Friday, 17 November 2017
Medicinal plants still comprise a nebulous cloud in biomedical science. We know they have been used since the dawn of man, but there are precious few good quality scientific studies that support their use. Unlike pharmaceutical drugs, plant medicines consist of many different molecules that interact together in the body to have a variety of, poorly understood, pharmacological effects. Despite variably successful attempts to identify single molecules in plants for drug development, we should acknowledge that the whole is greater than a single part. There is an increasing number of clinical studies which strongly imply that root, leaf, and flower extracts of medicinal plants can influence the brain and are effective at treating cognitive disorders. This article series will examine plants where we have double-blind, placebo-controlled studies to support their medicinal influence on the human brain.
St. John’s wort is a commonly known plant that is native to Europe and yields bright yellow flowers. Its name comes from flowering around St. John’s day on the 24th June. St. John’s wort has been used as long ago as the ancient Greeks, and the physician Dioscorides (40–90AD) used it in the treatment of sciatica. However, St. John’s wort has become known as less of a treatment for nerve pain and more so for depression, with multiple double-blind, placebo-controlled trials confirming its antidepressant properties. Authors typically compare St. John’s wort with mainstream anti-depressant drugs and find it has a preferable side effects profile. It is not without its downsides however, as excessive use has been linked to serotonin syndrome, sun sensitivity, and easy skin burning, and more generally with increased pharmaceutical drug metabolism by the liver. This means St. John’s wort may not be suitable for applications alongside other pharmaceutical drugs, and it is contraindicated with serotonin reuptake inhibitors.
American skullcap is a member of the mint family that is native to North America and grows wild in meadows and swamps. It was used by the Native Americans as a sedative and America’s 19th century physicians, the Eclectics, widely used the herb for complaints involving an overactive nervous system such as insomnia, anxiety, and epilepsy. A human double-blind, placebo-controlled study supports skullcap’s application against anxiety, and a mood elevating effect has also been noted. Herbalist’s view both St. John’s wort and American skullcap as ‘nervine tonics’, meaning that they act upon the nervous system medicinally and are also considered to have a long-term renewing effect. While, this claim is yet to be verified by scientific studies, it certainly warrants further investigation.
Ashwagandha, the root of which is a popular home remedy in India, is a plant native to India that is mentioned in the traditional Ayurvedic medical text, the Charaka Samhita, approximately 2000 years ago. Here it is recommended as a tonic for emancipation, reproductive ability, and longevity. In Ayurveda, it is classified as a ‘rasayana herb’, a class of plant that are considered to restore and support long-term health and that overlaps to some degree with the Western definition of a ‘tonic herb’. Two double-blind, placebo-controlled human studies support ashwagandha’s role in the reduction of anxiety. It’s wide-ranging medicinal properties are supported by two additional well-controlled, human clinical studies on osteoarthritis and subclinical hypothyroidism. The emerging picture is that ashwagandha possesses a wide range of medicinal properties that will likely be better understood in the future. Ashwagandha has been well-tolerated across clinical trials, with a side effect profile similar to placebo.
Auddy B, Hazra J, Mitra A, Abedon B, and Ghosal S. A standardized Withania somnifera extract significantly reduces stress-related parameters in chronically stressed humans: A double-blind, randomized, placebo-controlled study. J Am Nutraceutical Assoc. 2008;11:50–6. Access here.
