Depression Is Real – And It Hurts – Recovery Takes Time – Part VII

As I near the end of my ECT sessions, it is time for an update. As I said when I began this series on depression, PTSD, and all of my other assorted maladies, I am keeping it real and sharing my experience with all of you in hopes that my experience will help someone traverse the playing field that is mental health treatment in the United States – and trust me, it is treacherous field too!

ECTs are winding down for me. Tomorrow is number 10 of 12. I have not really noticed much of a difference since beginning. Several of the others that I have been going with have expressed that they are feeling less depressed than when they started. Unfortunately, I have not noticed improvement personally. All of my physicians have told me that they are not surprised by my lack of progress at this point as my depression has been resistant to all medications and therapies up to this point.

A bit about the ECTs that I have been undergoing. As I said earlier, I really have not noticed any changes in my mood or disposition. I am still quite depressed. The ECTs themselves are quite easy. Essentially, I do no eat or drink anything after midnight. I wake up. Shower and head to the main operating suite up on the fifth floor. I sprawl out across a gurney and await the sweet night night juice to be pushed into my picc line. Then off to sleep for a couple of hours. During my little nap a low current of electricity is put into my brain. This in theory resets the brain so that the depression is gone.

Electroconvulsive therapy (ECT) is a valuable therapeutic modality in psychiatric clinical practice.1)Development of various pharmacological agents with patient friendly profile restricted the use of ECT in current clinical practice. However, it is still commonly used in the management of depression, acute manic episode, catatonia, and treatment resistant schizophrenia.2) ECT has mood stabilizing property superior than pharmacotherapy in the management of depressive episode, manic episode as well as mixed episode in bipolar affective disorder.3) The therapeutic response achieved through administration of ECT is usually quicker than existing psychotropic medications. The initial use of seizure for a therapeutic purpose (management of psychiatric disorder) was based on an observation which was indicative of an important biological underpinning behind the therapeutic efficacy of ECT. In early part of last century, the glial cell density in the brain of patients suffering from schizophrenia was compared with those with epilepsy. The number of glial cells in the brain of patients with epilepsy was higher than those suffering from schizophrenia, indicating the role of seizure in maintaining the density of glial cells. This biological observation has given birth to the idea that induction of seizure may help in restoring the glial cell number causing improvement in the psychiatric illness.4) ECT was finally developed through series of experiments for seizure induction (initially by injecting epileptogenic chemicals, subsequently using electric stimuli for seizure induction) over past two centuries. Extensive web search in the Medline database using the keywords “Electroconvulsive therapy”, “ECT”, and “Neurobiology” was done. All relevant studies published till the end of July 2016 in English language were analyzed with focus on mechanism of action of ECT.

Seizures induced in human brain were demonstrated to be effective in treating psychiatric disorders as early as initial half of the last century. Yet, how this seizure activity in brain operates to ameliorate neuropsychiatric symptoms is still not completely understood. Since the very inception of electroconvulsive shock (ECS) use in clinical practice, various theories have been proposed to unravel this enigma. Growing knowledge base has helped in safer application of ECT with lesser adverse events, and a better understanding of the underlying mechanism might help in further improvisation of this therapy. Moreover, the importance of knowing the mechanism also lies in the fact that there have been voices raised time and again labeling ECT as inhumane treatment modality, questioning its mechanism of action. Studies have been performed on experimental animals, human subjects as well as cadaveric brain in attempts to elucidate the possible mechanisms.Go to:


Mechanism of Action of ECT

Numerous psychological, psychoanalytical and biological theories have been put forward as an endeavor to explain the therapeutic effect of ECT. Biological theories proposed, can broadly be classified into neurophysiological, neuro-biochemical, and neuroplasticity theories depending upon the effect of ECS on various aspects (functional, compositional and structural) of brain as well as underlying neuronal and glial tissues. This review aimed at understanding the developments in biological models explaining mechanisms of action of ECT.

Neurophysiological Hypotheses

The electrical impulse from ECT electrodes traverses through intermediary tissue to stimulate neurons in brain by altering their internal electrical milieu and concentration of ions.5) Group of depolarized neurons fire simultaneously to produce a convulsion, that has been suggested to exert a therapeutic effect in various neuropsychiatric disorders. The factors determining areas of brain that get activated, includes the particulars of seizure (induced), site of electrode placement as well as patient related variables.6,7)Generalized seizure encompasses critical brain structures such as cortex, sub-cortex, thalamus, basal ganglia and limbic system. However, certain brain areas are more strikingly involved than others.8)Notwithstanding these differences, Postictal Suppression Index (PSI) and Burst Suppression (BS) index have been identified as robust measures that can predict adequacy of seizures in ECT. Kranaster et al.9)had reported BS index as a marker comparable with PSI.9) After multiple sessions of ECT the BS index reduces, which reflects the anticonvulsant effect of ECT.9)

Changes in cerebral blood flow and regional metabolism

A variety of studies have shown ECT to alter the cerebral blood flow and glucose metabolism, using neuroimaging techniques such as positron emission tomography (PET), single photon emission computed tomography (SPECT) and functional magnetic resonance imaging (fMRI). Regional cerebral blood flow (rCBF) tends to increase immediately in the areas of brain with seizure activity and follows the seizure generalization pattern.6) In addition, the changes in rCBF vary depending on the type of seizure, with generalized seizures causing higher variations in rCBF than missed ones.6,8) There is a subsequent decline in rCBF shortly after ECT-induced seizures.10)

Alterations in global as well as rCBF have been demonstrated in mood disorders, psychosis as well as in population at higher risk of developing psychosis.11,12) Regarding absolute levels of blood flow research findings are inconsistent. This variability might be attributable to the differences in parameters been measured, patient characteristics, illness features, treatment received and the imaging modalities used.13)Mounting evidences in patients with depression (unipolar as well as bipolar depression) indicate significant hypometabolism in frontal gyrus.14,15) Furthermore, Hosokawa et al.14) showed difference in glucose metabolism pattern in patients with bipolar and unipolar depression in the form of hypometabolism in right anterior cingulate cortex (ACC) in the former, and the later exhibiting hypometabolism in right temporal gyrus, right insula, and left cingulate.

There is enormous literature, which supports the notion that ECT brings about changes in rCBF and regional metabolism. A post-ECT reduction in rCBF and glucose utilization in the cortex (particularly in dorsolateral and medial prefrontal cortex, superior frontal regions and temporal cortex) along with increase in flow across the amygdala, parahippocampal gyri, pons and other limbic/para-limbic structures has been reported in patients with depression.15,16) However, several studies report contradictory findings in this regards. Yatham et al.17) reported no significant change in blood flow. Conversely, increased rCBF had also been reported after an ECT course.18,19) Mervaala et al.18) using SPECT showed increased metabolism in right temporal and bilateral parietal cortices.

Most of the above evidences are suggestive of definite changes in rCBF following ECT in patients suffering from major psychiatric disorders. These amendments in rCBF have association with metabolism in different brain areas which are related to therapeutic outcome.

Changes in blood brain barrier

During the ictal phase of ECT induced seizure, there occurs an up-surge in blood pressure, consequently, there may occur break in the continuity of blood brain barrier (BBB) transiently.20) During this process, certain neuro-chemicals may get released from circulation to brain parenchyma which brings out specific changes (increased brain derived neurotrophic factor [BDNF] levels, angiogenesis, neurogenesis) in the microenvironment of the brain. The breach in BBB occurs only after repeated application of ECS. Accordingly, the alteration in BBB integrity may be unrelated to the brain changes following single session of electroconvulsive stimulus as evident from studies on experimental animals.20)

Electroencephalography changes

Electroencephalography (EEG) reflects the functional integrity of the cerebral cortex. EEG changes in specific brain areas during and after ECT may predict about clinical outcome as well as helps in understanding the underlying biological mechanisms of ECT. Studies correlating the therapeutic effect of ECT with EEG changes are limited. Slowing of waveform has been the commonest EEG finding, and might be associated with the clinical outcome. Some evidences suggest post-ECT delta activity in prefrontal cortex as a predictor of clinical response, irrespective of the mode of ECT.21,22) The onset of therapeutic response depends upon the rapidity as well as the extent of slowing of EEG waves.23) The ictal EEG changes on bilateral ECT (in comparison to unilateral ECT) is found to be more synchronous, symmetrical, uniform with high amplitude and have significant post-ictal suppression.24) Differences exist in EEG pattern among different subtypes of depression (unipolar depression, bipolar depression and psychotic depression). These differences in the EEG characteristics fade out with application of ECT.25) A recent study by Zhao et al.26) revealed decrease in alpha activity in the fronto-temporal cortex following a series of ECT. Increase in theta (4–7 Hz) activity was also reported in certain brain areas. McCormick et al.27) using low-resolution electromagnetic tomography analysis, showed sub-genual anterior cingulate cortex (SgACC) as the site of theta activity. Raised theta activity was shown to be associated with decline in psychotic symptoms in patients with psychotic depression. Additionally, the extent of decreased theta activity in the SgACC prior to treatment was positively associated with antipsychotic response of ECT.27)

Neurobiochemical Hypotheses

ECT modulates the process of neurotransmission and influences the expression as well as release of a great variety of neurochemicals in brain including transcription factors, neurotransmitters, neurotrophic factors, and hormones.28) It has an effect on transmission of almost all the major neurotransmitters in brain such as serotonin, dopamine, acetyl-choline, endogenous opioids, epinephrine and nor-epinephrine, etc.29,30)During chemical neurotransmission, it acts at multiple levels including the neurotransmitter synthesis, neurotransmitter release, binding of neurotransmitters to their receptors as well as their reuptake.30)

Genetic changes

Animal experiments have revealed altered expression of various target genes following acute as well as serial electroconvulsive stimulations. These genes might encode for various transcription factors, structural proteins as well as neuropeptides found in brain. For instance, Dyrvig et al.31) showed increased expression of genes c-FosEgr1Neuritin 1BDNFSnap29Synaptotagmin IIISynapsin IPsd95 and Npy in rodent brain post-ECS. Similarly Kaneko et al.32) demonstrated significantly increased expression of TCF7 (transcription factor 7) gene using microarray analysis of mRNA derived from peripheral blood in patients with catatonic schizophrenia following repeated ECT.

