a lost labor supply, high unemployment rates, frequent sick days, and lost productivity at work. In the European Union (EU), the total cost of mental health is estimated to be 800 billion euros annually, which accounts for 3% to 4% of the gross domestic product of the EU. In Canada, the monetary cost of decreased productivity associated with poor mental health is more than $15 billion, one-third of the total cost associated with mental illness.

The overall employment rate for people with mental illness is 10% to 15% lower than people without mental illness; people with mental illness are two to three times more likely to be unemployed. In the United States alone, workers with mental health disorders are 50% more likely to experience involuntary job loss and 30% more likely to leave a job voluntarily than healthier counterparts.

Women, young adults, and individuals with low levels of education are the most likely to experience mental illness. Most mental health disorders are mild to moderate, with depression, anxiety, and substance use disorders being the most common conditions. However, many mental health conditions coexist with physical comorbidities, which also negatively affect productivity.

The occurrence of mental illness among young adults is particularly worrisome, according to the OECD report, since young adults are at increased risk for leaving the job market completely or never entering it at all. In OECD member nations, mental illness accounts for one-third to one-half of new disability claims for workers. Among young adults, the proportion is 70%.

Luckily, research also indicates that individuals with mental illness who receive treatment can increase productivity and performance in the workplace. However, more than half of the people who suffer from mental illness receive no treatment — a social and policy-based struggle around the world that has already gained attention in recent years.

Many factors influence how mental health affects workplace performance, including psychological demands of the job itself, job security (or insecurity), and family and social support. According to the OECD, interventions to improve the economic burden of mental health should focus on improved working conditions and support for non-work-related stress. Additionally, the OECD recommends an atmosphere of mental health prevention, rather than reacting to acute episodes of poor mental health. Prevention and early identification of mental illness will improve the chances of young adults entering the workforce and maintaining long-term employment.

The misconceptions and stigma associated with mental illness at work prevent sufferers from disclosing their condition and receiving proper treatment. Particularly in the current economy, workers are even less likely to reveal anything that would make them appear to be a less-than-ideal employee. But, also in this economy, employers would be wise to take care of their employees and ensure productivity and quality job performance by keeping workers secure, happy and (mentally) healthy.

References

Czaba?a C, Charzy?ska K, & Mroziak B (2011). Psychosocial interventions in workplace mental health promotion: an overview. Health promotion international, 26 Suppl 1 PMID: 22079937

Dewa CS, & Lin E (2000). Chronic physical illness, psychiatric disorder and disability in the workplace. Social science & medicine (1982), 51 (1), 41-50 PMID: 10817467

Dewa CS, Thompson AH, & Jacobs P (2011). The association of treatment of depressive episodes and work productivity. Canadian journal of psychiatry. Revue canadienne de psychiatrie, 56 (12), 743-50 PMID: 22152643

Marchand A, & Blanc MÈ (2011). Occupation, work organisation conditions and the development of chronic psychological distress. Work (Reading, Mass.), 40 (4), 425-35 PMID: 22130060

OECD. Sick on the job? Myths and realities about mental health at work. 2011.

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Shyness and Social Phobia

Jennifer Gibson, PharmD — Sun, 18 Dec 2011 12:00:37 +0000

Personalities come in all shapes and sizes. Boisterous and docile. Flamboyant and reserved. Extroverted and introverted. Sociable and shy. But, when does a normal variation in personality characteristic, such as shyness, become a medical condition? Not as often as you might think, according to a new study that observed little connection between shyness and social phobia among adolescents.

The results, published in Pediatrics, were based on findings from the National Comorbidity Survey-Adolescent Supplement. The survey included face-to-face interviews of more than 10,000 nationally-representative adolescents aged 13 to 18 years in the United States. The investigators assessed the participants’ levels of shyness and social phobia based on validated diagnostic interviews and criteria, including the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition.

Overall, nearly half (47%) of the adolescents self-reported that they were shy. However, only 12% of these youth met the criteria for a diagnosis of social phobia at some point in their lifetime. An additional 5% of adolescents who did not find themselves to be shy met the criteria for social phobia.

Adolescents with social phobia were two to three times more likely to experience related conditions, such as anxiety disorders, posttraumatic stress disorder, major depression, and substance use disorders compared to shy youth. However, those with social phobia were not more likely than those who were shy to receive treatment for mental health conditions or take medications in general.

Social phobia in childhood is a complex condition, involving multiple etiologies, including genetic and environmental factors. Social phobia involves a feeling of loss of control, behavioral inhibition, and fear and avoidance of social situations. Social phobia, once diagnosed, is often effectively treated with a combination of psychosocial and pharmacological interventions. Some studies claim that shyness in childhood predicts social phobia later in life, though there are many precursors to social phobia. Still, many children who are shy grow to live phobia-free lives. In the National Comorbidity Survey, 26% of adult women claimed to be “very shy” in childhood and adolescence, and 19% of men claimed the same. Of these, 53% of women and 40% of men met diagnostic criteria for any anxiety or mood disorder, including social phobia, later in life. But, more than 50% of adults with social phobia were not shy growing up.

