Welcome to a New Medicine Website!

This is a new medicine website that critically reviews all aspects of medicine on an ongoing basis, provides basic and important information for the public and experts. This is not a website, just repeating the current knowledge in different disciplines of medicine, but critically reviews the shortcomings with proposals for revisions in the medical diagnostics, treatment, prevention and suggestions for the future research in each topic. Unfortunately medicine that has been in existence since the antiquity, it has not evolved as much a the other field of science, perhaps for not being profitable for capitalism to invest sufficiently in the health of their people as much as other industries. Hopefully this website along others as such would open the path to the future of medicine, where prevention of diseases will be the primary agenda so humans can enjoy the best of health and not being the subjects of profit making for entrepreneurs, hence fulfill the Hippocratic oath “preserve the purity of my life and my arts.”!

Throughout the history, humans have been able to discover and invent mainly through right questioning and critic, that is the purpose of this website.  Whenever we have followed an idea or belief rigidly, then we were stuck in dogma and any progress had stagnated,like many centuries of dark ages before the scientific revolution.  Through right questioning and critic of our current knowledge in medicine, this site will revisit the field and will attempt to bring on new perspectives on different medical conditions. 

Dr. Mostafa Showraki, MD, FRCPC                                                                       Lecturer, School of Medicine, University of Toronto                                        Author: ADHD:Revisited Book Adhdrevisited.com/medicinerevisited.com       

*All the contents of this website is copyright protected under the international law and registered with the Canadian intellectual property office and cannot be copied, including many new ideas, concepts, proposals and terminologies used throughout its articles, without the author’s permission and mentioning the references.

Your >250,000 hits shows that:

You care about the demise of our being before we extinct not by our wars or earth collision by asteroids or else, but by microbial invasions who have ruled the earth for billions of years!                          Mostafa Showraki

The only good is knowledge and the only evil is ignorance. Socrates

 All truths are easy to understand once they are discovered; the point is to discover them. Galileo Galilei

Perfect as the wing of a bird may be, it will never enable the bird to fly if unsupported by the air. Facts are the air of science. Without them a man of science can never rise. Ivan Pavlov

Synopses:                                                                                                                           Summary and easy read of lengthy articles that you can find under “Synopses” above in the home menu bar

Coming soon:

Brain Tumours: When our most precious organ is invaded

Autoimmune Disorders: Relapsing-Remitting Vs. Progressive


The majority of autoimmune disorders like cancers are progressive and fatal. The exceptions seem to be only autoimmune demyelinating disorders and its most common type, Multiple Sclerosis (MS) that in majority of cases have a relapsing-remitting course and a better prognosis. Although MS at the onset could manifest as a clinically isolated syndrome, it soon takes the form of either relapsing-remitting or progressive (primary). Later on in the course of illness a minority of the relapsing-remitting MS (RRMS) may change its course to progressive and poor prognosis and this group is classified secondary progressive MS (SPMS) against the primary progressive MS (PPMS) that has a progressive course from the onset (1)

 Unfortunately it has not yet been sufficiently questioned and studied why MS and other similar autoimmune demyelinating disorders possess could have a relapsing-remitting course and a better prognosis, while the nature of autoimmune disorders are generally progressive with morbidity and mortality. Autoimmune disorders that like cancers as detailed in other articles on this site are the results of microbial invasions, and no microbes such as bacteria or viruses invade our beings to fool around, remit and relapse. So then why if autoimmune demyelinating disorders such as MS are also the byproducts of microbial invasions such as EBV (Epstein Barr Virus), have a remission and relapse course while the invasion targets our most precious organ, the brain. In fact the answer when probe to it well lies in our brain, not the invaders. It’s the brain that protects itself and fights back against the invasion and strives to undo the damage. This interesting fact that so far seems to happen only in the brain and at least to the myelin sheaths of the brain is a very new discovery in the very recent years. But this has not yet been applied in the explanation of the relapsing-remitting course of autoimmune demyelinating disorders such as MS, and this article could be the first.

The Brain fights back:

While the great majority of brain cells are essentially stable throughout life, oligodendrocyte precursor cells (OPCs) that generate new oligodendrocytes hence new myelin sheaths have been observed widespread in the brain even in adult life (2). The myelin or myelin sheaths that cover the nerve cell axons act as the nervous system wires for the conduction of information from one neuron to the other, or one area of the brain to the other. The white matters or the highways of the brain are basically made of the myelin and myelin sheaths that are the targets of microbial invasions in the autoimmune demyelinating disorders such as MS. Generally the process of myelination or the generation of myelin and myelin sheaths that start early in the third trimester, continues throughout adolescence and early adult life that contribute and correspond to the continuation of the general brain development until mid-20s (3). The reason or need for the long development of the brain through ongoing myelination is building its widespread communication infrastructures for learning, skills developments and other higher cortical functions that create cognitive and skills maturity.  

Our brain that is the only organ of the body that its growth or development continues until mid-20s would remain stable or stationary from then on generally if no efforts in further learning or skill developments happen on the part of the individual or demands from his or her environment. In fact it has been shown that while the human white matter oligodendrocytes show very little turnover during life, the gray matter oligodendrocytes, that link more with higher cognitive functions, continue to be added until the fourth decade. In other word the brain like the rest of the body organs would stop in its development or regeneration without any stimulation or trigger. Learning new subjects, skills, or use of the brain actively in problem solving, inventions and creations triggers the new brain development locally corresponding to the specific area of the brain that has been stimulated (4-10)

 In the case of invasion or damage of the brain, it has been known for long in TBI (Traumatic Brain Injury) and stroke that the intact parts of the brain over time take over the tasks of the damaged parts by neuro-regeneration and re-myelination. Myelin degeneration that is the pathognomonic of autoimmune demyelinating disorders such as MS and leads to reduction in the existing mature or adult oligodendrocyte and the number of internodes on the myelin sheath in animal studies have been shown to be associated with debris accumulation in microglia that trigger new myelin regeneration or re-myelination through the birth of new oligodendrocyts from oligodendrocyte precursor cells (OPCs) in live imaging studies. The new oligodendrocyts and internodes that soon become stable and integrate with the existing cells and nodes have been shown to enhance by neural activity and young brain age. That is why at the extreme old age or inactive brain, degeneration and engulfment of myelin by microglia occur with no new regeneration, hence cognitive and other high cortical functions decline (11-14).

The role of cortical re-myelination in disease, specially autoimmune demyelinating disorders such as MS seems to contribute to the relapsing-remitting course of these illnesses, specifically when noticing that the new individual oligodendrocytes form their internodes within a few hours. This well explains the autoimmune demyelinating disorders and MS’ fluctuating symptoms and overall their better prognosis compared to any other autoimmune disorders. The cortical more than the spinal cord’s myelin is correlated with the synaptic and structural plasticity of the brain so more stimulated for regeneration by neural or cortical activities. Therefore it could be plausible in the autoimmune demyelinating disorders such as MS, other than immune fostering treatments, any brain cortical activities that could prompt re-myelination could enhance remission (7,8,10,15).  

 The onset of progressive MS may be more relevant to the patient’s age than the duration of a pre-progression relapsing disease course. About one third of RRMS patients may never develop a progressive disease course. Age-of-progression-onset is similar between BOPMS and PPMS. Switching from relapses to progression in MS is an age-dependent process independent of pre-progression disease course or disease duration. Almost all patients with MS develop progressive disease course before age 75 (or by 35 years post-MS onset). Recent imaging studies suggest that myelination of the compact white matter ends by the 4th decade followed by a slow degeneration in the white matter tracts in the following decades. Continued white matter tract repair (myelin and axons) may compensate for degeneration in previously damaged areas of the CNS until the end of 4th decade. An advancing degenerative phenotype afterwards is possibly reflected by the clinical progression surfacing in the 5th decade. PPMS patients with visual or brainstem/cerebellar onset had a significantly younger age at progression. SPMS patients with motor onset have a significantly higher age at progression and longer time to progression. Time to progression is significantly shorter in SPMS patients with higher age at disease onset. In summary the progression in MS is an age dependent process independent of relapses (11-15).

Of importance in any brain autoimmune or degenerative disorders, such as MS and Alzheimer’s Disease is also the role of microglia that rise to defense as the resident macrophages of the brain for the lack of any antibodies in the brain. Recent studies have revealed an expanding array of functions for microglia during brain development and in the adult brain for maintenance of the homeostasis after neurodegeneration resulting from infection and brain injury. Studies have shown that the cellular activities of microglia extend beyond their well-established role as immune sentinels and effectors to include synaptic organization, control of neuronal excitability, phagocytic debris removal and trophic support for brain protection and repair (16-19).

Unlike other organs and tissues of the body, aging affects the brain differently and by the brain regions differentially. First of all as discussed earlier, the brain growth or development mostly in the form of arborization and myelination continues until mid-20s and in some parts of the brain until the fourth decade. More importantly the different regions of the brain are not affected equally but differentially by aging and degenerative disorders. Moreover there are compelling evidences that microglia have phenotypic diversity in the healthy adult brain and also aging and degenerative diseases have a region-dependent impact on the brain. For example the microglia in the cerebellum hold a higher immune vigilant state and lower density so requiring each cell to survey a larger volume of tissue. In contrast the cortical and striatal microglia are similar to each other, while hippocampal microglia has an intermediate profile. Similarly the white matter microglia exist in a relatively less quiescent basal state than their grey matter counterparts, which could contribute to the more vigilant profile of microglia in the white matter-enriched cerebellum (20-21)

 Another factor is the genomic integration of endogenous retroviruses (ERVs) and other retrotransposons that although normally inactive, deficiencies in innate immunity could predispose to their reactivation. The cerebellum and hippocampus are more susceptible to the retrotransposition in the human brain and thus more immune vigilant and having higher expression of anti-viral interferon networks. Therefore more caudal regions of the CNS such as the cerebellum may be more vulnerable to age- or disease-related inflammatory degeneration if this heightened alertness is poorly controlled. However, the extra-alert phenotype may confer protective functions through increased vigilance and efficiency in removing potentially harmful agents, such as in the case of lower susceptibility of the cerebellum to amyloid deposition during ageing. Similar but to a lesser degree susceptibility to aging and degeneration has been shown in the hippocampal microglia. The cerebellum also along with caudate and putamen suffer from earlier atrophy in relapse-remitting than in primary-progressive MS. Also the demyelination is five times more in the cerebellar grey matter than the white matter (22-27).


Natural Interception in the course of MS:

It has been shown that myelin formation depends not alone on genetic programing, but environmental influence, experience, learning and exercise, plus other multiple intracellular and extracellular factors that all make myelination in the central nervous system a dynamic than a static process. Myelination has also been shown to depend on the sleep-wake cycle and up-regulation of myelin-related genes during sleep. Therefore poor and disturbed sleep-wake cycle and chronic insomnia could affect myelination and its regeneration substantially. It has been shown that the sleep loss could affect the node of Ranvier length, hence the nerve conduction in the brain. Therefore sleep is vital in promoting the white matter integrity. In recent years, a growing body of evidence has shown that myelin and the cells that form it, from OPCs to mature myelinating oligodendrocytes, are remarkably dynamic and responsive to the neurons they ensheathe. Artificially induced neuronal activity using selective optogenetic stimulation in premotor cortex can generate a rapid and robust proliferation of OPCs followed by increased myelination in the deep cortex and subcortical white matter within the stimulated circuit (28-36).

 Myelination and re-myelination especially in response to the environmental stimulus is time or period-dependent along the line of brain development, so the younger the brain the more impact. As discussed earlier all parts and structures of the brain including the white matter and myelination are task and stimulus-dependent, e.g. exercise, learning and training, such as piano playing, learning to read, mastering juggling, and many others. To date, studies have demonstrated the dynamic influence of exogenous environmental stimuli on multiple regions of the brain. This environmental influence positively and negatively impacts programs governing myelination, and acts on myelinating oligodendrocyte (OL) cells across the entire human lifespan. Therefore the acquisition of new skills so to maintain a more active and dynamic brain would ensue in more plasticity including more myelination and re-myelination of the brain. The white matter of the brain which occupies almost half the volume of the human brain with its myelination not only genetically correspond to developmental behavioral and functional milestones, but later on in life to the environmental stimulus (37-45).

Similarly while brain injuries or insults to the brain, such as microbial invasions in the case of autoimmune disorders, e.g. MS causing damage to the plasticity of the brain including its myelination, any positive stimulus could help in its cellular regeneration and recovery. The pioneer work of the OPC proliferation reduction as a result of the blockade of action potential propagation in the optic nerve showed well how myelin is regulated by functional neuronal inputs, and can therefore participate in activity-dependent CNS plasticity (46). Over the lifespan, DTI (Diffusion Tensor Imaging) that identifies the conduction velocity and health of myelination or the white matter increases during normal brain development, but conversely decreases during typical age-related demyelination. DTI during learning a complex motor skill, such as juggling, has been shown to improve WM architecture when practiced regularly. Study of a second language in adults also influences WM plasticity as identified with DTI. These changes reflect learning-related increases in myelination (47-50).