The epigenetic modifications brought about by ECT have also been suggested to account for the therapeutic effects of ECT.33) Electroconvulsive activity has been demonstrated to induce the gene Gadd45b (growth arrest and DNA-damage-inducible protein 45 beta) that has role in demethylation at the regulatory regions of genes for fibroblast growth factor 1 (FGF-1) and BDNF, factors involved in regulation of neurogenesis.34,35) Gadd45b mediates ECT-induced dendritic proliferation in nascent neurons of hippocampal dentate gyrus.35,36)

Electroconvulsive seizure improves neuronal connectivity at the hippocampus. Single electroconvulsive stimulus produces increased expression of specific proteins like—striatal enriched protein tyrosine phosphatase (STEP61), which dephosphorylates tyrosine from the N-methyl-D-aspartate (NMDA) receptor and extracellular signal regulated kinase 1/2 (ERK 1/2) resulting in internalization of the receptors.37) This physiological change has been observed in the hippocampus of rats.

Electroconvulsive seizures induce transcriptional regulation of various histone proteins, DNA modifying enzymes (DNA methyltransferase and DNA demethylase) and methyl-cytosine-phosphate-guanine-binding proteins within the hippocampus as seen in experimental animals (rats).38) ECT produces remodelling of the chromatins by various mechanisms. The therapeutic effects may be mediated through down-regulation of c-fos and up-regulation of BDNF.39) Another epigenetic mechanism explains the involvement of histone deacetylase enzyme that leads to post-transcriptional changes leading to down-regulation of NMDA receptor signaling pathways leading to effects of ECT.40)

However the evidences explaining possible role of ECT in modifying the epigenetic mechanisms to bring out the therapeutic effect is limited to experimental animals.

Neurotrophic factors

There is increasing evidence for role of neurotrophic factors in growth and development of brain structures as well as in pathophysiology and treatment of psychiatric disorders. ECT has been shown to change the levels of various biochemical mediators including these neurotrophic factors to effect neuroplastic changes in the brain. This trophic activity involves both neuroprotection as well as increased neuronal proliferation. Even single electroconvulsive stimulus produces proliferation of neurons at the dentate gyrus of hippocampus and newly formed neurons may survive for months.41,42) It has been hypothesized that ECS prevents cell death through activation of survival signal pathways, and inhibition of pro-apoptotic signaling. Animal studies have shown, repeated ECS to increase proliferative signals such as the Cdk2-pRB-E2F1 cell cycle pathway and ERK pathway in brain cortex.43,44) In addition, ECS decreases bcl-XS gene mediated neuronal apoptosis.45) Moreover, ECS produces down regulation of c-Myc, an intracellular protein involved in neuronal apoptosis. c-Myc, promotes apoptosis in response to various stimuli (in association of Bcl-2 group of proteins) and has a regulatory role on cellular proliferation and differentiation.44,46) In the frontal cortex of rat, Jeon et al.44) demonstrated ubiquitin-proteasomal degradation of c-Myc after repeated ECS. Bad, a pro-apoptotic factor responsible for apoptosis also got inactivated by ECS. This trophic effect of ECS blocking apoptosis may be responsible for the therapeutic effect.44)

Among neurotropic factors BDNF has been widely studied for its putative role in mediating the effects of ECT. BDNF is a nerve growth factor classified under neurotrophin class, mediates neuronal growth, proliferation, repair and survival.47,48) In rats, Nibuya et al.49) demonstrated ECS to enhance the expression of hippocampal BDNF mRNA. Further pre-clinical studies on rodents support the finding of ECS altering the levels of BDNF, proteins and the tyrosine kinase receptor B (TrkB) mRNA in different brain areas.50) Recent meta-analyses validate low serum BDNF (sBDNF) concentrations in depressed patients which get normalized by ECT and antidepressant treatment. A dose-response effect of ECS on BDNF has also been hypothesized.47,51,52) These studies however disproved consistent association between sBDNF concentrations and the symptom severity or clinical response in depression.47,51) In contrast several researches suggest post-ECT improvements in illness not to be associated with increase in sBDNF levels.53,54) Differential BDNF expression in different areas of brain is believed to be responsible for antidepressant action of electroconvulsive seizures.55) In rats, Taliaz et al.56) demonstrated the antidepressant-like effect of ECT. The effect was more dependent on ECT induced significant reduction of ventral tegmental area (VTA) BDNF expression rather than elevated hippocampal BDNF expression. Earlier researches also pointed to this contrasting BDNF action in the hippocampus and the VTA.56) It has also been hypothesized that BDNF expression differs according to duration post-ECT and further research to establish this correlation has been advised.57)

Studies also show post-ECS increased expression of vascular endothelial growth factor (VEGF), glial cell-line derived neurotrophic factor (GDNF) and basic FGF-2.5860) There is growing support regarding their involvement in causation of psychiatric illnesses.6164)

VEGF has a role in endothelial proliferation, angiogenesis, vaso-permeability, and has neurotrophic actions.60) In animal models there had been robust VEGF induction in hippocampus post ECS. VEGF was shown to be essential and sufficient to induce the proliferation of quiescent neural progenitor cell. Genetic variation of VEGF influences human hippocampal morphology suggest that effects of VEGF as reported in rodent models extend to humans.65) Similarly, it was reported to be significantly increased in depressed patients after ECT.66) It has also been hypothesized that VEGF may be involved in increasing antidepressant drug concentration in brain by down-regulating P-glycoprotein (a drug efflux transporter) at the brain-blood barrier.60)

GDNF is a neurotrophic agent from transforming growth factor β (TGF β) family of neurotrophins. It has a role in survival of dopaminergic neurons.67) Low serum GDNF has been reported in major depressive disorder (MDD) patients, levels of which improved following ECT. Zhang et al.68) reported significantly increased serum GDNF levels in MDD patients showing response to ECT. Accordingly, GDNF was hypothesized to have a role in mediating effects of ECT.

Studies have demonstrated down-regulation of expressions of FGF-2 transcripts in MDD, more so in untreated patients. Researchers also proposed FGF-2 to have an endogenous antidepressant and anxiolytic property and its increased expression to promote response to antidepressant therapies.69) Definite evidences for their role in mediating the effect of ECT are lacking, and it has been speculated that increase in the expression might just be an unrelated compensatory response.

Several other biochemical mediators have been proposed to play a role in ECT functioning. A recent study supports the possible involvement of tissue plasminogen activator (TPA) for the therapeutic effect of ECT.2) Electrical stimulation of brain enhances the expression of glutamate decarboxylase-65 isoform in the GABAergic neurons releasing TPA, which results in amplification of neurogenesis in limbic system, modulation of synaptic plasticity and neurotransmission.2)

ECT changes blood levels of various other molecules associated with mood disorders such as CD40L, interleukin (IL)-8, IL-13, EGF, insulin like growth factor (IGF)-1, pancreatic polypeptide, stem cell factor, sortilin-1 etc. The changes in blood levels were more prominent after acute ECT treatment. However, robust evidence regarding their role in mediating ECT action is lacking.57)

Immune system

Ongoing researches hinted towards a possible involvement of immune system in mediating the effects of ECT.29) A higher level of inflammatory mediators and activated immune cells in blood and cerebrospinal fluid (CSF) has been reported in patients with depression.70) Polymorphisms in genes related to immune system may predispose individuals to develop major depression. Inflammatory mediators implicated include C-reactive protein, IL-6, IL-1, and tumor necrosis factor α, etc. Similar pro-inflammatory states have been described in other psychiatric illnesses such as schizophrenia. Dysregulation of these immune mediators have been suggested to alter neurotransmitter synthesis and their blood levels through alterations in tryptophan-kynurenine pathway.71) Moreover, Guloksuz et al.72) have shown ECT to favour metabolites with neuro-protective properties. ECT temporarily increases expression of certain inflammatory cytokine genes. However, multiple sessions of ECT leads to a decline in the levels of inflammatory mediators.