Another recent study, published by the Journal of the American Academy of Child and Adolescent Psychiatry, reports that the lifetime prevalence of social phobia is 9%. More than half of those affected suffer from generalized social phobia and the rest suffer from the non-generalized subtype. Less than one percent of those affected with social phobia are diagnosed with performance-only phobia. As the names suggest, persons with generalized social phobia are anxious in nearly all social situations. Alternatively, non-generalized social phobia affects sufferers only in specific situations. Performance-only social phobia is a category of non-generalized social phobia. Compared to adolescents with non-generalized social phobia, those with generalized social phobia have a younger age of symptom onset, higher levels of disability and clinical severity, and more comorbidities related to the disorder.

The authors of the Pediatrics study conclude that social phobia is a disabling and impairing psychiatric disorder that is distinct from normal shyness. Unfortunately, few seek treatment for social phobia. Though little overlap was found between shyness and social phobia in this study, the evaluation did underscore the significance of social phobia as a defined medical diagnosis.

References

Burstein M, Ameli-Grillon L, & Merikangas KR (2011). Shyness versus social phobia in US youth. Pediatrics, 128 (5), 917-25 PMID: 22007009

Burstein M, He JP, Kattan G, Albano AM, Avenevoli S, & Merikangas KR (2011). Social phobia and subtypes in the national comorbidity survey-adolescent supplement: prevalence, correlates, and comorbidity. Journal of the American Academy of Child and Adolescent Psychiatry, 50 (9), 870-80 PMID: 21871369

Cox BJ, MacPherson PS, & Enns MW (2005). Psychiatric correlates of childhood shyness in a nationally representative sample. Behaviour research and therapy, 43 (8), 1019-27 PMID: 15967173

Ginsburg GS, Kendall PC, Sakolsky D, Compton SN, Piacentini J, Albano AM, Walkup JT, Sherrill J, Coffey KA, Rynn MA, Keeton CP, McCracken JT, Bergman L, Iyengar S, Birmaher B, & March J (2011). Remission after acute treatment in children and adolescents with anxiety disorders: Findings from the CAMS. Journal of consulting and clinical psychology, 79 (6), 806-13 PMID: 22122292

Hitchcock CA, Chavira DA, & Stein MB (2009). Recent findings in social phobia among children and adolescents. The Israel journal of psychiatry and related sciences, 46 (1), 34-44 PMID: 19728571

Schutters SI, Dominguez MD, Knappe S, Lieb R, van Os J, Schruers KR, & Wittchen HU (2011). The association between social phobia, social anxiety cognitions and paranoid symptoms. Acta psychiatrica Scandinavica PMID: 22077136

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Risk Factors for Recurrence of Depression

Jennifer Gibson, PharmD — Sat, 10 Dec 2011 12:27:50 +0000

Depression is a common mental health disorder that negatively affects daily functioning and quality of life. Unfortunately, depression is often a recurrent disorder. Current treatment guidelines are based on clinical features of the disease, but new evidence points to sociodemographic and psychosocial characteristics that influence the severity and prognosis of depression. Specifically, a study published in the Canadian Medical Association Journal highlights smoking and a feeling of lack of control over one’s life as significant predictors of a negative long-term prognosis of depression.

The population-based survey evaluated nearly 600 people aged 16 or older who participated in a national health survey. The national survey included more than 17,000 participants, and the subjects in this evaluation were those who had reported a major depressive episode in the first year of the survey. The participants were followed for six years. More than half (64.5%) of the participants were women, and, at baseline, the average age of the group was approximately 39 years. Most of the participants were white (91.7%) and earned a middle to high income (81.5%). Nearly two-thirds had achieved greater than a high school education.

Over the follow-up period, slightly more than half (55.3%) of the survey population experienced repeated episodes of depression. The authors evaluated numerous physical, emotional, psychological, social, and demographic characteristics of the participants to examine their association with depressive episodes. Daily smoking and low mastery (feeling that life circumstances are beyond one’s control) were significant predictors of recurrent depression. A history of depression, which is already a well-established risk factor for future episodes of depression, was also significantly related to recurrent depressive episodes in this study. The association between risk factors and depressive episodes varied with the severity of depression.

Due to the nature of the study and the small sample size, the direction of effect and causal mechanisms are unclear. However, interventions that promote smoking cessation and increase mastery may provide positive mental health outcomes. Smoking cessation has obvious health benefits, and high levels of mastery are linked to regular physical activity, a healthy diet, decreased metabolic risk factors, and a decreased risk of death from cardiovascular factors. In fact, high levels of mastery at baseline were protective against recurrent episodes of depression in this population.

