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How to cite this article:Singh O how to get kamagra prescription P http://jurain.com/portrait-n%c2%b02.html. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity suicide is how to get kamagra prescription one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went into a frenzy as newspapers, how to get kamagra prescription news channels, and social media were full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the how to get kamagra prescription process, reputations of many people associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly started getting distress calls from their patients in despair how to get kamagra prescription with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill how to get kamagra prescription person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's how to get kamagra prescription mental condition and illness and also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is how to get kamagra prescription even a more urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental how to get kamagra prescription health professionals were called by media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints how to get kamagra prescription perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally how to get kamagra prescription unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves how to get kamagra prescription with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media.

Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made how to get kamagra prescription – professional, personal, or as a representative of an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, how to get kamagra prescription Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 094, West Bengal IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain.

However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time.

Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions.

These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT.

In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes.

A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al. Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al.

That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression.

It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus. The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe.

It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage.

Metabolic Neuroimaging Studies. Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT.

Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations.

The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT.

Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT.

This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder.

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration. However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory.

Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered.

However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons. Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question.

However, in light of enduring ECT survivor accounts, there is a need to design studies that specifically answer this question.Financial support and sponsorshipNil.Conflicts of interestThere are no conflicts of interest. References 1.Payne NA, Prudic J. Electroconvulsive therapy. Part I.

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Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A. A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24.

77.Brodaty H, Hickie I, Mason C, Prenter L. A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

Electroconvulsive therapy and risk of dementia in patients with affective disorders. A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr.

Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

How to http://luxurypropertiesofmarcoisland.com/2011/06/marco_island_luxury/ cite this article:Singh O P kamagra wholesale. Aftermath of celebrity suicide – Media coverage and role of psychiatrists. Indian J Psychiatry 2020;62:337-8Celebrity kamagra wholesale suicide is one of the highly publicized events in our country. Indians got a glimpse of this following an unfortunate incident where a popular Hindi film actor died of suicide.

As expected, the media went into a frenzy as newspapers, news channels, and social media were kamagra wholesale full of stories providing minute details of the suicidal act. Some even going as far as highlighting the color of the cloth used in the suicide as well as showing the lifeless body of the actor. All kinds of personal details were dug up, and speculations and hypotheses became the order of the day in the next few days that followed. In the process, reputations of many people kamagra wholesale associated with the actor were besmirched and their private and personal details were freely and blatantly broadcast and discussed on electronic, print, and social media.

We understand that media houses have their own need and duty to report and sensationalize news for increasing their visibility (aka TRP), but such reporting has huge impacts on the mental health of the vulnerable population.The impact of this was soon realized when many incidents of copycat suicide were reported from all over the country within a few days of the incident. Psychiatrists suddenly kamagra wholesale started getting distress calls from their patients in despair with increased suicidal ideation. This has become a major area of concern for the psychiatry community.The Indian Psychiatric Society has been consistently trying to engage with media to promote ethical reporting of suicide. Section 24 (1) of Mental Health Care Act, 2017, forbids publication of photograph of mentally ill kamagra wholesale person without his consent.[1] The Press Council of India has adopted the guidelines of World Health Organization report on Preventing Suicide.

A resource for media professionals, which came out with an advisory to be followed by media in reporting cases of suicide. It includes points forbidding them from putting stories in prominent positions and unduly repeating them, explicitly describing the method used, providing details about the site/location, using sensational headlines, or using photographs and video footage of the incident.[2] Unfortunately, the advisory seems to have little effect in the aftermath of celebrity suicides. Channels were full of speculations about the person's mental kamagra wholesale condition and illness and also his relationships and finances. Many fictional accounts of his symptoms and illness were touted, which is not only against the ethics but is also contrary to MHCA, 2017.[1]It went to the extent that the name of his psychiatrist was mentioned and quotes were attributed to him without taking any account from him.

The Indian Psychiatric Society has written to the Press Council of India underlining this concern and asking for measures to ensure ethics in reporting suicide.While there is a need for engagement with media to make them aware of the grave impact of negative suicide reporting on the lives of many vulnerable persons, there is even a more kamagra wholesale urgent need for training of psychiatrists regarding the proper way of interaction with media. This has been amply brought out in the aftermath of this incident. Many psychiatrists and mental health professionals were called by kamagra wholesale media houses to comment on the episode. Many psychiatrists were quoted, or “misquoted,” or “quoted out of context,” commenting on the life of a person whom they had never examined and had no “professional authority” to do so.

There were even stories with byline of a psychiatrist where the content provided was not only unscientific but also way beyond the expertise of a psychiatrist. These types of viewpoints perpetuate stigma, myths, and “misleading concepts” about psychiatry and are detrimental to the image of psychiatry in addition kamagra wholesale to doing harm and injustice to our patients. Hence, the need to formulate a guideline for interaction of psychiatrists with the media is imperative.In the infamous Goldwater episode, 12,356 psychiatrists were asked to cast opinion about the fitness of Barry Goldwater for presidential candidature. Out of 2417 respondents, 1189 psychiatrists reported him to be mentally unfit while none had actually examined him.[3] This led to the formulation of “The Goldwater Rule” by the American Psychiatric Association in 1973,[4] but we have witnessed the same phenomenon at the time of presidential candidature of Donald Trump.Psychiatrists should be encouraged to interact with media to provide scientific information about mental illnesses and reduction of stigma, but “statements to the media” can be a double-edged sword, kamagra wholesale and we should know about the rules of engagements and boundaries of interactions.

Methods and principles of interaction with media should form a part of our training curriculum. Many professional societies have guidelines and resource books for interacting with media, and psychiatrists should familiarize themselves kamagra wholesale with these documents. The Press Council guideline is likely to prompt reporters to seek psychiatrists for their expert opinion. It is useful for them to have a template ready with suicide rates, emphasizing multicausality of suicide, role of mental disorders, as well as help available.[5]It is about time that the Indian Psychiatric Society formulated its own guidelines laying down the broad principles and boundaries governing the interaction of Indian psychiatrists with the media.

Till then, it is desirable to be guided by the following broad principles:It should be assumed that no statement goes “off the record” as the media person is most likely recording the interview, and we should also record any such conversation from our endIt should be clarified in which capacity comments are being made – professional, personal, or as a representative of kamagra wholesale an organizationOne should not comment on any person whom he has not examinedPsychiatrists should take any such opportunity to educate the public about mental health issuesThe comments should be justified and limited by the boundaries of scientific knowledge available at the moment. References Correspondence Address:Dr. O P SinghAA 304, Ashabari Apartments, O/31, Baishnabghata, Patuli Township, Kolkata - 700 kamagra wholesale 094, West Bengal IndiaSource of Support. None, Conflict of Interest.

NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_816_20Abstract Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage.

This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods.

These include structural, functional, and metabolic neuroimaging. Body fluid biochemical marker studies. And follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain.

However, there is a lack of evidence at present to suggest that ECT causes brain damage.Keywords. Adverse effect, brain damage, electroconvulsive therapyHow to cite this article:Jolly AJ, Singh SM. Does electroconvulsive therapy cause brain damage. An update.

Indian J Psychiatry 2020;62:339-53 Introduction Electroconvulsive therapy (ECT) as a modality of treatment for psychiatric disorders has existed at least since 1938.[1] ECT is an effective modality of treatment for various psychiatric disorders. However, from the very beginning, the practice of ECT has also faced resistance from various groups who claim that it is coercive and harmful.[2] While the ethical aspects of the practice of ECT have been dealt with elsewhere, the question of harmfulness or brain damage consequent upon the passage of electric current needs to be examined afresh in light of technological advances and new knowledge.[3]The question whether ECT causes brain damage was reviewed in a holistic fashion by Devanand et al. In the mid-1990s.[4],[5] The authors had attempted to answer this question by reviewing the effect of ECT on the brain in various areas – cognitive side effects, structural neuroimaging studies, neuropathologic studies of patients who had received ECT, autopsy studies of epileptic patients, and finally animal ECS studies. The authors had concluded that ECT does not produce brain damage.This narrative review aims to update the evidence with regard to whether ECT causes brain damage by reviewing relevant literature from 1994 to the present time.

Framing the Question The Oxford Dictionary defines damage as physical harm that impairs the value, usefulness, or normal function of something.[6] Among medical dictionaries, the Peter Collins Dictionary defines damage as harm done to things (noun) or to harm something (verb).[7] Brain damage is defined by the British Medical Association Medical Dictionary as degeneration or death of nerve cells and tracts within the brain that may be localized to a particular area of the brain or diffuse.[8] Going by such a definition, brain damage in the context of ECT should refer to death or degeneration of brain tissue, which results in the impairment of functioning of the brain. The importance of precisely defining brain damage shall become evident subsequently in this review.There are now many more tools available to investigate the structure and function of brain in health and illness. However, there are obvious ethical issues in designing human studies that are designed to answer this specific question. Therefore, one must necessarily take recourse to indirect evidences available through studies that have been designed to answer other research questions.

These studies have employed the following methods:Structural neuroimaging studiesFunctional neuroimaging studiesMetabolic neuroimaging studiesBody fluid biochemical marker studiesCognitive impairment studies.While the early studies tended to focus more on establishing the safety of ECT and finding out whether ECT causes gross microscopic brain damage, the later studies especially since the advent of advanced neuroimaging techniques have been focusing more on a mechanistic understanding of ECT. Hence, the primary objective of the later neuroimaging studies has been to look for structural and functional brain changes which might explain how ECT acts rather than evidence of gross structural damage per se. However, put together, all these studies would enable us to answer our titular question to some satisfaction. [Table 1] and [Table 2] provide an overview of the evidence base in this area.

Structural and Functional Neuroimaging Studies Devanand et al. Reviewed 16 structural neuroimaging studies on the effect of ECT on the brain.[4] Of these, two were pneumoencephalography studies, nine were computed tomography (CT) scan studies, and five were magnetic resonance imaging (MRI) studies. However, most of these studies were retrospective in design, with neuroimaging being done in patients who had received ECT in the past. In the absence of baseline neuroimaging, it would be very difficult to attribute any structural brain changes to ECT.

In addition, pneumoencephalography, CT scan, and even early 0.3 T MRI provided images with much lower spatial resolution than what is available today. The authors concluded that there was no evidence to show that ECT caused any structural damage to the brain.[4] Since then, at least twenty more MRI-based structural neuroimaging studies have studied the effect of ECT on the brain. The earliest MRI studies in the early 1990s focused on detecting structural damage following ECT. All of these studies were prospective in design, with the first MRI scan done at baseline and a second MRI scan performed post ECT.[9],[11],[12],[13],[41] While most of the studies imaged the patient once around 24 h after receiving ECT, some studies performed multiple post ECT neuroimaging in the first 24 h after ECT to better capture the acute changes.