Hypothalamic-pituitary-adrenal (HPA) axis

ECT has been hypothesized to enhance release of hormones from hypothalamus into CSF and blood through excitation of diencephalic structures.73) There is a transient and selective increase in secretion of adrenocorticotrophic hormone, cortisol and prolactin that returns to baseline in few hours following ECT. Evidences indicate disturbed levels of stress hormones in patients with mood disorder. In patients with depression, studies have consistently reported HPA axis hyper-function. This is evident in form of elevated cortisol levels and decreased cortisol suppression on dexamethasone suppression test. High cortisol levels have negative impact on neurogenesis, gliogenesis and are related to atrophy of structures such as hippocampus.74) The zone nearby node of Ranvier (i.e., paranode) in neurons has been suggested to be especially vulnerable to corticosteroids and stress related injury. It is considered as a crucial site of glial-neuronal interaction and dysfunctions there might result in neuropsychiatric manifestations.75) ECT has been shown to reduce the cortisol levels to normal among patients with MDD in due course. Whether these changes in levels of hormones have therapeutic implications or are manifestations of ECS related stress and to secondary other changes in brain is still unclear.73) It is also not known for sure that how changes in hormone levels affect amelioration of symptoms related to psychiatric illnesses. However, ECT has been demonstrated to reduce cortisol induced inhibition of neuroplasticity.76,77)

Mono-aminergic neurotransmitters

Disturbed monoaminergic neurotransmission has been proposed since long in depressed patients. Post mortem studies have demonstrated increased α2-adrenoceptor binding due to decreased release of noradrenaline in brain of suicide victims. Results from studies on rodents suggest that the therapeutic effect of ECS may be mediated through an increased release of noradrenaline indicated by a compensatory reduction in α2-adrenoceptor binding.78) The decreases in α2-adrenoceptor binding were more pronounced in areas of frontal cortex having robust connections with amygdala and hippocampus, the structures involved in processing of emotions and memory, respectively. In MDD patients dopamine transporter binding is reduced in the substantia nigra, striatum, thalamus, and anterior cingulate. ECT series has been shown to elevate levels of CSF homovanillic acid and 5-hydroxyindoleacetic acid, the metabolites of monoamine neurotransmitters.79) Transiently increased dopamine receptor binding has also been reported.80) Moreover, ECT has been proposed to modulate dopaminergic receptors and enhance dopamine neurotransmission in brain.


Serotonergic neurotransmitter system is well known to have implications in disorders of mood and psychosis. Various antidepressants targeting this system have been developed. Serotonin transporter (5-HTTLPR) and norepinephrine transporter (NET182C) polymorphisms have been suggested to be associated with ECT treatment response.81) However, studies conducted on rodents in past using radio-ligands or measuring serotonin (5-hydroxytryptamine; 5-HT) release have provided ambiguous results regarding effect of ECS on receptor sensitivity.82) Findings of human studies measuring post ECT blunting of cortisol response over 5-HT1A receptor agonist treatment were also contradicting. Researchers reported both increased response as well as no change in 5-HT1A receptor sensitivity. Antidepressant medications are associated with initial decline in 5-HT1A receptor down-regulation, before resetting of serotonergic system occurs in neurons. Likewise, a recent PET study on MDD patients showed a post ECT decrease in 5-HT1A receptor binding in various brain areas such as orbito-frontal cortex, ACC, hippocampus and amygdala.83) However, Saijo et al.82) using [carbonyl-11C]-WAY100635 a 5-HT1A antagonist with high affinity, reported unchanged 5-HT1A receptor binding in depressed patients receiving ECT. Moreover, a study using neuroendocrine challenge test in patients undergoing ECT, could not find association between illness improvement and serotonergic function.84) Similar to antidepressants, ECT also down-regulates 5-HT2 receptors globally, in the brain of patients with MDD.85) Reduction in 5-HT2 receptor density is suggested to have antidepressant action. Robust evidences for the direct involvement of serotonergic system in ECT are lacking at this point of time. Further research in this domain might throw light on implications of serotonergic system in ECT action.

Neuropeptide Y

Neuropeptide Y (NPY) has roles in emotional regulation, processing of memory, maintaining circadian rhythms, and regulation of appetite. Moreover, it also has anticonvulsant action and gets released in response to seizure stimulation. This effect is achieved through inhibitory effect of NPY on glutamatergic neurons. Diminished NPY levels have been reported in various psychiatric disorders such as depression with suicidality, bipolar disorder and schizophrenia.86) Repetitive spontaneous seizures have been shown to be associated with increased expression of NPY mRNA and peptide release throughout the mossy fiber pathway in cortex as well as hippocampus, not found otherwise.87) ECT has been shown to be associated with elevated NPY levels in CSF of patients with depression.79) Present evidences suggest that NPY may be involved with mechanism of action of ECT.


Glutamate is the most abundant excitatory neurotransmitter in human brain. Excessive release of glutamate is associated with overstimulation of extrasynaptic NMDA receptors leading to calcium influx inside neurons subsequently causing excitotoxic neuronal damage. The cystine glutamate antiporter located on astrocytes is involved in cystine uptake into cell in return for glutamate release. Cystine gets reduced to cysteine, a substrate for the synthesis of glutathione which has antioxidant properties. Extracellular glutamate excess competitively prevents cystine uptake inside cell, triggering oxidative stress related cellular death.88) Increased glutamate/GABA ratio was observed in prefrontal cortex and hippocampus in rodent model of depression (learned helplessness).89) Elevated glutamate levels in frontal cortex were also reported through post-mortem studies.90) Contrarily, other researchers have demonstrated reduced glutamate levels in dorso-lateral prefrontal cortex (DLPFC), amygdala, ventromedial prefrontal cortex (VMPFC) as well as in ACC in patients with depression.91,92) However, a recent study in depressed patients elucidated distinct glutamate levels in different areas of brain.93,94) Bernard et al.95)demonstrated significantly altered expression of glutamate receptor and transporter gene on post-mortem analysis of locus ceruleus in levels in MDD patients. In MDD patients, altered expression of glutamate receptors genes in hippocampus has also been reported.96) Furthermore, impaired AMPA receptor mediated glutamatergic neurotransmission has been shown in patients with schizophrenia.97) Thus, altered glutamatergic transmission has been implicated to have role in psychiatric disorders.

Dong et al.98) in experiment on rats showed ECT to lower down the levels of increased glutamate significantly in hippocampus of depressed animals. Moreover, stimulation threshold of NMDA receptors was reduced and the expression of NMDA receptor was up-regulated in the rat brain following ECT.98)Similarly, ECT has been reported to rectify glutamatergic alterations in specific areas of brain (i.e., DLPFC) in patients with depression.92,99) In addition, ECT increases glutamate levels in subgenual ACC and lowers the levels in left hippocampus in patients with depression. This glutamate normalizing action of ECT relates with improvement in disorders of mood.93)

Neuroplastic Changes

In psychiatric disorders alterations in volume of brain structures has been consistently reported. Studies have also demonstrated ECT to trigger changes in volume of whole brain as well as its components such as gray matter, white matter and other brain structures.100,101) These changes are more pronounced in areas with greater connection to prefrontal cortex and other limbic structures involved in regulation of mood.102104) ECT brings about neuroplastic changes at synapse (synaptogenesis), neurons (neurogenesis), dendrites (dendrogenesis), vasculature (angiogenesis), as well as glial cells and their processes (gliogenesis). Neuroplastic changes have been noticed as early as after a single electroconvulsive stimulus. In rodents, ECS enhances markers of glial activation within hours of its application.105) In experimental animals, repeated ECS instigates long lasting, mossy fiber sprouting in limbic structures of brain. This change was not associated with neuronal loss, ruling out it being just a compensatory activity.106) ECT in rodents (rats) may produce 30% increase in the population of endothelial cell by means of endothelial cell proliferation.107) The increase in angiogenesis may be related to the metabolic activity of specific brain regions.

A great deal of research has been performed pertaining to the neuroplastic effect of ECT in patients with MDD. Moreover, significant modulations in volume of brain substructures such as hippocampus, amygdala, anterior cingulate gyrus and medial and inferior temporal cortex have been reported with ECT.101,108110) However, the evidences regarding nature and extent of alterations as well as their correlation with response are contradicting.

In patients with MDD, MRI studies have reported increase in hippocampal volume (normalization) after a course of ECT.101,102) The ECT induced incremental changes in volume of hippocampus as well as amygdala can be observed within 72 hours of treatment initiation. Furthermore, smaller baseline hippocampus volume had been suggested to be associated with greater post ECT clinical response.103)However, several other studies do not support this finding.111,112) Abbott et al.102) showed ECT response and symptom improvement to be associated with increase in hippocampal functional connectivity (FC) rather than change in hippocampal volume. Additionally, FC changes were not found to correlate with hippocampal volume changes.

Several researches have also reported significant volume change in amygdala with ECT.103) Moreover, pretreatment volume as well as extent of enlargement had been suggested to relate with improvement of clinical symptoms of depression. Ota et al.101) reported change in right amygdala volume to relate with improvement of clinical symptoms of depression. Instead, Ten Doesschate et al.111) held left amygdala volume to have a greater predictive value. However, evidences regarding these associations are conflicting and require further exploration.

Neuroimaging studies have also revealed, ECT to modify the FC of brain areas. Mounting evidences suggest alterations in connectivity within functional networks as well as between distinct networks, among patients with depression. These networks are associated with top down regulation of attention and mood (fronto-parietal network), processing of emotion (the affective network and the ventral attention network) as well as internally or externally oriented attention (default mode [DM] network and dorsal attention network).113) In depression communication is impaired in both task-negative and task-positive networks. Studies have shown hyperconnectivity pattern in DM network in depression.113,114) Connolly et al.115)studied resting state FC of SgACC in patients with MDD and revealed increased FC of SgACC with amygdala as well as insula. Moreover, connectivity was decreased between the SgACC and left precuneus; thus, highlighting impairment in above mentioned networks.115) Reduction of FC within fronto-parietal network also occurs in patients with MDD.113) Likewise, altered FC in DM network, salience network (the affective network and the ventral attention network) and dorsal attention network has been demonstrated in patients with schizophrenia.116,117)

