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

Image via ostill / Shutterstock.

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Astrocytes are not electrically active in the classic way that neurons are. They were, therefore, long assumed not to play any active roles in neural signalling. However, experimental methods that allowed for the measurement of calcium release from cells, demonstrated that astrocytes communicated, not through electricity and voltage, but through calcium signalling. Calcium is involved in, but not necessarily responsible for neural signalling. By altering the calcium concentrations around a cell, the astrocytes can influence, but not initiate neural signalling. It could change the likelihood of a neuron firing, the speed at which a neuron could fire, or the size and strength of a connection between two neurons. Calcium, therefore, can add a level of sophistication in signalling to the otherwise binary code of neural processing.

In addition to playing complex roles in the brain, scientists grossly underestimated their size and reach. For many years, scientists used GFAP (glial fibrillary acidic protein), a protein known to be found on astrocytes, in order to view them under a microscope. Using GFAP, astrocytes look like stars: a cell body with processes extending into points. However, over the past decade, scientists began looking at astrocytes by injecting a dye into the cell that would stain the entire cell from the inside. These experiments showed that these initial GFAP-labelled processes actually branch into ever smaller processes, extending across a much greater area than previously seen. Astonishingly, GFAP had been labelling a mere 15% of the entire cell. The sheer extent of these cells is impressive. A single astrocyte in the human brain may have connections with as many as two million neurons. Their processes extend to every corner of the brain and spinal cord.

Astrocytes play a number of important roles in the developing, healthy, and diseased brain. They are involved in cerebral blood flow and metabolism, water transport, act as neural stem cells in neural development, and respond to damage in the brain. In addition, an increasing  number of functions for astrocytes in signalling and information processing have been proposed. Some of these new roles, such as the ability of astrocytes to release neurotransmitters, just like neurons, remain controversial. However, the sheer size and complexity of these cells suggests astrocytes form a sophisticated and interconnected network across the entire brain.

The human brain is significantly more complex than any other animal’s. And yet, other than increasing in number, neurons remain relatively similar across species, regardless of cognitive ability. Astrocytes, on the other hand, become larger, more complex, and more diverse in addition to more numerous as species go up the evolutionary chain. Could these long-underestimated cells be responsible for the complex cognitive tasks that separate the human brain from other animals?

References

Hamilton, N., & Attwell, D. (2010). Do astrocytes really exocytose neurotransmitters? Nature Reviews Neuroscience, 11 (4), 227-238 DOI: 10.1038/nrn2803

Freeman, M. (2010). Specification and Morphogenesis of Astrocytes Science, 330 (6005), 774-778 DOI: 10.1126/science.1190928

Giaume, C., Koulakoff, A., Roux, L., Holcman, D., & Rouach, N. (2010). Astroglial networks: a step further in neuroglial and gliovascular interactions Nature Reviews Neuroscience, 11 (2), 87-99 DOI: 10.1038/nrn2757

Nag S (2011). Morphology and properties of astrocytes. Methods in molecular biology (Clifton, N.J.), 686, 69-100 PMID: 21082367

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Individuals who are obese and/or with alterations of insulin homeostasis, including diabetes, are at an increased risk of developing dementia and Alzheimer’s disease. The risk of vascular dementia is increased 2 to 2.5 fold in people with type 2 diabetes, that of developing Alzheimer’s disease is 1.5 to 2 fold. The association between type 2 diabetes and Alzheimer’s disease is particularly pronounced in carriers of the apolipoprotein E epsilon 4 allele. Carriers of this allele who also have type 2 diabetes have a two-fold increased risk of developing Alzheimer’s disease compared to those who have the allele but not diabetes.

The neurocognitive effects of diabetes are most clearly visible in children and the elderly. In people with type 1 diabetes, changes are seen in the first five to seven years of life when the brain is developing. The elderly, over 65 years of age in whom the brain undergoes neurodegenerative changes are also particularly vulnerable to the neurocognitive effects of diabetes. These neurodegenerative changes include generalized brain atrophy, with larger lesions than those found in controls without diabetes, often in subcortical areas of the brain. Leukocaryosis, also known as white matter hyperintensive lesions are usually seen in people of the age of 80, but appear earlier and are more extensive in the brains of people with diabetes. MRIs often shows atrophy of the amygdala in people with diabetes. Finally patients with diabetes often have extensive amyloid plaques that are otherwise characteristic of Alzheimer’s disease.

