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Saturday, 30 June 2018
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Thursday, 28 June 2018
Asperger’s Syndrome: Hallmark of Genius, or Just Another Form of Autism?
Isaac Newton, Albert Einstein, Charles Darwin—what unites these three exceptional individuals? It is widely accepted that all three were geniuses, but there is something else. These days, neuroscientists believe that all three suffered from a specific neurological disorder called Asperger’s syndrome.
The whole definition of the term “neurological disorder” implies that something is going wrong in the brain. However, there is a growing recognition of the fact that when it comes to the processes in our brain, “going wrong” does not necessarily mean “going bad”. Our brain is too complicated a mechanism to be interpreted in simplistic terms. Some neurological disorders produce a peculiar state of mind often associated with high artistic and scientific achievements.
Asperger’s Syndrome (AS) is a developmental and neurological disorder that is often associated with symptoms of social withdrawal, motor clumsiness, and impaired communication skills. The Diagnostic and Statistical Manual of Mental disorders (DSM-5) classified AS in the same category as Autism Spectrum Disorder (ASD). It is often referred to as ‘High-functioning’ Autism (HFA), as individuals with AS are more intellectually capable and show less severe abnormalities compared to ASD subjects.
The story of AS and autism started in the 1940s, when two Viennese Scientists, Leo Kanner and Hans Asperger, described a syndrome observed in some children, with the unique characteristics of social isolation, impaired communication skills, and restrictive and obsessive interests. Both scientists used the term ‘autistic’ in their reports. While Kanner’s syndrome was published right away in 1943, Asperger’s report was written in German and remained undiscovered until 1991 when it reappeared in Uta Frith’s textbook Autism and AS.
Research and publications on Asperger’s syndrome reached its peak during 2000-2012. Different research groups proposed a set of criteria for AS diagnosis. While several of these criteria were overlapping, WHO’s International Classification of Diseases and Disorders set the following key characteristics that can be diagnostic for Asperger’s Syndrome:
- Qualitative social impairment involving dysfunctional social adaptivity, impaired non-verbal communication for interaction and lack of social reciprocity.
- Restrictive pattern of interest, motor clumsiness, repetitive behavior, and extreme obsessiveness to specific rituals.
- AS patients must show age-specific, normal cognitive and linguistic development.
Interestingly, the father of Asperger Syndrome, Hans Asperger, described AS patients to be characteristically distinct from ASD subjects. He characterized them as intellectually-able, abstract-loving, and even overachieving in some specific cognitive domains.
Decades after Asperger’s observation, recent studies have also found that AS patients often demonstrate high verbal IQ, strong grammatical skills and they often outperform others in fluid reasoning although they are reported to show a delayed reaction time with poor performance IQ, specifically in symbol coding and processing speed.
Surprisingly, AS is more common than classical autism. Epidemiological surveys report that about 4 out of every 10,000 children are autistic whereas about 25 out of 10,000 children are diagnosed with AS. AS is more common in boys than girls. No scientific explanation behind this observation exists at present.
Like with many other syndromes, no single specific cause is responsible for AS. Rather, a milieu of factors is associated with its development.
Children diagnosed with AS show a genetic pattern, like in autism, where at least one of the parents (most often the father) is diagnosed with AS or at least have some hallmark AS characteristics. The relatives of AS children are known to have anxiety or depression related disorders.
An important causal factor behind the development of AS might be the altered level of neurotransmitters. In AS patients, higher levels of N-Acetyl Aspartate/Choline (precursor of acetylcholine) intake and increased dopamine levels were reported, suggesting an overall altered dopaminergic neurotransmitter composition in major areas of the brain. Intranasal injection of oxytocin, a neuropeptide, was shown to improve facial emotion recognition abilities in AS patients.
Apart from alterations in neurotransmitter levels, neuroimaging studies show that there are structural changes in major areas of the brain that could be associated with the development of Asperger’s Syndrome. Altered grey and white matter volumes were observed in major brain regions, and an abnormal thickness of the hippocampus, amygdala, and anterior cingulate cortex was reported to be the major contributing factor for dysregulated cognitive functions in AS.
Some researchers also proposed that environmental factors can contribute indirectly to the development of AS. Viral or bacterial infection and smoking during pregnancy particularly increases the risk factor, although no concrete evidence supporting these views was found.
Due to the substantial number of overlapping similarities between Asperger’s Syndrome and Autism, it is very easy to confuse one with the other.
Studies in recent decades showed differences between AS and ASD on both quantitative and qualitative levels. The AS subjects displayed age-specific or earlier verbal development, meticulous speech ability, higher desire for social reciprocation, and supreme imagination compared to ASD patients.
On a cognitive level, AS subjects are more perceptive, they possess superior verbal performance and visual-spatial ability compared to ASD patients.
But the major limitations of these studies is the huge variability within the study groups and contradictions in the data patterns, as with age, the distinction between AS and ASD significantly reduces. It is particularly difficult to categorize AS from other disorders as there are no known biomarkers specific to AS only.