ECT normalizes resting state FC of brain networks.102,118) It has been shown to normalize decreased hippocampal connectivity in patients with MDD. Furthermore, the elevation of connectivity was reported to correlate with symptom improvement in depression.102) The decline in resting-state FC has been observed as early as after single ECT session.104) ECT was also shown to normalize (by increasing) network connectivity between posterior DM and dorso-medial prefrontal cortex (DMPFC) as well as between posterior DM and left DLPFC.119) Connectivity in parahippocampal gyri as well as VMPFC, the components of DM, subsides to normalize with ECT.120) The DM network have implications in depressive ruminations and impaired top-down regulation; thus, normalizing changes in FC may help in ameliorating symptoms of depression.119,121) Cano et al.104) reported decreased FC between intra-limbic structures (amygdala and SgACC) and increased FC between limbic–prefrontal networks (right amygdala and right DLPFC) after ECT. They suggested that FC changes occur initially in intra-limbic networks and subsequently extend to limbic-prefrontal networks. Changes in resting state FC in several brain structures (such as ACC, thalamus and hippocampus) are associated both with ECT application as well as clinical improvement.118) Accordingly, of the various FC changes that occur with ECT all might not be specific to a diagnosis or relate with clinical improvement.122)Go to:


Decades of research performed to elucidate the mechanism of ECT outlined a vast field of study that may involve numerous intricate biologic processes, including alterations in neuroplasticity, levels of various neurotrophic factors and neurotransmitters, FC, immune mechanisms, neuroendocrine function as well as epigenetic processes. Despite the evidences explaining neurobiological mechanisms of ECT, inconsistent research findings preclude from drawing firm inferences. This attributable to lacunae in present literature, such as lack of homogeneity in research methodology and study population, small to moderate sample size and lack of control group in numerous studies. Moreover, the cause-effect relationship between findings and therapeutic effects of ECT could not be established with absolute certainty and even it is also not very prudent to assume about a single mechanism that can explain the therapeutic effect of ECT.

The future researches focusing on neurobiologic mechanisms of ECT need to address following areas of concern; use of control groups, homogenous study methodology in a larger study population and to attend the grey areas where contrasting evidences exist.Go to:


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Loving Someone With Depression

If someone you love is dealing with depression you might feel helpless, confused, overwhelmed, hopeless, frustrated, or even angry. You simply might not know what to do.

We’ve rounded up tips on how to be there for your loved one from Health Stories Project community members who suffer from depression. Here’s what they had to say:

Listen. Offer an ear and your empathy without judgment or unrealistic advice.

“Depression feels like a hole. When you are in it you can’t see the other side. So, when a friend or family member insists that we focus on a brighter side that we can’t see, they aren’t being helpful. People tend to want to ‘fix’ problems, but support can be just listening without offering advice.” — Amanda

“Never say, ‘Oh things will get better.’ Simply let them know you are there for them; and you have to mean it.” — RLA

“Listen to them. Tell them you understand that they don’t feel like doing anything, let alone going and talking with strangers about it. Ask them what they need help with. Offer to take them for help and to see a therapist. Let them know all therapists are people, too. Some therapists even have been diagnosed with depression. I am a therapist and that’s how I know all about what depression is and what it feels like from the inside out. Let them know it’s good for them to find a therapist they like, so they feel comfortable talking with them.” — Juliet

Be understanding and supportive — not just emotionally, but practically too.

“People need understanding and support instead of judgment and criticism. Respect their needs and boundaries.” — Lorraine

“Support is vital; so is encouragement and medication reminders.” – Michele

“A small act of kindness, coupled with patience, can make my day.  Engaging in empathetic listening without trying to ‘fix us’ can make a world of difference.” — Bonnie

“Just be patient with them. If you text or call your loved one once a day it could make their day.  “ — Drake

“Be supportive. Offer to accompany them to daily appointments and errands (for a limited time). Be available to talk, accept what they tell you (it’s his/her mind) and make frequent phone calls to show support, even if they are brief. Encourage therapy!” — Lydia

“Support them and don’t lie to them. Don’t treat them as if they are crazy and stupid.” – Tina

“Be there for them — don’t let them be alone.” — Tracy

“Hug me, help me with things that need to be done, and text just to ask me how I am doing.” — Sandy

“Be supportive with love and compassion, and refrain from telling them what they need. Offer suggestions only.” — Lewellyn

Educate yourself about depression and other mental illnesses. The more you know, the more of an ally you can be.

“Educate, educate, educate!  Educate yourself and share with everyone you know. Advocate for people suffering from different types of mental illnesses all over the world. No two people will suffer the same way even with the same diagnosis(s). Again, educate, pray, and share, and you will be helping stop the stigma.” — Anita

“I am starting to become part of the neurodiversity movement.  People need to understand that what we have is just a disability that requires us to learn coping skills to manage it, just like anyone else. Loved ones need to educate themselves on the condition and how it affects people.” — Bonnie

“Learn, be patient and accepting, lose the criticism, don’t badger, and helpfully support healthy activity and self-care. Do it with your family member and work together towards both of your health goals. Don’t treat the other like they’re the one with the ‘problem.’ Don’t make the other feel like they are a burden.” — Philip

“Learn more about mental illness and be patient. I didn’t have much support because it wasn’t talked about and folks explained it as weakness and a failure. I know different now.” — Kathy

Find help for yourself too. Therapy and support groups offer a place to express your feelings and learn how to cope.

“I grew up with a schizophrenic mother. I was just told she was sick. It wasn’t until high school that I realized just how bad things were.  There really wasn’t anything I could do and it left me feeling really helpless. Just keep in mind that it is an illness.  It’s OK to talk to someone — you are not alone.” — Alisa

Always remember to see your loved one as more than their illness.

“Accept us for who we are and quit focusing on who you think we should be.” — Bonnie

“Treat them as a whole person, not just a label. Don’t use their diagnosis as an excuse, but it can help you understand and empathize with them. The weaknesses can be built into strengths; for example, once I learned I did not make eye contact, I could start practicing it.” — Chris

“Tell your loved one with this condition that you love them and can see them and you know they are not their symptoms; those symptoms are medically treatable so they can feel like themselves again.” — Juliet

5 Meaningful Ways You Can Increase Mental Health Awareness


Let’s face it. We still have a long way to go when it comes to raising mental health awareness.

Mental health is a topic that is very much “in” right now if you are a movie star or a professional athlete, but that doesn’t always trickle down to the rest of us.

For us plebeians, common suffers of mental illness are we, daily conversations about mental heath are a necessity.

For most humans, physical health comes up in conversation pretty much every single day, so why not mental health?

The answer is stigma–that amorphous, dark cloud that hangs ever so ominously over our heads.

But it doesn’t need to be this way.

Stigma goes away when we talk about it. Stigma doesn’t like the light of our words.

Stigma, when all is said and done, is a coward.

So let’s talk about mental health. Here are 5 creative ways to raise mental health awareness.

1. You go first.

This option is, arguably, the scariest.

But it’s the one I’ve found to be most rewarding. When I openly talk about my mental health, whether on Twitter, in the workplace, or at a public event, I give others the permission to do the same.

There is almost nothing as powerful as the simple act of going first.

When you go first, you model the behavior you expect to see from others. Also, you tether others in your web of safety; you demonstrate that you are opening up a judgment-free zone.

2. Speaking of Twitter, did you know that it’s a fantastic place to open up about your mental health?

Did you know there is an entire, welcoming community already tweeting about mental health on a daily basis?

There are people of varying ethnicity, of all gender and sexual orientations, of narrow and broad identities, all talking about mental health.

It really is a beautiful thing.

I’ve seen people hiding behind the safety of a false Twitter persona open up and share their true selves over time. I’ve read tweets from doctors and nurses, students and lawyers, battle-hardened advocates and mental health warriors new to the scene.

And the best part?

All of these individuals have unique stories. No two stories are exactly the same. Sure, you can identify trends and start to spot common symptoms and diagnoses, but each story is made up of its beautiful idiosyncrasies.

3. You build up your courage by starting small.

Start by talking with a trusted friend or family member. Choose your favorite one. Choose someone you know won’t discredit you–or choose a person who, if they accidentally dismiss what you say, you know, deep down, treats you with the best of intentions.

These people are out there.

When I was first becoming a mental health advocate, I started small. I found the National Alliance on Mental Illness (NAMI), and I signed up to take a class. It was a course designed to help me better understand how to support a family member living through a mental health crisis.

In the process, I found my tribe, a community of mental health advocates who freely shared their experiences, all with a general willingness to be positive and helpful.

Find those people first–because once you’ve found your people, you’ll have the winds of the community at your back. You’ll have forward momentum.

Then, when you’re ready to ride the winds to find a path of your own, you’ll know that you can always go back to your community to recharge.

4. Or don’t speak at all. Write something.

For some people, having conversations about anything–let alone mental health–is a daunting proposition. Whether you’re an introvert (I’m an ambivert, so a part-time introvert) or you have social anxiety, or you just like being a hermit-crab-variety recluse, speaking in public about mental health is not going to be a natural and enjoyable experience.

So write something down instead. Write it for yourself at first. Write it on a plain old piece of paper.

What matters is that you write it.

Because writing changes how your mind works.

When you write something, you clarify your thinking. You also free up mental space by getting the words out of your head and onto the page. Like anything else in life, the more you write, the easier it will get.

It used to take me hours to write a single blog post. Now I can typically crank one out in about 30 minutes. I’m not going to get into the science here, but your brain is made up of unfathomably amazing things called neurons, and as you perform the same tasks over and over, the neurons in your brain shoot electrical impulses to each other.

The old saying is: Neurons that fire together, wire together.

You can build this habit. You can write about mental health enough that it literally becomes part of who you are.

And it’s easier to talk about something when it becomes part of your identity.

5. When something is part of your identity, it is easier to talk about it.

Why do people love posting so much on social media platforms like Facebook and Instagram? No, it’s not because they are addicted by massive, super-evil corporations, although that could certainly be part of it.

It’s because we are humans–and humans love to express themselves. It’s part of who we are. We’re wired to communicate our thoughts, emotions, values, and customs to those who pass into our view.