The occurrence of amyloid plaques in the brains of people with diabetes points to a link between the pathophysiology of Alzheimer’s disease and diabetes. In patients with insulin resistance, too much insulin enters the brain. Both insulin and amyloid are metabolized by the insulin degrading enzyme (IDE). Since IDE has a much higher specificity for insulin than amyloid, the overabundance of insulin in the brain effectively blocks the clearance of amyloid and so promotes plaque formation. In summary, diabetes appears to accelerate the aging process of the brain by increasing atrophy and reducing the cognitive reserve.

So, do these pathophysiological changes in the brain lead to cognitive impairment? In people with type 1 diabetes, the reduced cognitive performance becomes apparent in childhood in the form of reduced psychomotor ability or speed, attention, memory and verbal IQ scores. The factors that most affect the intelligence of people with type 1 diabetes are age at diagnosis and glycemic control. Diagnosis before the age of 4 is associated with impaired executive skills, attention, and processing speed, most likely because the development of the brain is disrupted by the metabolic disturbance caused by diabetes. Notably, academic performance improves with better glycemic control.

In people with type 2 diabetes, the neurocognitive deficits are decreased psychomotor speed complex motor function, executive functions, memory skills, immediate and delayed recall, verbal fluency, attention, visuospatial ability. These deficits were recently assessed by Whitehead and colleagues, who tested whether neurocognitive speed or inconsistency was the better clinical marker of type 2 diabetes. Patients with type 2 diabetes performed slower and more inconsistently than the non-diabetic control subjects. In a longitudinal study, Espeland and colleagues observed the decline of cognitive function and fine motor speed. The study assessed women between the ages of 65 and 80 years, 179 with type 2 diabetes and 1984 non-diabetics. The study found a significantly accelerated of decline for verbal knowledge and verbal memory, but the use of oral diabetes medications was associated with relatively better cognitive function.

References

S Roriz-Filho J, Sá-Roriz TM, Rosset I, Camozzato AL, Santos AC, Chaves ML, Moriguti JC, & Roriz-Cruz M (2009). (Pre)diabetes, brain aging, and cognition. Biochimica et biophysica acta, 1792 (5), 432-43 PMID: 19135149

Whitehead BP, Dixon RA, Hultsch DF, & MacDonald SW (2011). Are neurocognitive speed and inconsistency similarly affected in type 2 diabetes? Journal of clinical and experimental neuropsychology, 33 (6), 647-57 PMID: 21416426

Espeland MA, Miller ME, Goveas JS, Hogan PE, Coker LH, Williamson J, Naughton M, Resnick SM, & Whisca Study Group (2011). Cognitive function and fine motor speed in older women with diabetes mellitus: results from the women’s health initiative study of cognitive aging. Journal of women’s health (2002), 20 (10), 1435-43 PMID: 21819251

Image via MARKBZ / Shutterstock.

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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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You might have cruised through classes at school, or you might have struggled and wondered how your peers managed to pass their classes so effortlessly. In the first case, perhaps you met your match at university when you found you were no longer at the top of the class. In the second, perhaps you had just spent your life assuming some people were born smarter than others. In both cases you are treating intelligence as if it were a static trait — you’re born with a fixed quantity of it, and that quantity never changes.

It’s a disheartening mindset to have. While successes are to be celebrated, failures – especially when they occur one after the other — begin to be regarded as inevitable. You might start to feel boxed in or imagine a glass ceiling is capping your intelligence while others whoosh past on a seemingly limitless supply of the stuff.

Caroline Dweck’s 2007 study has the potential to make you feel better. Her research uncovered that your performance as a student is not a function of your perceived intelligence levels. In fact, those so-called “intelligence levels” aren’t very level at all. Dweck’s research shows that those who are brought up to believe they can constantly work at developing their intelligence tend to do so, and as a result perform better in classes than those who believe there’s an upper limit on how smart they are.

The latter is characteristic of a “fixed mind-set” and you might have experienced it yourself when faced with a new task that requires some added effort on your part. It is likely to be exacerbated when an individual’s past experience has meant he or she has managed to overcome challenges easily, and without putting much work in. In the school or university scenario, this means that you may have been able to “naturally” perform well in a subject in the past, but when faced with a new, challenging task within that subject found yourself stuck. In this situation, you might find yourself confronted by thoughts of insecurity and self-doubt, and may imagine your belief in your own intelligence was unfounded. But take heart — that is simply not the case.