A single study by Coffey et al. Followed up the patients for a duration of 6 months and repeated neuroimaging again at 6 months in order to capture any long-term changes following ECT.[10]The most important conclusion which emerged from this early series of studies was that there was no evidence of cortical atrophy, change in ventricle size, or increase in white matter hyperintensities.[4] The next major conclusion was that there appeared to be an increase in the T1 and T2 relaxation time immediately following ECT, which returned to normal within 24 h. This supported the theory that immediately following ECT, there appears to be a temporary breakdown of the blood–brain barrier, leading to water influx into the brain tissue.[11] The last significant observation by Coffey et al. In 1991 was that there was no significant temporal changes in the total volumes of the frontal lobes, temporal lobes, or amygdala–hippocampal complex.[10] This was, however, something which would later be refuted by high-resolution MRI studies.

Nonetheless, one inescapable conclusion of these early studies was that there was no evidence of any gross structural brain changes following administration of ECT. Much later in 2007, Szabo et al. Used diffusion-weighted MRI to image patients in the immediate post ECT period and failed to observe any obvious brain tissue changes following ECT.[17]The next major breakthrough came in 2010 when Nordanskog et al. Demonstrated that there was a significant increase in the volume of the hippocampus bilaterally following a course of ECT in a cohort of patients with depressive illness.[18] This contradicted the earlier observations by Coffey et al.

That there was no volume increase in any part of the brain following ECT.[10] This was quite an exciting finding and was followed by several similar studies. However, the perspective of these studies was quite different from the early studies. In contrast to the early studies looking for the evidence of ECT-related brain damage, the newer studies were focused more on elucidating the mechanism of action of ECT. Further on in 2014, Nordanskog et al.

In a follow-up study showed that though there was a significant increase in the volume of the hippocampus 1 week after a course of ECT, the hippocampal volume returned to the baseline after 6 months.[19] Two other studies in 2013 showed that in addition to the hippocampus, the amygdala also showed significant volume increase following ECT.[20],[21] A series of structural neuroimaging studies after that have expanded on these findings and as of now, gray matter volume increase following ECT has been demonstrated in the hippocampus, amygdala, anterior temporal pole, subgenual cortex,[21] right caudate nucleus, and the whole of the medial temporal lobe (MTL) consisting of the hippocampus, amygdala, insula, and the posterosuperior temporal cortex,[24] para hippocampi, right subgenual anterior cingulate gyrus, and right anterior cingulate gyrus,[25] left cerebellar area VIIa crus I,[29] putamen, caudate nucleus, and nucleus acumbens [31] and clusters of increased cortical thickness involving the temporal pole, middle and superior temporal cortex, insula, and inferior temporal cortex.[27] However, the most consistently reported and replicated finding has been the bilateral increase in the volume of the hippocampus and amygdala. In light of these findings, it has been tentatively suggested that ECT acts by inducing neuronal regeneration in the hippocampus – amygdala complex.[42],[43] However, there are certain inconsistencies to this hypothesis. Till date, only one study – Nordanskog et al., 2014 – has followed study patients for a long term – 6 months in their case. And significantly, the authors found out that after increasing immediately following ECT, the hippocampal volume returns back to baseline by 6 months.[19] This, however, was not associated with the relapse of depressive symptoms.

Another area of significant confusion has been the correlation of hippocampal volume increase with improvement of depressive symptoms. Though almost all studies demonstrate a significant increase in hippocampal volume following ECT, a majority of studies failed to demonstrate a correlation between symptom improvement and hippocampal volume increase.[19],[20],[22],[24],[28] However, a significant minority of volumetric studies have demonstrated correlation between increase in hippocampal and/or amygdala volume and improvement of symptoms.[21],[25],[30]Another set of studies have used diffusion tensor imaging, functional MRI (fMRI), anatomical connectome, and structural network analysis to study the effect of ECT on the brain. The first of these studies by Abbott et al. In 2014 demonstrated that on fMRI, the connectivity between right and left hippocampus was significantly reduced in patients with severe depression.

It was also shown that the connectivity was normalized following ECT, and symptom improvement was correlated with an increase in connectivity.[22] In a first of its kind DTI study, Lyden et al. In 2014 demonstrated that fractional anisotropy which is a measure of white matter tract or fiber density is increased post ECT in patients with severe depression in the anterior cingulum, forceps minor, and the dorsal aspect of the left superior longitudinal fasciculus. The authors suggested that ECT acts to normalize major depressive disorder-related abnormalities in the structural connectivity of the dorsal fronto-limbic pathways.[23] Another DTI study in 2015 constructed large-scale anatomical networks of the human brain – connectomes, based on white matter fiber tractography. The authors found significant reorganization in the anatomical connections involving the limbic structure, temporal lobe, and frontal lobe.

It was also found that connection changes between amygdala and para hippocampus correlated with reduction in depressive symptoms.[26] In 2016, Wolf et al. Used a source-based morphometry approach to study the structural networks in patients with depression and schizophrenia and the effect of ECT on the same. It was found that the medial prefrontal cortex/anterior cingulate cortex (ACC/MPFC) network, MTL network, bilateral thalamus, and left cerebellar regions/precuneus exhibited significant difference between healthy controls and the patient population. It was also demonstrated that administration of ECT leads to significant increase in the network strength of the ACC/MPFC network and the MTL network though the increase in network strength and symptom amelioration were not correlated.[32]Building on these studies, a recently published meta-analysis has attempted a quantitative synthesis of brain volume changes – focusing on hippocampal volume increase following ECT in patients with major depressive disorder and bipolar disorder.

The authors initially selected 32 original articles from which six articles met the criteria for quantitative synthesis. The results showed significant increase in the volume of the right and left hippocampus following ECT. For the rest of the brain regions, the heterogeneity in protocols and imaging techniques did not permit a quantitative analysis, and the authors have resorted to a narrative review similar to the present one with similar conclusions.[44] Focusing exclusively on hippocampal volume change in ECT, Oltedal et al. In 2018 conducted a mega-analysis of 281 patients with major depressive disorder treated with ECT enrolled at ten different global sites of the Global ECT-MRI Research Collaboration.[45] Similar to previous studies, there was a significant increase in hippocampal volume bilaterally with a dose–response relationship with the number of ECTs administered.

Furthermore, bilateral (B/L) ECT was associated with an equal increase in volume in both right and left hippocampus, whereas right unilateral ECT was associated with greater volume increase in the right hippocampus. Finally, contrary to expectation, clinical improvement was found to be negatively correlated with hippocampal volume.Thus, a review of the current evidence amply demonstrates that from looking for ECT-related brain damage – and finding none, we have now moved ahead to looking for a mechanistic understanding of the effect of ECT. In this regard, it has been found that ECT does induce structural changes in the brain – a fact which has been seized upon by some to claim that ECT causes brain damage.[46] Such statements should, however, be weighed against the definition of damage as understood by the scientific medical community and patient population. Neuroanatomical changes associated with effective ECT can be better described as ECT-induced brain neuroplasticity or ECT-induced brain neuromodulation rather than ECT-induced brain damage.

Metabolic Neuroimaging Studies. Magnetic Resonance Spectroscopic Imaging Magnetic resonance spectroscopic imaging (MRSI) uses a phase-encoding procedure to map the spatial distribution of magnetic resonance (MR) signals of different molecules. The crucial difference, however, is that while MRI maps the MR signals of water molecules, MRSI maps the MR signals generated by different metabolites – such as N-acetyl aspartate (NAA) and choline-containing compounds. However, the concentration of these metabolites is at least 10,000 times lower than water molecules and hence the signal strength generated would also be correspondingly lower.

However, MRSI offers us the unique advantage of studying in vivo the change in the concentration of brain metabolites, which has been of great significance in fields such as psychiatry, neurology, and basic neuroscience research.[47]MRSI studies on ECT in patients with depression have focused largely on four metabolites in the human brain – NAA, choline-containing compounds (Cho) which include majorly cell membrane compounds such as glycerophosphocholine, phosphocholine and a miniscule contribution from acetylcholine, creatinine (Cr) and glutamine and glutamate together (Glx). NAA is located exclusively in the neurons, and is suggested to be a marker of neuronal viability and functionality.[48] Choline-containing compounds (Cho) mainly include the membrane compounds, and an increase in Cho would be suggestive of increased membrane turnover. Cr serves as a marker of cellular energy metabolism, and its levels are usually expected to remain stable. The regions which have been most widely studied in MRSI studies include the bilateral hippocampus and amygdala, dorsolateral prefrontal cortex (DLPFC), and ACC.Till date, five MRSI studies have measured NAA concentration in the hippocampus before and after ECT.

Of these, three studies showed that there is no significant change in the NAA concentration in the hippocampus following ECT.[33],[38],[49] On the other hand, two recent studies have demonstrated a statistically significant reduction in NAA concentration in the hippocampus following ECT.[39],[40] The implications of these results are of significant interest to us in answering our titular question. A normal level of NAA following ECT could signify that there is no significant neuronal death or damage following ECT, while a reduction would signal the opposite. However, a direct comparison between these studies is complicated chiefly due to the different ECT protocols, which has been used in these studies. It must, however, be acknowledged that the three older studies used 1.5 T MRI, whereas the two newer studies used a higher 3 T MRI which offers betters signal-to-noise ratio and hence lesser risk of errors in the measurement of metabolite concentrations.

The authors of a study by Njau et al.[39] argue that a change in NAA levels might reflect reversible changes in neural metabolism rather than a permanent change in the number or density of neurons and also that reduced NAA might point to a change in the ratio of mature to immature neurons, which, in fact, might reflect enhanced adult neurogenesis. Thus, the authors warn that to conclude whether a reduction in NAA concentration is beneficial or harmful would take a simultaneous measurement of cognitive functioning, which was lacking in their study. In 2017, Cano et al. Also demonstrated a significant reduction in NAA/Cr ratio in the hippocampus post ECT.

More significantly, the authors also showed a significant increase in Glx levels in the hippocampus following ECT, which was also associated with an increase in hippocampal volume.[40] To explain these three findings, the authors proposed that ECT produces a neuroinflammatory response in the hippocampus – likely mediated by Glx, which has been known to cause inflammation at higher concentrations, thereby accounting for the increase in hippocampal volume with a reduction in NAA concentration. The cause for the volume increase remains unclear – with the authors speculating that it might be due to neuronal swelling or due to angiogenesis. However, the same study and multiple other past studies [21],[25],[30] have demonstrated that hippocampal volume increase was correlated with clinical improvement following ECT. Thus, we are led to the hypothesis that the same mechanism which drives clinical improvement with ECT is also responsible for the cognitive impairment following ECT.