We form our identities on the stuff of communication.

So when mental health becomes part of your identity, it becomes much easier to consider sharing your mental health story online.

But, it’s important to note that there is a risk to doing this. And it’s why most people stick to posting “safe” things on social media, things that are guaranteed to get lots of “likes,” “retweets,” “hearts,” or whatever other newfangled status symbol the social media gods dream up next.

The risk of posting about your mental health identity is that there, inevitably, will be people who don’t like that identity–people who want to bring you down.

But this is the risk you run, and in my estimation, it’s healthy risk.

Any rewarding pursuit involves its own risks.

I’ll leave you with an almost unbelievable story about a experience I had writing on Facebook about my newfound mental health identity.

Several years ago, I wrote a long Facebook post about some of my struggles with anxiety and depression. I had been volunteering as a mental health advocate for about a year. I had found my tribe. I had done the steps that served as a precursor for this moment.

So I posted something much longer–and much more vulnerable–than anything I usually saw on Facebook. I didn’t expect anything, I just wanted to share it and see what happened.

It felt good to get it all out. And then I waited.

Later that day, I saw I had a notification for a new Facebook message. It was from a friend who ran in the same social circles and was more an acquaintance than anything.

He told me that my story really meant a lot to him, and he asked me I would meet up with him to talk about mental health.

When we met up later that weekend, I could tell he was very nervous. He shifted his hands in his lap and stumbled over his first few words.

I immediately told him I would be happy to talk about anything he wanted to talk about, no judgment whatsoever.

What followed was a gushing of words. He told me about a history of panic attacks, information he hadn’t even shared with his best friend.

I felt very sad–sad because he never felt safe enough to share this, and sad that we live in a world that creates the dark cloud of stigma.

I validated absolutely everything he told me. I told him there was nothing to be ashamed of.

His entire body brightened almost instantly. The conversation soon shifted from his own story to an idea he had for a mental health nonprofit.

I told him it was a great idea–and that he should start it. A week later, he had.

Today, that nonprofit funds mental health treatment for youth in Montana, and I sit on the board.

And it didn’t take much. I don’t feel I did much of anything at all. But I consistently come back to this as one of the most life-affirming moments I’ve ever experienced. I have goosebumps as I write this.

I found my tribe. I discovered who I am. I went first, and I continue to go first.

So that others may go first as well. So that we all can raise mental health awareness.

Depression Is Real – And It Hurts – The Stigma Is Real Too! Part VI

According to The Merriam-Webster Dictionary, stigma is defined as:
a mark of shame or discredit. (“Stigma.” 2019. In Retrieved March 15, 2019 - As illogical as it may sound, some illnesses bear a stigma. In my experiences the stigma has been created due to lack of understanding of the disease or disease process. This is especially true when it comes to the stigma associated with mental illness in America.

I know a few readers are already rolling their eyes at this topic. To those readers I issue a challenge – finish reading this blog post. Yep, set your stereotypes aside and attempt to understand what the stigma is that so many with mental illnesses face every day of their lives. Try to understand why mental illness is still a closeted set of disorders. It, the stigma, really is a big deal.

One of the biggest stigmas associated with mental illness is blaming the individual with mental illness for their mental illness. Just like an individual who has a cold or the flu cannot be the cause of their own illness, a person suffering with mental illness cannot be the cause of their own illness. Saying things such as “get over it,” “deal with it,” and “you are just over reacting,” or “you’re not going through anything the rest of us are not going through” are not helpful to the individual with mental illness.

Other stigmatizing attitudes contain some core assumptions. Media analyses of film and print have identified three common misconceptions about people with mental illness: they are homicidal maniacs who should be feared; they are rebellious, free spirits; or they have childlike perceptions of the world that should be marveled.

Public stigma comprises reactions of the general public towards a group based on stigma about that group. Although we are used to distinguishing between groups in society and to label these groups with different attributes, this is not a self-evident process. Most human differences are mainly ignored and socially irrelevant in Western societies of our time. For example, the color of one’s car or the size of one’s shoes do not matter for most people under most circumstances. However, other personal features like skin-color, sexual orientation or income are often relevant to one’s social appearance. There is obviously a social selection of which human qualities matter socially and which do not.

It is often taken for granted to distinguish between different groups in society and to label human differences accordingly. However, every demarcation of groups requires an oversimplification. Even with obvious attributes like skin-color, there is no clear demarcation line between, for example, ‘black’ and ‘white’. Even more so, there is no sharp line between mental health and mental illness.

That cultural attitudes to behavior and (mental) illness change substantially over time is another aspect of the social selection of human differences in creating groups. Whether patterns of behavior, thinking and feeling are being noticed at all and if so, whether they are described in moral, psychosocial or medical terms is influenced by societal discourse and usually varies over time. Attention deficit hyperactivity disorder is an example of a label that was unknown a few decades ago and is likely to change again.

It is further important to note that labeling often implies a separation of ‘us’ from ‘them’. This separation easily leads to the belief that ‘they’ are fundamentally different from ‘us’ and that ‘they’ even are the thing they are labelled. ‘They’ become fundamentally different from those who do not share a negative label, so that ‘they’ appear to be a completely different sort of people. Our use of language is revealing regarding the use of labels to distinguish ‘us’ from ‘them’. For example, it is common to call someone a ‘schizophrenic’ instead to call her or him a person with schizophrenia. For physical illness, things are often handled differently and people usually say, a person has cancer. The person afflicted with cancer remains one of ‘us’ and has an attribute, while the ‘schizophrenic’ becomes one of ‘them’ and is the label we affix to the person. In this way, language can be a powerful source and sign of stigmatization.

Given this background of distinguishing between groups, labeling and separating ‘us’ from ‘them’, social psychology has identified different cognitive, emotional and behavioral aspects of public stigma: stereotypes, prejudice, and discrimination (see Table 1). It is important for both theoretical research and practical initiatives to understand these components. Stereotypes are knowledge structures known to most members of a social group. Stereotypes are an efficient way to categorize information about different social groups because they contain collective opinions about groups of persons. They are efficient in the sense that they quickly generate impressions and expectations of persons who belong to a stereotyped group.

Table 1

Public StigmaSelf Stigma
Negative belief about a group: Negative belief about self such as:
Incompetence Incompetence
Character WeaknessCharacter Weakness
Agreement with belief ofAgreement with belief of
Negative emotionof negative emotional response
Anger Low self-efficacy
FearLow self-esteem
Behavior response to prejudice such as:
Avoidance of work and housing
Withholding help
Behavior response to prejudice
such as:
 Fails to pursue work and
housing opportunities
 Does not seek help from others

People do not necessarily agree with the stereotypes they are aware of. Many persons may, for example, be aware of stereotypes of different ethnic groups but do not think these stereotypes are valid. Prejudiced persons, on the other hand, endorse these negative stereotypes (“That’s right! All persons with mental illness are violent“) and have negative emotional reactions as a consequence (“They all scare me”). Prejudice leads to discrimination as a behavioral reaction. Prejudice that yields anger can lead to hostile behavior. In the case of mental illness, angry prejudice may lead to withholding help or replacing health care with the criminal justice system. Fear leads to avoidant behavior. For example, employers do not want persons with mental illness around them so they do not hire them. This association between perceived dangerousness of persons with mental illness, fear, and increased social distance has been validated for different countries, including Germany, Russia, and the United States.

Stereotypes and prejudice alone are not sufficient for stigma. In addition, social, economic and political power is necessary to stigmatize. For example, if individuals with mental illness form stereotypes and prejudices against staff in a mental health service, this staff is unlikely to become a stigmatized group because the persons with mental illness simply do not have the social power to put serious discriminatory consequences against the staff into practice.

In summary, public stigma consists of these three elements – stereotypes, prejudice and discrimination – in the context of power differences and leads to reactions of the general public towards the stigmatized group as a result of stigma.

Self-stigma refers to the reactions of individuals who belong to a stigmatized group and turn the stigmatizing attitudes against themselves. Like public stigma, self-stigma comprises of stereotyping, prejudice and discrimination (Table 1). First, persons who turn prejudice against themselves agree with the stereotype: “That’s right; I am weak and unable to care for myself!” Second, self-prejudice leads to negative emotional reactions, especially low self-esteem and self-efficacy. Also self-prejudice leads to behavior responses. Because of their self-prejudices, persons with mental illness may fail to pursue work or independent living opportunities. If they fail to reach this goal this is often not due to their mental illness itself but due to their self-discriminating behavior. How can self-stigma arise? Many persons with mental illness know the stereotypes about their group such as the belief that people with mental illness are incompetent. But, as in public stigma, knowledge alone does not necessarily lead to stigma, if persons are aware of the stereotypes but do not agree with them. Thus, fortunately for many persons with mental illness, awareness of stereotypes alone does not lead to self-stigma.

Now that we have identified exactly what stigma is, let’s shift gears to the impact of the stigma.