Smoking and mastery are simple and straightforward to assess in routine clinical practice. According to the authors of the current study, these novel prognostic factors may offer new avenues for treatment of depression and prevention of recurrent depressive episodes.

References

Colman I, Naicker K, Zeng Y, Ataullahjan A, Senthilselvan A, & Patten SB (2011). Predictors of long-term prognosis of depression. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 183 (17), 1969-76 PMID: 22025655

Howland RH, Wilson MG, Kornstein SG, Clayton AH, Trivedi MH, Wohlreich MM, & Fava M (2008). Factors predicting reduced antidepressant response: experience with the SNRI duloxetine in patients with major depression. Annals of clinical psychiatry : official journal of the American Academy of Clinical Psychiatrists, 20 (4), 209-18 PMID: 19034753

Katon W, Unützer J, & Russo J (2010). Major depression: the importance of clinical characteristics and treatment response to prognosis. Depression and anxiety, 27 (1), 19-26 PMID: 19798766

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Mixed Messages from Mom – Maternal Psychological Health Influences Fetal Development

Jennifer Gibson, PharmD — Mon, 05 Dec 2011 12:00:14 +0000

Pregnancy is far from a stress-free time of life. But, most mothers try their best to provide a healthy, happy placental home for nine months, knowing that anything she does to or for herself, she does to her growing fetus. The placental environment is sensitive to many foods, drinks, medications, and even activities, and the effects of many of these (think smoking and drinking) have long-term negative consequences. But, in addition to these external influences, internal factors, including psychological health and hormone levels, affect fetal development. A new study to be published in an upcoming issue of Psychological Science claims that, in fact, consistency of maternal mental health is more important in fetal outcomes than whether or not the mother is actually healthy.

The study, whose findings were published early through a press release by the Association for Psychological Science, examined how a mother’s mental state, specifically signs and symptoms of depression, influenced the development of babies, both before and after birth. Interestingly, the babies with the best developmental outcomes were those who grew in a consistent environment. That is, babies whose mothers were healthy both before and after birth and babies whose mothers were depressed both before and after birth had higher developmental scores than babies whose mothers went from healthy to depressed or depressed to healthy during or after birth.

Related studies by the same team of researchers revealed that anxiety during pregnancy, and its related fluctuations in hormones, predicts infant development and temperament. The higher the levels of cortisol, which indicate elevated levels of stress, at different points during pregnancy were significantly associated with negative reactivity and impaired adaptation to stress in infants. Maternal cortisol levels were also related to a more difficult temperament, behavioral and emotional problems, and delayed motor and cognitive development in infants. There is also evidence that cortisol levels during pregnancy result in differences in brain structures in infants.

So, what is a mom to do? Clearly, a lifetime of emotional and psychological connections to her baby begins in the womb, and unstable mental health places the child at risk for developmental, emotional, and cognitive impairment. But, so far, none of these studies have been able to prove if these connections are transient, persistent, or progressive. And, levels of stress and depression are only part of a myriad of conditions and environmental factors that influence development in offspring.

Throughout life, maternal-child interactions are dynamic and influenced by numerous internal and external factors. The current research underscores just how early these interactions start. And, it emphasizes that consistency is key. As the authors note, a cynical interpretation would be to let women who are depressed or anxious stay that way, in order to provide a consistent fetal environment. But, a more pragmatic approach would be to screen mothers-to-be before pregnancy for mental health conditions that may affect their babies later in life. And, monitoring of children at risk for psychological or developmental issues will lead to early intervention and treatment.

Maybe the bottom line is that fetuses should start preparing themselves early for a lifetime of mixed messages from mom.

References

Blair MM, Glynn LM, Sandman CA, & Davis EP (2011). Prenatal maternal anxiety and early childhood temperament. Stress (Amsterdam, Netherlands), 14 (6), 644-51 PMID: 21790468

Buitelaar JK, Huizink AC, Mulder EJ, de Medina PG, & Visser GH (2003). Prenatal stress and cognitive development and temperament in infants. Neurobiology of aging, 24 Suppl 1 PMID: 12829109

Change in mother’s mental state can influence her baby’s development before and after birth. Press release Nov. 9, 2011.