Whether this is a purely neuroinflammatory response or a neuroplastic response or a neuroinflammatory response leading to some form of neuroplasticity is a critical question, which remains to be answered.[40]Studies which have analyzed NAA concentration change in other brain areas have also produced conflicting results. The ACC is another area which has been studied in some detail utilizing the MRSI technique. In 2003, Pfleiderer et al. Demonstrated that there was no significant change in the NAA and Cho levels in the ACC following ECT.

This would seem to suggest that there was no neurogenesis or membrane turnover in the ACC post ECT.[36] However, this finding was contested by Merkl et al. In 2011, who demonstrated that NAA levels were significantly reduced in the left ACC in patients with depression and that these levels were significantly elevated following ECT.[37] This again is contested by Njau et al. Who showed that NAA levels are significantly reduced following ECT in the left dorsal ACC.[39] A direct comparison of these three studies is complicated by the different ECT and imaging parameters used and hence, no firm conclusion can be made on this point at this stage. In addition to this, one study had demonstrated increased NAA levels in the amygdala following administration of ECT,[34] with a trend level increase in Cho levels, which again is suggestive of neurogenesis and/or neuroplasticity.

A review of studies on the DLPFC reveals a similarly confusing picture with one study, each showing no change, reduction, and elevation of concentration of NAA following ECT.[35],[37],[39] Here, again, a direct comparison of the three studies is made difficult by the heterogeneous imaging and ECT protocols followed by them.A total of five studies have analyzed the concentration of choline-containing compounds (Cho) in patients undergoing ECT. Conceptually, an increase in Cho signals is indicative of increased membrane turnover, which is postulated to be associated with synaptogenesis, neurogenesis, and maturation of neurons.[31] Of these, two studies measured Cho concentration in the B/L hippocampus, with contrasting results. Ende et al. In 2000 demonstrated a significant elevation in Cho levels in B/L hippocampus after ECT, while Jorgensen et al.

In 2015 failed to replicate the same finding.[33],[38] Cho levels have also been studied in the amygdala, ACC, and the DLPFC. However, none of these studies showed a significant increase or decrease in Cho levels before and after ECT in the respective brain regions studied. In addition, no significant difference was seen in the pre-ECT Cho levels of patients compared to healthy controls.[34],[36],[37]In review, we must admit that MRSI studies are still at a preliminary stage with significant heterogeneity in ECT protocols, patient population, and regions of the brain studied. At this stage, it is difficult to draw any firm conclusions except to acknowledge the fact that the more recent studies – Njau et al., 2017, Cano, 2017, and Jorgensen et al., 2015 – have shown decrease in NAA concentration and no increase in Cho levels [38],[39],[40] – as opposed to the earlier studies by Ende et al.[33] The view offered by the more recent studies is one of a neuroinflammatory models of action of ECT, probably driving neuroplasticity in the hippocampus.

This would offer a mechanistic understanding of both clinical response and the phenomenon of cognitive impairment associated with ECT. However, this conclusion is based on conjecture, and more work needs to be done in this area. Body Fluid Biochemical Marker Studies Another line of evidence for analyzing the effect of ECT on the human brain is the study of concentration of neurotrophins in the plasma or serum. Neurotrophins are small protein molecules which mediate neuronal survival and development.

The most prominent among these is brain-derived neurotrophic factor (BDNF) which plays an important role in neuronal survival, plasticity, and migration.[50] A neurotrophic theory of mood disorders was suggested which hypothesized that depressive disorders are associated with a decreased expression of BDNF in the limbic structures, resulting in the atrophy of these structures.[51] It was also postulated that antidepressant treatment has a neurotrophic effect which reverses the neuronal cell loss, thereby producing a therapeutic effect. It has been well established that BDNF is decreased in mood disorders.[52] It has also been shown that clinical improvement of depression is associated with increase in BDNF levels.[53] Thus, serum BDNF levels have been tentatively proposed as a biomarker for treatment response in depression. Recent meta-analytic evidence has shown that ECT is associated with significant increase in serum BDNF levels in patients with major depressive disorder.[54] Considering that BDNF is a potent stimulator of neurogenesis, the elevation of serum BDNF levels following ECT lends further credence to the theory that ECT leads to neurogenesis in the hippocampus and other limbic structures, which, in turn, mediates the therapeutic action of ECT. Cognitive Impairment Studies Cognitive impairment has always been the single-most important side effect associated with ECT.[55] Concerns regarding long-term cognitive impairment surfaced soon after the introduction of ECT and since then has grown to become one of the most controversial aspects of ECT.[56] Anti-ECT groups have frequently pointed out to cognitive impairment following ECT as evidence of ECT causing brain damage.[56] A meta-analysis by Semkovska and McLoughlin in 2010 is one of the most detailed studies which had attempted to settle this long-standing debate.[57] The authors reviewed 84 studies (2981 participants), which had used a combined total of 22 standardized neuropsychological tests assessing various cognitive functions before and after ECT in patients diagnosed with major depressive disorder.

The different cognitive domains reviewed included processing speed, attention/working memory, verbal episodic memory, visual episodic memory, spatial problem-solving, executive functioning, and intellectual ability. The authors concluded that administration of ECT for depression is associated with significant cognitive impairment in the first few days after ECT administration. However, it was also seen that impairment in cognitive functioning resolved within a span of 2 weeks and thereafter, a majority of cognitive domains even showed mild improvement compared to the baseline performance. It was also demonstrated that not a single cognitive domain showed persistence of impairment beyond 15 days after ECT.Memory impairment following ECT can be analyzed broadly under two conceptual schemes – one that classifies memory impairment as objective memory impairment and subjective memory impairment and the other that classifies it as impairment in anterograde memory versus impairment in retrograde memory.

Objective memory can be roughly defined as the ability to retrieve stored information and can be measured by various standardized neuropsychological tests. Subjective memory or meta-memory, on the other hand, refers to the ability to make judgments about one's ability to retrieve stored information.[58] As described previously, it has been conclusively demonstrated that anterograde memory impairment does not persist beyond 2 weeks after ECT.[57] However, one of the major limitations of this meta-analysis was the lack of evidence on retrograde amnesia following ECT. This is particularly unfortunate considering that it is memory impairment – particularly retrograde amnesia which has received the most attention.[59] In addition, reports of catastrophic retrograde amnesia have been repeatedly held up as sensational evidence of the lasting brain damage produced by ECT.[59] Admittedly, studies on retrograde amnesia are fewer and less conclusive than on anterograde amnesia.[60],[61] At present, the results are conflicting, with some studies finding some impairment in retrograde memory – particularly autobiographical retrograde memory up to 6 months after ECT.[62],[63],[64],[65] However, more recent studies have failed to support this finding.[66],[67] While they do demonstrate an impairment in retrograde memory immediately after ECT, it was seen that this deficit returned to pre-ECT levels within a span of 1–2 months and improved beyond baseline performance at 6 months post ECT.[66] Adding to the confusion are numerous factors which confound the assessment of retrograde amnesia. It has been shown that depressive symptoms can produce significant impairment of retrograde memory.[68],[69] It has also been demonstrated that sine-wave ECT produces significantly more impairment of retrograde memory as compared to brief-pulse ECT.[70] However, from the 1990s onward, sine-wave ECT has been completely replaced by brief-pulse ECT, and it is unclear as to the implications of cognitive impairment from the sine-wave era in contemporary ECT practice.Another area of concern are reports of subjective memory impairment following ECT.

One of the pioneers of research into subjective memory impairment were Squire and Chace who published a series of studies in the 1970s demonstrating the adverse effect of bilateral ECT on subjective assessment of memory.[62],[63],[64],[65] However, most of the studies conducted post 1980 – from when sine-wave ECT was replaced by brief-pulse ECT report a general improvement in subjective memory assessments following ECT.[71] In addition, most of the recent studies have failed to find a significant association between measures of subjective and objective memory.[63],[66],[70],[72],[73],[74] It has also been shown that subjective memory impairment is strongly associated with the severity of depressive symptoms.[75] In light of these facts, the validity and value of measures of subjective memory impairment as a marker of cognitive impairment and brain damage following ECT have been questioned. However, concerns regarding subjective memory impairment and catastrophic retrograde amnesia continue to persist, with significant dissonance between the findings of different research groups and patient self-reports in various media.[57]Some studies reported the possibility of ECT being associated with the development of subsequent dementia.[76],[77] However, a recent large, well-controlled prospective Danish study found that the use of ECT was not associated with elevated incidence of dementia.[78] Conclusion Our titular question is whether ECT leads to brain damage, where damage indicates destruction or degeneration of nerves or nerve tracts in the brain, which leads to loss of function. This issue was last addressed by Devanand et al. In 1994 since which time our understanding of ECT has grown substantially, helped particularly by the advent of modern-day neuroimaging techniques which we have reviewed in detail.

And, what these studies reveal is rather than damaging the brain, ECT has a neuromodulatory effect on the brain. The various lines of evidence – structural neuroimaging studies, functional neuroimaging studies, neurochemical and metabolic studies, and serum BDNF studies all point toward this. These neuromodulatory changes have been localized to the hippocampus, amygdala, and certain other parts of the limbic system. How exactly these changes mediate the improvement of depressive symptoms is a question that remains unanswered.

However, there is little by way of evidence from neuroimaging studies which indicates that ECT causes destruction or degeneration of neurons. Though cognitive impairment studies do show that there is objective impairment of certain functions – particularly memory immediately after ECT, these impairments are transient with full recovery within a span of 2 weeks. Perhaps, the single-most important unaddressed concern is retrograde amnesia, which has been shown to persist for up to 2 months post ECT. In this regard, the recent neurometabolic studies have offered a tentative mechanism of action of ECT, producing a transient inflammation in the limbic cortex, which, in turn, drives neurogenesis, thereby exerting a neuromodulatory effect.

This hypothesis would explain both the cognitive adverse effects of ECT – due to the transient inflammation – and the long-term improvement in mood – neurogenesis in the hippocampus. Although unproven at present, such a hypothesis would imply that cognitive impairment is tied in with the mechanism of action of ECT and not an indicator of damage to the brain produced by ECT.The review of literature suggests that ECT does cause at least structural and functional changes in the brain, and these are in all probability related to the effects of the ECT. However, these cannot be construed as brain damage as is usually understood. Due to the relative scarcity of data that directly examines the question of whether ECT causes brain damage, it is not possible to conclusively answer this question.

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Psychol Med 2003;33:1277-84. 35.Michael N, Erfurth A, Ohrmann P, Arolt V, Heindel W, Pfleiderer B. Neurotrophic effects of electroconvulsive therapy. A proton magnetic resonance study of the left amygdalar region in patients with treatment-resistant depression.