As far as mental illness is concerned, stigmas seem to be widely supported by the general public. This is true for the United States and for other Western nations including Norway, Greece, or Germany while levels of stigmatisation may differ between nations. Unfortunately, research suggests that public attitudes toward people with mental illness seem to have become more stigmatizing over the last decades: Survey research suggests that a representative 1996 population sample in the US was 2.5 times more likely to endorse dangerousness stigma than a comparable 1950 group, i.e. perceptions that mentally ill people are violent or frightening substantially increased ( Phelan, J.C., Link, B.G., Stueve, A., and Pescosolido, B.A. Public conceptions of mental illness in 1950 and 1996: What is mental illness and is it to be feared?. J. Health Soc. Behav. 2000; 41: 188–207) . A recent German study also found increasing stigmatizing attitudes towards people with schizophrenia ( Angermeyer, M.C. and Matschinger, H. Causal beliefs and attitudes to people with schizophrenia. Trend analysis based on data from two population surveys in Germany. Br. J. Psychiatry. 2005; 186: 331–334) . On the other hand, the use of outpatient psychotherapy in the US increased between 1987 to 1997, at least among people about 60 years old, among the unemployed and persons with mood disorders (Olfson, M., Marcus, S.C., Druss, B., and Pincus, H.A. National trends in the use of outpatient psychotherapy. Am. J. Psychiatry. 2002; 159: 1914–1920). It has been speculated that the increased use of psychotherapy in these groups may be due to decreased stigmatisation especially of mood disorders. However, the link between stigma and use of psychotherapy was not assessed in this study, psychotherapy was very broadly defined including treatments of only one or two sessions, and the overall use of psychotherapy did not change in this period. In addition, being in psychotherapy may not necessarily mean to consider oneself having a ‘mental illness’ or to be considered ‘mentally ill’ by one’s environment, so different stigmata may apply and change independently over time. Another sobering fact is that mental health professionals equally support stigmatizing views ( Gray, A.J. Stigma in psychiatry. J. R. Soc. Med. 2002; 95: 72–76; Lauber, C., Anthony, M., Ajdacic-Gross, V., and Rössler, W. What about psychiatrists’ attitude to mentally ill people?. Eur. Psychiatry. 2004; 19: 423–427; Page, S. Social responsiveness toward mental patients: The general public and others. Can. J. Psychiatry. 1980; 25: 242–246; Sartorius, N. Stigma: what can psychiatrists do about it?. Lancet. 1998; 352: 1058–1059).

Two deleterious consequences of stigma can only briefly be mentioned here. First, public stigma results in everyday-life discriminations encountered by persons with mental illness in interpersonal interactions as well as in stereotyping and negative images of mental illness in the media ( Wahl, O.F. Media madness: Public images of mental illness. Rutgers University Press, New Brunswick, NJ; 1995). Second, structural discrimination includes private and public institutions that intentionally or unintentionally restrict opportunities of persons with mental illness (Corrigan, P.W., Markowitz, F.E., and Watson, A.C. Structural levels of mental illness stigma and discrimination. Schizophr. Bull. 2004; 30: 481–491). Examples of structural discrimination are discriminatory legislation or allocation of comparatively fewer financial resources into the mental health system than into the somatic medical system (Corrigan, P.W. and Watson, A.C. Factors that explain how policy makers distribute resources to mental health services. Psychiatr. Serv. 2003; 54: 501–507;
Matschinger, H. and Angermeyer, M.C. The public’s preferences concerning the allocation of financial resources to health care: Results from a representative population survey in Germany. Eur. Psychiatry. 2004; 19: 478–482) . It is important to note that for example a person with schizophrenia may experience structural discrimination whether or not someone treats her or him in a discriminatory way because of some stereotype about schizophrenia ( Link, B.G. and Phelan, J.C. Conceptualizing stigma. Annu. Rev. Sociol. 2001; 27: 363–385) .

In this blog post, I want to focus on two other negative consequences of stigma that are both related to the way a person with mental illness reacts to the experience of being stigmatized in the society: Self-stigma/empowerment and fear of stigma as a reason to avoid treatment. I focus on these two aspects because both are highly relevant for clinicians working in the mental health field. By this I do not imply that stigma is only an individual problem. In contrast I believe stigma to be primarily a social problem that should be addressed by public approaches (Mills, C.W. The sociological imagination. Oxford University Press, Oxford; 1967). Still, until stigma has been reduced in society, all clinicians should be aware of the meaning and consequences of stigma for individuals with mental illness.

Research has shown that empowerment and self-stigma are opposite poles on a continuum ( Corrigan, P.W. Empowerment and serious mental illness: Treatment partnerships and community opportunities. Psychiatr. Q. 2002; 73: 217–228)_. At one end of the continuum are persons who are heavily influenced by the pessimistic expectations about mental illness, leading to their having low self-esteem. These are the self-stigmatized. On the other end are persons with psychiatric disability who, despite this disability, have positive self-esteem and are not significantly encumbered.

Many persons who are discriminated against and suffer from public stigma do not experience self-stigma while others do. Correspondingly, the evidence is equivocal on this point: Some studies suggest that people with mental illness, who are generally well aware of the prejudices against them, show diminished self-esteem ( Wright, E.R., Gronfein, W.P., and Owens, T.J. Deinstitutionalization, social rejection, and the self-esteem of former mental patients. J. Health Soc. Behav. 2000; 41: 68–90). On the other hand, other surveys did not find that awareness of common stereotypes leads to diminished self-esteem in persons with mental illness. Even more amazingly, some stigmatized minority groups show increased self-esteem, including persons of color ( Hoelter, J.W. Factorial invariance and self-esteem: Reassessing race and sex differences. Soc. Forces. 1983; 61: 834–846) and people with physical disabilities (Llewellyn, A. Self-esteem in children with physical disabilities. Dev. Med. Child Neurol. 2001; 43: 70–71). Being stigmatized may stimulate psychological reactance so that instead of applying the common prejudices to themselves persons oppose the negative evaluation which results in positive self-perceptions. This fact that some react with righteous anger to stigma, while others are indifferent to stigma and yet another group self-stigmatizes has been called the paradox of self-stigma and mental illness (Corrigan, P.W. and Watson, A.C. The paradox of self-stigma and mental illness.Clin. Psychol. Sci. Pract. 2002; 9: 35–53). Why do people react so differently to public stigma? Corrigan and colleagues developed a model of the personal response to mental illness stigma (Fig. 1).

Many persons who are discriminated against and suffer from public stigma do not experience self-stigma while others do. Correspondingly, the evidence is equivocal on this point: Some studies suggest that people with mental illness, who are generally well aware of the prejudices against them, show diminished self-esteem ( Wright, E.R., Gronfein, W.P., and Owens, T.J. Deinstitutionalization, social rejection, and the self-esteem of former mental patients. J. Health Soc. Behav. 2000; 41: 68–90). On the other hand, other surveys did not find that awareness of common stereotypes leads to diminished self-esteem in persons with mental illness. Even more amazingly, some stigmatized minority groups show increased self-esteem, including persons of color ( Hoelter, J.W. Factorial invariance and self-esteem: Reassessing race and sex differences. Soc. Forces. 1983; 61: 834–846) and people with physical disabilities (Llewellyn, A. Self-esteem in children with physical disabilities. Dev. Med. Child Neurol. 2001; 43: 70–71). Being stigmatized may stimulate psychological reactance so that instead of applying the common prejudices to themselves persons oppose the negative evaluation which results in positive self-perceptions. This fact that some react with righteous anger to stigma, while others are indifferent to stigma and yet another group self-stigmatizes has been called the paradox of self-stigma and mental illness (Corrigan, P.W. and Watson, A.C. The paradox of self-stigma and mental illness.Clin. Psychol. Sci. Pract. 2002; 9: 35–53). Why do people react so differently to public stigma? Corrigan and colleagues developed a model of the personal response to mental illness stigma (Fig. 1).

Figure 1

Persons with a stigmatizing condition like serious mental illness perceive and interpret their condition and the negative responses of others. The collective representations in the form of common stereotypes influence both the responses of others and the interpretation of the stigmatized. Persons with a stigmatizing condition who do not identify with the stigmatized group are likely to remain indifferent to stigma because they do not feel that prejudices and discrimination actually refer to them (Fig. 1). However, those who identify with the group of the mentally ill apply the stigma to themselves ( Jetten, J., Spears, R., and Manstead, A.S.R. Intergroup norms and intergroup discrimination: Distinctive self-categorizationand social identity effects. J. Pers. Soc. Psychol. 1996; 71: 1222–1233). Their reaction is moderated by perceived legitimacy. If they consider the stigmatizing attitudes to be legitimate, their self-esteem and self-efficacy are likely to be low ( Rüsch N, Lieb K, Bohus M, Corrigan PW. Personal response of women with mental illness to public stigma: self-stigma empowerment, and the role of perceived legitimacy. Psychiatr Serv (in press)); (Schmader, T., Major, B., Eccleston, C.P., and McCoy, S.K. Devaluing domains in response to threatening intergroup comparisons: Perceived legitimacy and the status value asymmetry. J. Pers. Soc. Psychol. 2001; 80: 782–796). If, on the other hand, they regard public stigma to be illegitimate and unfair, they will probably react with righteous anger.(Fig. 1). People who are righteously angry are often active in empowerment efforts, targeting the quality of services.

Related to empowerment and self-stigma is the issue of stigma and disclosure. To disclose one’s mental illness may have both significant benefits, e.g. possibly increased self-esteem and decreased distress of keeping one’s illness a secret, and costs, e.g. social disapproval. Whether or not individuals decide to disclose will depend on context and their sense of identity (Corrigan, P.W. and Matthews, A.K. Stigma and disclosure: Implications for coming out of the closet. J. Ment. Health. 2003; 12: 235–248). For instance, if a woman with mental illness does not consider her illness a relevant part of her identity, she will be unlikely to tell her relatives about her mental illness, especially if those have repeatedly made stigmatising remarks about mental illness. If, on the other hand, a man with mental illness who is active in self-help groups and regards his mental illness as an important part of his life has trustworthy colleagues that have not shown discriminating behavior against people with mental illness, he is more likely to disclose his mental illness at work.