Davis EP, Glynn LM, Schetter CD, Hobel C, Chicz-Demet A, & Sandman CA (2007). Prenatal exposure to maternal depression and cortisol influences infant temperament. Journal of the American Academy of Child and Adolescent Psychiatry, 46 (6), 737-46 PMID: 17513986

Davis EP, & Sandman CA (2010). The timing of prenatal exposure to maternal cortisol and psychosocial stress is associated with human infant cognitive development. Child development, 81 (1), 131-48 PMID: 20331658

de Weerth C, van Hees Y, & Buitelaar JK (2003). Prenatal maternal cortisol levels and infant behavior during the first 5 months. Early human development, 74 (2), 139-51 PMID: 14580753

Huizink AC, Robles de Medina PG, Mulder EJ, Visser GH, & Buitelaar JK (2003). Stress during pregnancy is associated with developmental outcome in infancy. Journal of child psychology and psychiatry, and allied disciplines, 44 (6), 810-8 PMID: 12959490

Sandman CA, Davis EP, Buss C, & Glynn LM (2011). Exposure to Prenatal Psychobiological Stress Exerts Programming Influences on the Mother and Her Fetus. Neuroendocrinology PMID: 21494029

Sandman CA, Davis EP, Buss C, & Glynn LM (2011). Prenatal programming of human neurological function. International journal of peptides, 2011 PMID: 21760821

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The Concern with Self-Confidence

Jennifer Gibson, PharmD — Fri, 02 Dec 2011 12:00:23 +0000

People want to feel good about themselves. From the time children are young, they are told to believe in themselves and be confident. As they grow, children are showered with sometimes-undue praise in an effort to boost their self-esteem and self-confidence. They, in turn, learn to give themselves positive feedback and tell themselves they have done a great job. However, unrealistic self-assessments of performance do not boost self-esteem, but, instead, lead to depression, according to a study recently published in the American Psychological Association’s journal Emotion.

Researchers in the United States and Hong Kong evaluated four groups of high school and college-aged students. The groups were asked to take academic tests and then rate and compare their own performance with other students. The students also completed questionnaires to assess symptoms of depression. In two of the groups, investigators provided false feedback regarding performance to the students. That is, the high-performing students were told they had performed poorly, and the low-performing students were told they had performed well.

Across all four experimental groups, the students who rated their own performance as higher than it actually was were significantly more likely to have symptoms of depression. The authors claim that psychological distress is obvious after false self-praise because people’s inadequacies and vulnerabilities are made apparent. Students who accurately rated their own performance (both high and low performers) did not exhibit symptoms of depression.

Another conclusion of the authors is that inaccurate self-assessments prevent improvement. In this study, accurately self-rated high performers were able to recognize their strengths — arguably, an important life skill. Likewise, the self-rated low performers recognized their weaknesses and acknowledged their need to improve performance in the future — another important skill. Inaccurate self-assessments prevent this awareness, and, the authors claim, prevent low performers from acknowledging the areas in which hard work and dedication could lead to improved performance.

This study supported previous research (and common sense) that people like to hold favorable views of themselves across social and intellectual domains, and people are inaccurate judges of how their performance compares to others. In fact, the less skilled or competent people are at a given task, the more inaccurate their self-assessments. But, an objective perception of performance will improve mental well-being more than arbitrarily believing that one’s own performance is always high.

Today’s society values building up self-esteem and self-confidence. Children are not allowed to have their feelings hurt and there are no winners or losers at many youth sporting events anymore. How do these children ever grow into adults who learn to recognize their own strengths and weaknesses? Of course, children should not be belittled or disparaged, but setting unrealistic expectations of high performance does just as much damage as constant criticism of performance and abilities. Not every child will be the next major league sports star, the next rocket scientist, or the next musical or artistic genius, and setting realistic expectations early may improve their well-being and mental health.

References

Burson KA, Larrick RP, & Klayman J (2006). Skilled or unskilled, but still unaware of it: how perceptions of difficulty drive miscalibration in relative comparisons. Journal of personality and social psychology, 90 (1), 60-77 PMID: 16448310

Kim YH, & Chiu CY (2011). Emotional costs of inaccurate self-assessments: both self-effacement and self-enhancement can lead to dejection. Emotion (Washington, D.C.), 11 (5), 1096-104 PMID: 21942697

Kruger J, & Dunning D (1999). Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments. Journal of personality and social psychology, 77 (6), 1121-34 PMID: 10626367

Moore DA, & Healy PJ (2008). The trouble with overconfidence. Psychological review, 115 (2), 502-17 PMID: 18426301

Pronin E (2008). How we see ourselves and how we see others. Science (New York, N.Y.), 320 (5880), 1177-80 PMID: 18511681

Moore DA, & Small DA (2007). Error and bias in comparative judgment: on being both better and worse than we think we are. Journal of personality and social psychology, 92 (6), 972-89 PMID: 17547483

Image via Dmitry Naumov / Shutterstock.