Brock C, Whitehouse J, Tewfik I, and Towell T. (2014). American Skullcap (Scutellaria lateriflora): A Randomised, Double-Blind Placebo-Controlled Crossover Study of its Effects on Mood in Healthy Volunteers. Phytotherapy Research, 28(5), 692-698. DOI: 10.1002/ptr.5044
Castleman, Michael. “The new healing herbs.” Bantam Book, New York (2001): 465-471. ISBN: 1605298891
Chandrasekhar K, Kapoor J, and Anishetty S. A prospective, randomized double-blind, placebo-controlled study of safety and efficacy of a high-concentration full-spectrum extract of ashwagandha root in reducing stress and anxiety in adults. Indian Journal of Psychological Medicine 34.3 (2012): 255. DOI: 10.4103/0253-7176.106022
Dannawi M. Possible serotonin syndrome after combination of buspirone and St John’s Wort. Journal of Psychopharmacology 16.4 (2002): 401-401. DOI: 10.1177/026988110201600420
Hoffman, David. Holistic herbal. Element Books, 1988. ISBN: 1852300248
Laakmann G, Schüle C, Baghai T, and Kieser M. St. John’s wort in mild to moderate depression: the relevance of hyperforin for the clinical efficacy. Pharmacopsychiatry 31.S 1 (1998): 54-59. DOI: 10.1055/s-2007-979346
Markowitz JS, Donovan JL, DeVane CL, Taylor RM, Ruan Y, Wang JS, and Chavin KD. Effect of St John’s wort on drug metabolism by induction of cytochrome P450 3A4 enzyme. Jama 290.11 (2003): 1500-1504. DOI: 10.1001/jama.290.11.1500
Ramakanth GS, Uday Kumar C, Kishan PV, and Usharani P. A randomized, double blind placebo controlled study of efficacy and tolerability of Withaina somnifera extracts in knee joint pain. Journal of Ayurveda and integrative medicine 7.3 (2016): 151-157. DOI: 10.1016/j.jaim.2016.05.003
Scudder, John. Specific Medication and Specific Medicines, 1870. ISBN:
Sharma AK, Basu I, and Singh S1. Efficacy and Safety of Ashwagandha Root Extract in Subclinical Hypothyroid Patients: A Double-Blind, Randomized Placebo-Controlled Trial. The Journal of Alternative and Complementary Medicine (2017). DOI: 10.1089/acm.2017.0183
Szegedi A, Kohnen R, Dienel A, and Kieser M. Acute treatment of moderate to severe depression with hypericum extract WS 5570 (St John’s wort): randomised controlled double blind non-inferiority trial versus paroxetine. Bmj 330.7490 (2005): 503. DOI: 10.1136/bmj.38356.655266.82
Woelk, Helmut. Comparison of St John’s wort and imipramine for treating depression: randomised controlled trial. Bmj 321.7260 (2000): 536-539. PMCID: PMC27467
Wolfson P and Hoffmann DL. An investigation into the efficacy of Scutellaria lateriflora in healthy volunteers. Alternative therapies in health and medicine 9.2 (2003): 74. PMID: 12652886Read More Here..
Thursday, 16 November 2017
UN leaders appeal for immediate lifting of humanitarian blockade in Yemen – lives of millions are at risk
When we are confronted with the acts of excessive and unprovoked violence, we can’t help but wonder what is wrong with individuals committing such crimes. Think of serial killers: what motivates them? Both researchers and society, in general, have wanted to know how to explain the extreme brutality observed in some people. In most cases, they have no mental disorders that could explain their behavior. Even without going to the extremes, most of us did at some point in life come across people whose level of aggressiveness seemed beyond any reasonable explanation. Think of a hooligan looking for any excuse to pick a fight and beat someone up. Or a young boy torturing a defenseless animal with a smile on his face. Multiple theories were invented to this end, ranging from religious explanations (satanic possession) to scientific and psychological theories that involve a variety of mental disorders or problems with brain development.
The idea that excessive aggressiveness and criminal tendency might be heritable traits gained popularity with the publication of Dr. Cesare Lombroso’s book “Criminal Man” in 1878. In the book, Lombroso introduced the concept of the “born criminal”. He also developed the field of criminal anthropology that studied specific anatomical differences between normal and criminal individuals. Lombroso’s theory contributed to the science of eugenics that played a crucial role in the Nazi ideology of selective breeding of a superior race and the policy of exterminating the Untermenschen.