While the model of self-stigma, originating in social psychological research on other stigmatized groups (e.g. people of color, people with physical diseases), is useful to understand the different ways people react to stigma, three aspects have to be included to take into account the special case of mental illness. First, self-stigma resulting in decreased self-esteem and self-efficacy must be distinguished from decreased self-esteem during depressive syndromes that are common not only in affective disorders. Second, reaction to stigmatizing conditions depends on the awareness of having a mental illness, which may be impaired during episodes of, for instance, a psychotic condition.( Rüsch, N. and Corrigan, P.W. Motivational interviewing to improve insight and treatment adherence in schizophrenia. Psychiatr. Rehabil. J. 2002; 26: 23–32). Third, the reaction to a stigmatizing environment is dependent on one’s perception of the subtle stigmatizing messages from other people. This social cognition may be impaired in serious mental illness such as schizophrenia. (P.W. Corrigan, D.L. Penn (Eds.) Social cognition and schizophrenia. American Psychological Association Press, Washington DC; 2001).

Most people who live with mental illness have, at some point, been blamed for their condition. They’ve been called names. Their symptoms have been referred to as “a phase” or something they can control “if they only tried.” They have been illegally discriminated against, with no justice. This is the unwieldy power that stigma holds.

Stigma causes people to feel ashamed for something that isout of their control. Worst of all, stigma prevents people from seeking the help they need. For a group of people who already carry such a heavy burden, stigma is an unacceptable addition to their pain. And while stigma has reduced in recent years, the pace of progress has not been quick enough.

All of us in the mental health community need to raise our voices against stigma. Every day, in every possible way, we need to stand up to stigma. If you’re not sure how, here are nine ways folks on my inpatient unit responded to the question: “How do you fight stigma?

Talk Openly About Mental Health

“I fight stigma by talking about what it is like to have bipolar disorder and PTSD on Facebook. Even if this helps just one person, it is worth it for me.” – Patient 1

Educate Yourself And Others

“I take every opportunity to educate people and share my personal story and struggles with mental illness. It doesn’t matter where I am, if I over-hear a conversation or a rude remark being made about mental illness, or anything regarding a similar subject, I always try to use that as a learning opportunity and gently intervene and kindly express how this makes me feel, and how we need to stop this because it only adds to the stigma.” – Patient 2

Be Conscious Of Language

“I fight stigma by reminding people that their language matters. It is so easy to refrain from using mental health conditions as adjectives and in my experience, most people are willing to replace their usage of it with something else if I explain why their language is problematic.” – Patient 3

Encourage Equality Between Physical And Mental Illness

“I find that when people understand the true facts of what a mental illness is, being a disease, they think twice about making comments. I also remind them that they wouldn’t make fun of someone with diabetes, heart disease or cancer.” – Patient 4

Show Compassion For Those With Mental Illness

“I offer free hugs to people living outdoors, and sit right there and talk with them about their lives. I do this in public, and model compassion for others. Since so many of our homeless population are also struggling with mental illness, the simple act of showing affection can make their day but also remind passersby of something so easily forgotten: the humanity of those who are suffering.” – Patient 5

Choose Empowerment Over Shame

“I fight stigma by choosing to live an empowered life. To me, that means owning my life and my story and refusing to allow others to dictate how I view myself or how I feel about myself.” – Patient 6

Be Honest About Treatment

“I fight stigma by saying that I see a therapist and a psychiatrist. Why can people say they have an appointment with their primary care doctor without fear of being judged, but this lack of fear does not apply when it comes to mental health professionals?” – Patient 7

Let The Media Know When They’re Being Stigmatizing

“If I watch a program on TV that has any negative comments, story lines or characters with a mental illness, I write to the broadcasting company and to the program itself. If Facebook has any stories where people make ignorant comments about mental health, then I write back and fill them in on my son’s journey with schizoaffective disorder.” – Patient 8

Don’t Harbor Self-Stigma

“I fight stigma by not having stigma for myself—not hiding from this world in shame, but being a productive member of society. I volunteer at church, have friends, and I’m a peer mentor and a mom. I take my treatment seriously. I’m purpose driven and want to show others they can live a meaningful life even while battling [mental illness].” – Patient 9

This is what our collective voice sounds like. It sounds like bravery, strength and persistence—the qualities we need to face mental illness and to fight stigma. No matter how you contribute to the mental health movement, you can make a difference simply by knowing that mental illness is not anyone’s fault, no matter what societal stigma says. You can make a difference by being and living #StigmaFree!

Depression Is Real – And It Hurts – Treatment Begins – Meds and ECTs – Part V

Over the past few weeks I’ve been sharing my experiences with mental illness and depression specifically. Today I will be talking about the treatment of my depression including electroconvulsive therapy (ECT) and medications. I am going to begin with the statement that some of the treatments I have agreed to try have been questioned by providers I consult for second and third opinions. Another thing that I am going to say is that the stigma attached to mental illness is unreal! More on that a bit later though. . .

When I began seeing my mental health provider at the University Hospital in 1987, I was uncertain what to expect. Although I had been seen briefly in the past by a psychiatrist, I was not medication compliant, I missed appointments more regularly than I attended them. I lied to my therapist and psychiatrist both so I would not end up in the hospital – which realistically looking back now, I needed to be!

One of the biggest mental health challenges in Iowa is that funding was gutted two years ago. This substantially reduced the number of providers at all levels as well as forced the closing of the state mental institutions. This budget cut dripped directly down to me. I placed my call to the University Adult Psychiatry Clinic to schedule my intake appointment on June 8, 2017; the appointment was scheduled for July 20, 2018 – over a year later. Anyone other than me see a problem with waiting over 365 days to see ANY doctor? Ughhhhhh!!!!!!!!!!!

Fast forward to the first appointment with Margaret. I entered the clinic alone because it was the one appointment I attend at the University alone. Following check-in and vitals, I met my new practitioner. I immediately felt at ease and trusted Margaret. I cannot explain it nor give any reason that I should have trusted her as a complete stranger, but that is my reality.

Margaret is a nurse practitioner with prescribing privileges. She is a kind spirit, so very kind. She allowed me to lead the conversation asking questions when she needed clarification or explanation. In the past therapists and psychiatrists had directed the conversations during our appointments. Margaret was a breath of fresh air. I asked her why she was a shrink. She s aid because she truly wanted to help people. I believed her then and I know she has helped me so much over the past 8 months too.

Meds are often the first line of treatment for mental health issues.

I was prescribed Adderal for the ADHD, Hydroxyzine for the anxiety, and Prazosin for the nightmares and PTSD symptoms, Duloxetine for depression, and Haloperidol to help with quieting the voices and noise in my head as well as assist with getting to sleep. From here I am going to fast forward to this inpatient stay.

Suffice it to say that the medications alone did not work. I became more depressed than I had ever been in my life. I attempted to take my own life because I was so depressed and hopeless. I begged for the physicians at Genesis and the University to both figure something out and fix me.

Those that follow this blog already know that I am writing this from the comfort of the University of Iowa Hospitals and Clinics. I was admitted via self-committal on March 1, 2019. I agreed to be admitted under the guise of getting my meds checked over more thoroughly and adjusted as needed.

The first few days were boring and I slept long and hard. The Tuesday after I was admitted the staff physician came with my resident physician and broached the subject of ECT treatments. Like many in the US, I thought that ECT (electro convulsive therapy) had been out lawed long long ago. Nope. I was wrong. They have, just like other areas of medicine, made great strides to make the ECT process pain free. The ECTs, I learned that fateful Tuesday afternoon, are conducted under general anesthesia. y’all KNOW how I love a good nap!

Needless to say, I agreed to undergo 8-12 ECT treatments at the University. So far the worst side effect that I have experienced is an upset stomach and a bit of a headache. Not bad at all.

Now I’m going to delve into what ECTs are and what they are not. ECTS are not electroshock therapy. LOL.

For some people with severe or hard-to-treat depression, electroconvulsive therapy (ECT) is the best treatment. This treatment, sometimes referred to as “electroshock therapy,” is often misunderstood and incorrectly portrayed by popular media as a harsh, cruel treatment. In reality, it is a painless medical procedure performed under general anesthesia that is considered one of the most effective treatments for severe depression. It can be lifesaving.

ECT works quickly, which is why it’s often the treatment of choice for people with highly severe, psychotic, or suicidal depression. For these people, waiting for antidepressants or therapy to work might be dangerous. However, the drawback is that the effects of ECT usually don’t last, and further treatments will likely be necessary.

No one is sure how ECT helps certain psychiatric disorders. It may promote changes in how brain cells communicate with each other at synapses and it may stimulate the development of new brain cells. ECT may flood the brain with neurotransmitters such as serotonin and dopamine, which are known to be involved in conditions like depression and schizophrenia.

What happens during an ECT procedure?

Before ECT, patients are asked not to eat or drink from midnight the night before treatment.     

During the procedure, the patient receives a short acting anesthetic agent which puts the patient to sleep for approximately 5-10 minutes. A muscle relaxant is also used during the procedure to stop the patient’s muscles from moving during the seizure. Cardiac monitoring pads are placed on the patient’s chest to check on the cardiac status during and after the procedure. Four electrodes are placed on specific areas of the patient’s head. Two electrodes of these electrodes are for monitoring the brain waves. The other two are for delivering a short, controlled set of electrical pulses for a few seconds. The electrical pulses must produce a generalized seizure to be effective. Because patients are under anesthesia and have taken muscle relaxants, they neither convulse nor feel the current.

Patients awaken about 5 to 10 minutes after the end of the treatment. Patients are then moved to the recovery room and remain there until their blood pressure, pulse and breathing return to their pre-treatment levels. Usually this takes about 20 to 25 minutes.