More likely what you are experiencing is not “stupidity” or a limited intelligence level — it’s unfamiliarity. Without the prior experience of what it’s like to actually put an effort into learning something new, you might find yourself taking a more taxing path. This path leads you to the false conclusion that if a task is too difficult to do using just your “innate” intelligence levels, you cannot do it at all. This is a disappointing misconception because the truth is that you are fully equipped with the skills to rise to the challenge — you just haven’t had to use them yet.

Consider adopting the opposite “growth mind-set.” This relatively humble intellectual state focuses on learning rather than intelligence. The adoption of such a mindset means you ask questions in class, turn to peers and professors for help when you don’t understand something, and don’t look at every new challenge as an obstacle or a hurdle. It’s an empowering mentality to cultivate, and with it you realise there is nothing holding you back from achieving what you want to achieve.

Reference

Dweck CS. The Perils and Promises of Praise. Early Intervention At Every Age. 2007;65(2):34-39.

Image via Vladimir Koletic / Shutterstock.

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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

Image via Cresta Johnson / Shutterstock.

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The BBB plays an important role in brain diseases. A tightly closed BBB prevents drugs from crossing into the brain to treat diseases. And, breakdown of this barrier has been implicated in a wide variety of neurodegenerative diseases including epilepsy, multiple sclerosis, Parkinson’s, and Alzheimer’s. Furthermore, an opening of the BBB following stroke and brain trauma appears to exacerbate damage and lead to worsened outcomes. Therefore, scientists are increasingly interested in learning how to manipulate the barrier: temporarily opening the BBB to deliver drugs to the brain, and closing it to prevent damage from diseases.

The mechanisms of BBB opening and closing are not yet fully understood. The barrier is made up of so-called tight junctions between the endothelial cells lining the blood vessels. These tight junctions are formed by a series of proteins on the outside of the cells that interlock with each other, much like a zipper, creating a seal between cells. On the brain tissue side of the BBB, astrocytes, neurons, and pericytes are able to modulate the tightness of the seal in response to a variety of conditions. BBB opening appears to play a beneficial role following disease and trauma. It may help in clearing cellular debris remaining from extensive cell death, as well as the damaging proteins that aggregate in Alzheimer’s and Huntington’s. But, in a variety of neurodegenerative disorders, a loss of tight junction proteins causes the BBB to become leaky, which has been associated with a worsening of symptoms. In some neurodegenerative disorders such as stroke and multiple sclerosis, it appears that BBB opening also allows immune cells from the rest of the body into the brain, and these cells exacerbate the damage by attacking healthy cells. As with many complex responses to damage in the brain, it seems likely that a small opening is helpful, but a prolonged, chronic opening is detrimental.

Due to its complexity, research on the BBB is technically difficult. However, scientists are beginning to understand the complex role this structure plays and how its opening and closing may be manipulated. There are a number of therapies currently in development that utilize this greater understanding of the BBB. Therapies targeting the BBB present an exciting opportunity to develop novel and unique therapies to treat brain disorders by temporarily opening a closed BBB to deliver drugs to the brain and closing an open BBB to prevent further damage.

References

Neuwelt, E., Bauer, B., Fahlke, C., Fricker, G., Iadecola, C., Janigro, D., Leybaert, L., Molnár, Z., O’Donnell, M., Povlishock, J., Saunders, N., Sharp, F., Stanimirovic, D., Watts, R., & Drewes, L. (2011). Engaging neuroscience to advance translational research in brain barrier biology Nature Reviews Neuroscience, 12 (3), 169-182 DOI: 10.1038/nrn2995

Zlokovic, B. (2011). Neurovascular pathways to neurodegeneration in Alzheimer’s disease and other disorders Nature Reviews Neuroscience DOI: 10.1038/nrn3114

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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

Image via Chepko Danil Vitalevich / Shutterstock.

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To understand why emerging research about the diagnosis of binge eating disorder (BED) is increasingly being recognized in the psychiatric community, it is first critical to understand the behavioral phenomenon that is BED. Because of its close relationship to the better-understood (or at least more widely researched) condition of bulimia nervosa, it might be more effective for the purpose of an overview to describe how BED is distinguishable from bulimia. There appear to be notable differences that compel researchers to more thoroughly explore BED since it is closely linked to a pervasive issue in the US that doesn’t seem to be going anywhere anytime soon — obesity.