As there is not sufficient evidence of distinguishable characteristics for AS that can class the syndrome as ‘one biologically and clinically diagnosed entity’, the DSM-V in 2013 revised and categorized Asperger’s Syndrome as another variant of ASD. Although this decision was criticized by the scientific community, most of the researchers agreed that there is a need to conduct more studies that could help in distinguishing AS from other ASDs.
The most general misconception about Asperger’s syndrome or, as a matter of fact, about autism spectrum disorders in general, is that they develop because of poor parenting and a lack of bonding between parents and their child. This concept was even termed as ‘Refrigerator Mother’ to describe cold and distant parenting. But this notion was challenged from the 1960’s when research on these neurological disorders started to grow and scientists found that it is not parenting, but rather the genetic and neurological makeup of the child that is responsible for these syndromes. Even today, the belief that neurodevelopmental disorders are caused by a traumatic childhood are common. The reality, however, is more complicated than our guesses based on limited information.
References
Barahona-Correa, J. B. and C. N. Filipe (2015) A Concise History of Asperger Syndrome: The Short Reign of a Troublesome Diagnosis. Front Psychol 6: 2024. doi: 10.3389/fpsyg.2015.02024
Faridi, F. and R. Khosrowabadi (2017) Behavioral, Cognitive and Neural Markers of Asperger Syndrome. Basic Clin Neurosci 8(5): 349-359. doi: 10.18869/nirp.bcn.8.5.349
Weiss, E. M., B. Gschaidbauer, et al. (2017) Age-related differences in inhibitory control and memory updating in boys with Asperger syndrome. Eur Arch Psychiatry Clin Neurosci 267(7): 651-659. doi: 10.1007/s00406-016-0756-8
Image via BarbaraALane/Pixabay.
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Wednesday, 27 June 2018
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Tuesday, 26 June 2018
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Monday, 25 June 2018
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The 5 Second Rule: Task Initiation
The title—The 5 Second Rule: Transform Your Life, Work, and Confidence with Everyday Courage—intrigued me.
According to the publisher, Mel Robbins’s self-help book is “based on a simple psychological tool that the author developed to motivate herself. Using a technique that involves counting down backwards from five to one, she gave herself the extra push she needed to complete dreaded tasks, become more productive.”
Could this technique help solve my task-initiation problem?
I am a brain injury survivor. I have clusters of thin-walled blood vessels in my brain. Two of them bled. To prevent additional bleeds, I underwent brain surgeries, which left me with a number of challenging symptoms, including difficulties initiating tasks.
Though similar to procrastination in its end result, brain injury-related issues with task initiation feel very different. I am fully aware when I procrastinate, and I often laugh at myself in the process. When I procrastinate, I make conscious choices. Instead of working on the annual report, I choose to do the laundry, edit an essay, or take my dog for a walk. And when I run out of excuses or get too close to the deadline, I get started.
Trouble initiating tasks is more akin to the difficulty of shifting to a new undertaking after completing a long and involved project, when it feels almost impossible to switch to the next activity.
I usually have no idea that I’m having trouble initiating a task. I know with absolute certainty that I will get to the task—just not right now. In my mind, starting isn’t an issue, because this internal conviction that “of course I’ll do it” is so strong. It’s as if there’s a disconnect between the belief that I’ll do the task and the cognitive action required to actually initiate it. I’m not choosing to distract myself, and I’m not trying to postpone the inevitable. There’s simply no conscious awareness and no control over it.
Compounding the challenge is that brain injury-related task initiation problems don’t follow any recognizable pattern. They arise without warning and are frequently unrelated to the nature of the task, interfering equally with tasks I enjoy and those I’d rather avoid. They can last anywhere from several days to several years. They often end abruptly, for no apparent reason. When my brain releases me, I’m off and running, all signs of struggle gone, as if the problem never existed.
To combat my difficulties beginning an activity, my neuropsychologist suggested I keep a daily list and block off chunks of time in my calendar to work on those tasks. Fortunately, my brain injury brought on a level of rigidity—once an item is on that list, I feel compelled to address it.
Alas, identifying problematic tasks to include on the list is not straightforward, because the same “I know I’ll get to it” belief means there’s no problem, and it doesn’t occur to me that it belongs on the list. And I sometimes can’t initiate writing the list—I know I’ll write it, just not right now.
I’d recently been having trouble beginning a new essay on a topic I wanted to explore. It had been simmering in my mind for a while, and I felt ready to begin writing. But I couldn’t. I tried tricking my brain into cooperating by breaking the task into smaller and hopefully more manageable chunks.
I was able to sit down in front of my computer, but my brain refused to attempt the next task. Later, I managed to open a new file, but my mind wouldn’t move beyond that chunk. I left the file open, knowing I’d get to it (just not now). A few days later, I typed a title, but couldn’t start the body of the essay. I knew exactly how I wanted it to begin. The words were there. But I wasn’t.