Neuropsychopharmacology 2003;28:720-5. 36.Pfleiderer B, Michael N, Erfurth A, Ohrmann P, Hohmann U, Wolgast M, et al. Effective electroconvulsive therapy reverses glutamate/glutamine deficit in the left anterior cingulum of unipolar depressed patients. Psychiatry Res 2003;122:185-92.

37.Merkl A, Schubert F, Quante A, Luborzewski A, Brakemeier EL, Grimm S, et al. Abnormal cingulate and prefrontal cortical neurochemistry in major depression after electroconvulsive therapy. Biol Psychiatry 2011;69:772-9. 38.Jorgensen A, Magnusson P, Hanson LG, Kirkegaard T, Benveniste H, Lee H, et al.

Regional brain volumes, diffusivity, and metabolite changes after electroconvulsive therapy for severe depression. Acta Psychiatr Scand 2016;133:154-64. 39.Njau S, Joshi SH, Espinoza R, Leaver AM, Vasavada M, Marquina A, et al. Neurochemical correlates of rapid treatment response to electroconvulsive therapy in patients with major depression.

J Psychiatry Neurosci 2017;42:6-16. 40.Cano M, Martínez-Zalacaín I, Bernabéu-Sanz Á, Contreras-Rodríguez O, Hernández-Ribas R, Via E, et al. Brain volumetric and metabolic correlates of electroconvulsive therapy for treatment-resistant depression. A longitudinal neuroimaging study.

Transl Psychiatry 2017;7:e1023. 41.Figiel GS, Krishnan KR, Doraiswamy PM. Subcortical structural changes in ECT-induced delirium. J Geriatr Psychiatry Neurol 1990;3:172-6.

42.Rotheneichner P, Lange S, O'Sullivan A, Marschallinger J, Zaunmair P, Geretsegger C, et al. Hippocampal neurogenesis and antidepressive therapy. Shocking relations. Neural Plast 2014;2014:723915.

43.Singh A, Kar SK. How electroconvulsive therapy works?. Understanding the neurobiological mechanisms. Clin Psychopharmacol Neurosci 2017;15:210-21.

44.Gbyl K, Videbech P. Electroconvulsive therapy increases brain volume in major depression. A systematic review and meta-analysis. Acta Psychiatr Scand 2018;138:180-95.

45.Oltedal L, Narr KL, Abbott C, Anand A, Argyelan M, Bartsch H, et al. Volume of the human hippocampus and clinical response following electroconvulsive therapy. Biol Psychiatry 2018;84:574-81. 46.Breggin PR.

Brain-Disabling Treatments in Psychiatry. Drugs, Electroshock, and the Role of the FDA. New York. Springer Pub.

Co.. 1997. 47.Posse S, Otazo R, Dager SR, Alger J. MR spectroscopic imaging.

Principles and recent advances. J Magn Reson Imaging 2013;37:1301-25. 48.Simmons ML, Frondoza CG, Coyle JT. Immunocytochemical localization of N-acetyl-aspartate with monoclonal antibodies.

Neuroscience 1991;45:37-45. 49.Obergriesser T, Ende G, Braus DF, Henn FA. Long-term follow-up of magnetic resonance-detectable choline signal changes in the hippocampus of patients treated with electroconvulsive therapy. J Clin Psychiatry 2003;64:775-80.

50.Bramham CR, Messaoudi E. BDNF function in adult synaptic plasticity. The synaptic consolidation hypothesis. Prog Neurobiol 2005;76:99-125.

51.Duman RS, Monteggia LM. A neurotrophic model for stress-related mood disorders. Biol Psychiatry 2006;59:1116-27. 52.Bocchio-Chiavetto L, Bagnardi V, Zanardini R, Molteni R, Nielsen MG, Placentino A, et al.

Serum and plasma BDNF levels in major depression. A replication study and meta-analyses. World J Biol Psychiatry 2010;11:763-73. 53.Brunoni AR, Lopes M, Fregni F.

A systematic review and meta-analysis of clinical studies on major depression and BDNF levels. Implications for the role of neuroplasticity in depression. Int J Neuropsychopharmacol 2008;11:1169-80. 54.Rocha RB, Dondossola ER, Grande AJ, Colonetti T, Ceretta LB, Passos IC, et al.

Increased BDNF levels after electroconvulsive therapy in patients with major depressive disorder. A meta-analysis study. J Psychiatr Res 2016;83:47-53. 55.UK ECT Review Group.

Efficacy and safety of electroconvulsive therapy in depressive disorders. A systematic review and meta-analysis. Lancet 2003;361:799-808. 56.57.Semkovska M, McLoughlin DM.

Objective cognitive performance associated with electroconvulsive therapy for depression. A systematic review and meta-analysis. Biol Psychiatry 2010;68:568-77. 58.Tulving E, Madigan SA.

Memory and verbal learning. Annu Rev Psychol 1970;21:437-84. 59.Rose D, Fleischmann P, Wykes T, Leese M, Bindman J. Patients' perspectives on electroconvulsive therapy.

Systematic review. BMJ 2003;326:1363. 60.Semkovska M, McLoughlin DM. Measuring retrograde autobiographical amnesia following electroconvulsive therapy.

Historical perspective and current issues. J ECT 2013;29:127-33. 61.Fraser LM, O'Carroll RE, Ebmeier KP. The effect of electroconvulsive therapy on autobiographical memory.

A systematic review. J ECT 2008;24:10-7. 62.Squire LR, Chace PM. Memory functions six to nine months after electroconvulsive therapy.

Arch Gen Psychiatry 1975;32:1557-64. 63.Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction. A prospective three-year follow-up study.

Br J Psychiatry 1983;142:1-8. 64.Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.

Arch Gen Psychiatry 1981;38:89-95. 65.Squire LR, Wetzel CD, Slater PC. Memory complaint after electroconvulsive therapy. Assessment with a new self-rating instrument.

Biol Psychiatry 1979;14:791-801. 66.Calev A, Nigal D, Shapira B, Tubi N, Chazan S, Ben-Yehuda Y, et al. Early and long-term effects of electroconvulsive therapy and depression on memory and other cognitive functions. J Nerv Ment Dis 1991;179:526-33.

67.Sackeim HA, Prudic J, Devanand DP, Nobler MS, Lisanby SH, Peyser S, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;57:425-34. 68.Abrams R.

Does brief-pulse ECT cause persistent or permanent memory impairment?. J ECT 2002;18:71-3. 69.Peretti CS, Danion JM, Grangé D, Mobarek N. Bilateral ECT and autobiographical memory of subjective experiences related to melancholia.

A pilot study. J Affect Disord 1996;41:9-15. 70.Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects.

Ann N Y Acad Sci 1986;462:315-25. 71.Prudic J, Peyser S, Sackeim HA. Subjective memory complaints. A review of patient self-assessment of memory after electroconvulsive therapy.

J ECT 2000;16:121-32. 72.Sackeim HA, Prudic J, Devanand DP, Kiersky JE, Fitzsimons L, Moody BJ, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328:839-46.

73.Frith CD, Stevens M, Johnstone EC, Deakin JF, Lawler P, Crow TJ. Effects of ECT and depression on various aspects of memory. Br J Psychiatry 1983;142:610-7. 74.Ng C, Schweitzer I, Alexopoulos P, Celi E, Wong L, Tuckwell V, et al.

Efficacy and cognitive effects of right unilateral electroconvulsive therapy. J ECT 2000;16:370-9. 75.Coleman EA, Sackeim HA, Prudic J, Devanand DP, McElhiney MC, Moody BJ. Subjective memory complaints prior to and following electroconvulsive therapy.

Biol Psychiatry 1996;39:346-56. 76.Berggren Š, Gustafson L, Höglund P, Johanson A. A long-term longitudinal follow-up of depressed patients treated with ECT with special focus on development of dementia. J Affect Disord 2016;200:15-24.

77.Brodaty H, Hickie I, Mason C, Prenter L. A prospective follow-up study of ECT outcome in older depressed patients. J Affect Disord 2000;60:101-11. 78.Osler M, Rozing MP, Christensen GT, Andersen PK, Jørgensen MB.

Electroconvulsive therapy and risk of dementia in patients with affective disorders. A cohort study. Lancet Psychiatry 2018;5:348-56. Correspondence Address:Dr.

Shubh Mohan SinghDepartment of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh IndiaSource of Support. None, Conflict of Interest. NoneDOI. 10.4103/psychiatry.IndianJPsychiatry_239_19 Tables [Table 1], [Table 2].

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Kat Jercich is senior editor of Healthcare IT News.Twitter. @kjercichEmail. Kjercich@himss.orgHealthcare IT News is a HIMSS Media publication..

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Two weeks of outages Email messages forwarded to Healthcare IT News suggest weeks of uncertainty. On April 27, eMDs sent an email signed by CompuGroup Medical CEO Derek Pickell to hosted Aprima customers detailing the incident.According to the email, "A sophisticated criminal organization carried out a ransomware attack on some of the hosting vendor’s systems, disaster recovery site, and backups." "We do not have confirmation yet that this is a data breach, and if it was, which of our clients were kamagra wholesale impacted, but the eMDs Incident Response Team continues to follow all data integrity and appropriate government, regulatory, and notification protocols," the email continued. "eMDs will be sending a written data breach notice to any customer whose data has been confirmed to have been encrypted," it read. The email encouraged hosted customers to continue operating under HIPAA disaster kamagra wholesale protocols and contingency plans, including using paper-based workflows.

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We also have Aprima, in our kamagra wholesale cardiology group in Sarasota, Florida. We are still down ..." wrote one user on April 29. "We have patients that have been with us for many years and now it’s tough to help them," the user added in a different comment."I am down still will be [two] weeks this Thursday," wrote another on May 4. "As a solo practitioner I expect that I am a low priority." Problems appeared to persist for some customers even after their kamagra wholesale access was restored.

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When this connection happens, the kamagra is able to infect cells and multiply inside them. But monoclonal antibodies can slow or halt the by attaching to the viral spike protein before it reaches the ACE2 receptor. If this happens, the kamagra becomes harmless because it can no longer enter what is kamagra jelly our cells and reproduce.How Are Monoclonal Antibodies Created?. Monoclonal antibodies that neutralize the erectile dysfunction are complicated to manufacture and produce. They must be made inside cells taken from a hamster’s what is kamagra jelly ovary and grown in gigantic steel vats.