Though they examined slightly different diagnostic nuances, in recent years, research groups led by Striegel-Moore and Barry both compared women meeting criteria for purging bulimia nervosa and for BED. According to authors, data supports the view that BED is a disorder distinct from purging bulimia. Barry and colleagues found that there were some similarities between the groups (for example, body dissatisfaction) but that the significant differences noticed between women with bulimia and BED were associated with obesity status. Women with the BED were overwhelmingly found to be medically obese (having a body mass index of greater than thirty) compared with those women with bulimia. Also, bulimia sufferers scored higher on five personality disorder scales than BED patients.

Additionally distinguishing the two eating disorders involving binge-eating behaviors, a study was conducted comparing two community-based cohorts of young woman — one with bulimia and the other with BED — over a five-year period. At the five-year follow-up, the majority of women with BED had made a full recovery despite not having received any formalized treatment while results were much less promising for the group with bulimia. The study suggests an interestingly temporary component to BED.

The implications? To highlight a few: many statistically “normal” folks are affected by BED. In the US, the CDC reported in 2008 that 33.9% of adults age 20 years and over who are obese. In the general population, the prevalence of BED is between 1-3%. However, the prevalence of BED amongst obese individuals as well as in patients seeking help for weight loss is staggeringly greater (>25%). Therefore, the likelihood that those reading this article know someone meeting criteria for BED at some point in their life cycle is fairly great.

As for treatment, Charles Pull with the Department of Neuroscience at Luxembourg Hospital summarizes an in-depth examination of literature by suggesting that a combination of pharmacotherapy with psychotherapy is most efficacious in treating the disorder. He is clear, however, that more needs to be known to better determine appropriate treatment course.

If such a significant number of individuals in the US are touched by BED, that alone may be reason to better understand (and therefore further research) the disorder. What recent research is beginning to more firmly contribute regarding the previously less-understood of the eating disorders is that BED may largely be determined by genetic factors, racial and ethnic influences, and personality/character traits. If we continue to look at the factors that cause BED, along with effective ways to treat the disorder, we may well be on our way to addressing the elephant in the room in American culture –- obesity — in more substantive ways.

References

Barry DT, Grilo CM, & Masheb RM (2003). Comparison of patients with bulimia nervosa, obese patients with binge eating disorder, and nonobese patients with binge eating disorder. The Journal of nervous and mental disease, 191 (9), 589-94 PMID: 14504568

Brewerton T. Binge Eating Disorder: Recognition, Diagnosis, and Treatment. Medscape Psychiatry & Mental Health eJournal, 1997;2(3).

CDC. Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1960–1962 Through 2007–2008. Division of Health and Nutrition Examination Surveys, 2010.

Pull CB. Binge Eating Disorder. Current Opinion in Psychiatry, 2004;17(1).

Striegel-Moore RH, & Franko DL (2003). Epidemiology of binge eating disorder. The International journal of eating disorders, 34 Suppl PMID: 12900983

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The literature on the addictive properties is still rather sparse and replication of the existing studies would be beneficial. A preclinical study in rodents demonstrated that salv A produced a decrease in dopamine and dopamine transmission, the endogenous neurotransmitter associated with addiction, and no effect on locomotor activity (a common test for the stimulant effects of a drug). These depressive effects would seem to be contrary to the notion of salv A being an addictive drug. Furthermore, these effects may lend value to salv A and its analogs as potential pharmacotherapeutics for neuropsychiatric conditions including addiction and mood disorders.

Other studies have demonstrated the opposite effect, where low doses of salv A increase dopamine efflux, produce a conditioned place preference, and rats examined during intracerebroventricular self-administration will self-infuse the drug. The latter two tests are common preclinical assessments of the rewarding properties associated with a drug. There exists a discrepancy in the literature on whether salv A will substitute for LSD in rodent studies using drug discrimination. On such study in rodents demonstrated that salv A and LSD share similar stimulus properties which is contrary to previous reports.

Recently a controlled behavioral pharmacology investigation was conducted in humans to assess the physiological and subjective effects of salv A. It showed that salv A does not induce changes in blood pressure or heart rate although its subjective effects are similar to other hallucinogenic drugs. Given that salv A produces hallucinogenic effects similar to other known scheduled hallucinogens careful consideration needs to be given to legality of this substance.