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Silent Suffering – Nondisclosure of Depression Symptoms

Jennifer Gibson, PharmD — Sat, 26 Nov 2011 12:00:30 +0000

The lifetime prevalence of a major depressive disorder in the United States is nearly 20%. Unfortunately, many cases of depression are undiagnosed owing to nondisclosure of depression symptoms by patients. A new study evaluates the reasons for nondisclosure and emphasizes that we have a long way to go to erase the stigma associated with mental illness.

The study, published in the Annals of Family Medicine, was a follow-up survey of more than 1000 adults who had participated in a Behavioral Risk Factor Survey System. They were asked about reasons for nondisclosure of depression symptoms to their physician, as well as depression-related beliefs and demographic characteristics. Overall, 43% of the respondents reported at least one or more reasons for not disclosing symptoms of depression to their primary care physician. The most likely reason for nondisclosure was the fear that the physician would prescribe an antidepressant medication.

The reasons for nondisclosure among this sample varied according to demographic characteristics and depression history. For example, those with no history of depression were more likely to believe that depression did not fall under the purview of primary care. These individuals were also more fearful of being referred to a psychiatrist. Female gender, Hispanic ethnicity, and low socioeconomic status also predicted nondisclosure of depression symptoms.

The fact that depression symptoms are underreported and undertreated is not a new finding. Unfortunately, this is often due to the stigma associated with mental illnesses and disorders. As far as mental health treatment has come in the last few decades, most individuals have not let go of the individual stigma associated with depression and other disorders. On a population level, great strides have been achieved to reduce stigma and stereotypes associated with mental health, but, individually, many people are still willing to suffer in silence.

Concealing symptoms of depression has several consequences. The most obvious is, of course, that the depression remains untreated. However, the act of concealing symptoms also leads to decreased psychological well-being and physical health.

Interestingly, we are living in an era of social networks in which people continuously emote in public. But, these same people do not tell their physicians about legitimate psychological symptoms. A study of Facebook revealed that young adults commonly reveal symptoms consistent with depression in their displays. (Perhaps physicians need to be “friends” with their patients to truly assess their overall health and well-being.) Fortunately, many of these adults received an outpouring of support from online family and friends.

The bottom line is that people seem to not trust their physicians or the health care system enough to discuss issues that really matter. Is it the lack of time, the readiness to prescribe drugs, the stigma, or a loss of control that prevents full disclosure to primary care physicians? Essentially, the authors of the current study suggest that we still have a long way to go to make people understand what depression is and how it can be treated. Patients should be encouraged to share all symptoms — physical and psychological — with their physicians, and be an advocate for their own health.

References

Bell RA, Franks P, Duberstein PR, Epstein RM, Feldman MD, Garcia EF, & Kravitz RL (2011). Suffering in silence: reasons for not disclosing depression in primary care. Annals of family medicine, 9 (5), 439-46 PMID: 21911763

Garcia JA, & Crocker J (2008). Reasons for disclosing depression matter: the consequences of having egosystem and ecosystem goals. Social science & medicine (1982), 67 (3), 453-62 PMID: 18450349

Quinn DM, & Chaudoir SR (2009). Living with a concealable stigmatized identity: the impact of anticipated stigma, centrality, salience, and cultural stigma on psychological distress and health. Journal of personality and social psychology, 97 (4), 634-51 PMID: 19785483

Moreno MA, Jelenchick LA, Egan KG, Cox E, Young H, Gannon KE, & Becker T (2011). Feeling bad on Facebook: depression disclosures by college students on a social networking site. Depression and anxiety, 28 (6), 447-55 PMID: 21400639

Image via Krivosheev Vitaly / Shutterstock.

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Young at Heart – Depression and Cardiovascular Mortality in Young Adults

Jennifer Gibson, PharmD — Sun, 20 Nov 2011 13:07:07 +0000

Mental health and physical wellbeing are strongly interconnected. Specifically, depression is associated with increased cardiovascular morbidity and mortality, as well as an increased incidence of overweight, obesity, and type 2 diabetes. However, these links are mostly defined in older populations. For one of the first times, a new epidemiological study, published in the November issue of Archives of General Psychiatry, examines the risk of heart disease and depression in a younger age group.

The study evaluated a nationally-representative sample of nearly 8000 American adults, aged 17 to 39 years, who participated in the Third Health and Nutrition Examination Survey (NHANES III). The researchers linked the data to the National Death Index. The Diagnostic Interview Schedule assessed each participant’s history of depression and attempted suicide. At the beginning of the study, most of the participants were very healthy.

Over a follow-up period of almost 15 years, 51 participants died of cardiovascular disease (CVD), and 28 of the deaths were due to ischemic heart disease (IHD). In total, 538 participants had a history of depression, 419 reported suicide attempts, and 136 reported both.

After adjusting for multiple health and lifestyle factors, the risk of death from CVD was more than 2 times higher for people with depression than those without and more than 3 times higher for people with past suicide attempts than those with no reported attempts. The risk of death from IHD was nearly 4 times higher for people with depression, and more than 7 times higher for people with past suicide attempts.