Social environment also influences early myelin plasticity. Juvenile mouse studies of the prefrontal cortex have demonstrated that two weeks of social isolation could lead to alterations in Oligodendrocytes morphology, reduction in the myelin thickness, and deficits in working memory and sociability. Interestingly isolation in the adult mice had little effect on the myelin content, defining an important critical period in which juvenile social experience readily impacts regional brain development. Human studies on institutionally reared children have also demonstrated that severe neglect in early life compromises WM microstructure throughout the brain. However, early removal from adverse conditions and subsequent placement into high-quality foster care could promote more normative WM development, and therefore may support long-term motor, cognitive, and sensory remediation (51-58).

One of the oldest and most widely used experimental approaches to study the influence of experience on the brain is exposure to an enriched environment (59-61). Environmental enrichment (EE) refers to a complex and stimulating domain that challenges an organism to continuously adapt to its surroundings in a social, physical, and experiential manner. Early EE studies demonstrated widespread effects on numerous CNS cell types and under varied physiological conditions in both small and large mammals. Differential rearing in infant rhesus monkey shows that animals raised in larger groups demonstrate expansion of the CC (Corpus Callosum) and sustained improvement in cognitive performance versus age-matched, individually raised controls. In a model of Parkinson’s disease, young adult mice demonstrated an increase in new Oligodendrocyts(OLs) in the substantia nigra after a month of enriched housing. Similarly, EE increases OPC proliferation, and influences OPC number and cell fate in the amygdala of adult mice. EE also improves spatial learning in the aged rats by increasing the volume and length of myelinated fibers, volume of myelin sheaths, and total CC volume. Further, EE promotes progenitors derived from an endogenous pool of neural stem cells to generate OLs in a murine model of MS, with consequent enhanced re-myelination of lesions and reduced functional impairment (62-64).

Music is a multisensory form of EE that imparts cognitive (learning), auditory (listening), and motor (playing) stimulation, whereby simultaneous collaboration between multiple areas of the brain coordinate an organized response. Musical performance alters WM architecture and it has been shown that professional pianists who began playing during adolescence demonstrate improved WM integrity and WM plasticity, as shown in DTI. These studies have also revealed that these WM changes are relative to the amount of time spent practicing, and that specific WM regions are uniquely sensitive to piano playing during childhood, adolescence, and adulthood. This suggests age-specific regional plasticity in myelinating tracts, and functional adaptation within a critical period of development in WM undergoing maturation. Further, despite less overall training hours than adults, the larger number of involved brain regions correlated with practice during childhood, is a strong evidence the influence of early experience on WM plasticity. Pragmatically, these WM changes serve as a foundation to build upon with future experience. This adaptive response to music also occurs in the WM tracts of the adult, and in disease, emphasizing how life experiences – in this case learning could alter myelination and are influenced by the environment (65-68).

 Interacting with and adapting to our environment forms the basis for learning. Dynamic and influential learning involving WM occurs throughout life, but is especially critical during development, as organisms establish the infrastructure and patterns of circuitry in the brain. At the same level, any mental exercise or brain fitness such as cognitive training and stimulation that improves mental function, shapes and preserves WM integrity in the aging individuals that could be applied as treatment modalities in degenerating diseases such as Alzheimer’s disease and MS. Like music, meditation could improve myelination and WM efficiency in the areas of the brain such as the anterior cingulate cortex as it has been shown in DTI studies.

Physical activity not only improves the brain function and cognition, but also protects the brain from the detriments of aging. Voluntary exercise in mice enhances differentiation of OPCs into mature OLs, and increases oligodendrogenesis in the intact thoracic spinal cord after only a week of activity. Recent studies also confirm an impact of cardiorespiratory fitness on WM in older humans. DTI studies have shown positive relationship between fitness and spatial working memory that is mediated by WM microstructure. On the contrary, sedentary behavior in adults reduces WM integrity, but exercise is beneficial for WM health, and memory-related brain networks (69-79).

The nutritional environment impacts brain structure and function, and gross deviations in nutritional status are implicated in many neurological disorders. OLs, especially OPCs, have tremendous energy requirements. Synthesis and maintenance of myelin by OLs is a metabolically taxing process, and thus adequate dietary intake of a number of key elements is crucial to successful myelination. Iron deficiency is the most common nutritional health problem in the world, and has been linked to persistent hypo-myelination. This has important clinical implications during development, as the neurological sequelae (behavioral disorders, decreased cognitive ability, poor school performance) are long-lasting. Developmental disturbances in myelin synthesis and composition are not corrected with iron repletion. In the models of MS, MRI and histological iron distribution reveal that iron maintains myelin integrity and plays an important role in re-myelination and repair. Interestingly, age-related iron accumulation in the striatum is linked to demyelination and a reduction in declarative memory (80-84).

Essential fatty acids (EFAs) also play a key role in the structural integrity of myelin. Because the body cannot synthesize EFAs, they must be obtained from dietary intake. EFAs help build the myelin sheath, and their deficiency during infancy can delay brain development as well as accelerate the deterioration of cognitive processing in the adult (86).

Additionally, obesity is associated with reduced myelin. BMI is negatively correlated to WM integrity in multiple regions of the brain, including the CC, and has been implicated in the reduction of OL and OPC numbers in the murine spinal cord. Encouragingly, 7 weeks of exercise training reversed these reductions in the OL population. Obesity-related loss of WM integrity is prevalent in the limbic system and tracts connecting the frontal and temporal lobes, and could compound the effects of age-related cognitive decline. The reciprocal relationship between diet, exercise, and myelinogenesis highlights that adequate nutrition is required for normal brain development and plays a central role in myelin homeostasis (86-88).

Socialization tremendously impacts neurological development. Environmental resources like healthcare, education, and housing have a cause and effect relationship on the brain throughout life, and individual differences in cognition, emotion, and psychological wellbeing can be attributed to deviations in these social parameters. Early environmental adversity studies have demonstrated that rhesus monkeys raised in isolation and are detached from their environment, could be hostile and could not form adequate social attachments. Similarly, recent studies investigating social influence on WM plasticity have found that monkeys exposed to early life stress, particularly a disrupted infant-mother bond, demonstrate reductions in myelin and WM integrity, and elevations in plasma cortisol levels after maltreatment. These WM alterations are especially evident in regions of the brain associated with motor integration and emotional regulation (89-91).

 Murine studies also implicate neglect as a cause of reduced myelination in the prefrontal cortex. Two weeks of social impoverishment reduced myelin thickness and simplified OL morphology, and importantly, social reintegration in young adult mice did not lead to recovery. Further, DTI of language and limbic pathways reveals microstructural WM abnormalities in orphanage-reared children. Importantly, these changes correlate with the period of deprivation and time spent in the orphanage, i.e. in a deprived environment, and could misshape the trajectory of cognitive and behavioral neurodevelopment (92-93).


It has been and it is still an enigma about the remission and relapse of autoimmune disorders (or any disorders) that’s the most common in the case of autoimmune demyelinating disorders, popularly Multiple Sclerosis (MS). Since at least two thirds of MS have a relapsing-remission course with an unknown reasons or sufficient explanations, this illness is a gold guiding marker to understand the relapsing-remitting illnesses if any more and above all understanding the defense of the brain against invasions. Since the question of pathogenesis of relapse and more importantly the remission has not been answered clearly or even worse has not been sought in the research arena, to find the answer if any, one needs to read between the lines and mostly in the basic neuroscience research as there are not many of such in the MS research field.

Therefore in this paper, I have surfed the neuroscience research that include mostly animal counterpart subjects to discern the answer to the remission and relapse of autoimmune demyelinating disorders such as MS. Although it has been hypothesized that remission in MS is driven by a small heat shock protein, αB crystalline that decreases the production of TH1- and TH17-type cytokines from auto-reactive T cells (94), it seems that the nature and the infrastructure of the brain holds a significant role as discussed above in the remission phases of MS.

 Oligodendrocyte precursor cells (OPCs) throughout the life generate new oligodendrocytes hence new myelin sheaths, particularly when triggered by an injury to the white matter of the brain, or in normal brain by stimulation from neural activities. Therefore in any demyelinating disease such as MS, the POCs are called into action the brain repairs itself, hence causes remissions. In fact the remission in MS starts first after the initial lesion of MS and the first isolated symptom, then the microbe e.g. EBV attacks back and causes relapse. This remission and relapse cycle will continue until one, the brain or microbe wins the battle.

The current available treatments of MS that involve monoclonal antibodies and fostering the immune system that are relatively effective, might not yield to a full recovery. Therefore it seems to be prudent to stimulate the brain and in this case the oligodendrocytes and their precursors to regenerate the damaged myelin and the myelin sheaths and lead to longer remission and hopefully full recovery. This importance could be accomplished either with neural stimulations e.g. DBS (Deep Brain Stimulation) (95-96) or simply by increasing the patient’s physical and mental activities to stimulate the brain and the POCs to repair itself, promote remission and lead to recovery (47, 49, 54, 56, 58). Also the correction of any trace element such as iron, B12 and essential fatty acids that are vital for the nutrition and wellbeing of the brain could enhance remission (80-85).

More important than any treatment, we need to move towards strategies for the prevention or lowering the prevalence of demyelinating diseases such as MS. To achieve so, first of all the body and mind need to be active, so there would be less chance of degenerations to demand treatments as detailed earlier. Secondly the provision of an enriched environment of rearing from early childhood or even farther before during conception for the fetus and lack of any stressful and adversarial life events on the developing brain could ensure a healthier brain, hence less damage and diseases, such as MS (59-64).

Dr.Mostafa Showraki, MD, FRCPC                                                                Lecturer, School of Medicine, University of Toronto                               Author: ADHD: Revisited Book, Amazon Kindle Books                   www.adhdrevisited.com/www.medicinerevisited.com


  1. Lublin FD, et al. (2014) Defining the clinical course of multiple sclerosis. Neurology. 83 (3): 278–286.
  2. Swire M, Ffrench-Constant C. (2018). Seeing Is Believing: Myelin Dynamics in the Adult CNS. Neuron. 98(4):684-686.
  3. Stadelmann, C, Timmler S, Barrantes-Freer A, Simons M. (2019)Myelin in the Central Nervous System:Structure, Function and Pathology. Physiological Reviews. 99 (3): 1381–1431.
  1. Auer F, Vagionitis S, Czopka T. (2018) Evidence for myelin sheath remodeling in the CNS revealed by in vivo imaging. Curr. Biol. 28: 549-559.
  2. Czopka T, Ffrench-Constant C, Lyons D.A. (2013) Individual oligodendrocytes have only a few hours in which to generate new myelin sheaths in vivo. Dev. Cell. 25: 599-609.
  3. Hill R.A, Li A.M, Grutzendler J. (2018) Lifelong cortical myelin plasticity and age-related degeneration in the live mammalian brain.Nat. Neurosci. 21: 683-695.
  4. Hughes E.G, Orthmann-Murphy J.L, Langseth A.J, Bergles D.E. (2018) Myelin remodeling through experience-dependent oligodendrogenesis in the adult somatosensory cortex. Nat. Neurosci. 21: 696-706.
  5. McKenzie I.A, Ohayon D, Li H, de Faria J.P, Emery B, Tohyama K, Richardson W.D. (2014) Motor skill learning requires active central myelination. Science. 346: 318-322.
  6. Sampaio-Baptista C, Johansen-Berg H. (2017) White matter plasticity in the adult brain.Neuron. 96: 1239-1251.
  1. Bengtsson SL, Nagy Z, Skare S, Forsman L, Forssberg H, Ullén F.(2005) Extensive piano practicing has regionally specific effects on white matter development. Nat Neurosci. 8(9):1148-50.
  2. Tutuncu M, Tang J, Zeid NA, et al. (2013) Onset of progressive phase is an age-dependent clinical milestone in multiple sclerosis. Mult Scler. 19(2):188–198.
  1. Confavreux C, Vukusic S. (2006) Natural history of multiple sclerosis: a unifying concept. Brain. 129(Pt 3):606–16.
  2. Tremlett H, Zhao Y, Devonshire V. (2009) Natural history comparisons of primary and secondary progressive multiple sclerosis reveals differences and similarities. J Neurol. 256(3):374–81.
  3. Koch M, Mostert J, Heersema D, De Keyser J. (2007) Progression in multiple sclerosis: further evidence of an age dependent process. J Neurol Sci. 255(1-2):35–41.
  4. Westlye LT, Walhovd KB, Dale AM, et al. (2010) Life-span changes of the human brain white matter: diffusion tensor imaging (DTI) and volumetry. Cereb Cortex. 20(9):2055–68.
  5. Grabert K, Michoel T, Karavolos MH, et al.(2016) Microglial brain region-dependent diversity and selective regional sensitivities to aging. Nat Neurosci. 19(3):504–516.
  1. Paolicelli RC, et al. (2011) Synaptic pruning by microglia is necessary for normal brain development. Science. 333(6048):1456-8.
  2. Schafer DP, et al. (2012) Microglia sculpt postnatal neural circuits in an activity and complement-dependent manner.