References

Braida D, Limonta V, Capurro V, Fadda P, Rubino T, Mascia P, Zani A, Gori E, Fratta W, Parolaro D, & Sala M (2008). Involvement of kappa-opioid and endocannabinoid system on Salvinorin A-induced reward. Biological psychiatry, 63 (3), 286-92 PMID: 17920565

Carlezon WA Jr, Béguin C, DiNieri JA, Baumann MH, Richards MR, Todtenkopf MS, Rothman RB, Ma Z, Lee DY, & Cohen BM (2006). Depressive-like effects of the kappa-opioid receptor agonist salvinorin A on behavior and neurochemistry in rats. The Journal of pharmacology and experimental therapeutics, 316 (1), 440-7 PMID: 16223871

Gehrke BJ, Chefer VI, & Shippenberg TS (2008). Effects of acute and repeated administration of salvinorin A on dopamine function in the rat dorsal striatum. Psychopharmacology, 197 (3), 509-17 PMID: 18246329

Johnson, M., MacLean, K., Reissig, C., Prisinzano, T., & Griffiths, R. (2011). Human psychopharmacology and dose-effects of salvinorin A, a kappa opioid agonist hallucinogen present in the plant Salvia divinorum Drug and Alcohol Dependence, 115 (1-2), 150-155 DOI: 10.1016/j.drugalcdep.2010.11.005

Peet, M., & Baker, L. (2011). Salvinorin B derivatives, EOM-Sal B and MOM-Sal B, produce stimulus generalization in male Sprague-Dawley rats trained to discriminate salvinorin A Behavioural Pharmacology, 22 (5 and 6), 450-457 DOI: 10.1097/FBP.0b013e328349fc1b

Drug Enforcement Administration. SALVIA DIVINORUM AND SALVINORIN A (Street Names: Maria Pastora, Sage of the Seers,
Diviner’s Sage, Salvia, Sally-D, Magic Mint). December 2010.

Image via Doug Stacey / Shutterstock.

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Microglia, it turns out, actually play an important role in keeping the brain healthy. Improved microscopy has been able to show that while these cells appear to be “resting”, they, in fact, have very fine processes extending out from the cell bodies constantly searching the brain for damage. It has been estimated that every few hours the entire human brain has been checked for health. Like a sentry in a watchtower, in order to stay in this surveillance state microglia require a constant, “all is well,” signal from the surrounding cells. If they fail to receive this signal, the microglia jump into action to investigate the problem.

If damage has occurred, microglia are also capable of a sophisticated range of responses depending on the level of damage. If the damage is small, cells can send out a “find me” signal. The microglia are activated to a protective state and seek out these cells. They attempt to stabilise the damage and protect the nearby neurons. However, if the damage is greater or more dangerous to surrounding tissue, these cells will send out an “eat me” signal. The microglia then become fully activated to a toxic state. They can kill infected cells before infection spreads and clear any debris from damaged or dying cells.

Microglia thus must effectively decide whether to protect or destroy cells in response to insults. Unfortunately, as the brain ages, these cells seem to become less efficient at reacting. The same signal that induces microglia to a protective state in a young brain may induce a fully activated, toxic state in an older brain. It appears that in older brains, microglia overreact to damage and disease. Instead of protecting brain tissue from further damage, they aggravate the problem by becoming fully activated and attacking healthy brain cells.

Microglia are, therefore, a very interesting target for therapies for all neurodegenerative diseases such as Parkinson’s Disease, Alzheimers Disease, multiple sclerosis, stroke, and so on. The goal of many scientists is now to differentiate the types of signals that control the states of activation of microglia and exploit these in creating new drugs. While calming the microglia into a protective state will not cure the underlying neurodegenerative disorders, it could slow the damage and disease progression. This may even help the brain repair some of the damage, recover lost tissue, and ease the symptoms of these diseases.

References

Kettenmann, H., Hanisch, U., Noda, M., & Verkhratsky, A. (2011). Physiology of Microglia Physiological Reviews, 91 (2), 461-553 DOI: 10.1152/physrev.00011.2010

Nimmerjahn, A. (2005). Resting Microglial Cells Are Highly Dynamic Surveillants of Brain Parenchyma in Vivo Science, 308 (5726), 1314-1318 DOI: 10.1126/science.1110647

Hanisch, U., & Kettenmann, H. (2007). Microglia: active sensor and versatile effector cells in the normal and pathologic brain Nature Neuroscience, 10 (11), 1387-1394 DOI: 10.1038/nn1997

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So support for caregivers of family members should not be targeted solely to those who provide care to family members with dementia; caregivers of family members without dementia but other illness and impairments suffer as well. A variety of support services are available to caregivers though, including local support groups, magazines, newsletters, and conferences.

Many family caregivers must work for pay outside the home and/or care for their children. These responsibilities, in addition to family caregiving, can leave little time for caregivers to pay heed to their own health and well-being, with consequences that impair their ability to sleep, exercise, and cook healthy meals.