When the researchers divided the group by gender, women with a history of depression had a 3-fold increased risk of death from CVD and a 14-fold increased risk of death from IHD. Correspondingly, men with a history of depression had 2- and 3-fold increased risks of death from CVD and IHD, respectively. However, these results were not statistically significant, likely due to the small number of events that occurred in the entire population.

The authors concluded that depression and a history of suicide attempts are significant independent predictors of heart disease mortality in young adults. This underscores previous research that suggests psychological health foretells vulnerability to heart disease. The authors suggest that clinicians must be more mindful of assessing mental health and cardiovascular health in routine practice, even among younger populations.

The findings of the study are limited by the relatively small number of events that occurred during the study period. And, the conclusions are not based on age, so mortality data may be skewed by older participants.

Still, the fact remains that depression and other mental health disorders can indicate an increased risk for heart disease. While depression is common among young adults, screening for cardiovascular health is not. Enhanced monitoring for and prevention of cardiovascular risk factors following a diagnosis of depression may be warranted, even in young populations.

References

Ludescher B, Machann J, Eschweiler GW, Thamer C, Maenz C, Hipp A, Claussen CD, & Schick F (2011). Active depression is associated with regional adiposity in the upper abdomen and the neck. International journal of psychiatry in medicine, 41 (3), 271-80 PMID: 22073766

Rubin RR, Gaussoin SA, Peyrot M, DiLillo V, Miller K, Wadden TA, West DS, Wing RR, Knowler WC, & Look AHEAD Research Group (2010). Cardiovascular disease risk factors, depression symptoms and antidepressant medicine use in the Look AHEAD (Action for Health in Diabetes) clinical trial of weight loss in diabetes. Diabetologia, 53 (8), 1581-9 PMID: 20422396

Rutledge T, Linke SE, Krantz DS, Johnson BD, Bittner V, Eastwood JA, Eteiba W, Pepine CJ, Vaccarino V, Francis J, Vido DA, & Merz CN (2009). Comorbid depression and anxiety symptoms as predictors of cardiovascular events: results from the NHLBI-sponsored Women’s Ischemia Syndrome Evaluation (WISE) study. Psychosomatic medicine, 71 (9), 958-64 PMID: 19834049

Shah AJ, Veledar E, Hong Y, Bremner JD, & Vaccarino V (2011). Depression and history of attempted suicide as risk factors for heart disease mortality in young individuals. Archives of general psychiatry, 68 (11), 1135-42 PMID: 22065529

Image via Alex Staroseltsev / Shutterstock.

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Sibling Risk of Autism

Jennifer Gibson, PharmD — Thu, 10 Nov 2011 12:00:24 +0000

The causes of and risk factors for autism spectrum disorders (ASD) are not fully understood. But, new data reports that the risk of recurrence among siblings with autism is substantially higher than previously believed.

Until recently, the risk of recurrence of ASD was estimated to be between 3% and 10% for children with a sibling diagnosed with any type of autism. Most of these studies were small and affected by selection bias or reporting limitations. A new longitudinal study published by Pediatrics is the largest study of this type to date and used a long follow-up period and prospective investigation techniques to mitigate these limitations.

For the study, the investigators enrolled 664 infants who had at least one sibling diagnosed with ASD. Six percent of the infants had more than one affected sibling. Eighty-four percent of the siblings were male. The average age of the infants at the time of enrollment was 8 months. Slightly more than half (56%) the infants were male and 40% of the infants were third-born or later in their respective families.

The study reported that nearly 19% of infants with a sibling with ASD will also be diagnosed with ASD by age 36 months, an estimate that is much higher than previously believed. Male infants were nearly 3 times as likely to develop ASD as females. Infants with multiple affected siblings were more than twice as likely to develop ASD compared to those with only one affected sibling. The risks were not affected by age at enrollment, gender or functioning level of the older sibling, or other demographic factors.

The authors conclude that these higher-than-expected rates of recurrence have implications for infant screening and genetic counseling. Pediatricians, the authors assert, should be more vigilant about screening for ASD in children with affected older siblings, and parents with children already diagnosed with ASD should be advised of the risk of recurrence if planning on having more children. However, a clear gene-based link to autism is likely a long way from being identified.

The characteristics of ASD are highly variable among children, as are the rate and severity of development. Though some risk factors and markers of future disability are present in children younger than 1 year old, identification of ASD in infants is extremely difficult. Special assessment tools specific to this population provide the best chance for early identification and intervention, which are critical to successful ASD therapy. Children at high-risk for ASD should be monitored early and often and referred for treatment at the first identification of signs of ASD.