Neuron. 74(4):691-705.

  1. Neumann H, Kotter MR, Franklin RJ. (2009) Debris clearance by microglia: an essential link between degeneration and regeneration. Brain. 132(Pt 2):288-95.
  1. Gehrmann J, Matsumoto Y, Kreutzberg GW.(1995) “Microglia: intrinsic immuneffector cell of the brain”. Brain Research. Brain Research Reviews. 20 (3): 269–87.
  2. Hart AD, Wyttenbach A, Perry VH, Teeling JL. (2012) Age related changes in microglial phenotype vary between CNS regions: grey versus white matter differences. Brain Behav Immun. 26(5):754-65.
  3. Lee KH, Horiuchi M, Itoh T, Greenhalgh DG, Cho K. (2011) Cerebellum-specific and age-dependent expression of an endogenous retrovirus with intact coding potential. Retrovirology. 8:82.
  4. Baillie JK, et al. (2011) Somatic retrotransposition alters the genetic landscape of the human brain. Nature. 479(7374):534-7.
  5. Damani MR, et al. (2011) Age-related alterations in the dynamic behavior of microglia. Aging Cell. 10(2):263-76.
  6. Goh JO. (2011) Functional Dedifferentiation and Altered Connectivity in Older Adults: Neural Accounts of Cognitive Aging. Aging Dis. 2(1):30-48.
  7. Eshaghi A, Marinescu RV, Young AL, et al. (2018) Progression of regional grey matter atrophy in multiple sclerosis. Brain. 141(6):1665–1677.
  8. Gilmore CP, Donaldson I, Bö L, Owens T, Lowe J, Evangelou N.(2009) Regional variations in the extent and pattern of grey matter demyelination in multiple sclerosis: a comparison between the cerebral cortex, cerebellar cortex, deep grey matter nuclei and the spinal cord. J Neurol Neurosurg Psychiatry. 80(2):182-7.
  9. Szulc-Lerch KU, et al. (2018) Repairing the brain with physical exercise: Cortical thickness and brain volume increases in long-term pediatric brain tumor survivors in response to a structured exercise intervention. Neuroimage Clin. 18:972–985.
  10. Adkins DL. (2015) Cortical Stimulation-Induced Structural Plasticity and Functional Recovery after Brain Damage. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects.
  11. Chen YH, et al. (2018) Exercise Ameliorates Motor Deficits and Improves Dopaminergic Functions in the Rat Hemi-Parkinson’s Model. Sci Rep. 8(1):3973.
  12. Toritsuka M, Makinodan M, Kishimoto T. (2015) Social Experience-Dependent Myelination: An Implication for Psychiatric Disorders. Neural Plast. 2015:465345. doi:10.1155/2015/465345
  13. de Vivo L, Bellesi M.(2019) The role of sleep and wakefulness in myelin plasticity. Glia. 67(11):2142–2152.
  14. Fields R. D. (2015). A new mechanism of nervous system plasticity: Activity dependent myelination. Nature Reviews. Neuroscience, 16, 756–767.
  15. Fields RD. (2008)White matter in learning, cognition and psychiatric disorders. Trends Neurosci. 31(7):361-70.
  16. Forbes T. A., & Gallo V. (2017). All wrapped up: Environmental effects on myelination. Trends in Neurosciences, 40, 572–587.
  17. Gibson E. M., et al. (2014) Neuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain. Science, 344, 1252304.
  18. McKenzie I. A., et al. (2014) Motor skill learning requires active central myelination. Science, 346, 318–322.
  19. Xiao L., et al. (2016) Rapid production of new oligodendrocytes is required in the earliest stages of motor skill learning. Nature Neuroscience, 19, 1210–1217.
  20. Scholz J., et al. (2009) Training induces changes in white matter architecture. Nature Neuroscience, 12, 1370–1371.
  21. Zatorre RJ, Fields RD, Johansen-Berg H. (2012) Plasticity in gray and white: neuroimaging changes in brain structure during learning. Nat Neurosci. 15(4):528-36.
  22. Scholz J, Klein MC, Behrens TE, Johansen-Berg H. (2009) Training induces changes in white-matter architecture. Nat Neurosci. 12(11):1370-1.
  23. Engel A, et al. (2014) Inter-individual differences in audio-motor learning of piano melodies and white matter fiber tract architecture. Hum Brain Mapp. 35(5):2483-97.
  24. Zatorre RJ, Fields RD, Johansen-Berg H. (2012)Plasticity in gray and white: neuroimaging changes in brain structure during learning. Nature Neurosci. 15:528–536.
  25. Mitew S, Hay CM, Peckham H, Xiao J, Koenning M, Emery B. (2014)Mechanisms regulating the development of oligodendrocytes and central nervous system myelin. 276:29–47.
  26. Emery B, Lu QR. (2015)Transcriptional and epigenetic regulation of oligodendrocyte development and myelination in the central nervous system. Cold Spring Harb Perspect Biol. 7(9):a020461.
  27. Barres BA, Raff MC. (1993)Proliferation of oligodendrocyte precursor cells depends on electrical activity in axons. 361(6409):258–260.
  28. Mangin JM, Li P, Scafidi J, Gallo V. (2012)Experience-dependent regulation of NG2 progenitors in the developing barrel cortex. Nature Neurosci. 15(9):1192–1194.
  29. Lebel C, Gee M, Camicioli R, Wieler M, Martin W, Beaulieu C.(2012) Diffusion tensor imaging of white matter tract evolution over the lifespan. 60:340–352.
  30. Scholz J, Klein M, Behrens T, Johansen-Berg H. (2009)Training induces changes in white matter architecture. Nature Neurosci. 12(11):1367–1368.
  31. Hosoda C, Tanaka K, Nariai T, Honda M, Hanakawa T.(2013) Dynamic neural network reorganization associated with second language vocabulary acquisition: a multimodal imaging study. J Neurosci. 33(34):13663-72.
  32. Makinodan M, Rosen KM, Ito S, Corfas G. (2012)A Critical Period for Social Experience-Dependent Oligodendrocyte Maturation and Myelination. 337:1357–1360.
  33. Bick J, Zhu T, Stamoulis C, Fox NA, Zeanah C, Nelson CA. (2015)Effect of early institutionalization and foster care on long-term white matter development: a randomized clinical trial. JAMA Pediatr. 169(3):211–219.
  34. Young K, Psachoulia K, Tripathi R, Dunn S-J, Cossell L, Attwell D. (2013) Oligodendrocyte dynamics in the healthy adult CNS: evidence for myelin remodeling. 77:873–885.
  35. McKenzie IA, et al. (2014) Motor skill learning requires active central myelination. Science. 2014 Oct 17; 346(6207):318-22.
  36. de Lange AG, et al. (2016) White matter integrity as a marker for cognitive plasticity in aging. Neurobiol Aging. 47():74-82.
  37. Dietz K, Polanco J, Pol S, Sim F. (2016) Targeting human oligodendrocyte progenitors for myelin repair. Exper Neurol. 283(B):489–500.
  38. Hughes E, Kang S, Fukaya M, Bergles D. (2013) Oligodendrocyte progenitors balance growth with self-repulsion to achieve homeostasis in the adult brain. Nature Neurosci. 16(6):668–676.
  39. Ontaneda D, Thompson A, Fox R, Cohen J. (2017) Progressive multiple sclerosis: prospects for disease therapy, repair, and restoration of function. 389:1357–1366.
  40. Diamond MC, et al. (1964) The effects of an enriched environment on the histology of the rat cerebral cortex. J Comp Neurol. 123():111-20.
  41. Kempermann G, Kuhn HG, Gage FH. (1997) More hippocampal neurons in adult mice living in an enriched environment. Nature. 386(6624):493-5.
  42. Sánchez MM, Hearn EF, Do D, Rilling JK, Herndon JG. (1998) Differential rearing affects corpus callosum size and cognitive function of rhesus monkeys. Brain Res. 812(1-2):38-49.
  43. Okuda H, et al. (2009) Environmental enrichment stimulates progenitor cell proliferation in the amygdala. J Neurosci Res. 87(16):3546-53.
  44. Zhao YY, et al. (2012) Enriched environment increases the myelinated nerve fibers of aged rat corpus callosum. Anat Rec (Hoboken). 295(6):999-1005.
  45. Magalon K, Cantarella C, Monti G, Cayre M, Durbec P.(2007) Enriched environment promotes adult neural progenitor cell mobilization in mouse demyelination models. Eur J Neurosci. 25(3):761-71.
  46. Zatorre RJ, Chen JL, Penhune VB. (2007) When the brain plays music: auditory-motor interactions in music perception and production. Nat Rev Neurosci. 8(7):547-58.
  47. Han Y, et al. (2009) Gray matter density and white matter integrity in pianists’ brain: a combined structural and diffusion tensor MRI study. Neurosci Lett. 459(1):3-6.
  48. Imfeld A, Oechslin MS, Meyer M, Loenneker T, Jancke L. (2009) White matter plasticity in the corticospinal tract of musicians: a diffusion tensor imaging study. Neuroimage. 46(3):600-7.
  49. Steele CJ, Bailey JA, Zatorre RJ, Penhune VB. (2013) Early musical training and white-matter plasticity in the corpus callosum: evidence for a sensitive period. J Neurosci. 33(3):1282-90.
  50. Metzler-Baddeley C, et al. (2014) Improved Executive Function and Callosal White Matter Microstructure after Rhythm Exercise in Huntington’s Disease. J Huntingtons Dis. 3(3):273-83.
  51. Sampaio-Baptista C., et al. (2013) Motor skill learning induces changes in white matter microstructure and myelination. J Neurosci. 33(50):19499-503.
  52. Xiao L, et al. (2016) Rapid production of new oligodendrocytes is required in the earliest stages of motor-skill learning. Nat Neurosci. 19(9):1210-1217.
  53. Engvig A, et al. (2012) Memory training impacts short-term changes in aging white matter: a longitudinal diffusion tensor imaging study. Hum Brain Mapp. 33(10):2390-406.
  54. Tang YY, Hölzel BK, Posner MI.(2015) The neuroscience of mindfulness meditation. Nat Rev Neurosci. 16(4):213-25.
  55. Posner MI, Tang YY, Lynch G. (2014) Mechanisms of white matter change induced by meditation training. Front Psychol. 5:1220.
  56. Tang YY, Lu Q, Fan M, Yang Y, Posner MI. (2012) Mechanisms of white matter changes induced by meditation. Proc Natl Acad Sci U S A. 109(26):10570-4.
  57. Kang DH, et al. (2013) The effect of meditation on brain structure: cortical thickness mapping and diffusion tensor imaging. Soc Cogn Affect Neurosci. 8(1):27-33.
  58. Oberlin LE, et al. (2016) White matter microstructure mediates the relationship between cardiorespiratory fitness and spatial working memory in older adults. Neuroimage. 131():91-101.
  59. Burzynska AZ , et al. (2014) Physical activity and cardiorespiratory fitness are beneficial for white matter in low-fit older adults. PLoS. 9(9):e107413.
  60. Tian Q, et al. (2014) Physical activity predicts microstructural integrity in memory-related networks in very old adults. J Gerontol A Biol Sci Med Sci. 69(10):1284-90.
  61. Connor JR, Menzies SL. (1996) Relationship of iron to oligodendrocytes and myelination. Glia. 17(2):83-93.
  62. Todorich B, Pasquini JM, Garcia CI, Paez PM, Connor JR. (2009) Oligodendrocytes and myelination: the role of iron. Glia. 57(5):467-78.
  63. Algarin C, et al. (2017) Differences on Brain Connectivity in Adulthood Are Present in Subjects with Iron Deficiency Anemia in Infancy. Front Aging Neurosci. 9:54.
  64. Stephenson E, Nathoo N, Mahjoub Y, Dunn JF, Yong VW. (2014) Iron in multiple sclerosis: roles in neurodegeneration and repair. Nat Rev Neurol. 10(8):459-68.
  65. Steiger TK, Weiskopf N, Bunzeck N.(2016) Iron Level and Myelin Content in the Ventral Striatum Predict Memory Performance in the Aging Brain. J Neurosci. 36(12):3552-8.
  66. Yehuda S, Rabinovitz S, Mostofsky DI. (2005) Essential fatty acids and the brain: from infancy to aging. Neurobiol Aging. 26 Suppl 1():98-102.
  67. Xu J, Li Y, Lin H, Sinha R, Potenza MN.(2013) Body mass index correlates negatively with white matter integrity in the fornix and corpus callosum; a diffusion tensor imaging study. Hum Brain Mapp. 34(5):1044–1052.
  68. Yoon H, et al. (2016) Interplay between exercise and dietary fat modulates myelinogenesis in the central nervous system. Biochimica et Biophysica Acta. 1862(4):545–555.
  69. Kullmann S, Schweizer F, Veit R, Fritsche A, Preissl H. (2015) Compromised white matter integrity in obesity. Obes Rev. 16(4):273-81.
  70. Piccolo LR, Merz EC, He X, Sowell ER, Noble KG. (2016) Pediatric Imaging, Neurocognition, Genetics Study. Age-Related Differences in Cortical Thickness Vary by Socioeconomic Status. PLoS One. 11(9):e0162511.
  71. Howell BR, et al. (2013) Brain white matter microstructure alterations in adolescent rhesus monkeys exposed to early life stress: associations with high cortisol during infancy. Biol Mood Anxiety Disord. 3(1):21.
  72. Liu J, et al. (2012) Impaired adult myelination in the prefrontal cortex of socially isolated mice. Nat Neurosci. 15(12):1621-3
  73. Makinodan M, Rosen KM, Ito S, Corfas G. (2012) A critical period for social experience-dependent oligodendrocyte maturation and myelination. Science. 337(6100):1357-60.
  74. Champagne DL, et al. (2008) Maternal care and hippocampal plasticity: evidence for experience-dependent structural plasticity, altered synaptic functioning, and differential responsiveness to glucocorticoids and stress. J Neurosci. 28(23):6037-45.
  75. Steinman, L. (2009) A molecular trio in relapse and remission in multiple sclerosis. Nat Rev Immunol9, 440–447.
  76. Brandmeir NJ, Murray A, Cheyuo C, Ferari C, Rezai AR. (2019) Deep Brain Stimulation for Multiple Sclerosis Tremor: A Meta-Analysis. Neuromodulation. 2019 Nov 22. doi: 10.1111/ner.13063. [Epub ahead of print]
  77. Abboud H, Hill E, Siddiqui J, Serra A, Walter B. (2017) Neuromodulation in multiple sclerosis. Mult Scler. 23(13):1663-1676.