Galvanized into action by Robbins’ five second rule, I was determined to try it the next morning.
As I finished getting dressed, I thought about working on the essay. “5-4-3-2-1” and there I was, at my computer, tapping away, the essay taking form just as I’d imagined it.
Every time my inner voice suggested I needed to take a breather, before I had time to question my motive, I applied the five second rule. “5-4-3-2-1” and I was back on track. After finishing a first draft, I wondered about working on another troublesome essay. Five seconds later, I was back at the keyboard. Feeling like I was on a roll and afraid that I’d fall prey to my damaged brain if I paused, I moved on to sending email queries about speaking engagements and book events.
The next problematic item that came to mind gave me pause—I needed to grade a pile of essays. This time, the five second rule failed, because common sense kicked in. I had reached my limit—fatigue overwhelmed me and my brain blanked out. I absolutely had to rest, or I’d be in no shape to do anything.
I came away from that day feeling good about myself. I’d been more productive than I’d been in a long time. But I was also exhausted. Applying the five second rule had thoroughly drained me.
I have since realized that the five second rule doesn’t work for me exactly the way Mel Robbins explained it. I haven’t abandoned it, but as with so many other things post-injury, I am learning to adapt it to my particular circumstances. I have to pace myself, and as soon as I recognize the early signs of fatigue, I use the rule to take a nap.
My conclusion?
The five second rule rules.
References
Robbins, M. (2017). The 5 Second Rule: Transform your Life, Work, and Confidence with Everyday Courage. Savio Republic. ISBN-10: 1682612384
Image via JESHOOTScom/Pixabay.
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Saturday, 23 June 2018
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Are Dyslexics More Entrepreneurial?
Dyslexia is rather common: it is estimated that around 5-10% of individuals are dyslexic. Despite an apparent disability, some are famous, like Tom Cruise or Richard Branson. Obviously, they do not suffer from a lack of intelligence and are, in fact, quite successful in the business world. So what is going on in their brains? Are they developing some compensatory mechanisms that help them to do things better?
Epidemiological research studies indicate that dyslexics develop coping strategies to compensate for their weaknesses, which helps them in later life. The resilience that they acquire while in school often helps them to be more successful in developing a business, in being an entrepreneur.
Statistics show that there are twice more dyslexics among entrepreneurs when compared to the general population. However, dyslexics are uncommon in higher management. They also tend to have a different business management style. Thus, they do better in startups and are better at handling particular types of businesses.
Dyslexia is usually first identified when a child goes to school and struggles with scrambled text. Dyslexic children have difficulty in reading texts, interpreting them, and explaining the meaning of the text to others, even though they can be very intelligent otherwise. Dyslexia often results in poor academic performance, undue pressure, and psychological trauma. Each dyslexic child needs to learn to cope with these challenges.
Although dyslexic children are as intelligent as their peers at school, they are often labeled as less capable. Children with dyslexia are often targets of bullying in school. Poor self-image at school often leads to worsening of self-esteem in many of these kids. As helping dyslexic children is not easy, they are often left to themselves.
What’s going on in the dyslexic brain? Neurological basis of dyslexia
As a common disorder, dyslexia is the subject of multiple studies. Researchers agree that those living with dyslexia may have differences in the brain relative to non-dyslexic children, and these differences are the subject of intense clinical research. The recent explosion in brain imaging technology is helping us gain a deeper understanding of the matter.
The neurological theory of dyslexia is one of the earliest. The theory was proposed about a century ago when British physicians Morgan and Hinshelwood described dyslexia as a “visual word blindness.”
The study of adults living with brain trauma in the left parietal region demonstrated that many of these people develop reading difficulties. They find it challenging to process the optical image of letters. Thus, the early theory was that those with dyslexia have developmental defects in the parietal region of the brain.
Left parietal involvement was also somewhat confirmed during pathological examination of the brains of those who died at an earlier age and were known to be dyslexic.
Another important theory focuses on delayed brain lateralization in dyslexia. It is thought that some people have weak or insufficient brain lateralization that hinders the understanding of languages. This theory was the subject of multiple studies in the second half of last century.
The latest research into the neurophysiology of those living with dyslexia seems to indicate that dyslexia is phonological in nature: dyslexics have difficulty in manipulating the phoneme parts of speech. It is possible that there are developmental issues in the visual tract or other visual mechanisms in the brain may be contributing to the difficulty.
Apart from defects in a specific subsystem of the vision pathway, researchers think that there are other brain developmental issues involved as well. It is entirely possible that people with dyslexia have temporal processing impairment, and therefore they are not able to process information fast enough. Thus, dyslexia is considered the result of multi-system deficits
In conclusion
Dyslexia is probably the result of deficits in the brain at multiple levels. There is an impaired phoneme discrimination resulting in difficulty in understanding spelling. Visual perceptual impairment leads to further worsening of word recognition, and phonological awareness impairment causes speech disturbances. In the center of all this is delayed temporal processing. The end result is delayed speech development, difficulties in reading and comprehending texts, and poor academic performance.