Intensive family caregiving can also mean the caregiver decreases his/her work hours, resulting in lost wages. And as we learned above, the emotional consequences of caregiving include depression, as well as anxiety. Depression, not surprisingly, tend to be especially high in caregivers of family members with dementia who are also accusative, suspicious, and/or wander away from home.

So does personality play a role in the stress of caregiving? Yes.

The consequences associated with being a caregiver are related to caregivers’ personalities. Caregivers who are extraverted and conscientious tend to show more signs of physical health and mental health, whereas caregivers who are Neurotic tend to show worse signs of physical health and mental health.

And when asked to report on their own physical health and mental health, caregivers who are open and agreeable tend to report the highest levels. Depression in particular is worse for neurotic caregivers, and least problematic for extraverted caregivers. So personality is clearly associated with the strain of being a family caregiver.

Yet these findings are based on correlational research, so it isn’t clear if personality traits cause health outcomes, health outcomes cause or at least magnify personality traits, or some other third variable, such as a person’s coping style, contributes to both health outcomes and personality. More experimental research is needed to determine such.

There is some longitudinal research on coping styles though, as they relate to caregivers’ personality traits and anxiety levels. Anxiety levels are related to the ways in which caregivers cope with the seemingly endless burdens placed upon them by the needs of an ill or impaired family member. Coping strategies take many forms, and three common types are described below:

• Emotion-Focused (e.g., social support, humor, and finding meaning in the situation)
• Problem-Focused (e.g., help from others, advice, and planning)
• Dysfunctional (e.g., venting, denial, and substance abuse)

Problem-focused coping helps individuals feel in control of a stressful situation, but unfortunately, research indicates that Neurotic caregivers are less likely to engage in this type of coping strategy. And longitudinal research reveals that anxiety does not escalate over time for caregivers who use positive emotion-focused coping strategies, which is also used infrequently by Neurotic caregivers.

So caregivers may wish to change the way they cope with the stressors of caring for a loved one, for the sake of the family member’s well-being, as well as their own.

References

Chappell NL, & Dujela C (2009). Caregivers–who copes how? International journal of aging & human development, 69 (3), 221-44 PMID: 20041567

Cooper, C., Katona, C., Orrell, M., & Livingston, G. (2008). Coping strategies, anxiety and depression in caregivers of people with Alzheimer’s disease International Journal of Geriatric Psychiatry, 23 (9), 929-936 DOI: 10.1002/gps.2007

Fisher, G., Franks, M., Plassman, B., Brown, S., Potter, G., Llewellyn, D., Rogers, M., & Langa, K. (2011). Caring for Individuals with Dementia and Cognitive Impairment, Not Dementia: Findings from the Aging, Demographics, and Memory Study Journal of the American Geriatrics Society, 59 (3), 488-494 DOI: 10.1111/j.1532-5415.2010.03304.x

Gaugler, J., Kane, R., Kane, R., & Newcomer, R. (2005). The Longitudinal Effects of Early Behavior Problems in the Dementia Caregiving Career. Psychology and Aging, 20 (1), 100-116 DOI: 10.1037/0882-7974.20.1.100

Löckenhoff, C., Duberstein, P., Friedman, B., & Costa, P. (2011). Five-factor personality traits and subjective health among caregivers: The role of caregiver strain and self-efficacy. Psychology and Aging, 26 (3), 592-604 DOI: 10.1037/a0022209

Melo, G., Maroco, J., & de Mendonça, A. (2011). Influence of personality on caregiver’s burden, depression and distress related to the BPSD International Journal of Geriatric Psychiatry, 26 (12), 1275-1282 DOI: 10.1002/gps.2677

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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.

Image via kwest / Shutterstock.

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If both the past and the external world exist only in the mind, and if the mind is controllable – what then?
— George Orwell, in 1984

The concept of brainwashing was first used to describe certain obscure procedures carried out in early Communist China, but the idea of “cleansing the mind” can be traced back all the way to fourth century Confucian thinkers.

In Popular Western culture, the word immediately evokes George Orwell’s dystopian novel 1984 and experiments by Nazi scientists and the CIA, as well as Soviet intelligence services. Science’s interest in the possibility of controlling the mind dates back some 20 years before Orwell’s publication of his novel. The first published research on the subject was Chaffee and Light’s A Method for Remote Control of Electrical Stimulation of the Nervous System from 1934. The article recounted experiments carried out on animals using brain implants and electric waves to control brain and motor functions, including getting a monkey to sleep or inducing gastric secretions in a dog.