The antibodies that these cells manufacture must then be extracted and purified. Unfortunately these monoclonal antibodies, which have been used for other illnesses for years, are often quite expensive.Regeneron’s two antibodies are targeted to the spike protein of erectile dysfunction – the protrusions on the surface of kamagra that give it a crown-like look and are critical for infecting human cells.One of Regeneron’s two antibodies is a replica, or clone, of an antibody harvested from a person who recovered from erectile dysfunction treatment. The second antibody was identified in a mouse what is kamagra jelly that was biologically engineered to have a human immune system. When this mouse was injected with the spike protein, its human immune system generated antibodies against it. One of the most effective mouse antibodies was then harvested and used to form part of this therapy.Eli Lilly’s monoclonal antibody therapy, bamlanivimab, was identified from a blood sample taken from one of the first what is kamagra jelly U.S.

Patients who recovered from erectile dysfunction treatment.Both companies have in place large-scale manufacturing with robust, global supply chains in place to produce the monoclonal antibodies, with many global manufacturing sites to ramp up supply. Eli Lilly has received FDA approval, and Regeneron is still awaiting approval. Unfortunately, there will likely be a shortage of the antibodies in the early going of approvals.Monoclonal Antibodies what is kamagra jelly Plus a treatmentMonoclonal antibodies will be able to complement treatments by offering rapid protection against . When they are given to an individual, monoclonal antibodies provide instantaneous protection for weeks to months. treatments take longer to provide protection since what is kamagra jelly they must challenge the immune system.

But the advantage of a treatment is that they usually provide long-term protection.Regeneron’s and Eli Lilly’s products are both delivered by intravenous injection, after which the patient must be monitored by health care professionals. Since they offer immediate protection, the implications to treat or provide protection to high-risk populations is immense.These medicines have the potential to treat what is kamagra jelly infected patients or prevent of essential health care and public health professionals on the front line of this kamagra. Monoclonal antibodies could also be useful for older people, young children and immunocompromised people for whom treatments either don’t work or can be dangerous.Rodney E. Rohde is a professor clinical laboratory science at Texas State University. This article appeared on The Conversation and is what is kamagra jelly republished under a Creative Commons license.

Read the original here.Face coverings and social distancing are necessary for keeping the novel erectile dysfunction at bay, but are kamagra-related precautions affecting our ability to ward off other ailments down the road?. Health experts may not be able to say for sure yet, but what is kamagra jelly there are ways to balance the two interests. Pro tip?. Get outside (preferably a good distance from people who don't live in your household) and take a deep breath. Your microbiome what is kamagra jelly will thank you.

What is the Microbiome?. Our bodies play host to a wide array of microorganisms that make their home on our what is kamagra jelly skin and inside our guts, airways and other organs. Their presence is so significant that the number of bacteria in our guts is actually greater than the number of human cells in the human body. The organisms' collective DNA is known as the microbiome and scientists have studied its effect on everything from our social lives to our mental health.Put simply. The microbiome provides the immune system what is kamagra jelly with information about potential intruders.

It clues our body in on what is and isn't a threat and helps prepare our white blood cells for battle. Some of the microbiome is built up what is kamagra jelly shortly after birth. A trip down the birth canal followed by months of breastfeeding helps babies form their unique microbiome, but exposure to the natural environment in those first few years of life is crucial as well, experts say. €œAll of these organisms provide data for the immune system,” says Graham Rook, an immunologist and professor emeritus at University College London. €œIt's like what is kamagra jelly the brain.

It has to have data. And just like the brain, it needs the data early in life.” If the body fails to get the right messages about its environment, it may go rogue and attack things it shouldn't, what is kamagra jelly leading to conditions like allergies, asthma and autoimmune disorders. Since the first few years of life are most crucial, Rook is especially concerned that if young children are not leaving their homes, they are not getting the exposure to microbes they need. €œThat is why confining an infant to a high-rise apartment during erectile dysfunction treatment lockdowns is likely to be detrimental,” says Rook. €œThe microbiome of a modern apartment is not a useful exposure.” The Daycare what is kamagra jelly TestA recent study comparing different daycare settings in Finland demonstrated that simply enriching the outdoor play areas with elements of the natural environment had a positive effect on the microbiomes in children.

For four weeks in 2016, young children played on segments of forest floor and sod placed on top of the existing gravel. Instructors at the schools also engaged the children in activities such as planting gardens, resulting in average daily exposure of 90 minutes per day.The results indicated an increase in microbe biodiversity on the skin and in the guts of the what is kamagra jelly children, and a corresponding bump in immune system function. The study offers hope that even children in urban environments can build their microbiomes with some exposure to the natural world. Animals Can Help Bring Exposure, Too “The most evidence-based strategy for improving your microbiome from an immunity [and] asthma perspective is to get a cow,” says Rob Knight, a University of California, San Diego professor and co-founder of the American Gut Project. €œBut that isn’t especially practical if you live in an apartment in the city.”In studies completed by scientist Erika von Mutius, life on a farm and bacteria carried by cows, specifically, appeared to have the best benefit to humans, Knight what is kamagra jelly says.

Dogs and cats that spend time outdoors can also bring in some good microbes, experts say, which provides another reason to adopt a pet while sheltering in place. Diet Also Plays a PartKnight says a diet promoting microbiome diversity would include a diverse what is kamagra jelly range of plants and fermented foods, with limits on sugar and salt. Rook adds that although building a healthy microbiome can be most crucial in the early years, studies indicate that adults can be affected as well.“Sick adults have less diverse gut microbiomes,” Rook says, adding that a diverse diet and time in the natural environment are key to bolstering health. While it is true that humans pick up “data” from other humans and that is a missing piece of the equation now, Rook notes that he is far more concerned about young children who are not leaving their homes and getting exposure to microbes in their natural environments. And if you're worried that a lack of colds this year might lead what is kamagra jelly to an immune system unprepared for next year's kamagraes, experts say that's not exactly how it works.

€œThere’s no evidence that exposure to pathogens per se is good,” Knight says. €œCurrent thinking is that exposure to a wide range of harmless organisms from other people and the environment is what is kamagra jelly good.”So, while the long-term health effects of social distancing might not be fully understood yet, embracing a lifestyle that includes healthy food choices and time spent outdoors may be the best tools at our disposal right now. Rook also suspects that mask-wearing doesn't inhibit the ability to absorb what is needed from the outside world. €œPlenty of small particles from the natural environment are wafting into the lungs,” what is kamagra jelly he says.If you’re feeling anxious or depressed right now, you’re not alone. Daily pressures can trigger stress, and our reaction to those stressors can set off symptoms of anxiety or depression or both.In fact, 79 percent of adults say that the kamagra is adding stress to their lives, according to a recent survey by the American Psychological Association (APA).Normal anxiety is a warning system that alerts us to threats and helps us prepare for challenges.

Depression is a major mental illness that negatively changes how we feel, think and act — it’s not just feeling sad. The two share common symptoms what is kamagra jelly. Both anxiety and depression hurt our ability to concentrate, trigger restlessness and fatigue, and disrupt sleep. They share similar biological mechanisms in the brain, and both can be triggered by social stressors, says Vaile Wright, senior director what is kamagra jelly for health care innovation for the APA.“It’s totally normal to feel abnormal right now,” says Wright. €œWe need to give ourselves some grace, and not judge ourselves for not doing as well as we hope.”When we can't get rid of our stressors, we can improve how we react to feeling anxious or overly worried.

We just need to figure out which tools work best for us, and use them consistently.Mirror, MirrorFor starters, we can shore up our mental health by connecting to our emotions every day. This self-check can include asking ourselves questions what is kamagra jelly like, “How am I today?. € or “Was I triggered today in any way?. € Just the act of saying, “I feel anxious right now,” activates the parts of our brain that helps us organize and regulate our emotions, and also what is kamagra jelly calms the emotional part of the brain, says Alejandra Gonzalez Rodriguez, a family and marriage therapist at the University of Wisconsin School of Medicine and Public Health in Madison. Making this a daily habit is not easy, says Gonzalez Rodriguez, because we’ve lost our natural transitions.

Getting up, traveling to work, taking the kids to school. She suggests starting new routines by adding in habits aimed to make us feel well, and sticking to them.“Every person has to develop their own sense of ownership over this,” Gonzalez Rodriguez says.We can make positive what is kamagra jelly changes by prioritizing what Wright calls the “foundational four”. Healthy food, exercise, adequate sleep and social connections (even if the latter looks different right now).If this advice sounds straight from a parenting handbook, Wright says adults are not that different from children. €œWhen children what is kamagra jelly are hungry, they are not rational. When they are tired, they are not rational,” she says.

€œIt really is that basic.”Carrying around anxiety and depression can make the changes we need for good mental health seem overwhelming. Wright suggests sticking to a basic routine, like getting up and going to bed at the same what is kamagra jelly time and keeping regular mealtimes. Having this foundation in place keeps our emotions balanced enough to find and add stress-reducing coping skills. Toolbox for the SensesWright encourages people what is kamagra jelly to create a toolbox of activities that engage your mind, body and senses, such as puzzles and games, walking or other exercises, taking a hot bath or lighting a scented candle. Assembling a collection of activities from each of these categories that you can rely on is important for your mental health, she says.

The trick with exercise is to find something you will crave, because it takes more willpower to force yourself to do something you don’t like, says Charles Raison, a psychiatrist and researcher specializing in depression at the University of Wisconsin School of Medicine and Public Health. €œIn the abstract, we all want to exercise, but we may not want to put on what is kamagra jelly those running shoes and head outside,” he says. If you don’t feel motivated enough to move, heating your body in a hot bath for 30 minutes, about an hour or so before bedtime, doesn’t call for much discipline but will raise your mood, says Raison. Just keep the water hot, but not so hot what is kamagra jelly you burn yourself.Improve sleep by making your bedroom as cool, dark and quiet as possible. In the morning, expose yourself to light.

Step outside for a few minutes — even cloudy days provide enough light to lift our mood. If you what is kamagra jelly need more of a boost, talk to your doctor about using light therapy. You can also try meditation or mindfulness exercises. These can help us banish destructive thoughts what is kamagra jelly and help manage the stress that triggers anxiety and depression.kamagra SOSUnfortunately, not everything we try at home will help. We may not always recognize when our own anxiety or depression reaches the breaking point, because the progression can be so slow.Be on the lookout for early signs of too much stress, such as irritability in ways not normal for you, like snapping at your family.

Notice if you go several weeks without getting much sleep, or have started drinking to cope.If stress starts to interfere with your life in a big way — you can’t work, you’re skipping classes, you’re not taking care of yourself or your family, and especially if you’re starting to feel life is not worth living or you’re having thoughts of hurting yourself — get help right away, says Raison.You can call your doctor or insurance company for a referral. You can also find therapists through an online locator, such as what is kamagra jelly the one at Psychology Today. If none of those work, try asking friends and family if they have seen anyone or have recommendations, says Wright. You can get immediate help through the National Suicide Prevention Lifeline at 1-800-273-8255.Finally, remember that we all need to cut ourselves some slack, says Wright.“People what is kamagra jelly can expect to have good days and bad days, and that is OK. The trick is, once you’ve had ice cream for lunch, and you’ve just doomscrolled all day, just remember, the next day is a new day,” says Wright.Chances are, you know at least one person with a cat or dog allergy.