References

Muhle R, Trentacoste SV, & Rapin I (2004). The genetics of autism. Pediatrics, 113 (5) PMID: 15121991

Ozonoff S, Young GS, Carter A, Messinger D, Yirmiya N, Zwaigenbaum L, Bryson S, Carver LJ, Constantino JN, Dobkins K, Hutman T, Iverson JM, Landa R, Rogers SJ, Sigman M, & Stone WL (2011). Recurrence Risk for Autism Spectrum Disorders: A Baby Siblings Research Consortium Study. Pediatrics PMID: 21844053

Tager-Flusberg H (2010). The origins of social impairments in autism spectrum disorder: studies of infants at risk. Neural networks : the official journal of the International Neural Network Society, 23 (8-9), 1072-6 PMID: 20800990

Yoder P, Stone WL, Walden T, & Malesa E (2009). Predicting social impairment and ASD diagnosis in younger siblings of children with autism spectrum disorder. Journal of autism and developmental disorders, 39 (10), 1381-91 PMID: 19449096

Image via ZouZou / Shutterstock.

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Is Giftedness Nothing More than Good Genes?

Jennifer Gibson, PharmD — Mon, 07 Nov 2011 12:00:04 +0000

Most people want to believe that if they work hard, and practice, practice, practice, they can be the next great musician, artist, sports star, math genius, or whatever other fill-in-the-blank talented person they aspire to be. A new article discounts that egalitarian view of success and claims that hard work alone may not lead to greatness.

In the latest installment of the nature-versus-nurture discussion, psychologists claim that practice only accounts for half the success of great performance. Certain tasks and abilities, however, are defined by genetics, they posit. You either have gifted genes, or you don’t. And, if you don’t, practice can only take you so far.

For the study, published in Current Directions in Psychological Science, researchers evaluated 57 piano players with varying levels of experience — from virtual beginners to virtuosos. Each pianist was asked to sight-read of piece of music he or she had never seen before. Scoring a point for the “nurture” side of the debate, those with more hours of practice did do better at sight-reading. But — score one for “nature” — the number of hours of practice only predicted half of the differences in performance.

Working memory capacity — the ability to store and process information simultaneously — is an important factor in learning, comprehension, reasoning, and overall intellectual capability. And, working memory capacity is substantially heritable. In this piano-playing study, working memory capacity significantly impacted sight-reading performance. The authors believe it may be due to the fact that a higher capacity influenced how many notes ahead a player could read as he or she played.

The authors do not insist that talent is all innate. Deliberate practice can overcome shortfalls or limitations in heritable or genetic abilities. But, innate intellectual ability makes a big difference in what one will be able to achieve.

Knowledge and skills acquired through experience cannot be discounted in music, sports, academics, or the arts. And, deliberate practice does predict success to some degree. Essentially, the heritable factors related to intelligence set limits to success. No causal relationship between unique genes and talent, success, or giftedness has been uncovered, and most scientists believe that a combination of innate abilities and motivation, training, and support influence the success of exceptional individuals.

So, child prodigies and successful geniuses, be thankful for what you were born with, and continue to work hard. For the rest of the population, you can still get to Carnegie Hall (or wherever else you want to go) with practice, practice, practice. You may just have to practice a little harder.

References

Ericsson KA, Krampe RT, & Heizmann S (1993). Can we create gifted people? Ciba Foundation symposium, 178 PMID: 8168368

Ericsson KA, Nandagopal K, & Roring RW (2009). Toward a science of exceptional achievement: attaining superior performance through deliberate practice. Annals of the New York Academy of Sciences, 1172, 199-217 PMID: 19743555

Hambrick, D., & Meinz, E. (2011). Limits on the Predictive Power of Domain-Specific Experience and Knowledge in Skilled Performance Current Directions in Psychological Science, 20 (5), 275-279 DOI: 10.1177/0963721411422061

Koziol LF, Budding DE, & Chidekel D (2010). Adaptation, expertise, and giftedness: towards an understanding of cortical, subcortical, and cerebellar network contributions. Cerebellum (London, England), 9 (4), 499-529 PMID: 20680539

Meinz EJ, & Hambrick DZ (2010). Deliberate practice is necessary but not sufficient to explain individual differences in piano sight-reading skill: the role of working memory capacity. Psychological science, 21 (7), 914-9 PMID: 20534780

Winner E (2000). The origins and ends of giftedness. The American psychologist, 55 (1), 159-69 PMID: 11392860

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Criminalization of HIV Exposure

Jennifer Gibson, PharmD — Sat, 05 Nov 2011 00:02:51 +0000

Approximately 1.2 million people in the United States are infected with the human immunodeficiency virus (HIV). Roughly 20% of these don’t even know they are infected. What is more startling is that nearly 100% of the people infected with HIV don’t know they might be criminals.