Electromagnetic Control (EMR)

In 1964, electromagnetic-response researcher Dr. José Delgado from Cordoba, Spain, performed one of the most spectacular public acts of thought control ever, climbing into a bullring and halting the bull in its tracks by pushing a button that controlled an electrode implanted in his brain.

In the US, research on EMR techniques was largely carried out under the wing of the CIA, and the information was classified as top secret for several decades. However, in the 1990s, the US military admitted having worked on developing EMR weapons. When the USSR’s system collapsed, Russian “mind control” research was exposed. Named acoustic psycho-correction, the Russian research program involved developing the capability to control minds and alter behavior through the transmission of:

specific commands via static or white noise bands into the human subconscious without upsetting other intellectual functions.

MK-ULTRA

Within the CIA’s program MK-ULTRA, the infamous Dr. Ewen Cameron used electro-shock therapy, LSD and other psychotropic drugs and various forms of psychological torture on children and adults, trying to de-program the brain in order to re-program it with new information. The aims of these experiments were varied, including the extraction of information from spies and war prisoners and the programming of individuals to carry out counter-espionage missions and attacks, without their consent.

MK-ULTRA was proven to have performed all sorts of damaging tests and experiments on humans without their consent, with devastating effects for their lives, in many cases, including death and suicide.

Weapons Targeting the Brain

As early as 1994, Dr. Barbara Hatch Rosenberg referred to non-lethal weapons in the Bulletin of the Atomic Scientists:

Many of the non-lethal weapons under consideration utilize infrasound or electromagnetic energy (including lasers, microwave, or radio-frequency radiation, or visible light pulsed at brain-wave frequency) for their effects. These weapons are said to cause temporary or permanent blinding, interference with mental processes, modification of behavior and emotional response, seizures,severe pain, dizziness, nausea and diarrhea, or disruption of internal organ functions in various other ways… The current surge of interest in electromagnetic and similar technologies makes the adoption of a protocol explicitly outlawing the use of these dehumanizing weapons an urgent matter.

According to the latest issue of Synesis, which was entirely devoted to Neurotechnology in National Security, Intelligence and Defense, drugs that can be useful in combat or special operations include:

• cognitive and motor stimulants
• somnolent agents
• mood altering agents, some of which can induce paranoia in larger doses
• “affiliative” agents
• convulsants

The review of the current military implications of neurotechnology goes on to affirm that,

while some of these agents can be used to enhance the neuro-cognitive and motor performance of (one’s own) troops (e.g., low does of stimulants, mood altering drugs, etc), others have apparent utility against hostile forces (e.g., somnolent, psychotogenic, af? liative, and convulsant agents).

With the first of these objectives in mind, the US military implemented the Comprehensive Soldier Fitness program earlier this year, which uses cognitive behavioral principles, instead of drugs, to “better prepare” soldiers and families for war. Although this type of “programming” is seen as a less harmful form of mind control, the program has also encountered many detractors.

The Smirnov Way

In 2007, the US Department of Homeland Security closed a deal with Moscow’s Psychotechnology Research Institute. Now run by his widow, Professor Russalkina, the institute’s achievements were largely the work of Dr. Igor Smirnov.

Using electroencephalography (EEG), Smirnov had measured brain waves to create a map of the subconscious. Later, he used recorded subliminal messages to physically alter that landscape by means of the power of suggestion. Some of Smirnov’s reported experiments include using visual and aural subliminal messages to re-program a drug addict to become more interested in the upcoming birth of his son than in securing his next dose of heroin.

The Homeland Security Department became more interested in the Institute’s work on account of their Semantic Stimuli Response Measurements Technology (SSRM) Tek project. This is a software-based “mind reading” technology which tests a subject’s involuntary responses to subliminal messages. The idea is to use it, for example, at airport screening posts, flashing subliminal images, such as photos of Bin Laden and the World Trade Center, as part of an innocent videogame. Passengers’ involuntary responses are said to be different for regular people and those plotting a terrorist attack.

Although there are companies working on further research and the practical implementation of SSRM Tek, such as Canada’s NORTHAM Psychotechnologies, it hasn´t been used for mass-screening at airports as yet.

The Future

Ever since tetraplegic patient Matthew Nagle was able to control a cursor with his brain, through neural implants in 2004, it would seem logical that the reverse processes of having external agents controlling the mind should no longer be the stuff of science fiction.