Reactive Depression: Lost in Translation!


The old classification of depression into Reactive and Endogneous that are still observed in the clinical practice cannot all be accommodated under the current rubric of Major Depression. This is because psychiatric nosology under DSM and its latest 5th edition is still descriptive, and not etiologic. In this article both reactive and endogenous categories of depression are revisited from the perspective of today’s understanding of etiological pathways. From an epigenetic perspective, the old dichotomy of Reactive vs. Endogenous are inter-related through the impact of the environment (e.g. stress). This includes familial or prenatal depression, where the environmental impact is before birth, or childhood depression where the early life stress is the precipitating factor to the genetic susceptibility. In conclusion, searching for both environmental impact (e.g. stressors) and genetic predispositions in depression, even at a clinical level could help clinicians with better therapeutic decisions.

 The differentiation of major depression into ‘reactive (stress-induced)’ vs. ‘endogenous (e.g. genetic)’ dates back to the German psychiatrist, Kurt Schneider (Schneider, 1920) who borrowed the term ‘endogenous’ from Emil Kraepelin. The differentiation was an early attempt at an etiological classification of depression (Mendels & Cochrane C, 1968). Despite the extensive use of these terms and despite the popularity of the catecholamine deficiency hypothesis of depression (Schildkraut, 1965) and the effectiveness of tricyclic antidepressants that began with the introduction of imipramine in the 1950’s, psychiatric nosology then gave up on the attempt of classifying depressions according to etiology.

 Although the aim of DSM-III in 1980 was for psychiatry to do what the rest of medicine does, to classify disease according to cause, this proved impossible and a non-etiological, purely descriptive system was devised that relied on categories based on symptoms and their severity. DSM-III divided the depressions into major and minor (DSM-III, 1980). Almost four decades later, DSM5 continues to be descriptive and non-etiological (DSM5, 2013). This has continued despite research that points to distinguishable pathways leading to the symptoms of major depression (Ghaemi & Vohringer, 2011; Malki et al. 2014; Mizushima et al. 2013; Parker 2000).

In this article an attempt depression is reviewed on a pathophysiological basis through 1) the impact of stressful events and their timing 2) gene-environment interactions and 3) biological circuits affected by different kinds of depression. The generic term of “depression” that has been used in this paper, refers mostly to major or unipolar depression, though it can at times also applies to minor depression and dysthymia. This article also excludes the normal reaction of mood to stress below clinical level of severity and dysfunction.

The timing of the stress onset:

In reference to stress leading to depression, there is a major differentiation between an early childhood adversary or later in life (adulthood) stress. While these two types of depression, one with an early onset in childhood or adolescence, and the other one with a later onset in adulthood, could be referred to as “Reactive Depression”, they are fundamentally different. (Hazel NA., et al., 2008) This differentiation between reactive depression in the past decade has been recognized in the literature as “Juvenile” and “adult” onset with different pathophysiological pathways that perhaps demand different treatment pathways as well. (Jaffee SR, et al., 2002; Weissman MM, 2002)

Read the full text here:

Autoimmune Disorders: Relapsing-Remitting Vs. Progressive

Anxiety & Depression Survey

Struggling with Anxiety more than usual so that causes dysfunctions in one or more areas of life seems to be very common and more than the current statistics in DSM5 (Diagnostics and Statistics of Manual of Mental Disorders) 5th edition. Please take a few minutes and answer the following survey as an attempt to identify the true rate or prevalence of the common anxiety disorder that’s medically known as GAD (Generalized Anxiety Disorder). To a get close estimate of the prevalence of this condition, we ask everyone who visits this site to fill out the survey even if you don’t have no history of anxiety or depression. 

Thank You.  

1. How old are you?

2. Do you usually get anxious, tense or stressed upon performance such as in school upon tests, exams, presentations or interviews?


3. Do you usually get anxious, tense or stressed in social situations, crowds or with strangers?


4. Do you dislike and usually try to avoid anxiety provoking situations?


5. Are you a worrier and do you anticipate the worst of the situations?


6. Have you found difficult to control your anxiety and worries?


7. Are you usually restless or feeling keyed up or on edge?


8. Do you feel easily fatigued?


9. Do you usually have difficulty concentrating or experience your mind going blank?


10. Are you usually irritable?


11. Do you usually have muscle tension?


12. Do you usually have any sleep disturbances such as difficulty falling or staying asleep, or having restless, unsatisfying sleep?


13. Have you ever had any anxiety or panic attacks with uncomfortable physical symptoms such as heart race, sweating, shortness of breath, chest pain, dizziness, shakes?


14. Has your anxiety caused dysfunction in any parts of your social, occupational, or any other important parts of your life?


15. Have you ever had any episode of depression?


16. Has your depression been long for more than 2 weeks?


17. Has your depression been reactive to your stress, anxiety and situational?


18. Have you been helpless towards the situations that you could not control?


19. Have you ever become hopeless towards life?  


20. Have you ever been suicidal?


21. Have you ever attempted suicide?


22. Have you ever been diagnosed with GAD (Generalized Anxiety Disorder)?


23. Have you ever been diagnosed with Major Depression?


24. Have you thought or been told that you have mood swings?


25. Have you ever been diagnosed with Bipolar Disorder?


26. When did you first experience your anxiety?


27. When did you first experience your depression?


28. Have you ever sought medical help for your mood condition?


29. Have you ever been in psychotherapy?


30. Have you ever taken any antidepressants?


31. Have you ever taken any tranquilizers such as Lorazepam (Ativan), Clonazepam, Diazepam?


32. Have you ever taken any other psychiatric medications?


33. Have you tried more than a few times to use alcohol or street drugs for alleviation of your mood condition and which one of the following?


34. Does anybody else in your family suffers from anxiety and worries?


Stem Cell Therapy: Does it work and for what?


Stem cells are the primordial or original cells that give rise to life and being of a living thing, from animals and humans. Zygote formed from the fusion of sperm and oocyte is the first line of stem cell that is “totipotent” meaning it gives rise to embryonic stem cells and from there to epiblast and embryonic germ stem cells, that are all “pluripotent” meaning they form all the differentiated cell types of a given tissue. These pluripotent stem cells lineage give rise to the primordial germ cells that form all the tissues from skin to bone marrow and all other body tissues. The aim of stem cell therapy over the past half a century has been to induce pluripotent stem cells (IPS) in different body tissues to repair or replace the damaged tissues and cells of specific organ or parts of the body in vitro (in lab) and in vivo (in live beings) (1-2).

 Bone marrow transplant has been the earliest stem cell therapy in the treatment of leukemia and lymphoma and has been widely clinically practiced over almost half of a century all over the world with quite success. Later on umbilical cord blood storage and use for transplants has been clinically practiced, while other forms of stem cell therapy such as the use of induced pluripotent stem cells (IPS) for a wider treatment of cancers and autoimmune disorders of different organs and tissues have been mostly experimental. Another common clinical use of bone marrow transplants has been in chemotherapy of cancers, to introduce the hematopietic stem cells within the bone marrow to replace the destroyed healthy cells by chemotherapy. The most common side-effects of bone marrow and other transplants traditionally has been graft vs. host reaction that rejects the transplant. Another stem cell therapy, “Prochymal” based on allogenic stem cells therapy using mesenchyme stem cells has been used recently in the management of such transplant rejections (3-4).

 While in the past it was thought that the stem cells are basically in bone marrow and umbilical cords and most organs and tissues unlike the epidermis of the skin do not possess the capacity of renewal, in recent years it has become apparent that some other tissues in fact contain stem cells for potential renewal (5). One main reason of the delay in the stem cells therapy has been lack of recognition of different stem cells across different tissues with different potential capacities unlike the progenitor bone marrow and umbilical cord stem cells. As explained above while many of these stem cells are pluripotent, most are multipotent or unipotent, meaning having the capacity of their own specific tissue cells regeneration (6-7). In fact and with a comprehensive perspective, cancer cells could be considered as stem cells for their capacity of turnover and proliferation. This fact has been known and discussed as early as late 80s, but only recently has received widespread attention and acceptance. The cancer stem cell concept is important for opening a new venue to the novel approaches in anti-cancer therapies that instead of killing all or partial cancer cells with the potential of regrowth, to target the cancer stem cells for final cure with no possibility of relapse (8-9).

 The advancement in stem cell research over years has led to the distraction and culture of progenitor or totipotent stem cells in vitro first from the animal models such as mouse, and now from the human’s blastocysts, with the ability of generation all the differentiated cells of a being such as human, hence “cloning” that puts the science in the jeopardy of Frankenstein as it has long been anticipated and infuriated (10-11). Other than blastocysts, the progenitor or embryonic stem cells with capacity of generating differentiated tissues of the whole being, it has been shown that epiblasts first from mouse and now humans could created such pluripotency (12-14). Moreover and morally riskier is the capability of adult stem cells to be reprogrammed to a pluripotent state, through transferring the adult nucleus into an oocyte or by fusion with a pluripotent cell. The most famous example of this cloning has the creation of “Dolly” the sheep by transferring of a somatic nucleus into an oocyte (15-18).

 From a therapeutic not creational standpoint, the ability of regenerating new cells in the damaged and destroyed tissues is the art and science of IPS (induced pluripotent stem cells). Despite knowing for long that some amphibians could naturally regenerate limbs, eye or other injured body parts, therapeutic regeneration or regrowth of damaged or destroyed tissues medically by IPS is quite recent (2, 19-20). Since the original retrovirus-mediated induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by some defined factors in 2006-2007 (21), rapid progress has been made to generate iPS cells from adult human cells (22), a range of tissues that can be reprogrammed (23), and from patients with specific diseases (24). The number of transcription factors required to generate iPS cells has also been reduced (25), and the efficiency of iPS cell generation has increased (26), and techniques have been devised without viral vectors integration (27).

 From Research to the bed side:

Read the full text here:

Stem Cell Therapy: Does it work and for what?

ADHD:Subtypes or one Type?