Although Lombroso was eventually proven wrong, the concept that criminal behavior might be linked with genes survived. Evidence that criminal and violent behaviors run in some families was a particularly strong argument to investigate the issue further. These investigations produced rather interesting discoveries.
The question to what degree the predisposition for crime might be genetically determined was first answered by a twin study performed in Denmark. Twins are ideal subjects for genetic research: identical twins have exactly the same sets of genes, while non-identical twins are as similar to each other as usual brothers and sisters. However, both identical and non-identical twins, if brought up together, can be considered as having the same upbringing. The study compared the rate of crime offenses among the identical twins with this rate in non-identical twins. It turned out that a Danish man with an identical twin who has a criminal record is 50% more likely to be an offender himself, as compared with the average Danish man. In non-identical twins, the chances of both of them having the criminal records are 15-30% higher than the average for the population. The findings definitely point to a degree of genetic predisposition. In addition, another study performed in Sweden has shown that when the identical twins were brought up separately, the chances of developing a criminal career were higher among children from parents with criminal records, even when the children were brought up in law-abiding adopted families.
Twin studies can detect correlations but certainly can’t help in finding out which genes are behind these correlations. The study performed in the Netherlands provided important information on the possible identity of such genes. Researchers have studied genetic defects in one particular family with 14 males spanning 4 generations that displayed an unusually high level of aggression and criminal offenses. The subjects in question had very low IQ (around 85) and were prone to impulsive behavior and physical and sexual violence. The researchers found a specific hereditary defect in the family: the gene for monoamine oxidase A (MAOA) was mutated. Mutation prevented the enzyme from working properly. This is important as this enzyme is responsible for breaking down neurotransmitters, including serotonin, dopamine, and noradrenaline. A lack of MAOA activity leads to the rising of neurotransmitter levels in the brain and they, in turn, cause the over-excitation of neurons. The gene for MAOA is located on the X chromosome, and this explains why high levels of aggression were observed only in males. Meanwhile, females have a second X chromosome with the non-mutated functional version of the gene.
An important question, which sparked fierce ethical debate, is to what extent criminal behavior might indeed be genetically programmed. This is a classic discussion of nature vs nurture. To what extent do our genes make us who we are? We easily accept the fact that some people are born smarter or physically stronger than the rest of us. We know that genes are involved in making these individuals who they are. Genes responsible for stronger muscles or better brain connections allow these people to excel where others may struggle. Nonetheless, the idea that some of us are born with a predisposition for a higher level of aggression or reduced empathy appears very unpalatable to many people. However, this idea makes perfect biological sense. We evolved as hunter-gatherers, and at this stage of our evolutionary history, aggressiveness was crucially important for survival. Genetically, we didn’t change since the Stone Age. And this aggressiveness still plays an important role in our society, from competition in the workplace to multiple armed conflicts around the world. Aggression levels, like many other human behavioral traits, can be genetically determined to a degree. This means that there is variability: in some people, the level of aggressiveness is very low, while in others it can be quite high.
Aggressiveness still doesn’t equal crime: although violent crime requires a perpetrator to be aggressive, the two things are not the same. Social factors still play a key role when it comes to the expression of aggressive behavior. It works the same way with other genetic attributes. A born athlete will never reach his Olympic dream and could turn into a couch potato if they don’t train. Most scientists, even the very successful ones, are not born geniuses: they simply worked and studied hard. Similarly, people with a predisposition for higher levels of aggression are at higher risk of becoming criminals when they are exposed to the social factors that lead them in that direction.
Baum ML (2013) The Monoamine Oxidase A (MAOA) Genetic Predisposition to Impulsive Violence: Is It Relevant to Criminal Trials? Neuroethics 6, 287-306. doi: 10.1007/s12152-011-9108-6.