Roughly 10–20 percent of people what is kamagra jelly worldwide exhibit some form of allergic symptoms to these common household pets. Given how common allergies to other species are, you may wonder. Can the opposite be true?. Could a cat or dog have an what is kamagra jelly allergic reaction to their owner, or to humans in general?. Maybe, says Douglas Deboer, a dermatologist at the School of Veterinary Medicine at the University of Wisconsin-Madison.

There has been some what is kamagra jelly research and experiments that suggest the possibility that pets can be allergic to humans, but nothing conclusive. If there are cats or dogs with these allergies, they are extremely rare.“Anything’s possible,” Deboer says. €œBut it seems clear that it is not very common, if it exists at all.”Deboer, whose research focuses on skin diseases and allergic reactions in household animals, says reactions to dogs or cats typically occur when someone is allergic to the animal’s dander, flakes of dead skin cells shed from the body. So, in the event that pets what is kamagra jelly can have allergic reactions to human beings, those reactions would stem from exposure to human dander. Deboer says there have been allergy tests done on household pets, but most of these test results are negative.

A very small amount of tests, roughly less than 2 percent, show a reaction to human dander.However, Deboer what is kamagra jelly says that’s far from a conclusive result. Allergy tests aren’t perfect, and have a fairly high rate of false positives. Humans who have grappled with food allergies and elimination diets might be able to predict the next step. To confirm that a household pet is actually allergic to humans, you would need what is kamagra jelly to isolate them from people and find demonstrable evidence that their conditions improve. Then, the pet would need to be brought back to an environment with humans to confirm it made their condition worse.

Given the difficulty of performing a test where what is kamagra jelly cats would be completely isolated from humans for a significant length of time, there haven’t been any conclusive studies that have proven a human-induced allergy in a cat.Elia Tait Wojno, an immunologist at the University of Washington, says that allergy testing for dogs and other pets is quite rare, which is part of the reason why it's unclear if these animals can be allergic to humans. Generally speaking, even when a dog is demonstrating clear signs of atopic dermatitis or skin allergies, veterinarians will often prescribe them allergy management medication rather than running a full allergy test to determine the root cause. So, it becomes difficult to understand, on a population level, how many dogs have allergies and what they are actually allergic to. That said, although the existence of human allergies in cats and dogs is up for debate, what is kamagra jelly there is evidence to suggest that household pets can be allergic to one another. Although it’s not common, there have been cases where cats, who are more prone to develop allergic asthma symptoms, have shown allergies to dogs.Tait Wojno says that, like human allergies in pets, it’s an area where scientists have relatively little understanding.

She hopes further research will reveal more what is kamagra jelly about how allergies manifest in household animals. €œI think that's an area of ongoing research that will be important as we learn how to treat these allergies better,” Tait Wojno says.Every year, around 3.2 million cats are placed in U.S. Animal shelters, according to the American Society for the Prevention of Cruelty to Animals. There are many reasons what is kamagra jelly why these pets are given up, but one of the most common is allergies. Cats are one of the most common allergy triggers in the world, with at least 10 percent of Americans exhibiting some symptoms.

These symptoms can be mild, but they can also cause serious health complications, particularly among younger children who are at risk of developing asthma what is kamagra jelly through prolonged exposure. And while there are a variety of ways to treat allergies, most of them only address the symptoms rather than removing the underlying cause. The only way to do that, for now, is to remove the cat itself. “With any disease, you want to address the root cause, rather than just the symptoms, and that's all that is available today,” says Gary Jennings, a biochemist and the CEO of Swiss biotech company HypoPet what is kamagra jelly. €œIt's suboptimal.” Luckily for cat lovers, researchers and companies like HypoPet are working on alternative treatments to cat allergies –– ones that treat the cat instead of the human.

And although this research is still in its beginning phases, don’t be surprised if cat what is kamagra jelly allergies become a thing of the past sometime soon. Allergy treatment for CatsHypoPet, which spun off from research conducted at the University of Zurich in 2014, aims to prevent household cats from producing a key allergen called Fel d 1. It’s a protein produced in various cat glands and is found in their saliva and on their skin. Fel d 1 is the primary cause of allergic reactions to what is kamagra jelly cats among humans. HypoPet is working on an experimental treatment called Fel-CuMV (or HypoCat), which incorporates particles from the cucumber mosaic kamagra attached to a Fel d 1 protein.

The treatment what is kamagra jelly tricks the cat’s immune system into recognizing the protein as a foreign intruder. This induces the production of antibodies that neutralize the Fel d 1 proteins, essentially eliminating their presence in the cat’s body. Although HypoPet has been developing this treatment since 2014, in the past year they’ve made accelerated progress toward their treatment what is kamagra jelly. In July 2019, they published a paper in the Journal of Allergy and Clinical Immunology reporting the results of a number of studies they did on the treatment’s effects on 70 cats, showing that it successfully induced a sustained antibody response in the felines. They also noted that cat saliva samples contained lower concentrations of the allergenic protein, and that overall, the treatment didn’t seem to harm the animals.

In March of this year, what is kamagra jelly they published the results of a long-term clinical study on 10 cat owners with feline allergies. The cats were vaccinated, and over the course of two years, the symptoms of the human allergy sufferers were tracked. Cat owners showed a significant reduction in their allergy symptoms, and they could spend longer periods of time directly interacting with their cats before developing symptoms, according to the work published in the what is kamagra jelly journal kamagraes. Recently, HypoPet began working with a new business partner. Jennings declined to name names, but says they’re one of the top global animal health companies.

They hope to get the treatment on the market what is kamagra jelly in the next two to three years, Jennings adds. Jennings says the HypoCat treatment is a practical solution for cat owners with allergies because of how long the antibiotic reaction lasts. After the initial vaccination, cats will only have to be vaccinated roughly every six months to a what is kamagra jelly year to maintain the effects. This treatment is a stark contrast to decongestant sprays or daily allergy pills, which require consistent use to effectively prevent allergy symptoms. “We think it’s going to be cost-effective and convenient for the cat owner,” Jennings says.

€œAnd we know it’s safe and well tolerated for the cat.” CRISPR what is kamagra jelly CatAnother preventative method for cat allergies is to delete the gene that produces Fel d 1 proteins altogether, effectively making the cat completely hypoallergenic. This method is being tested by a Virginia-based company, Indoor Biotechnologies, which researches and develops tools to measure different types of indoor allergens. President and CEO Martin Chapman, a former professor of what is kamagra jelly microbiology at University of Virginia, says the company has been researching CRISPR gene-editing software in cats for the last two years. The project, known as CRISPR Cat, is being led by biologist Nicole Brackett. Brackett says her research started by sequencing Fel d 1 from 50 cat tissue samples, and finding DNA regions that were consistent among the cats and were suitable to test CRISPR editing on.

Brackett then tested the CRISPR technology on a feline kidney cell line, using 10 different synthetic RNA guides targeting the genes that produce Fel what is kamagra jelly d 1. The project ended with a 50 to 55 percent success rate in editing the genes out of the samples. Because the what is kamagra jelly team was only working with cells, no cats were harmed. “50 to 55 percent efficiency is great,” Brackett says. €œEspecially because the cell type that we were using was not a very easy cell type to work with, and the target is a bit difficult as well.

So that was a great sign.” Brackett says her team is currently working on acquiring and testing samples from different what is kamagra jelly types of cats, such as big cats or wild cats, to compare the genetic structures and Fel d 1 production of different feline species. Because there isn’t that much research on cat allergens, Brackett hopes the project can shed more light on how Fel d 1 is produced among all feline species, as well as house cats. Brackett says there is some what is kamagra jelly concern that CRISPR technology could cause negative effects in the cats. The genetic scissors they use called Cas9 is only intended to cut or modify a specific part of the DNA, but it’s possible that it could change another part of the genome and cause unanticipated mutations in the cat. Fortunately, Brackett says there are several newly developed tools that improve gene-editing accuracy, which has helped to minimize the risk CRISPR has on its subject.

Chapman says the CRISPR technology has a major advantage over other forms of what is kamagra jelly potential allergy treatments because it’s the only method that removes allergy risk permanently. Others only reduce allergen levels temporarily, whereas CRISPR editing allows for the complete elimination of Fel d 1 proteins from a house cat. Furthermore, Chapman says the team hopes that their CRISPR research can determine the function of the protein what is kamagra jelly in the cat, and why it is produced in the first place. “If that were the case, then one could look for other alternatives to control the allergen,” Chapman says. €œSo that, big picture, is what we’re looking at.”.

When President Trump was diagnosed with erectile dysfunction treatment, one of the cutting-edge experimental therapies he received was a mixture of kamagra wholesale monoclonal antibodies. But now a treatment may soon be available. So are other kamagra wholesale therapies necessary or valuable?.

And what exactly is a monoclonal antibody?. Over the past few months, the public has learned about many treatments being used to combat erectile dysfunction treatment kamagra wholesale. An antiviral like remdesivir inhibits the kamagra from replicating in human cells.

Convalescent plasma from the blood of donors who have recovered from erectile dysfunction treatment may contain antibodies that suppress the kamagra and inflammation. Steroids like dexamethasone may modify and reduce the kamagra wholesale dangerous inflammatory damage to the lungs, thereby slowing respiratory failure.The FDA issued emergency use authorization for Eli Lilly’s monoclonal antibody, called bamlanivimab, and Regeneron is waiting for FDA’s green light for its antibody treatment. Monoclonal antibodies are particularly promising in therapy because they can neutralize the erectile dysfunction kamagra, which causes erectile dysfunction treatment, and block its ability to infect a cell.

This might be a lifesaving intervention in people who are unable to mount a strong natural immune response to the kamagra – those over 65 or with existing conditions kamagra wholesale that make them more vulnerable.I’ve worked in public health and medical laboratories for decades, specializing in the study of kamagraes and other microbes. Even when a treatment for erectile dysfunction treatment becomes available, I see a role for monoclonal antibody therapy in getting the kamagra under control.Why Should We Care?. Until a large percentage of a population has immunity to an infectious disease – either through a treatment or the unchecked spread through a community – the world must rely on other weapons in our war against the erectile dysfunction treatment kamagra.Along with the previously mentioned therapies, monoclonal antibodies can offer us another tool to neutralize the kamagra once it causes an .These man-made antibodies offer the world the possibility of immunotherapy similar to the use of convalescent plasma but with a more targeted and accurate action.