What makes a dyslexic a successful person?
From Leonardo da Vinci to Einstein, children with learning disabilities prove that there is a limited link between disability and intelligence. Children with dyslexia are at least equally intelligent to non-dyslexic children.
The higher success of individuals with dyslexia in certain professions is probably the result of resilience or compensatory mechanisms that they cultivate during the school days to overcome their difficulties.
Some of these kids may develop better skills for interacting with others. They may focus more on specific arts or sciences. Many of them may not concentrate on studies and instead start doing business at an early age. This means that they can be found in any profession, and in the long run they are equally successful.
The compensatory mechanisms developed at a young age may provide an edge over others in specific areas when the children grow up. Even though dyslexics may score poorly in school, they may outscore other children in practical life since they spend more time perfecting their verbal skills.
As an entrepreneur, dyslexics are known to be good at delegating tasks, they are excellent mentors, and they are often creative. All of these qualities usually make them more successful entrepreneurs, though they may not be that good in roles where there is less space for creativity.
Achieving success with dyslexia is perhaps about learning different skills, mastering different approaches to solving the tasks, and developing strategies to compensate for certain limitations.
References
Habib, M. (2000) The neurological basis of developmental dyslexia: An overview and working hypothesis. Brain, 123(12), 2373–2399. 10.1093/brain/123.12.2373
Locke, R., Scallan, S., Mann, R., & Alexander, G. (2015) Clinicians with dyslexia: a systematic review of effects and strategies. The Clinical Teacher, 12(6), 394–398. 10.1111/tct.12331
Logan, J. (2009) Dyslexic entrepreneurs: the incidence; their coping strategies and their business skills. Dyslexia, 15(4), 328–346. 10.1002/dys.388
Logan, J. (2018) Analysis of the incidence of dyslexia in entrepreneurs and its implications.
Toffalini, E., Pezzuti, L., & Cornoldi, C. (2017) Einstein and dyslexia: Is giftedness more frequent in children with a specific learning disorder than in typically developing children? Intelligence, 62, 175–179. 10.1016/j.intell.2017.04.006
Yu, X., Zuk, J., & Gaab, N. What Factors Facilitate Resilience in Developmental Dyslexia? Examining Protective and Compensatory Mechanisms Across the Neurodevelopmental Trajectory. Child Development Perspectives, 0(0). 10.1111/cdep.12293
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Monday, 18 June 2018
How Weather Influences the Brain?
We all know that the weather can strongly influence our mood and productivity. Many people feel better when the weather is nice and sunny. It is thus not surprising that people more often feel unhappy and depressed in winter. There is even a medical condition known as winter depression. Still, some researchers believe that our brain functions better during the cold days. In this article, I’ll briefly analyze what happens in our brain in relation to weather-related mood and mind changes.
Scientific studies indicate that weather conditions such as high temperature and humidity can impair mental performance by affecting brain neurochemistry. For instance, it is believed that thermal stress can cause cognitive impairment.
One recent study has investigated the impact of thermal stress on cognitive functions in soldiers spending at least one year in desert conditions. The evaluation of memory and cognitive functions indicated there is a decline in cognitive performance in hot climates when compared to normal weather. The decline was most pronounced for attention, concentration, verbal memory, and psychomotor performance.
Another recent study has investigated the impact of sand and dust storms on children’s cognitive function. Using mathematical analysis and word-recognition test scores, how prenatal exposure to sand and dust storms affects the cognitive performance of children was evaluated. The authors found a decline in both test scores, as well as a later beginning of counting and speaking in whole sentences in children prenatally exposed to storms. The findings imply that this kind of weather jeopardizes the cognitive functions of the next generation.
However, results from scientific research on the effects of temperature on cognitive functions are quite mixed and contradictory.
One study investigated how temperature affects the cognitive performance of subjects with multiple sclerosis. Healthy subjects were included as controls. The researchers correlated cognitive status with temperature in both study groups. In patients with multiple sclerosis, unlike in healthy subjects, the higher temperatures were associated with worsening cognitive status. These findings confirmed that warmer outdoor temperatures lead to a higher incidence of clinical exacerbation and T2 lesion activity in subjects with this condition (T2 lesions represent the white spots observed by MRI that are used to diagnose and track the progress of multiple sclerosis).
With regard to cognitive functions in cold weather, studies have shown both impairments and improvements.
For instance, one study investigated the impact of exposure to the cold and the following rewarming on working memory and executive functions in 10 young males. The results demonstrated a decline in the test results when the subjects were exposed to 10°C, and these impairments persisted for one hour during the rewarming period. Although the underlying mechanisms were not tested, the authors suggested that acute vascular changes in the brain could explain the observed changes. According to the authors, another explanation could be a deregulation of catecholamine levels, particularly important for complex attentional functions.