In a way, knowing everything that was achieved scientifically in terms of thought control and brain programming as early as the 1950′s and 60′s, many people wonder that very little progress has been made since Dr. Cameron’s times. However, one can naturally assume that the problem has much more to do with the secrecy of military programs than with a slow scientific development.

The ethical questions are, of course, the central issue here. While Dr. Smirnov claimed that he had often refused offers by Russian mob types to help them tweak reluctant business associates’ wills; many researchers have historically had no problem selling their information to the highest bidder.

In fact, the ethical problems associated with this type of research today have more to do with where the financing can come from. Although techniques that might permit control over the human brain’s reactions might be extremely beneficial to treat certain chronic psychiatric conditions, it has been largely military and intelligence services that have been willing to fund this research with a very different agenda altogether. Scientists are faced with the difficult choice between working for government organizations, knowing full well what their research will be used for, or cutting down their experiments, for lack of funding.

Today, the horrifying landscapes that Orwell imagined are all scientifically plausible — the thought police might be implemented and thought crime might be discovered by scanning a subject’s brain; there is no scientific impediment for all that. The question lies simply with who has access to the technology and what are they prepared to use it for.

References

Taylor, K. (2004). Brainwashing: the science of thought control. Oxford, Oxford University Press.

Hatch Rosenberg, B. “Non-lethal” weapons may violate treaties. Bulletin of the Atomic Scientists. 1994;(50)5:44.

Giordano, J, Wurzman, R. Neurotechnologies as weapons in national intelligence and defense – an overview Synesis [PDF], 2011.

Chomsky, N. (1989). Necessary illusions: Thought control in democratic societies. Toronto,
Canada: CBS Enterprises.

Schell BH (1994). The ominous shadow of the CIA has imprinted itself on the brain research community. The journal of the California Alliance for the Mentally Ill, 5 (1), 38-40 PMID: 11653317

Moreno, J.D. (2000) Undue risk: secret state experiments on humans. New York: W.H. Freeman and Co.

Image via Justin Huang / Shutterstock.

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At one point or another, we’ve all been on the receiving end of a poor or ill-fitting gift. How did you react to it? Or, more importantly, what did it mean to you in terms of your relationship with the giver? A study in recent years has explored exactly how men and women react upon receiving good and bad gifts.

A paper published in Social Cognition by Elizabeth Dunn and colleagues at the University of British Columbia explored the theory that while “good” gifts would reaffirm similarity between couples, poor gift-giving may cause partners to question their compatibility.

In the first experiment, participants met and chatted with a person of the opposite sex for four minutes. Afterward, they were instructed to select a gift for their new friend from a list of gift cards for various restaurants and stores. Would each participant evaluate their similarity to the person based on the gift they received?

Beforehand, each participant had ranked the gifts in the order in which they would personally prefer to receive them; the experimenter then used this information to persuade the participants when it came to gift-selecting. As a result, half of the participants chose their friend’s top choice, while the other half selected their friend’s second-to-last choice. Basically: half got what they wanted, and half did not.

Men who received the gifts they desired perceived themselves as more similar to their partner than those who did not. Women, however, seemed relatively unaffected by the appropriateness of the gift.

Dunn and colleagues performed a follow-up experiment, this time with men and women already in heterosexual relationships. Again, men who received poor gifts perceived less similarity to their partner. When asked how long they expected their relationship to last, those men predicted a shorter future with their girlfriend.

In an unexpected twist, women who received the poor gift from their boyfriend actually perceivedmore similarity with them, and predicted their relationship to last longer compared those women who received the good gift.

Dunn reason that perhaps the more “threatened” women feel in a relationship (in this case, internal conflict from receiving the poor gift), the more they try to protect against it. With the new relationship (experiment #1), there was not much to protect, hence the indifference to their partner. When, however, there is a substantial relationship to guard (experiment #2), women are more motivated to remedy the situation. Men did not display this effort, simply stating that they did not like the gift — and, by extension — their partner.

So the moral of the story is: if you want to stick with your honey, gift a woman a sock and a man their favorite Rolex. (Just kidding. Don’t. Seriously…don’t.)

References

Dunn, E., Huntsinger, J., Lun, J., & Sinclair, S. (2008). The Gift of Similarity: How Good and Bad Gifts Influence Relationships Social Cognition, 26 (4), 469-481 DOI: 10.1521/soco.2008.26.4.469

Image via Yelloj / Shutterstock.

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