The literature on pathophysiology of ADHD is quite inconsistent with mixed results to synthesize all the findings in any domain of neuropsychological, neuroanatomical, neurochemical or genetics to link them to the correspondent clinical phenotypes of the current ADHD subtypes. On a descriptive level, the symptomatology of two distinct ADHD subtypes of hyperactive-impulsive (ADHD-HI) and inattentive (ADHD-I) are quite different and hardly seem to come under the same disease entity as it has long been categorized by DSM classifications with no change in the recent DSM5 (1). While ADHD-I or ADD as it was labeled in the past, it is an “attention-deficit” disorder, ADHD-HI beyond an attention-deficit disorder, it is a behavioural disorder with cardinal symptoms of hyperactivity, impulsivity and behavioural disinhibition (2-4). As a result, the majority of research samples, hence the conclusions of the literature for clinical practice have relied heavily on the “combined subtype” that is an ill-defined combination of both subtypes. This ill-defined combined subtype usually is not consisted of 6 symptoms of either subtypes as required by DSM5, but some of the symptoms of each, in a mixed and arbitrary construct with no clear underlying pathophysiology as either subtypes. This contradicting fact has long caused an intense argument in the literature on the total validity of ADHD as a homogenous or single disorder with a single pathophysiology or two or more heterogeneous disorders with different pathophysiology (5-7), that I will attempt to review and explore in this paper.

 ADHD: Homogenous or Heterogeneous?

In fact throughout the history, ADHD has been a homogeneous condition, first described as “hyperkinetic” or “hyperactive” syndrome or disorder of children, with recognition of “impulsivity” as a component of hyperactivity first by Laufer et al. (8) in 1957. The second edition of DSM, i.e. DSM-II in 1968, (9) published by the APA, that for the first time recognized the condition as a disorder, labeled it as “hyperkinetic reaction of children”. It was not until the third edition of DSM (10) in 1980 that recognized the condition as an attention deficit with hyperactivity and labeled it as such, i.e. ADHD, that we started facing a combined and heterogeneous disorder. Unfortunately since then the research samples have been mostly undifferentiated or of combined subtype with rare comparison between the two subtypes, so to clarify any distinctions between the two if any.

 The few available comparison studies between the subtypes have shown that there is a distinct difference between the two with the conclusion of the most that ADHD is a heterogeneous condition with differences not only in symptomatology and the course of illnesses across the brain development, but differences in cognitive functions and different etiopathophysiology (11-12). Goth-Owens et al. (13) in their comparison study of 572 children and adolescents with pure inattentive subtype (ADD), combined type (ADHD-C) and non-ADHD controls, reported slower cognitive interference speed in the ADD vs. ADHD-C and controls comparisons. A similar result was reported by Carr et al. (14) who reported an attenuated attentional blink versus controls and ADHD-combined addressed in a sample of 145 ADD/ADHD and typically developing comparison adolescents (aged 13-17). A similar result has been reported by Solanto et al. (15 ) that predominantly inattentive subtype show worse performance than combined subtype and control groups on the WISC-III Processing Speed Index. This has made some researchers to question the validity of DSM current diagnostic criteria of ADHD to include two distinct subtypes of inattentive and hyperactive/impulsive under the same diagnostic umbrella. (16) Martel et al. (17) in comparison between the two subtypes, reported “a composite executive function factor was significantly related to inattentive but not hyperactive-impulsive symptoms.” The authors concluded “Executive function weakness in adolescent ADHD is specifically related to symptoms of inattention-disorganization.” Nigg et al. (18) also reported that symptoms of inattention-disorganization were uniquely related to executive functioning when hyperactivity-impulsivity controlled. “Inattention was associated with slower response speed, and hyperactivity-impulsivity with faster output speed. Results were not accounted for by IQ, age, gender, education level, or comorbid disorders.” Also Marshal et al. (19) found academic underachievement in a group of 6-12 years old with ADHD without hyperactivity. Friedman et al. (20) have reported that such cognitive deficits continue until late adolescence and Nigg et al. (21) who report their extensions to adulthood.

Read the full text here:

ADHD:Subtypes or one Type?

Hating Chemicals: Natural Medicines and Vitamins


Natural medicine or Alternative Medicine or the field of Naturopathy with their widespread health food stores that have filled up the shelves of pharmacies as well is based on the propaganda that medications are chemicals and unsafe and their own products natural and safe. The field of naturopathy and the natural or herbal medicines that have dominated the health products market and sell more than prescription medicines, is solely based on the notion that the prescribed medications are chemicals and theirs are not. The irony is that everything is chemical, the oxygen in the air that we breath (O2), the water that we drink (H2O), and all the food that we eat, and so on.

In fact the prescribed medications that are nowadays synthesized in pharmaceutical factories have been originally made out of plants, e.g. Digoxin for heart attacks, Atropine for pupillary dilatation and else, Codeine for pain relief, L-Dopa for treatment of Parkinson’s, Aspirin, Quinidine an anti-arrhythmic, Reserpine a hypotensive, Theophylline a diuretic, and Yohimbine an aphrodisiac among so many others. Investing and profiting from the popular lack of sufficient knowledge and also the mass suggestibility, the field of alternative medicine has gone so far that simple food items such as garlic, cranberry and fish oils have nowadays been packaged in capsules, tablets and sold to consumers (1-2).

Although the science of Medicine originated from the herbs and plants, it was not until the modern era that the real based evidence medicine as we know it developed a competitor as “alternative medicine” to promote the use of natural medicine and other forms of healings. This alternative medicine or “naturopathy” from the start by the Bavarian priest Sebastian Kneipp in late 19th century to Benedict Lust, the founder of naturopathy in US, started their propaganda against evidence-based or real medicine and medications, including vaccinations even in children and against killing infections such as small pox or chicken pox. Although naturopathy or alternative medicine cover an extensive area and different treatment modalities, e.g. acupuncture, aromatherapy, massage therapy, Chinese medicine, homeopathy, herbology, reflexology, Reiki and chiropractic, the focus here will be on the promotion of the use of natural or herbal medicines, vitamins, minerals and supplements that have become a huge profit making business and available everywhere even on the shelves of pharmacies and grocery stores (3).

 The efficacy and safety of herbal medicines:

In argument against the core of natural or herbal medicine that they are natural and safe while prescription medicines are not, there are numerous studies across the globe demonstrating evidence to the contrary. It is well known even to the lay people that one could get poisoned by food, consuming plants or even coming in touch with them. Mushroom poisoning and contact dermatitis by poison ivy are the two very common examples that almost everyone is aware of. A total of 216 medicinal plants belonging to 77 families in North and Central America and Caribbean have been reported as toxic. These herbal medicines and alike that have been promoted and used for different illnesses such as rheumatism, wound healing, flu, headache, dysentery, gastritis, constipation, diarrhea, body pains, cancer, antiseptic, digestive, diuretic, fever, infections, menopause, dysmenorrhea, postpartum, diabetes, asthma, anemia, inflammation, muscle relaxant, hair loss, seizures, hypertension, anxiety, depression, psychosis, weight loss or simply to purify body and the blood, have been reported to cause many side-effects and toxicities (4).

The list of these untoward effects and toxicities like the claimed positive effects are numerous, e.g. nephrotoxicity (toxicity of kidneys), hepatotoxicity ((toxicity of liver), dermatitis, hypertension, nausea, vomiting, diarrhea, muscle paralysis, cardiotoxicity (toxicity of heart), gastritis, even being carcinogenic, sleepiness, muscle paralysis, respiratory failure, neurotoxicity (toxicity of nerves and central nervous system), causing abortions, hallucinations (hearing voices or seeing visions), edema (swelling), hemorrhage, blurred vision, vertigo, stupor, confusion, being narcotic and addictive among others (5-16).

Other than the above gross and obvious toxicities, the herbal medicines could caused molecular and cellular toxicities (cytotoxicity), even mutagenicity and genotoxicity (causing gene mutations and toxicities). Some herbal medicines could also cause toxicities during pregnancy and reproduction and cause abortions. These facts are only the tip of the iceberg of the possible side-effects and toxicities of the herbal medicines as most people do not report to their physicians and refer to emergency rooms of hospitals when intoxicated. Moreover there are untoward interactions of the herbal or natural medicines with the prescription medications that again many patients do not report to their physicians or pharmacies when use these products in addition to their prescribed medications (17-20).

 The case of naturopathy or homeopathy and their broad advertisements in media, specially in social media, TV, and many journals are beyond control. Nowadays to skip the drug agency controls, many of these products are offered in the common food products such as drinks, teas and even candies and other snacks. Moreover the health benefits of certain herbs, vegetables, plants and food as simple as garlic or fish oil have been exaggerated and they have been produced and released into tablets, capsules and sold in the market at a much higher prices, instead of promoting these basic food items in meals. These propagandas have been at the cost of advertising against the consumption of some food health promoting foods that nowadays are missing from many people’s diet such as dairy products, eggs, lipids, red meat and fruits (21-22).

 Read the full text here:

Hating Chemicals: Natural Medicines and Vitamins

Fibromyalgia/Chronic Fatigue Syndrome: Controversy or Truth?


Fibromyalgia that is diagnosed and labelled by physicians in clinical practice and even research interchangeably with Chronic Fatigue Syndrome is still a controversy by some, while a clear diagnostic entity by others. As the label of fibromyalgia denotes, it is a condition of generalized body (musculoskeletal) and joint pains. The Chronic Fatigue Syndrome label indicates the patient suffering from a general body fatigue. These two labels if they are two conditions may overlap as some patients and present with both generalized symptom clusters. That is why the two conditions are considered by some as one and inter-related. While these conditions were misdiagnosed or under-diagnosed in the past, they may be over-diagnosed in the recent years. Either way the diagnosis of these conditions often is clinical and by history and physical examinations (only if muscle and joint tenderness present) as any lab or imaging tests are often non-conclusive. Therefore the pathophysiology of these conditions is still known by many as idiopathic, without any known aetiology or pathologic pathway(s).

 More than a controversy, Fibromyalgia and Chronic Fatigue Syndrome (FCFS) are elusive and the diagnosis by many could be descriptive and clinical by symptoms counting like major depression. But there is at least one or more types of FCFS that are associated with many other medical conditions, e.g. IBS (Irritable Bowel Syndrome), non-ulcer dyspepsia, esophageal dysmotility, interstitial cystitis, chronic prostatitis, vulvodynia, vulvar vestibulitis, temporomandibular joint syndrome, sickle cell anaemia, osteoarthritis to name a few. The association with some of these comorbidities that are known as autoimmune disorders, could easily classify this type (s) of FCFS as an autoimmune condition(s) (1). The common conception behind the pathogenesis of FCFS is over-focussing on the pain symptoms that could be due to super-sensitivity or hyperalgesia of the nociceptive process in the central nervous system. But here the focus will be more on the type or types of FCFS that have some true underlying pathologies (1-2). This or these pathological condition (s) are inflammatory, systemic throughout the body and associated with one or more inflammatory or autoimmune disorders (e.g. 3-4).

In the Search of a True Pathologic Fibromyalgia & CFS:

A Chronic Pain Syndrome or A Systemic Musculoskeletal Inflammation?

The first thing to reach the truth of FCFS is to separate these two different conditions that currently are diagnosed under the generic umbrella of fibromyalgia and chronic fatigue syndrome. First of all since both a chronic pain syndrome due to hyperalgesia or super-sensitivity of the nociceptive receptors in the central nervous system, and a systemic musculoskeletal inflammation could cause chronic fatigue syndrome, this secondary or post-morbid condition in this article will be excluded and the literature on fibromyalgia is solely explored (5-8).

 Although a systemic musculoskeletal inflammatory condition could cause chronic generalized body pain, but the reason for the pain is not hyperalgesia or hyper-sensitivity of the nociceptive receptors in the central nervous system, but peripheral inflammations. This inflammatory condition is separated and searched for its underpinning pathology as the true pathological fibromyalgia, as pain even a generalized type could be subjective and not a true objective and pathological condition. Even tenderness of the muscles and joints without any proof of underlying pathology such as inflammation could be all subjective. Therefore this subjective condition or Chronic Pain Syndrome that could be due to a hyperalgesia or hyper-sensitivity of the nociceptive receptors of the brain or in a simpler word due to hyper-perception of pain by an individual is separated from a true fibromyalgia in this paper. This sole pain condition that is simply subjective could be perhaps associated more with other subjective conditions such as depression or being influenced by psychosocial processes (9-12).

Fibromyalgia: A Systemic Musculoskeletal Inflammatory Condition  

Unfortunately since most samples of fibromyalgia studies are mixed with chronic pain syndrome and other subjective conditions without any underlying physical pathology, the physical findings of any inflammatory biomarkers are below the real level of the pathological reality of the condition. But despite this limitation, there are studies that have been able to show the presence of an underlying inflammatory process in the true cases of fibromyalgia.

Read the full text here:

Fibromyalgia/Chronic Fatigue Syndrome: Controversy or Truth?