Other findings suggest that winter helps to wake up our mind and makes us think more clearly. It is well known that the brain utilizes glucose as its main energy source. Thus, when glucose is depleted, brain functioning is jeopardized. Energy, i.e., glucose, is also used for the regulation of body temperature, especially in extremely hot or cold conditions. It seems that more energy (glucose) is needed to cool down than to warm up the body. Thus, warm temperatures are more likely to deplete glucose levels and thus impair brain function and clarity of thinking.
It has been suggested that high temperatures increase the risk of mental disorders, especially in the elderly.
One recent study has analyzed data on emergency admissions linked to mental diseases and daily temperatures over a period of more than 10 years in 6 different cities. The results indicated that high temperatures might jeopardize mental health and be responsible for the exacerbation of symptoms of mental diseases. For instance, according to the results, more than 30% of admissions for anxiety were attributed to hot temperatures. Exposure to hot temperatures leads to reactions in the body that may cause an increase in stress hormone levels and brain temperature. Additionally, extremely hot weather may deregulate the dopamine and serotonin levels (these neuromediators are important for the feeling of happiness).
According to widespread belief, weather can affect our mood. Although a lack of sunshine is commonly linked to seasonal depression, some researchers believe that not all individuals respond similarly to weather changes.
Research has linked an individual’s self-reported daily mood with the objective weather over a 30 day period. Large individual differences have been found in how people react to the weather. Accordingly, four distinct types of weather responders have been identified: summer lovers (i.e., a better mood with warmer weather and more sun), summer haters (i.e., a worse mood with warmer weather and more sun), rain haters (i.e., a bad mood on rainy days), and unaffected (i.e., no particular association between weather and mood). Interestingly, adolescents and their mothers are often the same type, suggestive of familial weather reactivity.
The analysis of both scientific and popular literature permits the conclusion that extreme weather conditions can affect our cognitive function and mood. Most likely, this is caused by a decline in the brain’s energy source (glucose), which needs to be used for thermoregulation. Also, it is evident that extreme temperatures affect the level of catecholamines in the brain (such as dopamine and serotonin). Still, it seems that there is some individual variability in the brain’s response to weather, and it may run in the family.
References
Saini, R., Srivastava, K., Agrawal, S., Das, R. C. (2017) Cognitive deficits due to thermal stress: An exploratory study on soldiers in deserts. Med Journal Armed Forces India. 73(4):370-374. doi: 10.1016/j.mjafi.2017.07.011.
Li, Z., Chen, L., Li, M., Cohen, J. (2018) Prenatal exposure to sand and dust storms and children’s cognitive function in China: a quasi-experimental study. The Lancet. Planetary Health. 2(5): e214-e222. doi: 10.1016/S2542-5196(18)30068-8.
Leavitt, V.M., Sumowski, J.F., Chiaravalloti, N., Deluca, J. (2012) Warmer outdoor temperature is associated with worse cognitive status in multiple sclerosis. Neurology. 78(13): 964-968. doi: 10.1212/WNL.0b013e31824d5834.
Muller, M.D., Gunstad, J., Alosco, M.L., Miller, L.A., Updegraff, J., Spitznagel, M.B., Glickman, E,L. (2012) Acute cold exposure and cognitive function: evidence for sustained impairment. Ergonomics. 55(7): 792-798. doi: 10.1080/00140139.2012.665497.
Lee, S., Lee, H., Myung, W., Kim, E.J., Kim, H. (2018) Mental disease-related emergency admissions attributable to hot temperatures. The Science of Total Environment.616-617: 688-694. doi: 10.1016/j.scitotenv.2017.10.260.
Klimstra, T.A., Frijns, T., Keijsers, L., et al. (2011) Come rain or come shine: individual differences in how weather affects mood. Emotion. 11(6): 1495-1499. doi: 10.1037/a0024649.
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Does Depression Accelerate Aging?
A clear association between depression, especially the major depressive disorder, oxidative stress, and accelerated aging is supported by research.
Depression, major depressive disorder more specifically, is one of the most striking problems of modern society. Millions of people worldwide suffer from depression, with many patients not experiencing relief from symptoms. Depression is associated with increased mortality from age-related conditions, such as cardiovascular disease and cancer. Researchers have suggested that depression is associated with increased oxidative stress and a disturbed immune response, which may accelerate aging and increase susceptibility to age-related disorders.
One of the proven indicators of cellular aging is the length of telomeres. Telomeres are nucleoprotein complexes that cap the end of chromosomal DNA and serve to protect chromosomal integrity. They become shorter with each round of replication and cell division, meaning that normally they become shorter with age. When telomeres reach a critically short length, the cells undergo apoptosis, i.e., programmed death. Leukocyte telomere length has been typically used in clinical studies as a marker of cellular aging. They shortening accelerates in the cells subjected to oxidative stress.