Preventing sexually transmitted diseases is a difficult public health challenge, and HIV prevention is no exception. The use of criminal laws to address issues of HIV transmission and exposure are examined in a recent overview of international legal issues related to HIV, published in Future Virology. The authors of the article assert that the laws are misguided public health policy and should be repealed or reformed.

As of 2010, 53 countries had HIV-specific laws that criminalized virus exposure or transmission. Many other countries use existing non-HIV-specific laws related to sexual assault to criminalize virus exposure. The laws have been used to impose harsh penalties on those who have spread the virus, but still leave many question unanswered. What is the degree of responsibility necessary to cause criminal prosecution? Is non-disclosure of HIV status really equivalent to rape, sexual assault, or the intent to cause harm? Do safe sex practices mitigate criminal sanctions?

In the US, 36 states and 5 territories have laws criminalizing HIV transmission exposure through sexual contact or intercourse. Through 2010, 36 HIV-specific laws in the US resulted in more than 350 prosecutions for HIV exposure and transmission; a high percentage of these resulted in imprisonment of the offender.

The authors of the article acknowledge that sex brings out the worst in policy-makers, and many of these laws are the result of moral judgments rather than sound scientific evidence. Criminalization of any vice, be it food, drink, or sex, rarely leads to less of it, and criminalization of HIV exposure has never been shown to prevent the spread of infection. Interestingly, HIV is not nearly as contagious as many other viruses, even sexually-transmitted ones, but in the public’s mind, the virus’s roots in homosexuality, promiscuity, drug use, and sex work earned it regulation based on fear and stigma.

There are surely cases of people infected with HIV who have malicious intent to cause harm to others, but these cases are rare. Most people living with HIV do not intend to knowingly, cruelly inflict harm on others. Human rights advocates, as represented by the authors of the current article, do not support the use of criminal laws to address HIV exposure if there is no significant risk of transmission or when reasonable measures have been taken to reduce the risk of transmission; additionally, after full disclosure of HIV status, if all parties involved consent to sexual contact, criminal intent is not supported.

The authors also claim that criminal HIV statutes undermine public health responses to HIV, making people less likely to accept HIV testing or care, since that would make them culpable in “knowingly” transmitting the virus. Ignorance is a defense in this case, it seems. Additionally, punishing or imprisoning a person infected with HIV does not prevent them from spreading the virus. Situations and living conditions in prisons actually facilitate virus transmission owing to uncontrolled and unsafe sex practices, unsafe tattooing equipment, and drug use.

The authors assert that the criminal justice system should be reserved for administering justice for the most heinous and serious of crimes against society, not improving public health. Criminalization of HIV exposure does not incapacitate criminals, rehabilitate offenders, or prevent future virus transmission. Moral judgments are getting in the way of evidenced-based policy decisions. All of the achievements in removing the stigma associated with HIV over the last 2 or 3 decades are negated by the criminalization of virus exposure. Shared responsibility for safe sex practices and improved prevention education among the most at-risk groups are needed to prevent HIV exposure, not more laws.

The CDC estimates that approximately 50,000 people are newly-infected with HIV each year in the US. What would the criminal justice system look like if each of these people could prosecute the person that infected them? Would society be safer or healthier as a result?

References

Centers for Disease Control and Prevention (CDC) (2011). HIV surveillance–United States, 1981-2008. MMWR. Morbidity and mortality weekly report, 60 (21), 689-93 PMID: 21637182

Csete, J., & Elliott, R. (2011). Criminalization of HIV transmission and exposure: in search of rights-based public health alternatives to criminal law Future Virology, 6 (8), 941-950 DOI: 10.2217/fvl.11.74

Dodds C, Bourne A, & Weait M (2009). Responses to criminal prosecutions for HIV transmission among gay men with HIV in England and Wales. Reproductive health matters, 17 (34), 135-45 PMID: 19962647

Dodds C, Hammond G, Weatherburn P, Hickson F, Keogh P, Reid D, Henderson L, & Jessup K (2008). Homosexually active men’s views on criminal prosecutions for HIV transmission are related to HIV prevention need. AIDS care, 20 (5), 509-14 PMID: 18484317

Dodds C, & Keogh P (2006). Criminal prosecutions for HIV transmission: people living with HIV respond. International journal of STD & AIDS, 17 (5), 315-8 PMID: 16643681

Mears A (2007). The criminalization of HIV transmission in England and Wales: a brief review of the issues arising. Current opinion in infectious diseases, 20 (1), 47-53 PMID: 17197881

Prejean J, Song R, Hernandez A, Ziebell R, Green T, Walker F, Lin LS, An Q, Mermin J, Lansky A, Hall HI, & HIV Incidence Surveillance Group (2011). Estimated HIV incidence in the United States, 2006-2009. PloS one, 6 (8) PMID: 21826193

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