When one is not enough: Multiple Autoimmune Syndrome


The world even the medical filed are all terrified by the cancers, while the autoimmune disorders are more prevalent across the globe. While the incidence of all cancers world wide is about 17 millions cases in 2018 that makes it .22%, the prevalence of only very common autoimmune disorders is over 3.45% or over 266 millions internationally, making them more than 15 times prevalent than the cancers. (1-2) The common autoimmune disorders that to some including physicians might not be recognized as such diseases in the above estimate of prevalence (with an average prevalence per 100,000 in brackets) are as follow: Diabetes type 1 in all ages (946); Hypo- and Hyper-Thyroidism (691); Rheumatoid Arthritis (381); Ulcerative Colitis (378); Crohn’s Disease (225); Psoriasis (197); Multiple Sclerosis (182); Uveitis (149); Polymyalgia Rheumaica (112), Celiac Disease (50); Sjogren Disease (48); Chronic active Hepatitis (45); SLE (Systmeic Lupus Erythematosus) (32); Vilitigo (29); Systemic Sclerosis (23); Alopecia (21); Addison’s Disease (18); Myasthenia Gravis (18); Primary Billiary Cirrhosis (12); and Systemic Vasculitis (10). (1)

 As discussed in a few articles on different cancers such as breast, prostate, ovarian and endometrial, lung, colorectal, skin cancers and leukemia on this site, cancers are mostly epigenetic than genetic (3-10). Of the epigenetic factors, microbial invasions are the frontiers on the assaults and causation of different cancers. The epigenetic factors such as infections as part of their offensive strategies, weaken the defensive power of the targeted organ, causing dysplasia, polyps or other benign forms of tumours before progressing to malignant cancers that are the killers of the assaulted organs. In a relatively similar process, autoimmune disorders are caused by epigenetic factors including microbial invasions. While cancers are localized assaults, autoimmune disorders are more generalized attacks of epigenetics to our living system.


It is not yet very clear to our scientific strive to differentiate at the onset of the invasion which disease will ensue at the end. It seems so far to our limited knowledge that the pathogeneses of either cancers or autoimmune disorders, or the impact of what organ or system of the body are multi-factorial. This depends on the invader, what organ or system it attacks or what is its specialty, and also on the condition of the targeted organ or body system. The control of the invaders is by avoidance (e.g. too much exposure to the sun in skin cancer), prevention (e.g. vaccinations when possible and available), early recognition of he early stages of the attack and recovery (e.g. surgical removal of polyps or benign tumours). But more importantly is the fostering of our body system to be more immune and protective against such invasions that are all around us and often could not be avoided. This strategy is about reinforcing our immune system that is perhaps the major defense against autoimmune disorders (3-15).   

 It is suspected that the incidence of autoimmune disorders are on the rise that could be due more to our less defensive immune system than the stronger environmental factors such as microbial invasions. It also seems that single autoimmune diseases are rising up to multiple autoimmune diseases or syndromes. This makes the hypothesis of increasing the rate of autoimmune disorders due to our poorer immune system seem more right as multiple autoimmune syndromes occur more in the subjects with less defensive or weaker immune system. In this article through a search into our available scarce knowledge data on this growing monster, I will attempt to bring these syndromes and their pathogenesis more to the light of recognition and hope to the arena of prevention (16-18).


Humans: More Knowledge, More Tools, More Vulnerable:

For the sake of simplicity and unified terminology with the rest of the field, the term of Multiple Autoimmune Syndrome (MAS) for any multiple autoimmune disorders that occur together in a person. The condition is so on the rise due to our defenseless immune system that the expert consider MAS when there are three or more of autoimmune disorders clamp together in an individual. About 25 percent of patients with autoimmune diseases have a tendency to develop additional autoimmune disorders. Surprisingly for whatever reason, MAS often involves one dermatological or skin condition such as alopecia, vitiligo or psoriasis (19).

 For long and before the discovery of MAS, the medical field was acknowledged of a few systemic autoimmune disorders, spreading to more than one organ of the body, and the most commonly known is SLE (Systemic Lupus Erythematous) that is a progression from skin lupus but spread beyond to the joints and more. Later on in the course of the history of medical knowledge, we recognized more concurrent autoimmune diseases in autoimmune hepatitis autoimmune bowel diseases, e.g. ulcerative colitis and crohn’s disease. Association of skin autoimmune diseases such as vitiligo and alopecia in MAS is another important and significant observation that could one day lead us to more understanding of the pathogenesis of these metastatic autoimmune disorders. Moreover on the epigenetic or the invader’s front, some such as cytomegalovirus by producing multiple autoantibodies are capable of spreading into different organs and causing MAS (20-21).


Read the full text here:

When one is not enough: Multiple Autoimmune Syndrome

Sport Injuries: When Young and Healthy Break

(To: My daughter Tiffany, Mohammad Ali, Rafael Nadal, Milos Raonic and all the injured athletes of the world) 


When my daughter, a junior tennis player, injured her wrist this summer it took her about two months to recover and get back to the game. Having had to retire from a few important tournaments, I realized more of the significance and self-destruction that sport injuries could cause to a person. We all know about the consequences of sport injuries in famous world sport leaders such as Mohammad Ali who developed Parkinson syndrome (not the disease but what’s called in medicine “Punch Drunk Syndrome” with Parkinson-like symptoms). Sport injuries are almost unavoidable in athletes, and in the tennis the fans know how many operations the current world number one, Rafael Nadal has had just on his knees, or Canadian Milos Ranoic broke his hip at age 20 by falling on the grass court in Wimbledon.

Different sports are more prone to injuries and different parts of the body are more common to injuries in different sports. For example tendonitis of the wrist, elbow, shoulders and injuries to the knees, ankles and foot are more common in tennis. But head injuries are more common in boxing and hockey, while foot, legs and knees injuries are more common in soccer. Overall some sports are more prone to injuries due to the nature of the sport and the behavior of the athletes and due to more lenient rules and prohibition executed by the specific sport authorities and the referees in some specific sports such as hockey. While the physical injuries are more obvious and attended to, the mental and emotional injuries due to the stress and expectations of the athlete performance by the athlete, coaches, fans and families should not be ignored(1).

We need not to forget that sport injuries do not occur only in professional athletes that comprise a small population in sports in general, but in many healthy youngsters who engage in sports curricular in schools or extra-curricular sport activities. There are more than 30 millions injuries alone in the United States in teenagers and children. We also need to realize that some sport injuries when befall on the neck and head could lead to permanent disabilities and loss of lives that often happen to the otherwise healthy and young ones. We need not to be scared and avoid the sports for ourselves and our children, as playing sport or exercise is the best that we or they can do as a guarantee for a healthy life, but we need to know how to do it right so to prevent injuries. Although this article is focused on sport injuries in the athletes of all ages and different levels, but ordinary people who engage in harsh and in-calculated exercises could have injuries as well (2).

In this article after classifying the common sport injuries, considering different age groups, in non-professionals and professionals, and across different sports, and also among ordinary people regarding over-use and improper injuries, prevention of such injuries will be discussed.

 Soft-Tissue Injuries:

Soft-tissue injuries are the most common type of injuries that include simple cuts, lacerations and bruises, easily seen by the naked eyes. But deep soft-tissue injuries that could affect tendons, muscles, blood vessels, nerves and could cause more pains, discomfort and longer disability mostly due to deep inflammations, may be ignored. The most common of these deep soft-tissue injuries are tendonitis and neuritis or neuralgic pains that demand longer and more specific treatments.  

  Read the full text here:


Asthma: A Tribute to Ernesto Che Guevara

(“I went to see an old woman with asthma, a customer at La Gioconda. The poor thing was in a pitiful state, breathing the acrid smell of concentrated sweat and dirty feet that filled her room, mixed with the dust from a couple of armchairs, the only luxury items in her house. On top of her asthma, she had a heart condition. It is at times like this, when a doctor is conscious of his complete powerlessness, that he longs for change: a change to prevent injustice of a system in which only a month ago this poor woman was still earning her living as a waitress, wheezing and panting but facing life with dignity. In circumstances like this, individuals in poor families who can’t pay their way become surrounded by an atmosphere of barely disguised acrimony; they stop being father, mother, sister or brother and become a purely negative factor in the struggle for life and, consequently a source of bitterness for the healthy members of the community who resent their illness as if it were a personal insult to those who have to support them….In those dying eyes there is a submissive appeal for forgiveness and also, often a desperate plea for consolation which is lost to the void, just as their body will be soon lost in the magnitude of mystery surrounding us.”)    

Ernesto Che Guevara,

Motorcycle diaries


Asthma that is the narrowing of the airways of lung, causing difficulty in  breathing with sound of wheeze, is a chronic disease often starts in childhood and is an interaction between the environmental allergens or pathogens and the individual lung’s susceptibility or genetic make up. This early onset asthma that often leads to asthma attacks, frightening the person and the relatives for the fear of inability in total breathing and death, is usually due to an allergic eosinophilic reaction of the lung airways, causing their narrowing due to thickness of their smooth muscle walls and also obstruction caused by reactive sputum (1-3).

 But not all asthma is an allergic eosinophilic reaction of the lung airways and there is a heterogeneity even in the inflammatory asthma known and reported since 1922 by Huber and Koessler (4). It has been shown and reported that any problems with the lung function such as reduced its function even as early as infancy could lead to late on obstructive lung disease such as asthma (5-6). At the same time, having a history of allergy or atopic sensitization as long as not related to such sensitivity in the lung airways, it will not necessarily lead to asthma in childhood. (7) Following an epigenetic model of causation in asthma, the airway hyper-responsiveness or sensitivity or overwhelming the lung airways with too much dust mites, heavy smoking specially at an early age could prolong the childhood asthma into adulthood and also cause exacerbations and further attacks (8).

 Other than the common allergic or eosinophilic asthma with an early onset in life and running a chronic course, microbial invasions of the lungs and respiratory airways, also contribute to asthma. There have been reports on neutrophilic and lymphocytic infiltrations of the lung airways among others causing the narrowing of the airways, hence asthma (9-10). Such infiltrations of other white blood cells even in the airways or sputum of allergic or eosinophilic asthma that for long thought to be due to T helper type 2 disease and as an allergic reaction, has more recently been shown to have an underlying immunologic susceptibility. This is the beginning of a new understanding of asthma and its genetic susceptibility as an immune or perhaps an early autoimmune disease (11-12).

Che Guevara: An Iconic Asthma Sufferer

Ernesto Guevara was an Argentine physician, who later on by his Cuban comrades was popularized as “Che”, meaning comrade or friend, and since then he has been known as Che Guevara. Before joining the Cuban revolution along with Fidel and Raul Castro and other guerillas, since he suffered from a severe asthma with frequent attacks from his childhood, causing him staying home sick often, he spent all his sick time reading a lot of everything from literature, poetry, philosophy, politics and else. He was also in love of photography and travelling, that his trip across South America, that he called one nation, on a motorcycle with his friend Alberto Granado, under the title of “The Motorcycle Diaries”, before his graduation from medical school and becoming a revolutionary, has been a popular book and film. Despite his severe asthma in his continental trip, he swam at night across Amazon river, a considerable distance of 4 kilometers (2.5 miles) when visiting and helping the lepers in a leper colony in Peru. He unlike the doctors and nurses in the colony, did not wear gloves to shake hands and touch the lepers, but bravely did so with his bare hands.


Read the full text here:


Sleep: Our yet not well discovered inner world!


As adults we spend or should if we dont one third of our time in sleep and as children up to half of their time. We all sleep when tired and when have a good sleep, we would feel rested. We therefore know that the sleep function is for restoration of physical tiredness or fatigue. But sleep is not just for restoration of physical fatigue, but for the restoration of the mental or brain fatigue as well. We may think that during the sleep, the body is totally shout down and in rest. But surprisingly the body is quite active in sleep and like a factory, does self-restoration or repair during the hours of sleep. In deep sleep, if we can get any, the physical restoration or repair is done and in REM (Rapid Eye Movement) or dream stage of sleep, the mental or brain restoration or repair is done. More importantly, many hormones such as growth hormone in children are secreted in sleep and mostly in deep sleep.

 In this paper, the architecture or different stages of sleep will be explored. Then the sleep-wake cycle that is a major component of our circadian rhythm and our body homeostasis and health balance will be exposed. Then the importance of sleep hygiene and lack of it and the disorders of sleep will be discussed. The treatment for sleep disorders and the most common one, insomnia or sleeping pills will not be discussed, as majority are of Benzodiazepine class of drugs, addictive and more habit forming and perpetuating the insomnia. The purpose of this article among the others on this site is more to understand the pathophysiologic process of every disease, so hopefully soon move towards the prevention. Finally what is a very dilemma and question for many, the world of dream and its interpretations will be explained.    


Stages of sleep:

During a night sleep of about 8 hours that is normal for adults, the body or brain goes through about 5 cycles, starting with the stage 1 that is the drowsiness or falling asleep stage lasting only a few minutes. Then the second stage that comprises about %45-50 of a normal adult sleep, that is still light and the person could be aroused by sounds and noises and it is the usual toss and turn stage of sleep. The second stage lasts about 40-45 minutes in each cycle that lasts normally 90 minutes. Then the deep sleep kicks in that is comprised of stages 3 & 4 and most adults do not get it much nowadays, while they need to have it at least %20 of their sleep. These stages of 3 & 4 or deep sleep is for the restoration of physical fatigue and if the person does not get it enough, he or she would not feel rested in the morning.