Multiple studies, including some meta-analysis, have questioned the association between leukocyte telomere length and major depressive disorder. For instance, one meta-analysis compared the length of telomeres between depressed and healthy individuals and found significantly shorter telomeres in groups with depression. A very recent prospective study including over 100 participants aged from 18 to 70 with or without major depressive disorder assessed telomere length at baseline and at two years follow-up. The authors concluded that individuals with major depressive disorder at baseline had significantly larger shortening of telomeres over the period of 2 years, supporting the association between depression and accelerated aging.
Major depressive disorder is typically classified as a mental illness, but its pathology is evident in cells throughout the body. According to some researchers, several biological mediators are deregulated in this disorder that contribute to accelerated aging. These changes affect levels of genetic and epigenetic mediators (i.e., the variants of genes), and biochemical mediators such as glucocorticoids and neurosteroids. This can alter immune functions, oxidative processes, and levels of factors regulating the metabolism of glucose and production of insulin.
It is evident that deregulation of some of these biological mediators leads to oxidative stress, which seems to be highly correlated with the aging process. Oxidative damage occurs when the body can’t cope with psychological and physical stressors. In other words, oxidative stress refers to the excessive production of free radicals that cannot be completely neutralized by the body’s antioxidative mechanisms. Elevated markers of oxidative stress, along with decreased antioxidant capacity, have been reported in subjects with depression.
Oxidative damage is associated with the aging process, while markers of oxidative stress correlate with the decreased activity of an enzyme called telomerase. This enzyme is responsible for extending the length of telomeres. When telomerase is absent, the telomeres shorten faster. Thus, the link between the depression and accelerated aging can partly be explained by an increased cellular oxidative stress.
Animal studies have also been conducted in order to elucidate the mechanisms underlying major depressive disorder-mediated accelerated aging. For instance, in one study, the researchers exposed rats to mild chronic stress in order to induce the symptoms of major depressive disorder. The animals that developed these symptoms were found to have shorter telomeres and decreased telomerase activity, along with an increase in oxidative damage and decreased antioxidant enzyme activity. In addition, damaged mitochondria and reduced mitochondrial DNA content were also reported in rats with depressive symptoms. This research provided clear cellular evidence of accelerated aging associated with major depressive disorder.
A group of researchers proposed that early treatment (i.e., in the first half of life) of psychiatric disorders, including depression, could extend life expectancy and significantly reduce the burden of age-related disorders (such as cardiovascular disease, cerebrovascular disease, and cancer). They demonstrated that the persistence of some psychiatric disorder from the ages of 11 to 38 years led to the dose-dependent shortening of telomere length by the age of 38. Analyses of blood samples collected at the age of 26 and 38 revealed an accelerated erosion of telomeric ends in males diagnosed with the psychiatric disorder such as depression. Interestingly, there was no such association in females with a psychiatric disorder in the interim assessment at the age of 26. This research points to the link between psychiatric disorders and accelerated biological aging, which may be particularly emphasized in men.
Recently, one study investigated the association between major depressive disorder and age-related changes of the basal ganglia. The basal ganglia are a set of subcortical structures involved in reward processing, which is often dysfunctional in subjects with major depressive disorder. Based on images from the brains of patients with depression and healthy controls, the authors assessed the grey matter volume of basal ganglia in their different parts. They found a negative correlation between the size of the putamen (a region of the basal ganglia located in the base of the forebrain) and age. Importantly, this association was twice as big in patients with major depressive disorder in comparison with healthy subjects. The finding of a greater age-related volume decrease in the depressed subjects, suggests that major depressive syndrome is clearly associated with accelerated aging.
It seems that although various biochemical mediators are responsible for the clear association between depression and accelerated aging, oxidative stress is the largest contributor to this phenomenon. Thus, it is most likely that cellular oxidative damage caused by different psychological and physical stressors represents the underlying mechanism of depression-related accelerated aging.