Patients who are given ECT on an outpatient basis must have someone drive them home after the procedure and stay with them until they go to sleep at night. People should not drive in the 24 hours following ECT.

How long is an ECT procedure?

A single ECT session usually lasts one hour. This includes the time the patient will be in the treatment room (approximately 15-20 minutes) and the time spent in the recovery room (approximately 20-30 minutes).

Typically, ECT (whether inpatient or outpatient) is given two to three times a week for a total of six to twelve sessions. Some patients may need more or fewer treatments.

These sessions improve depression in 70 to 90 percent of patients, a response rate much higher than that of antidepressant drugs.

Although ECT is effective, its benefits are short-lived. For this reason, patients take antidepressant medication after ECT or may continue receiving ECT periodically to prevent relapse.

What are the side-effects of ECT?

The immediate side effects of the procedure which may last for about an hour include:

  • Headaches
  • Nausea
  • Muscle aches and soreness
  • Disorientation and confusion

Patients may also develop memory problems. Memories formed closer to the time of ECT are at greater risk of being lost while those formed long before ECT are at less risk of being lost. The ability to form new memories is also impaired after a course of ECT treatments but this ability usually makes a full recovery in the weeks and months following the last treatment.

The most common side effect of ECT is short-term memory loss. However, some people report that they have long-term memory loss, as well. ECT also causes a brief rise in heart rate and blood pressureduring the procedure, so it may not be recommended in people with unstable heart problems. A physical examination and basic laboratory tests including an electrocardiogram (ECG) are necessary before starting ECT to assure that no medical problems are present that could interfere with the safe administration of ECT.

ECT can often work quickly, but 50% or more of the people who receive this treatment will relapse within several months if there is no subsequent treatment (for example, medicines) to prevent relapse. Your doctor will typically advise a medication regimen including antidepressants, or possibly additional periodic (“maintenance”) ECT sessions to help prevent relapse.

Tomorrow is my fourth ECT. So far so good! I will update again soon! ❤

Depression Is Real – And It Hurts Part IV — From Special K – Party Drug to Ketamine – Antidepressant

Back when I was a kid, rumor has it that I would drop $50-$100 for a couple of Special K doses to snort up my nose. Mind you, in my current state of mind, I lack the relevant information to either deny or admit such rumors. Suffice it to say that I have mutilated a few too many brain cells over the years coupled with my mental illnesses ya really do not want me telling ya about the 80’s! (LOL).

Seriously, one of the old school party drugs was Special K, we wanted to be in a dis-associative state of existence so that nothing was hurting our feelings or bruising our delicate and seemingly fragile egos. When looking for Special K one needed look no further than the dance floor so the story goes. Special K was a dance party drug because it made ya feel like ya were floating a bit – or so I have heard anyway.

Why party with Special K, you ask? Well a few of the effects of ketamine are:

  • At lower doses, ketamine produces a mild, trance-like or “floaty” feeling similar to nitrous oxide.
  • Higher doses produce hallucinogenic and dissociative effects, and may cause out-of-body experiences.
  • An out-of-body experience is often referred to as entering a “K-hole” and can be compared to a near death experience with sensations of rising above one’s body. Other users report being “teleported” to other locations. Many users find these experiences spiritually significant, while others find them frightening. (

After decades of kids ripping off their veterinarians to get the ketamine, the medical community began looking at ketamine for legitimate uses such as pain relief and the treatment of depression. Ketamine was originally created for use as an anesthetic, and is still used today for general anesthesia in infants, persons of poor health, and by veterinarians. Last week, the FDA approved a nasal spray made of esketamine the active component of ketamine the party drug. It seems quite logical to me too.

This is not snake oil. It’s not something that has to be stamped out. It’s something that has to be reined in.

Dr. Jeffrey Lieberman, Psychiatrist-In-Chief of Columbia University Medical Center

Although there have been dozens of antidepressants, they have come with barriers to effectiveness and a plethora of side effects that caused many to quickly become non-compliant. All of the previously available antidepressants are selective serotonin re-uptake inhibitors (SSRIs).
Selective serotonin reuptake inhibitors are a class of drugs that are typically used as antidepressants in the treatment of major depressive disorder and anxiety disorders. The exact mechanism of action of SSRIs is unknown. These drugs include: Paxil. Zoloft, Lexapro, and Prozac. Side effects of this class of meds include: insomnia, dry mouth, diarrhea, decreased libido, and erectile dysfunction.

Ketamine belongs to the same class of drugs as PCP, DXM, and nitrous oxide. This is commonly referred to as the class of drugs know as dissociative anesthetics. As an antidepressant, ketamine works in a very different manner than the SSRIs.

The experts aren’t quite sure how Ketamine works, but they do know it works differently than other commonly used antidepressants like Prozac, Zoloft, or Effexor. In general, Ketamine infused or inhaled activates certain neurotransmitter receptors and pathways which trigger rapid growth of new neurological connections. Some researchers believe that prolonged exposure to stress causes certain neurons to die off, resulting in depression, but Ketamine causes them to rapidly re-grow within hours, relieving the depressive symptoms.

There is speculation that depression results from the violation of the original blueprint of neurological brain connections due to mis-connections of certain critical synapses, and that Ketamine detaches the improper synapses allowing them to regrow and reattach according to the original non-depression blueprint. However, over many weeks or months the improper synapse connections gradually reform and so depression can reappear in some patients. This explains why these patients need to repeat Ketamine therapy every few weeks or months to restore the normal brain wiring and relieve recurrent depression.

Glutamate Pathway

There are other hints that Ketamine helps improve or inhibit several other mechanisms in the brain as well. Unlike other antidepressants, which work on serotonin or norepinephrine pathways, Ketamine works via the glutamate pathway. Glutamate is one of the most prominent neurotransmitters in the brain and regulates large regions of the nervous system. Overactivation of glutamate receptors may lead to long-term depression, and Ketamine works by blocking these glutamine receptors. Ketamine is also a powerful anti-inflammatory medication. Since depression has been linked to chronic inflammation, this may also be part of its antidepressant effect.

As you can see, this one-time party drug could be the miracle relief that so many sufferers of depression, such as my self who is currently hospitalized due to a bout of psychotic depression, have been praying for! For more information about this treatment, please contact your psychiatrist.

Ketamine gives hope to patients with severe depression.

To see Parts I to III of this series, please follow the links below:

Iowa Democratic Party Strives To Keep Up With Technology

Iowa, seems to be moving politics into the technology age… Finally! The Iowa Democratic Party has set forth a plan to allow registered Iowa voters who are Democrats of course to participate in the states first in the nation caucus via their computer.

A few of the nearly 20 Democratic Candidates for Presidenrt 2030

In the past, caucus participants gathered in local high school and junior high gymnasiums, libraries, diners, and even occasionally a bar or a persons dining room. Unlike a primary in which a person reports to a polling place and cast a single vote for his or her favorite candidate, caucus participants spend the cold in January or February evening and almost seemingly social event complete often times with coffee and cookies!

Andrew Yand Democratic Candidate for US President 2020

Once at the caucus these folks sit in groups and chat about their favorite candidate. Often times resulting in arguments I’m in support or against their favorite or least favorite candidate. Relatively early in the evening, the coccus chair person will call for an initial online account. This initial count is very public all of your friends family neighbors etc. can you see who you have aligned with as far as the Democratic presidential hopefuls. This alignment shows your support of your single favorite candidate. This initial alignment also demonstrates who is a little bit behind At the caucus location. Following the initial caucus account, group supporters I told him who is no longer viable as a group and they are forced to join forces with other account representatives within groups all groups reach the point of viability at the caucus location. Following the initial caucus account, groups of supporters I told him who is no longer viable as a group and they are forced to join forces with other camp representatives within groups all groups reach the point of viability. Often times the only three or four candidates are viable by the end of the caucus which may have begun with 10 to 20 candidates.

Typically the caucus takes an hour and a half to three hours to complete. The coxes take place across The entire state of Iowa in all 99 counties. At the end of the evening or whenever is the announced state wide after all of the caucus results are phoned into Des Moines.

Only because of the importance of relegated to the Iowa caucus, it is after all the first official vote in a presidential election anywhere in the country, Iowa remains an important political powerhouse state even though it has a relatively low population in comparison to other much much more populous states. You should be pointed out that the importance of Iowa generate millions of dollars in revenue in advertising office rentals lodging food etc. as each candidate comes through and hits many, if not all, of the 99 counties. Worth noting is the fact that the Iowa caucus across someplace between January 2 and February 14 every presidential cycle. The earliness of the Iowa caucus ensures the candidates must spend a great amount of time, energy, and money In the great state of Iowa. For this reason, many candidates such as Barack Obama who campaign in Iowa throughout 2007 in preparation for the Democratic primary and subsequent general election in which he was elected president.

The Iowa Democratic Party has submitted a proposal to the Democratic National Committee for review and approval. The proposal will allow caucus participants to attend from any internet connected device such as pc or smartphones. The online caucus will be open six night around the time of the in-person event is help.

It is unclear what safeguards have been put in place to ensure the fairness and the integrity of the Caucus. In my mind there are many many unanswered questions. What agency or agencies will be responsible for safeguarding the caucus? What penalties will be imposed for those who violate the rules? If United States of America could not keep a presidential election safe from the Russians in 2016, how are we going to keep a caucus save in 2020? Those are but a very very few of the questions that I have and I would like to have represented as for the Iowa Democratic Party address and a public forum at some point in the immediate future.

President Obama and JT Santana

As we prepare for the 2020 presidential election, which is sure to be a roller coaster ride as well as fast and furious, Iowa again is ready to welcome all Democratic and Republican contenders for the presidency of the United States of America.