The next stage of sleep in the cycle is REM (Rapid Eye Movement) sleep that is the dream stage of sleep when the individual enters the world of his or her dreams. This stage that comprises about 20-25% of a night sleep is very active not just for the eyes that moves fast as its term suggests, but the whole body physiology such as heart beat, respiration and else are active even more than in the waking state.  After the first cycle of sleep and REM, the brain may not start over from stage 1, unless someones sleep is very light and broken and keeps waking up in the middle of the night, or after a nightmare. So in a normal restful sleep, after the first cycle and REM, in the second cycle and thereafter, the brain starts from stage 2 and the rest. If the individuals sleep is light, he or she may not go much or at all through the deep sleep of stages 3 &4 that is very common in the modern era of sleepless nights. Therefore everybody gets mostly stage 2 and REM sleep even if one does not remember having any dreams. REM sleep due to its high brain and physiological activity, has the vital role of restoration of brain fatigue. Thats why people with many mind preoccupation or worries may have lots of dreams and even nightmares. The following figure shows how the body enters the different stages of sleep from a waking state and the repeated sleep cycles throughout a night sleep:

 Now in the following each stage of sleep will be discussed in more detail:

Read the full text here:


Training New Physicians:Towards the Future


Physicians or medical doctors who are in charge of our health and well-being world wide, are the products of different medical training standards around the world. The medical schools training could last from 5 to 8 years to graduate a general practitioner or GP. Many medical schools around the world accept the high school graduates after an entry exam into the medical schools that mostly last about 6 years. This could be true in many developed countries such as in Europe. But in US, Canada and UK that hold higher standards in medical training, the entry into medical school is much more sophisticated, longer and more competitive. The applicants in these countries, mostly need a bachelor degree principally in biological science or alike, passing a medical entry test, MCAT (Medical Colleges Admission Test), voluntary works, references, etc. to be accepted to medical schools that is highly competitive. In these countries, then the medical schools training is four years, all focused on medical sciences, from the basic to the clinical and specialties, concluding general practitioners. But there are no jobs or positions for GPs per se in these countries without any specialties, and the shortest training for these would be family practice that lasts two years that is equivalent of GPs in other countries, only after 6 years of post-graduate studies past high school. Therefore one could easily appreciate the difference in the quality of medical training across the globe that could be translated to the quality of medical care. (1-3)

 In many places in the world after graduation from medical schools, there might not be any final general exams of all the pre-clinical and clinical subjects for licensing to practice general medicine. But in US, Canada and UK there are several step exams during the medical school years and after graduation for licensing to practice medicine. In US there are three step of such exams, step 1, testing basic medical sciences in one-day of 8-hours session, step 2 consisted of two sub-steps of clinical knowledge (one-day of 9-hour test) and clinical skills (one-day of practical clinical skills assessment with mock patients). The final step licensing exam, or step 3 of USMLE (United States Medical Licensing Examination) assesses the capability of the application of basic medical and clinical sciences in a two-day exams, 7-hours the first day and 9-hours the second day including clinical skills assessment of 13 simulation cases across major medical disciplines. (4-5)

In Canada there is a similar licensing exams or MCCQE (Medical Council of Canada Qualifying Examination). The first part of MCCQE in 3.5 hours assesses the general medical knowledge, followed by 4-hours of clinical decision making scenarios assessment. The part 2 of MCCQE consists of an objective structured clinical examination in total simulated clinical sessions with patients, that could be taken after one year past the clinical training graduation.

 In England, unlike US and Canada but like many other parts of the world, entry into medical schools are right after graduation from high schools, though the competition is quite high and the rate of acceptance is not more than 10%. Other than traditional or multiple mini-interview, depending on the university, there is the United Kingdom Clinical Aptitude Test (UKCAT) required by most universities and Biomedical Admission Test (BMAT) required by five universities. The medical courses in English medical schools are “problem-based learning” and “lecture-based learning”, and consist of 2-3 years in pre-clinical and 3 years in clinical. The graduates after these 5-6 years of medical training are recognized as Foundation House officer (FHO) and are only permitted to work in supervised clinics and hospitals for one year before being granted independent license to practice as GP and fully register in the General Medical Council. (6-7)


Which system is better?

Is the straight entry from high school to medical school better or an entry after a four years under-grad university education? While entry into medical school in most parts of the world is probably the hardest among any other university courses, when entered most students graduate and there is not much scrutiny and not much failure. A major difference between the two systems is the age and maturity of the applicant. In the straight from high school entry with 6 years course, the applicant is younger and less mature, but in the other system entry after a bachelor degree, the applicant is four years older and more mature. At the same time in the first system of straight six years medical studies, two years basic medical sciences and four years of clinical, the students acquire more knowledge due to studying medicine two years longer. But in the four years course after a bachelor degree, unless those students who have studied four years of basic medical sciences, the rest have only four years to study medicine, including basic and clinical sciences. That is why in countries with this latter system such as US and Canada, there is no GP or licensure to practice after graduation from medical school, unless finishing a specialty training that equivalent to general practice is family practice in these countries that require an additional two years of training. At the end both system in regard with training, education and knowledge could be equivalent, but the only difference will remain age and maturity that the latter system could provide more better health care service due to age and maturity.(8-9)

 Are the licensing examinations well justified?

Read the full text here:


Heart Attack: The Killer of all

(In the memory of my father, a common man, but a poet)


Heart attack that medically known as Myocardial Infarction (MI) is the leading cause of death in the developed countries and the second in the developing world with over 12% of the cause of the death worldwide. The prevalence of such deaths due to heart failure after acute myocardial infarction from the 10% within 30 days and 20% in 5 years in the 70’s, have skyrocketed to 23% and 34%, respectively, in the 90’s. MI usually is a result of Coronary Artery Disease (CAD) of the blood supplies to the heart muscles, that is caused by the occlusion of these arteries by atherosclerotic or lipid plaques that finally rupture and leading to the necrosis or infarction of the cardiac muscles, impeding its pumping function, finally failure and death.


The accumulation of the atherosclerotic plaques which is a long or chronic process, after years warns the individual with symptoms of Angina, e.g. chest pain that my feel like heartburn, radiating to left arm, shoulder and other associated symptoms such as nausea and vomiting, shortness of breath, numbness on the left side, faint feeling and cold sweat, etc. While the precipitating process is long, the end result could be sudden and acute, causing sudden death in minutes even at times without warning or chest pain, so called silent MI or heart attack. In certain situations, MI could happen without a precipitating long process, by coronary arteries spasm due to the use of some illicit drugs such as cocaine and extreme cold among others. (1-2)


Why a beating heart stops?

A beating heart does not stop incessantly, as it looks in the heart attack or myocardial infarction to be sudden and acute. Underlying a stopping heart or attack that is seemingly acute and sudden, there are chronic or long-standing processes that lead to its standstill. There are more than one factor in the process that ends in the heart attack and understanding of these factors could help to prevent sudden death from heart attacks. Although there are many modern treatment modalities from angioplasty to coronary bypass, saving an infarcted or a partially or more complicated dead heart muscle, hence saving lives, the ultimate goal in this arena needs to be prevention of such fatal accidents, as there are many unfortunate instances such as my father’s that any treatment even advanced ones could be already too late!


While to many people, including the patients themselves and their clinicians, heart attack or myocardial infarction is interpreted as coronary arteries (blood supplies to heart itself) occlusion, there is a big and long-standing secret behind it. Moreover the great majority of myocardial infarctions are not fatal, whether treated or untreated, and understanding, prevention and treatment of the precipitating factors are crucial as subsequent attacks may kill the person if not the first one, like in the case of my father. Among many of these factors, there are comorbidities or other illnesses such as diabetes mellitus or hypertension, plus the size and location of the infarct that influence the clinical course, treatment and prevention. The exact anatomic territory infarcted and whether it includes the sinus node or AV node or important neuro-receptors; whether many small arteries are occluded (especially downstream of narrowed main coronary branches) are all important. Also whether the heart is hypertrophied, dilated, infected, or infiltrated; and whether there may be intra-cardiac, extra-cardiac, or intracranial neuro-pathological conditions that could destabilize cardiac electrical activity are needed to be identified. (3)


Moreover it is known that apoptosis plays a major role in myocardial infarction or ischemia, but it also occurs within the heart completely and independently of infarction. There is also the vexing dilemma that an effective coronary collateral circulation, which is determined primarily by trans-anastomotic pressure gradient, is made less effective by exactly those treatments that reestablish flow in an occluded coronary artery. Since thrombolysis and angioplasty are automatically considered urgent treatment for an occluded coronary artery, it is prudent to remember the complex causes that determine whether the patient lives or dies. (3)

Read the full text here:


Skin Cancer: When our good sun hurts! (In the memory of Bob Marley)


Skin cancers are divided into three main types of Basal cell carcinoma, Squamous cell carcinoma and Melanoma, based on the abnormal cell development and proliferation of the type of skin cells. While Basal-cell carcinoma grows slowly and is more localized to the skin tissue, Squamous-cell carcinoma is more aggressive and malignant and can lead to metastatic far distance spread to other body tissues and could be fatal. Melanomas that arise from the melanocytes or skin pigment cells, are the most aggressive, malignant and metastatic, that killed Bob Marley.


While the sun is the source of life on earth and our own life in different aspects depend on its shinning, such as regulation of our circadian rhythm, sleep-wake cycle, and the color of our skin, its excess could contribute to more than 90% of skin cancers cases. The risk nowadays are higher due to a thinner ozone layer, and also the increase fad of artificial tannings as another common source of ultraviolet radiation. The longer and more intense exposures, such as from childhood and the sensitivity of the skin’s subject, for example the white skins, the living zones, such as regions with intense sunshine like Australia and New Zealand, and also the less defensive immune system, the more risk of cancer. (1-2)

Despite all these, and the skin cancer being the most common of all cancers world wide, the early intervention of the skin cancers, even melanoma through removal of the locus of the cancer such as the mole, radiotherapy and medications, have increased the survival rate of all the skin cancers higher than other cancers, close to 90% recovery rate. That takes us to the sad story of Bob Marley, who due to his religious beliefs, refused the full treatment of his melanoma on his toe from 1977, so the cancer spread to his brain and killed him mercilessly on 11 May 1981, at age only 36 and deprived the whole art of music and his global friends form a longer legendary career. (3-5)

Bob Marley, a musical icon, the father of reggae and an international messenger of love and peace, who started with band “The Wailers” , and a national symbol for Jamaica, with all his spirituality, yet could not survive from a small mole on her toe that finally spread to his brain and killed him. His songs such as “One love”, “Is this Love”, “Redemption Song”, “Waiting in Vain”, “Satisfy my Soul”, “O’Woman don’t cry”, “Buffalo Soldier”, “I shot the Sherriff”, “Jamming” and more has no need for an introduction as he is know and loved still to this day by billions. He could easily be the only human’s messenger and representation in popular music and culture. Unfortunately his religious commitment to Rastafari, not to allow the amputation of his cancerous toe so to prevent the spread of the melanoma, deprived him of such a great life and his fans to enjoy his music years longer.


Sunlight: Good, Bad and Ugly

Read the full text here:


Anxiety or Depression: Chicken or Egg?!


In Medicine, the existing of more than one condition or disease is common and it is so called “Comorbidity”. This term by definition refers to the co-existence of two conditions without any relationship such as causal. In other word, comorbidity is the co-existing of two conditions in parallel with no relationship, or different pathophysiology and treatment paths. But in fact that is not the case in many situations, as one condition may give rise to another, or in a better sense, one is primary and the other is secondary. For example hypertension or high blood pressure can lead to stroke and its consequences such as hemiplegia, or diabetes as a primary condition could cause many complications as secondary conditions such as diabetic foot and poor vision, etc. The treatment of the primary condition such as diabetes or osteoporosis could prevent the secondary condition such as diabetic wounds and bone fractures.

 Although some of these co-conditions that are still commonly labeled as “comorbidity” are very obviously primary and secondary to each other with a causal or consequential relationship, some conditions specially in Psychiatry may not look that much related to each other. For example in ADHD, secondary conditions or complications such as depression, oppositional defiant and anti-social behaviours or disorders, substance use disorders, etc. while not much superficially related, they are in fact so, and treatment of ADHD would prevent majority of the others. For the first time, I coined the term “post-morbidity” in ADHD for these secondary conditions or complications that are still in the literature considered loosely “comorbidity” with no apparent causal relationships. (1-2)


A similar relationship exists between depression and anxiety that are commonly comorbid in psychiatry and it is still considered with no causal or temporal relationship as simply “comorbid” in the literature and among experts. If two conditions are causally related and not appreciated as such, it will affect their treatments and both conditions could be treated with two treatments, e.g. two or more medications. But if there is a causal relationship, the treatment of the primary condition would prevent and treat the secondary or “post-morbid” condition, while their pathophysiologic relationship is more appreciated and understood. In this paper, I will show for the first time that such a primary and secondary or “post-morbidity” relationship exists between depression and anxiety that has never to this date been recognized.