References
Lin, P.Y., Huang, Y.C., Hung, C.F. (2016) Shortened telomere length in patients with depression: A meta-analytic study. Journal of Psychiatric Research. 76: 84-93. doi: 10.1016/j.jpsychires.2016.01.015
Vance, M.C., Bui, E., Hoeppner, S.S., et al. (2018) Prospective association between major depressive disorder and leukocyte telomere length over two years. Psychoneuroendocrinology. 90: 157-164. doi: 10.1016/j.psyneuen.2018.02.015
Wolkowitz, O.M., Reus, V.I., Mellon, S.H. (2011) Of sound mind and body: depression, disease, and accelerated aging. Dialogues in Clinical Neuroscience. 13(1): 25-39. PMID: 21485744
Xie, X., Chen, Y., Ma, L., Shen, Q., Huang, L., Zhao, B., Wu, T., Fu, Z. (2017) Major depressive disorder mediates accelerated aging in rats subjected to chronic mild stress. Behavioural Brain Research. 329: 96-103. doi: 10.1016/j.bbr.2017.04.022
Shalev, I., Moffitt, T.E., Braithwaite, A.W., et al. (2014) Internalizing disorders and leukocyte telomere erosion: a prospective study of depression, generalized anxiety disorder, and post-traumatic stress disorder. Molecular Psychiatry. 19(11): 1163-1170. doi: 10.1038/mp.2013.183
Sacchet, M.D., Camacho, M.C., Livermore, E.E., Thomas, E.A.C, Gotlib, I.H. (2017) Accelerated aging of the putamen in patients with major depressive disorder. Journal of Psychiatry and Neuroscience. 42(3): 164-171. PMID: 27749245
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Acupuncture and Pain
Acupuncture is one of the oldest systems of traditional medicine. With roots in China, this medical system is more than 2000 years old. It differs from various other medical systems as it does not involve taking any herbs or substances. Instead, it involves inserting small needles at specific predefined points. From the 20th century onwards, it has continued to gain prominence in the Western world, although many remain skeptical about efficacy.
These days, researchers want to know the exact mechanism of action of any medical system. They only trust the therapy if it has been proven as effective in randomized placebo-controlled clinical trials. Acupuncture has been the subject of many such trials, and its usefulness has been established in certain pain-associated conditions, mood disorders, and even in some diseases of internal organs. This led to the recognition of this medical system by many healthcare providers and medical organizations. In the US, acupuncture is recognized as complementary medicine. The WHO also recommends it for a number of specific medical conditions.
Clinical evidence of efficiency
Hundreds of clinical trials provide evidence of the effectiveness of acupuncture in various medical conditions. Among the most relevant trials are the so-called German mega-trials named ARC, ART, COMP, and GERAC. The primary focus of these trials has been pain relief in various musculoskeletal conditions. GERAC and ART were high quality random clinical trials investigating low back pain. These trials compared real acupuncture with sham acupuncture and standard care. Sham acupuncture involved needling without the use of conventional acupuncture points. Whereas standard care included the use of physiotherapy, exercise therapy, and NSAIDs (non-steroidal anti-inflammatory drugs). Results were measured after three months, and the response was defined as adequate if there was an improvement of more than 33% on the pain scale (the Von Korff Chronic Pain Grade Scale). After 6-months, the response rate with real acupuncture was 47.6%, while it was 44.2% with sham acupuncture, and 27.4% with standard care. Though these trials clearly demonstrated the efficacy of acupuncture, they also showed the effectiveness of sham acupuncture. Researchers think that this phenomenon is linked to psychogenic factors involved with back pain.
Interestingly, similar results were also demonstrated in various trials in the US. Though these trials show the usefulness of acupuncture in painful conditions, they also illustrate the value of psychogenic factors. Therefore, it is not surprising that acupuncture had also proven its utility in treating mood disorders and sleep disorders.
In Chinese medicine, the use of acupuncture is not limited to pain-related conditions. Thus, there is need for more extensive trials across a diverse range of diseases. The existing data do indicate that acupuncture may be an alternative approach for many difficult to treat chronic ailments.
Possible mechanisms
One of the areas of debate regarding acupuncture has been the difficulty in explaining its mechanism of action. As per traditional explanation, acupuncture is used to correct the flow of energy (Qi) in the body. This life energy flows through the fixed paths or highways in our body called meridians. Practitioners of acupuncture believe that in disease conditions there is a blockade of energy highways or meridians. Acupuncture is about creating the balance between the internal forces called Yin and Yang. However, the trouble is that modern science is not able to demonstrate or even understand the concepts of Qi, Yin, Yang, and Meridians.
In the last few decades, practitioners of modern science have made various attempts to explain the mechanism of action of acupuncture, and they came up with multiple theories.
- Measurable effects of acupuncture: One of the explanations is that needling does cause local changes and alterations in reflexes. It also has systemic effects, as it changes the working of the autonomous nervous system. Thus, acupuncture affects blood pressure, heart rate, levels of various hormones, and changes the levels of neurotransmitters. All of this results in pain relief and other beneficial effects.
- Local mechanotransduction: This is a theory promoted by a French physician in 1961, who wrote that acupuncture points have lower local resistance when compared to surrounding skin. He wrote that while normal dry skin has a resistance of 200,000 to 2 million Ohms, acupuncture points have a resistance of just 50,000 Ohms. The believers in this theory say that acupuncture causes minute traumas at the points of needle insertion and thus stimulates survival mechanisms of the body. Needling stimulates homeostasis, anti-inflammatory responses, tissue regeneration, and much more.
- Neurohumoral theory: it has been demonstrated that acupuncture is useful in pain relief, and naloxone blocks its analgesic effect. Thus, researchers propose that needling at specific points leads to the release of endogenous painkilling opiate-like substances such as enkephalins, endorphins, dynorphins and some other neurotransmitters like serotonin and noradrenaline.
