Friday, 22 June 2018
Wednesday, 20 June 2018
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
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.
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.12293Read More Here..
Tuesday, 19 June 2018
Monday, 18 June 2018
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.
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.Read More Here..
Saturday, 16 June 2018
Friday, 15 June 2018
Thursday, 14 June 2018
Wednesday, 13 June 2018
Tuesday, 12 June 2018
Monday, 11 June 2018
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.
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: 27749245Read More Here..