Brunner HG; Nelen MR; van Zandvoort P; Abeling NGGM; van Gennip AH; Wolters EC; Kuiper MA; Ropers HH; van Oost BA (1993) X-linked borderline mental retardation with prominent behavioral disturbance: phenotype, genetic localization, and evidence for disturbed monoamine metabolism. Am. J. Hum. Genet. 52 (6): 1032–9. PMID 8503438.
Buades-Rotger, M., & Gallardo-Pujol, D. (2014). The role of the monoamine oxidase A gene in moderating the response to adversity and associated antisocial behavior: a review. Psychology Research and Behavior Management, 7, 185–200. doi: 10.2147/PRBM.S40458
Christiansen KO. Seriousness of criminality and concordance among Danish twins. In: Hood R, editor. Crime, Criminology and Public Policy. The Free Press; New York: 1974. pp. 63–77.
Farrington DP, Gundry G, West DJ (1975) The familial transmission of criminality. Med Sci Law 15(3):177-86. doi: 10.1177/002580247501500306
Hunter P (2010) The psycho gene. EMBO Rep. 11 (9): 667–9. doi: 10.1038/embor.2010.122.
Kendler, K. S., Lönn, S. L., Morris, N. A., Sundquist, J., Långström, N., & Sundquist, K. (2014). A Swedish national adoption study of criminality. Psychological Medicine, 44(9), 1913–1925. doi: 10.1017/S0033291713002638.
McDermott R et al. (2009) Monoamine oxidase A gene (MAOA) predicts behavioral aggression following provocation. Proc Natl Acad Sci USA 106, 2118–2123. doi: 10.1073/pnas.0808376106.
Taylor S (2013) Criminal Minds: The Infuence of the Monoamine Oxidase AGenotype and Environmental Stressors on Aggressive Behaviour. Burgmann Journal II, 71-77. link hereRead More Here..
Wednesday, 15 November 2017
Tuesday, 14 November 2017
Dissociative identity disorder (DID, commonly referred to as multiple personality disorder) is well known to the general public through multiple movies and books. However, the disease remains poorly understood and rather mysterious for the medical specialists. The definition of this disorder implies that a patient has at least two distinctive and relatively long-lasting identities (sometimes called “alters”) that manifest themselves in a person’s behavior. Their presence is accompanied by memory impairments that cannot be explained by usual forgetfulness.
However, there are no clear clinical criteria to help in the diagnostics. There is a whole range of dissociative disorders that range from daydreaming and lapses in attention to serious pathologies. The diagnostics rely on descriptive data rather than something measurable. This leads to lots of confusion, controversies, and inconsistencies.
Historically, the incidence of multiple personality disorder varied wildly. For a long time, the condition was considered among the rarest psychological disorders, with less than 100 cases described before 1944. The incidence of DID rose sharply in the 1970s–1980s, reaching 20,000 by the end of the century. In addition, this growth was accompanied by the increase in the number of alters reported in patients, from just one to 13–16 by the 1980s. These changes in the statistics might have been caused by increasing recognition of the disease symptoms among practitioners, but also led to the growing skepticism in the research community about the very existence of this distinct condition.
The variability on the geographic distribution of this condition is substantial too: the disorder is diagnosed in the US much more frequently than anywhere else. The overwhelming majority of publications on this condition originate from North America, making some researchers believe that DID is a purely American disease confined to this continent. This further adds to the skepticism of many health practitioners: there are no reasons to believe that qualified specialists capable of recognizing this condition are vastly underrepresented in other developed countries.
There is little clarity regarding what causes the disorder. The iatrogenic hypothesis suggests that DID can be a result of psychotherapeutic treatment, while the traumatogenic hypothesis states that the disease develops as a result of severe trauma, usually in childhood. Some researchers believe that most cases of DID are pseudogenic, i.e., simulated. There is an opinion that many patients want to believe that they have the disorder, to explain the inconsistencies in their own behavior.
The incidence of DID is 5–9 times higher in females compared to males. Again, there is no agreement among specialists regarding what causes such a big gender difference.