- Gate-control theory: This theory states that needling stimulates large myelinated nerve fibers. These fibers carry tingling sensations and feelings of warmth, and can inhibit the painful sensation that is transmitted to the brain by much smaller C-fibers via spinal tracts.
- Postsynaptic inhibition: This is another explanation, which states that acupuncture results in the inhibition of pain through a central mechanism via disinhibition of RAF. This phenomenon typically works in cases of extreme trauma like loss of limb. This central mechanism has a role in protecting the body from extreme stress and pain.
- Autonomous nervous system: Proponents of this theory suggest that acupuncture works by changing the balance of sympathetic and parasympathetic nervous system.
- Morphogenetic singularity theory: This is one of the more complicated hypotheses that tries to explain the existence of meridians. Advocates of this theory explain the presence of non-neural communication pathways in the body. During embryonic development, when neurons are not yet formed, cells must communicate among themselves to direct development. Meridians are just the remains of these early communication paths, which are still present in the adult body.
- Visualization: In recent years, fMRI methods have advanced a lot, and in many clinical studies it has been demonstrated that stimulation of various acupuncture points by needling results in activation of different brain centers, thus explaining the mechanism of action of acupuncture. It is believed that both the elements of morphogenetic singularity theory (meridians) and components of the neurohumoral response are involved in the stimulation of the brain.
It is obvious that various theories have been used to describe the mechanism of action of acupuncture, and most probably there is more than one mechanism is involved. Clinical trials do seem to indicate that acupuncture is beneficial in specific health conditions. But the way it works still remains a mystery.
References
Dong, B., Chen, Z., Yin, X., Li, D., Ma, J., Yin, P., … Xu, S. (2017. The Efficacy of Acupuncture for Treating Depression-Related Insomnia Compared with a Control Group: A Systematic Review and Meta-Analysis. BioMed Research International, 2017, 9614810. doi: 10.1155/2017/9614810
Kawakita, K., & Okada, K. (2014) Acupuncture therapy: mechanism of action, efficacy, and safety: a potential intervention for psychogenic disorders? Biopsychosocial Medicine, 8, 4. doi: 10.1186/1751-0759-8-4
White, A., & Ernst, E. (2004) A brief history of acupuncture. Rheumatology, 43(5), 662–663. doi: 10.1093/rheumatology/keg005
Wong MC, Shen HJ (2010) Science-based Mechanisms to Explain the Action of Acupuncture. Journal of the Association of Traditional Chinese Medicine (UK), 17(2), 5-10.
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"All Americans are just one bad tweet away from being fired"
"If you use Twitter, you too are a public figure. And one egregious tweet could blow up your life.
The political climate puts all employers on high alert when it comes to the words and behavior of their employees.
Many people are plugged into the news cycle all day long. One in five employers think staff is productive fewer than five hours a day, with most citing smartphone use as the culprit.
The First Amendment protects free speech, but it may not protect your job if you do or say anything that is contrary to the company’s values, even if it’s a joke.
Anyone with a public Twitter account is a de facto public figure.
“We have to be mindful of every word we speak and everything we write.” Even posting photographs or retweeting someone else’s tweet can be enough to get fired.
In fairness to American workers, it’s a double-edged sword: They’re often times encouraged to tweet and maintain an active social media presence."
References:
Like Roseanne, all Americans are just one bad tweet away from being fired https://buff.ly/2xB5bAm
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When advertising your physician practice: Google and Facebook dominate 73% of U.S. digital advertising market
"Imagine a not-too-distant future in which trustbusters force Facebook FB to sell off Instagram and WhatsApp. Imagine a time when Amazon’s cloud and delivery services are so dominant the company is broken up like AT&T. Imagine Google’s search or YouTube becoming regulated monopolies, like electricity and water.
Facebook Inc., Google parent Alphabet Inc. and Amazon.com Inc. are enjoying profit margins, market dominance and clout that, according to economists and historians, suggest they’re developing into a new category of monopolists.
Together, Google and Facebook take in 73% of U.S. digital advertising.
They also benefit from something historically unprecedented: the ability to get users to subsidize them with enormous quantities of free labor. Their systems are fueled by personal information, but instead of them hunting for it, people willingly provide it."
The reality is that if you choose to advertise your physician practice, there are 2 dominant channels:
- Google Ad Words https://www.google.com/ads
- Facebook Ads https://www.facebook.com/business/products/ads
Related articles for physicians advertising on Google and Facebook:
Online Advertising Challenges for Medical Clinics | Physicians Practice https://buff.ly/2JjF7i2
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Facebook Advertising Tips for Physicians | Physicians Practice https://buff.ly/2JnZuuv
References:
Tech’s Titans Tiptoe Toward Monopoly https://buff.ly/2H5SHAh
Healthcare and medicines - Advertising Policies Help https://buff.ly/2JmXVNa