While a treatment will ultimately help protect the public, vaccination kamagra wholesale will not be an instantaneous event, delivering treatment to 100% of the population. Nor do we know how effective it will be.The impact of a treatment also isn’t instantaneous. It takes several weeks to generate a powerful kamagra wholesale antibody response.

In the interim, monoclonal antibodies could help mop up kamagra that is multiplying in the body.Antibody 101An antibody is a Y-shaped protein naturally produced by our body’s immune system to target something that is foreign, or not part of you. These foreign bodies are called antigens and can be found on allergens, bacteria and kamagraes as well as other things like toxins or a transplanted organ.A monoclonal antibody treatment mimics the body’s natural immune response and targets foreign agents, like a kamagra, that infect or harm people. There are also monoclonal antibodies that pharmaceutical companies have designed that target cancer kamagra wholesale cells.

Monoclonal antibodies are one of most powerful types of medicine. In 2019 seven of the kamagra wholesale top 10 best-selling drugs were monoclonal antibodies.For President Trump, the experimental treatment made by the pharmaceutical company Regeneron included two antibodies.Typically the spike protein on the erectile dysfunction fits perfectly into the ACE2 receptor on human cells, a protein common in lung cells and other organs. When this connection happens, the kamagra is able to infect cells and multiply inside them.

But monoclonal antibodies can slow or halt the by attaching to the viral spike protein before it reaches the ACE2 receptor. If this happens, the kamagra becomes harmless because it can kamagra wholesale no longer enter our cells and reproduce.How Are Monoclonal Antibodies Created?. Monoclonal antibodies that neutralize the erectile dysfunction are complicated to manufacture and produce.

They must be made kamagra wholesale inside cells taken from a hamster’s ovary and grown in gigantic steel vats. The antibodies that these cells manufacture must then be extracted and purified. Unfortunately these monoclonal antibodies, which have been used for other illnesses for years, are often quite expensive.Regeneron’s two antibodies are targeted to the spike protein of erectile dysfunction – the protrusions on the surface of kamagra that give it a crown-like look and are critical for infecting human cells.One of Regeneron’s two antibodies is a replica, or clone, of an antibody harvested from a person who recovered from erectile dysfunction treatment.

The second antibody was identified in a mouse that was biologically engineered kamagra wholesale to have a human immune system. When this mouse was injected with the spike protein, its human immune system generated antibodies against it. One of the most effective mouse antibodies was then harvested and used to form part of this therapy.Eli Lilly’s monoclonal antibody therapy, bamlanivimab, was identified from a blood sample taken from one of the first U.S kamagra wholesale.

Patients who recovered from erectile dysfunction treatment.Both companies have in place large-scale manufacturing with robust, global supply chains in place to produce the monoclonal antibodies, with many global manufacturing sites to ramp up supply. Eli Lilly has received FDA approval, and Regeneron is still awaiting approval. Unfortunately, there will likely be a shortage of the antibodies in the early going of approvals.Monoclonal Antibodies Plus a treatmentMonoclonal antibodies will be able to complement treatments by offering rapid kamagra wholesale protection against .

When they are given to an individual, monoclonal antibodies provide instantaneous protection for weeks to months. treatments take longer to provide protection since they must challenge the immune kamagra wholesale system. But the advantage of a treatment is that they usually provide long-term protection.Regeneron’s and Eli Lilly’s products are both delivered by intravenous injection, after which the patient must be monitored by health care professionals.

Since they offer immediate protection, the implications to treat or provide protection to high-risk populations is immense.These medicines kamagra wholesale have the potential to treat infected patients or prevent of essential health care and public health professionals on the front line of this kamagra. Monoclonal antibodies could also be useful for older people, young children and immunocompromised people for whom treatments either don’t work or can be dangerous.Rodney E. Rohde is a professor clinical laboratory science at Texas State University.

This article appeared on The kamagra wholesale Conversation and is republished under a Creative Commons license. Read the original here.Face coverings and social distancing are necessary for keeping the novel erectile dysfunction at bay, but are kamagra-related precautions affecting our ability to ward off other ailments down the road?. Health experts may not be able to say for sure yet, but there are ways to balance the kamagra wholesale two interests.

Pro tip?. Get outside (preferably a good distance from people who don't live in your household) and take a deep breath. Your microbiome kamagra wholesale will thank you.

What is the Microbiome?. Our bodies play host to a wide array of microorganisms that make their home kamagra wholesale on our skin and inside our guts, airways and other organs. Their presence is so significant that the number of bacteria in our guts is actually greater than the number of human cells in the human body.

The organisms' collective DNA is known as the microbiome and scientists have studied its effect on everything from our social lives to our mental health.Put simply. The microbiome provides the kamagra wholesale immune system with information about potential intruders. It clues our body in on what is and isn't a threat and helps prepare our white blood cells for battle.

Some of the microbiome kamagra wholesale is built up shortly after birth. A trip down the birth canal followed by months of breastfeeding helps babies form their unique microbiome, but exposure to the natural environment in those first few years of life is crucial as well, experts say. €œAll of these organisms provide data for the immune system,” says Graham Rook, an immunologist and professor emeritus at University College London.

€œIt's like kamagra wholesale the brain. It has to have data. And just like the brain, it needs the data early in life.” If the body fails to get the right messages about its environment, it may go kamagra wholesale rogue and attack things it shouldn't, leading to conditions like allergies, asthma and autoimmune disorders.

Since the first few years of life are most crucial, Rook is especially concerned that if young children are not leaving their homes, they are not getting the exposure to microbes they need. €œThat is why confining an infant to a high-rise apartment during erectile dysfunction treatment lockdowns is likely to be detrimental,” says Rook. €œThe microbiome of a modern apartment is not a useful exposure.” The Daycare TestA recent study comparing different daycare settings in Finland demonstrated kamagra wholesale that simply enriching the outdoor play areas with elements of the natural environment had a positive effect on the microbiomes in children.

For four weeks in 2016, young children played on segments of forest floor and sod placed on top of the existing gravel. Instructors at the schools also kamagra wholesale engaged the children in activities such as planting gardens, resulting in average daily exposure of 90 minutes per day.The results indicated an increase in microbe biodiversity on the skin and in the guts of the children, and a corresponding bump in immune system function. The study offers hope that even children in urban environments can build their microbiomes with some exposure to the natural world.

Animals Can Help Bring Exposure, Too “The most evidence-based strategy for improving your microbiome from an immunity [and] asthma perspective is to get a cow,” says Rob Knight, a University of California, San Diego professor and co-founder of the American Gut Project. €œBut that isn’t especially practical if you live in an apartment in the city.”In studies completed by scientist Erika von Mutius, kamagra wholesale life on a farm and bacteria carried by cows, specifically, appeared to have the best benefit to humans, Knight says. Dogs and cats that spend time outdoors can also bring in some good microbes, experts say, which provides another reason to adopt a pet while sheltering in place.

Diet Also Plays a PartKnight says a diet promoting microbiome diversity would include a diverse range of plants kamagra wholesale and fermented foods, with limits on sugar and salt. Rook adds that although building a healthy microbiome can be most crucial in the early years, studies indicate that adults can be affected as well.“Sick adults have less diverse gut microbiomes,” Rook says, adding that a diverse diet and time in the natural environment are key to bolstering health. While it is true that humans pick up “data” from other humans and that is a missing piece of the equation now, Rook notes that he is far more concerned about young children who are not leaving their homes and getting exposure to microbes in their natural environments.

And if you're worried that a lack of colds this year might lead to an immune system unprepared kamagra wholesale for next year's kamagraes, experts say that's not exactly how it works. €œThere’s no evidence that exposure to pathogens per se is good,” Knight says. €œCurrent thinking is that exposure to a wide range of harmless organisms from other people and the environment is good.”So, while the long-term health effects of social distancing might not be fully understood yet, embracing a lifestyle that includes healthy kamagra wholesale food choices and time spent outdoors may be the best tools at our disposal right now.

Rook also suspects that mask-wearing doesn't inhibit the ability to absorb what is needed from the outside world. €œPlenty of small particles from the natural environment are wafting into the lungs,” he kamagra wholesale says.If you’re feeling anxious or depressed right now, you’re not alone. Daily pressures can trigger stress, and our reaction to those stressors can set off symptoms of anxiety or depression or both.In fact, 79 percent of adults say that the kamagra is adding stress to their lives, according to a recent survey by the American Psychological Association (APA).Normal anxiety is a warning system that alerts us to threats and helps us prepare for challenges.

Depression is a major mental illness that negatively changes how we feel, think and act — it’s not just feeling sad. The two share kamagra wholesale common symptoms. Both anxiety and depression hurt our ability to concentrate, trigger restlessness and fatigue, and disrupt sleep.

They share similar biological mechanisms in the brain, and both can be triggered by social stressors, says Vaile Wright, senior director for health care innovation for the APA.“It’s totally normal to feel abnormal kamagra wholesale right now,” says Wright. €œWe need to give ourselves some grace, and not judge ourselves for not doing as well as we hope.”When we can't get rid of our stressors, we can improve how we react to feeling anxious or overly worried. We just need to figure out which tools work best for us, and use them consistently.Mirror, MirrorFor starters, we can shore up our mental health by connecting to our emotions every day.

This self-check kamagra wholesale can include asking ourselves questions like, “How am I today?. € or “Was I triggered today in any way?. € Just the act of saying, “I feel anxious right now,” activates the parts of our brain that helps us organize and regulate our emotions, and also calms the emotional part of the brain, says Alejandra Gonzalez Rodriguez, a family and marriage therapist at the University of Wisconsin kamagra wholesale School of Medicine and Public Health in Madison.

Making this a daily habit is not easy, says Gonzalez Rodriguez, because we’ve lost our natural transitions. Getting up, traveling to work, taking the kids to school. She suggests starting new routines by adding in habits aimed kamagra wholesale to make us feel well, and sticking to them.“Every person has to develop their own sense of ownership over this,” Gonzalez Rodriguez says.We can make positive changes by prioritizing what Wright calls the “foundational four”.

Healthy food, exercise, adequate sleep and social connections (even if the latter looks different right now).If this advice sounds straight from a parenting handbook, Wright says adults are not that different from children. €œWhen children are kamagra wholesale hungry, they are not rational. When they are tired, they are not rational,” she says.

€œIt really is that basic.”Carrying around anxiety and depression can make the changes we need for good mental health seem overwhelming. Wright suggests sticking to a basic routine, like getting up kamagra wholesale and going to bed at the same time and keeping regular mealtimes. Having this foundation in place keeps our emotions balanced enough to find and add stress-reducing coping skills.