The potential reasons for the sharp increase in the incidence of DID were examined in the scientific literature. Although there are many possible explanations for this phenomenon, the iatrogenic explanation appears to be the most substantiated. The unusually large number of diagnosis in the 1980s were clustered around a small number of practitioners, many of whom used hypnosis as a therapeutic tool. It is quite possible that under the influence of hypnosis the patients with a higher level of suggestibility may start to believe that they are suffering from split personality disorder, and behave accordingly. The level of hypnotisability of people with the diagnosis of DID is known to be the highest among any clinical population.
The rise of the DID diagnosis numbers also correlated with the growing number of split personality cases in the criminal court cases. The defense on the basis of DID was rarely successful, as it was often assumed that the defenders simply pretend to have the disorder to avoid taking responsibility for their crimes.
An opinion exists that the manifestations of DID are simply the consequences of other disorders such as bipolar disorder, schizophrenia, and borderline personality disorder. Many patients diagnosed with DID have previous history of these and other psychiatric conditions. Another theory suggests that the manifestations of DID are the consequences of trauma. There is plenty of clinical cases in support of this theory, but not so much statistical data.
Nonetheless, it is well proven that people with DID are at higher risk of depression and suicide. The patients often suffer from post-traumatic stress disorder, substance abuse, anxiety and eating disorders. Such statistics are not uncommon in other psychiatric conditions, though.
Importantly, there is a shortage of proper neurological studies of this disorder. Nobody knows what exactly causes it and what kind of changes take place in the brains of patients diagnosed with this disease. The brain imaging data from patients with DID do not reveal any specific diagnostic patterns. Several studies demonstrated that the changes in personality state in the DID patients are associated with certain changes in the blood flow in the brain. There are also differences in the brain blood flow patterns between patients with DID and healthy control subjects. It remains uncertain if these differences can be used in the diagnostics.
The question of how real the majority of DID cases are is yet to be fully answered. In general, researchers agree that there are cases with very pronounced and obvious manifestations that would be rather hard to explain without invoking the concept of DID. However, when it comes to less severe cases, the diagnostic remains really problematic. This creates a problem for patients, as not knowing the specific diagnosis means the lack of clarity with treating the problem. Also, there is no consensus regarding how to treat the split personality disorder. Various psychotherapeutic and hypnotherapeutic techniques are currently used, but their efficacy remains unknown due to the absence of controlled randomised clinical trials. Clearly, there is a lot of room for further research in this field.
Maldonado, JR; Spiegel D (2008) Dissociative disorders — Dissociative identity disorder (Multiple personality disorder). In Hales RE; Yudofsky SC; Gabbard GO; with foreword by Alan F. Schatzberg. The American Psychiatric Publishing textbook of psychiatry (5th ed.). Washington, DC: American Psychiatric Pub.
Reinders AA (2008) Cross-examining dissociative identity disorder: Neuroimaging and etiology on trial. Neurocase. 14 (1): 44–53. doi:10.1080/13554790801992768.
Paris J (1996) Review-Essay: Dissociative Symptoms, Dissociative Disorders, and Cultural Psychiatry. Transcult Psychiatry. 33 (1): 55–68. doi:10.1177/136346159603300104.
Kihlstrom JF (2005) Dissociative disorders. Annual Review of Clinical Psychology. 1 (1): 227–53. doi:10.1146/annurev.clinpsy.1.102803.143925.
Piper A, Merskey H (2004) The persistence of folly: A critical examination of dissociative identity disorder. Part I. The excesses of an improbable concept. Canadian Journal of Psychiatry. 49 (9): 592–600. PMID 15503730.
Spiegel D, Loewenstein RJ, Lewis-Fernández R, Sar V, Simeon D, Vermetten E, Cardeña E, Dell PF (2011) Dissociative disorders in DSM-5. Depression and Anxiety. 28 (9): 824–852. doi:10.1002/da.20874.Read More Here..
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