Depression and Anxiety: Are they related?

Read the full text here:


Polypharmacy: When too much good is no good!


While medications from the time of antiquity have saved lives and do so more and more over time, have fostered health and increased longevity, too many medications or polypharmacy, particularly if it is not necessary, could cause more harms than benefits. Polypharmacy is seen in all age ranges and in all countries, but more in patients with comorbidities or more than one medical conditions, specially in the older population that is more risky and cause more harms and is more common in developing countries. Although it is assumed commonly that polypharmacy is used in comorbidity conditions, one would be surprised that it is common as well in single medical conditions, when physicians helplessly add to the number of medications to bring under control a non-responsive medial condition. (1-3)


The common and known unfavorable effects or harms of polypharmacy are adverse drug reactions, drug-drug interactions, low adherence to drug therapy and stopping all the medications by the patient, psychological dependency of the patient that only medications could help so not to resort to non-pharmacotherapy modalities if available, also physical dependency if the medication (s) are addictive, and finally the burden of the body tissues and organs by too many medications as foreign objects, specially on liver and kidneys that mostly metabolize the medications. In addition, it is also assumed that polypharmacy causes unnecessary health expenditure, directly due to redundant drug sales and indirectly due to the increased level of hospitalization caused by drug-related problems. Drug-related problems are reported to cause a substantial proportion of all emergency treatment and admissions to hospitals such as in elderly population. (4-7)

 Unfortunately many studies of polypharmacy have primarily been conducted on samples of elderly individuals admitted to hospitals or nursing homes, and only a few have been population-based studies, though some of these again have also been limited to elderly individuals. A recent register study showed that 2/3 of all individuals in a national population who were being prescribed with 5 or more drugs were < 70 years of age, indicating that multiple medication use is not only common in elderly population. A recent Swedish Prescribed Drug Registery in the period of 2005-2008 has shown an 8.2% increase in polypharmacy (>5 medications). (8-9)

In this article, we discuss first polypharmacy in different age groups, elderly, adults, children and adolescents, then across a few common medical disciplines, among comorbidities and single medical conditions.


Polypharmacy across life span:

In the above mentioned Swedish study of polypharmacy between 2005-2008, the prevalence of more than one medication in elderly (>70) was 80% on average, with more than 5 drugs averaged 45%, and more than 10 medications was about 13% on average. In adult age group, the prevalence of more than one medication was 30-40% in the age range of 20-49, but that jumped to > 50% in 50’s and to about 65% in 60’s. The use of more than 5 and 10 medications were rare until the 5th and 6th decades of life that was about 10% and 20%, but the use of more than 10 medications was still rare. In children and adolescence surprisingly the use of more than one medication was quite high about 18% in the first decade and 22% in the second decade of life. The number of individuals on polypharmacy and excessive polypharmacy over 5 medications were quite high, >4,500 in the first decade of life, >9,000 in the second, about 18,000 in the third, >35,000 in the fourth, close to 70,000 in the fifth, >138,000 in the sixth, >220,000 in the seventh decade of life, and in the elderly, 70-79 years old it was close to 250,000 and in the 80-89 years age group, it was >210,000. Surprisinlgy in all age groups the prevalance of polypharmacy has been increasing over years from 2005-2008. (9)

 Read the full text here:


Legalization and Medicalization of Marijuana: When Ignorance Harms!


Marijuana or cannabis extracted from cannabis plant possesses about 483 known compounds including at least 65 cannabinoids, most active THC (Tetrahydrocannabinol). The drug causes “high” or “stoned” feeling, euphoria and change in perception, that are used, mostly smoked for. But the drug has many other effects, or side-effects such as an increase in appetite, impairing cognition (attention, concentration, memory, thinking, learning, planning, etc.), dry mouth, impaired motor skills, red eyes, anxiety or its exacerbation and even paranoia and psychosis in susceptible individuals. Globally an average of 4% of the world population between the ages of 15 and 65 use marijuana. In 2015, 43% of Americans had used cannabis, which increased to 51% in 2016. All these data makes Marijuana, the most commonly used illegal drug both in the world and the United States. (1-2)  


Marijuana or Cannabis: Benefits Vs. Harms

Marijuana or Cannabis that is considered by lay people and lawmakers and some physicians to have potential medical benefits, and medical marijuana has been legislated in many parts of the world, is not as beneficial that is harmful. A recent meta-analysis found that cannabinoids that were originally justified in medical use for treatment of cancer chemotherapy-related nausea and vomiting, or in the treatment of pains and spasticity, showed inconclusive benefits for many of these indications such as improvement of appetite and weight, reduction in tic severity, and improvement of mood or sleep in such patients. On the flip side, cannabinoids and cannabis have acute and long-term adverse effects. In randomized controlled trials, cannabinoids increase the risk of total adverse events, serious adverse events, and dropout due to adverse events. Cannabis impairs cognition, and driving after cannabis use is associated with an increased risk of traffic accidents, including fatal accidents. Long-term cannabis use may lead to dependence, respiratory conditions, psychosis. Cannabis use during pregnancy may compromise certain pregnancy outcomes such as fetal growth, and use during adolescence may compromise neurodevelopment, social adjustment, and vocational success. (3-17)


Data from the Global Burden of Disease Study 2010 suggested that, during 2010, an estimated 13.1 million persons were dependent on cannabis; peaked in the 20- to 24-year age group, and was nearly twice as high in males as in females. Cannabis dependence was associated with 2,057,000 years of life lived with disability and the same number of disability-adjusted life-years. In Canada, these statistics were estimated to be 10,533 years of life lost due to premature mortality, 55,813 years of life lost due to disability, 66,346 disability-adjusted life-years, and 287 deaths in 2012. (3-6) Cannabis use has long been suggested to adversely affect cognition, and a recent systematic review concluded that verbal learning and memory and attention are functions that are most consistently impaired by acute and chronic cannabis use. (7) Psychomotor impairment occurs most obviously during acute intoxication but may be detected in chronic users, as well. The neuropsychological deficits probably arise from impairments that have been identified in hippocampal, prefrontal, subcortical, and other brain networks that subserve cognition. (8)


Read the full text here:


Self-abuse: Why some people abuse their bodies and minds?!


The term self-abuse first may bring to the mind self-harm, self-medicating, drugs abuse, masochism and so on. While these behaviours are common and life wasting, threatening, at times lethal, and important to be reviewed and discussed on its own, this article is not on this subject. This paper will review and discuss more masked and perhaps unrecognized types of human behaviours that are self-abusive, deteriorating and the causes of morbidities and in long-run even life shortening. These behaviours will be classified into sacrificing sleep; restricting or indulging eating behaviours; lack or extreme of physical activities; and unhealthy social activities through social media and virtual life.


Sacrificing Sleep:

More and more people in this era of rat race, profit hunger for a few and financial struggle for the rest, and also dependency on digitalism, social media and alike, cannot get enough of sleep or enough of a good and restful one. Therefore deliberately sacrificing one’s sleep to stay up on their gadgets, social media and else, or having sleep deprivation due to work and else has become an epidemic world wide. Therefore it is not uncommon to see many with sunken eye, fatigue, daytime sleepiness on the wheel, at work and school, or looking clumsy and even with weight gain as a result. (1)

 It is not just the amount and the hours of sleep that people do not get enough, but the quality of sleep! The sleep is comprised of different stages: Stage 1 (when feeling drowsy and sleepy); Stage 2 (or light sleep); Stage 3 & 4 (deep sleep); and REM (Rapid Eye Movement) sleep when one dreams. Every night our sleep goes through 4 to 5 of such a cycle, the first starting from 1-4 then REM, and so on. People who do not wake up in the middle of the night and have a sound sleep, they do not go back to stage 1 after the first cycle. Stage 2 of sleep is the prominent part of the sleep in normal adults, about 45-50% and deep or stages 3 & 4 comprises about 15% and REM about 25%. But most adults with sleep deprivation, insomnia, any other sleep disturbances and disorders, people with anxiety, depression, stress, worries, etc. do not get much of deep sleep or none. While REM sleep is for the restoration of mental fatigue, so anxious and worried people have more of it, stage 3 &4 that is deep or slow wave sleep is for the restoration of physical fatigue, so children get more of it due to their higher physical activities. (2)


Unfortunately even children and teens nowadays due to addiction to their gadgets and games, staying up till late at night, first of all do not get enough hours of sleep, and since they are not physically active, not much of deep or restful sleep. The case for children could be worse and life determining as the growth hormone and many others alike do secrete during stages 3, 4 and REM. The low secretion of growth hormone not only causes slow and poor physical growth, also the growth and development of the rest of the body organs, specially the brain. (3)

 Moreover sleep disturbances such as nightmares, sleep talking, sleep walking, night-terrors, sleep apnea, restless leg syndrome in sleep are becoming more and more common. Although many children, teens and even youngsters whose population of unemployment and dropping schools is on the rise, may sleep in the day and try to compensate their lack of night sleep, their sleep-wake cycle is deranged. The sleep-wake cycle or circadian rhythm, one of the important and vital cycles of life and nature, works on the rise and set of sun, so that is why melatonin a hormone that with addition of sunlight, gives us skin and hair color, and Vitamin D that gets activated by sun to deliver calcium to our bones are all dependent on a normal and healthy sleep-wake cycle. As a result as they say “Nothing is like a good night sleep”! (4-8)

 Read the full text here:


Biosensors and the personalized medicine: Towards the future


Humans have always watched and used animals and plants to detect danger and warning signs for climate changes and natural disasters. One of typical and popular of these had been the use of Canaries in coal mining even up until 1980’s as an early warning system of toxic gases such carbon monoxide, as the gas would kill the bird before affecting the miners. (1) This is the basis of “biosensors” that uses a biological element in an organism such as humans to detect and sense abnormality and diseases, or measuring certain functions. A common old such example is the “artificial cardiac pacemaker” that is implanted in the individual when the natural heart pacemaker for control of the heart beat is not working properly. Cardiac defibrillator also separately or at the same time could be implanted for the individuals with arrhythmia and at risk of cardiac failure. In the case of the pacemaker, when it does not detect normal heartbeat through its sensor, it will stimulate the ventricle of the heart with a short low voltage pulse that will normalize the heart beat. (2-3) Another popular type of biosensor in common use is the blood glucometer in diabetes. This biosensor uses the enzyme glucose oxidase that breaks down the glucose as a measure of blood glucose level. In brief, the biosensors through their transducer or detecting element, detects a measurable change in chemical, physiological or electrical system of the organism such as humans. (4) The blood glucose biosensor monitors blood sugar chemically, and the pacemaker detect abnormal heart beats physiologically and electrically.  

 The application of biosensors since the early use of cardiac pacemaker has evolved over the past half a century, and with more advancement in digitalism, the idea and research is extending to make the biosensors personalized and available to everyone into their digital gadgets such as their cell phones. While the personal gadgets such as cell phones already carry health monitor applications, including vital signs monitoring, the biosensors research’s goal is to bring to the hands of the individuals diagnostic and treatment tools. In this article, I will explore this area of research and advancement in medicine and will show the path towards the future of medicine that will be personalized. Since this area of medicine research is aggressively progressing and a detailed review of the subject is beyond the scope and space of this site, a concise review of a few areas of the biosensor development in a few fields of medicine will be conducted and presented.(5)

 Beyond pacemaker for our Hearts:

Since the heart is one of the most vital organs of the body and mortality due to the cardiac diseases such as heart attacks are still the leading cause, and since the invention of pacemaker saved so many lives in the past, the area of biosensors in cardiology is worth of advancement and consideration. Heart other than being the most vital organ of the body, is also the most active, working 24/7 even in sleep, so is a unique organ functioning physiologically, dynamically, electrically and magnetically. The artificial pacemaker that was adapted in invention from the natural heart pacemaker itself, was based on the electrical currency within the heart. To go beyond and use the biosensors for further diagnostic and treatment tools of the heart diseases, the research needed to invent more sophisticated devices to detect and control other functional parameters of the heart, e.g. physiological, dynamic and magnetics field of the heart beyond electrical conduction. Therefore these parameters such as oxygen saturation, blood flow pressure, its pH, cardiac output, temperature, and the sound of the heart beat all needed to be counted and put into the invention of these devices. (5)


Read the Full text here:


Welcome to a new Medicine site

Translate »