Toolbox for the SensesWright kamagra wholesale encourages people to create a toolbox of activities that engage your mind, body and senses, such as puzzles and games, walking or other exercises, taking a hot bath or lighting a scented candle. Assembling a collection of activities from each of these categories that you can rely on is important for your mental health, she says. The trick with exercise is to find something you will crave, because it takes more willpower to force yourself to do something you don’t like, says Charles Raison, a psychiatrist and researcher specializing in depression at the University of Wisconsin School of Medicine and Public Health.

€œIn the abstract, we all want to exercise, but we may not want kamagra wholesale to put on those running shoes and head outside,” he says. If you don’t feel motivated enough to move, heating your body in a hot bath for 30 minutes, about an hour or so before bedtime, doesn’t call for much discipline but will raise your mood, says Raison. Just keep the water hot, but not so hot you burn yourself.Improve kamagra wholesale sleep by making your bedroom as cool, dark and quiet as possible.

In the morning, expose yourself to light. Step outside for a few minutes — even cloudy days provide enough light to lift our mood. If you need more of a boost, kamagra wholesale talk to your doctor about using light therapy.

You can also try meditation or mindfulness exercises. These can kamagra wholesale help us banish destructive thoughts and help manage the stress that triggers anxiety and depression.kamagra SOSUnfortunately, not everything we try at home will help. We may not always recognize when our own anxiety or depression reaches the breaking point, because the progression can be so slow.Be on the lookout for early signs of too much stress, such as irritability in ways not normal for you, like snapping at your family.

Notice if you go several weeks without getting much sleep, or have started drinking to cope.If stress starts to interfere with your life in a big way — you can’t work, you’re skipping classes, you’re not taking care of yourself or your family, and especially if you’re starting to feel life is not worth living or you’re having thoughts of hurting yourself — get help right away, says Raison.You can call your doctor or insurance company for a referral. You can also find therapists through an online locator, such as the one at kamagra wholesale Psychology Today. If none of those work, try asking friends and family if they have seen anyone or have recommendations, says Wright.

You can get immediate help through the National Suicide Prevention Lifeline at 1-800-273-8255.Finally, remember that we all need to kamagra wholesale cut ourselves some slack, says Wright.“People can expect to have good days and bad days, and that is OK. The trick is, once you’ve had ice cream for lunch, and you’ve just doomscrolled all day, just remember, the next day is a new day,” says Wright.Chances are, you know at least one person with a cat or dog allergy. Roughly 10–20 percent of people worldwide exhibit some form kamagra wholesale of allergic symptoms to these common household pets.

Given how common allergies to other species are, you may wonder. Can the opposite be true?. Could a cat kamagra wholesale or dog have an allergic reaction to their owner, or to humans in general?.

Maybe, says Douglas Deboer, a dermatologist at the School of Veterinary Medicine at the University of Wisconsin-Madison. There has been some research and experiments that suggest the possibility that pets kamagra wholesale can be allergic to humans, but nothing conclusive. If there are cats or dogs with these allergies, they are extremely rare.“Anything’s possible,” Deboer says.

€œBut it seems clear that it is not very common, if it exists at all.”Deboer, whose research focuses on skin diseases and allergic reactions in household animals, says reactions to dogs or cats typically occur when someone is allergic to the animal’s dander, flakes of dead skin cells shed from the body. So, in kamagra wholesale the event that pets can have allergic reactions to human beings, those reactions would stem from exposure to human dander. Deboer says there have been allergy tests done on household pets, but most of these test results are negative.

A very kamagra wholesale small amount of tests, roughly less than 2 percent, show a reaction to human dander.However, Deboer says that’s far from a conclusive result. Allergy tests aren’t perfect, and have a fairly high rate of false positives. Humans who have grappled with food allergies and elimination diets might be able to predict the next step.

To confirm that a household pet is kamagra wholesale actually allergic to humans, you would need to isolate them from people and find demonstrable evidence that their conditions improve. Then, the pet would need to be brought back to an environment with humans to confirm it made their condition worse. Given the difficulty of performing a test where cats would be completely isolated from humans for a significant length of time, there haven’t been any conclusive studies that have proven a human-induced allergy in a cat.Elia Tait Wojno, an immunologist at the University of Washington, says that allergy testing for dogs and other pets is quite rare, which is part of the reason why it's unclear kamagra wholesale if these animals can be allergic to humans.

Generally speaking, even when a dog is demonstrating clear signs of atopic dermatitis or skin allergies, veterinarians will often prescribe them allergy management medication rather than running a full allergy test to determine the root cause. So, it becomes difficult to understand, on a population level, how many dogs have allergies and what they are actually allergic to. That said, although kamagra wholesale the existence of human allergies in cats and dogs is up for debate, there is evidence to suggest that household pets can be allergic to one another.

Although it’s not common, there have been cases where cats, who are more prone to develop allergic asthma symptoms, have shown allergies to dogs.Tait Wojno says that, like human allergies in pets, it’s an area where scientists have relatively little understanding. She hopes further research will reveal more about how allergies manifest kamagra wholesale in household animals. €œI think that's an area of ongoing research that will be important as we learn how to treat these allergies better,” Tait Wojno says.Every year, around 3.2 million cats are placed in U.S.

Animal shelters, according to the American Society for the Prevention of Cruelty to Animals. There are many reasons why these pets are given up, but kamagra wholesale one of the most common is allergies. Cats are one of the most common allergy triggers in the world, with at least 10 percent of Americans exhibiting some symptoms.

These symptoms can be mild, but they can also cause serious health complications, particularly among younger children who are at kamagra wholesale risk of developing asthma through prolonged exposure. And while there are a variety of ways to treat allergies, most of them only address the symptoms rather than removing the underlying cause. The only way to do that, for now, is to remove the cat itself.

“With any disease, you want to address the root cause, rather than just the symptoms, and that's all that is available today,” says Gary Jennings, a biochemist and the CEO kamagra wholesale of Swiss biotech company HypoPet. €œIt's suboptimal.” Luckily for cat lovers, researchers and companies like HypoPet are working on alternative treatments to cat allergies –– ones that treat the cat instead of the human. And although kamagra wholesale this research is still in its beginning phases, don’t be surprised if cat allergies become a thing of the past sometime soon.

Allergy treatment for CatsHypoPet, which spun off from research conducted at the University of Zurich in 2014, aims to prevent household cats from producing a key allergen called Fel d 1. It’s a protein produced in various cat glands and is found in their saliva and on their skin. Fel d 1 is the primary kamagra wholesale cause of allergic reactions to cats among humans.

HypoPet is working on an experimental treatment called Fel-CuMV (or HypoCat), which incorporates particles from the cucumber mosaic kamagra attached to a Fel d 1 protein. The treatment tricks the cat’s immune system kamagra wholesale into recognizing the protein as a foreign intruder. This induces the production of antibodies that neutralize the Fel d 1 proteins, essentially eliminating their presence in the cat’s body.

Although HypoPet has been developing this treatment since 2014, in the past year they’ve made accelerated kamagra wholesale progress toward their treatment. In July 2019, they published a paper in the Journal of Allergy and Clinical Immunology reporting the results of a number of studies they did on the treatment’s effects on 70 cats, showing that it successfully induced a sustained antibody response in the felines. They also noted that cat saliva samples contained lower concentrations of the allergenic protein, and that overall, the treatment didn’t seem to harm the animals.

In March of this year, they published the results of a long-term clinical study on 10 cat owners with feline kamagra wholesale allergies. The cats were vaccinated, and over the course of two years, the symptoms of the human allergy sufferers were tracked. Cat owners showed a significant reduction in their allergy symptoms, and they could spend longer periods of time directly interacting with their cats before developing symptoms, according to the work kamagra wholesale published in the journal kamagraes.

Recently, HypoPet began working with a new business partner. Jennings declined to name names, but says they’re one of the top global animal health companies. They hope to get the treatment on the market in the next kamagra wholesale two to three years, Jennings adds.

Jennings says the HypoCat treatment is a practical solution for cat owners with allergies because of how long the antibiotic reaction lasts. After the kamagra wholesale initial vaccination, cats will only have to be vaccinated roughly every six months to a year to maintain the effects. This treatment is a stark contrast to decongestant sprays or daily allergy pills, which require consistent use to effectively prevent allergy symptoms.

“We think it’s going to be cost-effective and convenient for the cat owner,” Jennings says. €œAnd we know it’s safe and well tolerated for the cat.” CRISPR CatAnother preventative method for cat allergies is to delete the gene that kamagra wholesale produces Fel d 1 proteins altogether, effectively making the cat completely hypoallergenic. This method is being tested by a Virginia-based company, Indoor Biotechnologies, which researches and develops tools to measure different types of indoor allergens.

President and CEO Martin Chapman, a former professor of microbiology at University of Virginia, says the company has been researching CRISPR gene-editing software in cats for kamagra wholesale the last two years. The project, known as CRISPR Cat, is being led by biologist Nicole Brackett. Brackett says her research started by sequencing Fel d 1 from 50 cat tissue samples, and finding DNA regions that were consistent among the cats and were suitable to test CRISPR editing on.

Brackett then tested the CRISPR technology on a feline kamagra wholesale kidney cell line, using 10 different synthetic RNA guides targeting the genes that produce Fel d 1. The project ended with a 50 to 55 percent success rate in editing the genes out of the samples. Because the kamagra wholesale team was only working with cells, no cats were harmed.

“50 to 55 percent efficiency is great,” Brackett says. €œEspecially because the cell type that we were using was not a very easy cell type to work with, and the target is a bit difficult as well. So that was a great sign.” Brackett says her team is currently working on acquiring and testing samples from different types of cats, such as big cats or wild cats, to compare the genetic structures and Fel d 1 production of different feline kamagra wholesale species.

Because there isn’t that much research on cat allergens, Brackett hopes the project can shed more light on how Fel d 1 is produced among all feline species, as well as house cats. Brackett says there is some concern that CRISPR technology could cause negative effects kamagra wholesale in the cats. The genetic scissors they use called Cas9 is only intended to cut or modify a specific part of the DNA, but it’s possible that it could change another part of the genome and cause unanticipated mutations in the cat.

Fortunately, Brackett says there are several newly developed tools that improve gene-editing accuracy, which has helped to minimize the risk CRISPR has on its subject. Chapman says the CRISPR technology has a major advantage over other forms of potential allergy treatments kamagra wholesale because it’s the only method that removes allergy risk permanently. Others only reduce allergen levels temporarily, whereas CRISPR editing allows for the complete elimination of Fel d 1 proteins from a house cat.

Furthermore, Chapman says the team hopes that their CRISPR research can determine kamagra wholesale the function of the protein in the cat, and why it is produced in the first place. “If that were the case, then one could look for other alternatives to control the allergen,” Chapman says. €œSo that, big picture, is what we’re looking at.”.